Teodora Olariu

Anaesthetics and emergencies in intensive

care

Arad - 2016
Scientific referents:

Prof. Liana Moș, Ph, D

Prof. Alexandru Dumnici, Ph, D

Descrierea CIP a Bibliotecii Naţionale a României

OLARIU, TEODORA
Anestezie şi urgenţe în terapie intensivă / Teodora Olariu.
- Ed. a 2-a, rev.. - Arad : "Vasile Goldiş" University Press,
2016
Conţine bibliografie
ISBN 978-973-664-798-7

616-089.5(075)
616-083.98(075)

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Introduction

The emergency medicine, the intensive care and the anaesthetics are basic disciplines, very
complex, that must be known with no exception, by the whole medical personnel.
Summary notions of cardio-respiratory resuscitation must be well handled by every person of
the civil society, in order to give the first aid, until the arrival of a medico-sanitary cadre.
The manual addresses the medical students from the 6th year of studies and also the medical
assistants from the 3rd year, but is also useful for the resident doctors of specialty.
In the manual are presented summary notions of many medical disciplines, which are
necessary in emergency situations, crucial or at the limit in which the sick persons find
themselves, and also the nursing of the hospitalized ones.
The second edition of the course Anaesthetics and Emergencies in Intensive Care compiles in
a great part notions included in the first edition but which come to complete a series of new
data which are used in present by this specialty.
In the new edition there were introduced some criteria of diagnostic for the donor in cerebral
death, general notions about the enteral alimentation of the critical patient, guides and
protocols included in the obligatory therapy of the sick person of intensive care.
Also a completion of the usual anaesthetic substances was made. Although completions were
brought, the manual compiles only general notions about anaesthetics and intensive care, in
conclusion, those who follow it will complete their educational base, theoretical with the
practical one and with the specialty books of this domain. I consider that this manual offers a
minimal data base by which the student can become more sensitive and accumulate
information about this specialty, which in the future he may practice, offering a lot of
professional satisfactions.
The ATI specialty is a multi-disciplinary science, which compiles an extremely vast and
complex pathology.
For practicing it a lot of fundamental notions are necessary from anatomy, physiology,
physiopathology, pharmacology, and also from medical, surgical specialties, but also multiple
notions of mathematics, informatics, physics, chemistry, communication, environment etc.
Of course not all the necessary notions can be comprised in this manual, but most certainly
this is a complex guide of orientation in the domain, which associated and conjugated with a
practical activity of quality and on time becomes sufficiently useful.
The greater balance is given to the subjects of emergency intensive care, of hydro-electrolytic
and hematic rebalancing and of maintaining the vital functions of the patients and of applying
the first steps which are necessary in the major emergencies.
In this conception, we have the chapters of major interest: the cardio-respiratory-cerebral
resuscitation, the comas, the respiratory, cardiac and renal insufficiency, the shock, the
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rebalancing and maintenance of the vital functions, the intoxications, the blood transfusion,
the monitoring of the critical patient...
In this manual it was given a significant attention to the symptomatology and to the
emergency therapeutic steps, in order to establish a fast and exact diagnostic, favouring the
practice of the first emergency steps for saving the patient in the hospital but also at the
domicile.
The first part of the course compiles the basic notions of the anaesthetics and intensive care,
which will be completed with the practical activity from the surgery room, from the intensive
care unit and from the service of receiving emergency.
The conditions in which the medico-surgical emergencies appear are very different and are
produced by worsened pathologic states, traffic and work accidents, natural disasters,
aggressions, traumatisms, intoxications, sports accidents, etc.
In all these situations, the emergency steps must be known and applied rapidly in the first
minutes of the event.
The manual respects the analytical program established for the students of the years of study 6
and 3, from the Faculty of General Medicine, Pharmacy and Dentistry from the “Vasile
Goldiș” Western University of Arad, also compiling a few supplementary chapters
consequent to the students’ demand.
The edition of 2008 is completed with the last medical novelties included in the analytical
program and guides which are used obligatory in the new therapy of the critical sick person.
Being convinced by the usability of this manual and by the words of the great professor
Iacobovici who once said:
“Nobody in the world has a greater responsibility than the one called to dispose of the life of
his own kind”, we can figure out that any delay or acquaintance of the situation, is paid by
the patient with his/her “LIFE”, the greatest GIFT that he/she received at birth.

The pain

Short history of the pain

The pain appears once with the arrival of the living matter. It is present in the vivid, animal
and vegetal world, remaining only for the manifestation to be different.
The animals manifest their pain through crispation, their retreat their limbs, they give forth
sounds, and they become agitated, aggressive. In the vegetal reign, the Indian researcher
Ingedis Chandra Bose, was demonstrating that also plants feel pain. While experiencing pain,
the leafage of the plants twist, they lose color, they seize to bloom etc.
For the human, the pain, is a symptom of sickness, it is a “guardian” of the health. Nowadays
it is said, that the persons who do not know pain due to some severe deficiencies, have
insensitivity to sickness, or “pain asymbolia or dissociation”.
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From the Greeks we were transmitted the words: alglas, algena, algesis, which left in the
Indo-European language the root “alg” found in many words from our language: algie (pain),
nevralgie (pain irradiated on the trajectory of a nerve), hiperalgie (great pain), hipoalgezie
(low intensity pain), analgezie (absence of the pain), analgetic (medicament which suppresses
the pain), algocalmin (Romanian analgesic).
The word “pain” derives from a Latin word: “dolor” which in other neo-Latin languages has
become: douleur (in French), dolore (in Italian), dolor (in Spanish and Portuguese).
The human pain appeared in the atemporal ties of the gods who were complaining about pains
produced by infectious or toxic factors (Horus was bitten by a scorpion).
Then it appears the pain provoked by the natural aggressions, then by the disorders of the
normal mechanisms of the organism and then by the torture of the knife in the stages of
beginning of the surgery.
Each human has a certain sensitivity to pain, which is given by multiple factors which depend
of the race, family education, religious, of the personal positive painful experience (when the
pain was well treated or negative (pain which was not treated efficiently).
In order to know the pain better as a symptom we must make a detailed anamnesis:
- How did the pain appear: suddenly or slowly?
- When did it appear?
- The localization of the pain?
- Intensity of the pain?
- Under what form did it appear: prick, itching, twinge, dagger?
- Permanent or colic?
- Localized or with irradiations?
- Whether it stops to analgesics or not?
- The rhythmicity of the pain (periodicity)
- If the pain is accentuated to mobilization and it stops while resting?
- If the pain is accompanied by other symptoms?
- If it stops to antalgics?
The pain is induced by a lesion, corporal aggression or pathologic deficiencies, which appear
in the tissues or in organs. There are more definitions of the pain, starting with some simple
ones, for example:
Aristotle was calling the pain “an experience opposite to the pleasure”.
The pain is a guide of diagnostic for the doctors.
The pain is “friend and enemy” (T. OIariu). It is a friend because it announces a sickness,
being a symptom and an enemy because a pathologic element was produced.
The definition accepted by the IASP Committee (International Association for the Study of
Pain) of taxonomy in the year 1994, being also the most complex, is stated as it follows: “Pain
is a degradable sensorial and emotional experience given by a veritable or potential tissue
lesion, or, by a description with terms, which refers to such a lesion (Meskey)”.
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Pain classification:
It is various and classified depending on:
1. The place of the lesion
- somatic
- superficial
- profound
- visceral (internal organ)
- central (medullar or cerebral lesions)
- psychical (psychogenic cause)
- mixed (neoplasm)
2. the place of apparition of the pain
- primary pain (main)
- secondary pain (irradiate on the trajectory of a nerve)
- referred pain (visceral referred on the somatic area)
3. the way of triggering
- pathologic pain
- experimental pain
4. depending on the evolution
- acute pain
- chronic pain
The pain disappears, if the cause disappears and if it is correctly treated.
If the lesion produced more pregnant morpho-functional modifications the pain persists for a
long time.
There are a lot of situations in which the pain appears (Nordembas):
a) the pain provoked by external factors, which has the following particularities:
- it always affects the tegument
- the pain has a short duration
- the pain can be avoided
- the nervous trajectory is intact
b) the pain caused by internal lesions when:
- the pain doesn’t affect the tegument
- the pain has a longer duration and it doesn’t disappear until the disappearance
of the cause
- the pain cannot be localized exactly
- the nervous system is not affected
c) the pain associated with the lesions of the nervous system, which has the following
particularities:

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 - the tegument is affected
- the pain is difficult to be localized
- the pain is of long duration
- the pain cannot be avoided
- the pain affects the nervous system and, it can be generalized.
d) The atypical pain, associated with the factors of environment, social, psychological.
Taking into consideration the nociceptors (the pain receptors), mechanics, chemical, thermic,
polymodal, we can affirm that there is:
- Primary pain (sharp, of short duration, well localized)
- Secondary pain (deaf, diffuse, extended)
The acute pain is considered a symptom and it announces a disorder in physiologic, is an
alarm terminal which announces a sickness.
The chronic pain is a disorder of the normal mechanism of protection against the internal and
external aggressions, we can already call in disease and it is maintained between 1-6 months
or maybe even years.

The chronic pain is divided in:

- chronic benign pain
- chronic neoplastic pain
No matter how the chronic pain induces with time the limitation of the physical activities,
social and mental, the respective persons, having perturbations of family behaviour and also
professional, depression, anxiety, anger, sleep perturbation, irritability, inappetence,
disappearance of the sexual desire (7% of the population).
The visceral pain is perceived as a discomfort and pain. The stimuli which produce the
visceral pain are different. For example: the myocardium is sensitive and it aches in case of
ischemia, but not to the mechanic stimuli; the small intestine can be sectioned or burned,
without producing pain, but the distortion, the traction produces pain.
The visceral pain is more profound, it appears as a prick and it is associated with an
autonomous activity (transpirations, arterial hypotension, nausea, vomiting, bradycardia. The
central pain, results from the lesions or dysfunction of the central nervous system (CSN) and
it is difficult to be treated sometimes even impossible.
The acute pain, is the form of pain in which no matter the aggressive stimuli (internal,
external, physiologic, artificial) excite the nociceptors which transmit central, the signal of the
aggression through nervous inflexions of different frequencies. The high and strong
frequencies, produce a great aggression, starting the alarm system, releasing the inhibiting or
excreting mechanism of the pain. In the transmission of the pain, there are some chemical
mediators and pain transmitters, at peripheral level and at the place of the lesion, in a central
level, and the sensation of pain depends of its interaction.

7
There are pain receptors (nociceptors), some are excretory others are inhibitory. Some
receptors produce important modifications in the neuronal activity and others produce only
insignificant changes. This is why the liberation of the transmitters and the activation of the
excitation receptors, determine the neural activity the increase of the liberation of the
transmitters and/or increase of the excitability of the neurons.
The activation of the inhibiting receptors will decrease the neuronal activation, will reduce the
liberation of the transmitters and will make the neurons to become less excitable.
The neuronal transmitters activate the receptors and the synthetic drops of excitation or
inhibition can activate and minimalize the activation of the endogenous transmitters or they
can block their receptors.
In the pain transmission, the excitatory receptors are involved, being determined both in the
generation of the pain and in its transmission, and the analgesia can be produced by the
stimulation or activation of the inhibiting systems, or by the block of the excitatory systems.
The increase of the excitatory systems produces the intensification of the pain resulting
hyperalgesia, which can be produced also through the reduction of the inhibition.
From a physio-pathologic point of view, in a process of excess of stimulation, it is produced
an aggression over the neuron, through an overproduction of excitation amino acids out of
which the glutamate and aspartate, are the best known and produce cellular oedema with the
death of the neuron.
In the case of the pain, after surgical interventions, cellular lesions are produced, which
liberate allogeneic substances (prostaglandins, substance P, bradykinines, histamines),
producing nociceptive influxes, after their receptors, by the nociceptors which transmit the
information through the nervous fibers A, B and C, by the nervous systems. The influxes are
transmitted at medullar level (the anterior part and antero-lateral of the marrow), inducing
reflex segmental responses; then the impulses are transmitted towards the nervous supra-
spinal centers through fascicules spino-thalamic and spino-reticular, where they provoke a
segmental and cortical response.
In the chirurgical or traumatic act (through aggression), is produced a muscular hypotonia
striate, skeleton-like, muscular spasms which take to the increase of the consume of O2 and
production of lactic acid, the sympatric neurons are stimulated (which produce tachycardia,
increase of the volume of systolic ejection with increase of the mechanic work of the heart
and with the increase of the consume of O2 of the myocardia muscle, hypotonia of the
digestive and urinary ways) the metabolism increases and also the consume of O2.
Post-operatory pain and other forms of pain create a state of anxiety, of fear, unrest, hate and
other hard feelings towards the ones who are nursing them, tagging them as being insensitive
to their pain. The insomnia accentuates this state.
Like this it appears, on pain respiratory dysfunctions, cardio-vascular, gastro-intestinal,
endocrine, metabolic, muscular and urinary.
The reception of the painful information.
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The receptor (nociceptor) is a nervous cell specialized or an aneural structure which has the
role of transforming the physical energy, the chemical or the thermal one in a nervous
excitation. The energy of the stimulus, qualitative or quantitative, is transformed in
electrochemical energy, which is a form of propagating the information for the living systems.
The nociceptors - mechanic: respond to the mechanic tissue deformations and are represented
by fibers A delta
- polymodal: they respond to the multiple stimuli and are represented by fibers
A delta, or amyelinic fibers
In order to receive the painful information there are 2 phases:
1. the lesion – tissue phase:
- any mechanic energy, thermic, chemical, electrical, is transformed in
electrochemical energy.
- At the level of the lesion chemical mediators are set free: acetylcholine, histamine,
serotonin, angiotensin, potassium ions, P substance, bradykinin, activated plasma.

2. The phase of activation of the receptor:

These activated mediators depolarize the receptor (nociceptor), with the condition for the
stimulus to be sufficiently large.
The minimum value of the stimulus, which is capable to make the polarization, is called
LIMEN
In this way, the receptor makes the codification of the information, which is transmitted on
anatomic ways, to the formations of integration and analysis from the central nervous system
(CSN). The transmission of the painful stimulus to the CNS, is made on two ways algo
conducting, which are of two types:
- peripheral – extranevraxial and
- central - intranevraxial
Terms:
Nociceptor = sensitive receptor, preferential for the noxious stimulus or potentially noxious.
Noxious = stimulus which provokes central lesion
Painful limen = minimal intensity of a stimulus that a subject can perceive
Limen or tolerance to pain = maximum intensity of a painful stimulus, that a subject tolerates
Hyperpatia = exaggerate response to the noxious stimuli
Wind-up = central sensitivity (spinal)

The physiopathology of the pain

The nociceptor system
The nociceptor fibers are afferent primary sensitive fibers.
Instead of the term painful it is used the word NOCICEPTION, term which is used also for
experimental studies on animals, which cannot express their pain verbally.
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The nociceptor fibers are classified as it follows:
The myelinised fibers A-delta-respond to the noxious fibers of great intensity. They have the
speed of 20 m/sec for conducting the great stimulus.
Non-myelinised fibers C-nociceptor polymodal, which respond to stimuli with high limen.
Stimulus: mechanic, chemical, thermal. From here the name of polymodals.
Both the fibers A-delta and the C fibers branch peripheral in free terminations specialized.
The A-delta fibers lose their myelin theca before ending in the epidermis, and the fibers C end
in the dermis.
There are two classes of nociceptors:
- mechanoreceptors with high stimulation limen (group A-delta)
- mechanoreceptors A-delta, the C polymodal fibers
Through their stimulation it is produced an intense pain. The persistent pain is produced by
the C fibers C.
The pain – localized (prick) = fast or primary pain, is mediated by the fibers A-delta and it is
transmitted through the neo-spino-thalamic tract (little influenced by the opioids)
- diffuse (burn = slow pain, is mediated by the C fibers (is influenced more by the
opioids).
The noxious stimuli are:
 thermic
 mechanic
 chemical

The classification of the nociceptive fibers

The C nociceptors (poly-modal): are sensitive fibers, thin, non myelinised which form the
majority of the fibers of the sensitive nerves and respond to the 3 stimuli.
The nociceptive A-delta neurons: are myelinised thin fibers (A fibers)-mecano-thermic.
Fibers A-beta thick myelinised: are fibers with decreased activation limen, produced by the
tactile and pressure stimuli of the tissue.
The pain is started by the stimulation of the receptors with high activation limen
(nociceptors). These activate the cells from the dorsal corn of the marrow, which send
projections towards the thalamus, the reticulate formation and hypothalamus.
On the trajectory of these ways there are neurons which modulate the painful sensitivity. But
the marrow of the spine contains inhibiting neurons in the dorsal corn.

The skin nociceptors

The mecanoreceptors with high activation limen: are thin myelinised fibers A-delta with free
nervous terminations, which respond to strong mechanic stimuli, and after the sensibilisation
also to heat.

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The polymodal receptors: are non myelinised C fibers with free nervous terminations and they
respond to mechanic strong stimuli but also to chemical thermic stimuli.

The somatic nociceptors extra-cutaneous

 the muscles, tendons, fascia, are C fibers which respond to chemical stimuli, heat,
contraction, strong pressure, ischemia.
 articulations: the A-delta fibers from the ligaments, articular capsule: they respond
to bradikinin and prostaglandins,
 the dental pulp: respond to strong heat, pressure, cold
 cornea – A-delta fibers
The somatic nociceptors are in the teguments, the skeleton musculature. The superficial pain
well localized, delimited with sharp character.

The visceral nociceptors.

They are found in the internal organs (thorax, abdomen). The visceral pain is weakly localized
it has a defence character, traction, projected as a dermatome.
They produce pain: ischemia, mesenteric distension, inflammation, spasm, dilatation of the
cavity organs.
They don’t produce pain: clamping, burns, sectioning.
The intra thorax viscera, intra-abdominal and pelvic transmit the pain on sympathetic way
through sensitive fibers.
The inhibiting neurons – they are neurons which liberate the GABA and modulate the
segmental inhibitor mechanism.
Ways of transmitting the pain
The neo-spinothalamic tract – with fast conduction and it projects in the posterior cores from
the thalamus
Th paleo-spinothalamic tract – projects in the medial cores from the thalamus and conducts
the emotive sensation, unpleasant which accompanies the pain.
The spinoreticular way – it has a role in the reaction of awakening, and it participates to the
motivational affective reaction which accompanies the pain.
The spinomesencephalic way – transmits the non-discriminative information and it can
activate the descendant inhibiting way.
The descendent inhibiting system - comprises serotonin inhibiting fibers and adrenergic
descendent inhibiting fibers.

The pain is led through the A-delta and C fibers but these fibers have also a neuro-secretory
function: after activating neuropeptides are released, such as: A neurokinin, calcitonin gene-
related peptide, sP, intestinal vasoactive peptide. These things trigger a neurogenic

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inflammation, with vasodilatations and plasmatic extravasation, mast degranulation. The
nociceptive pain appears through direct irritation of the somatic-visceral nociceptors.
For providing analgesia it is practiced the blockade of the nociceptive ways at various levels
(spinal nerve, spinal marrow, thalamus). For the analgesia we use different types of local and
general anaesthetics.
Surgical trauma causes neurogenic inflammation which induces prolonged sensitization of the
nociceptive ways.
Primary hyperalgesia is produced indicating the local phenomenon (at the level of the lesion)
and secondary hyperalgesia which refers to the sensitive change that occurs in the healthy
perilesional tissue (hyperalgesia is the phenomenon of increased intensity of the pain to a
normal painful stimulus).

Pain measurement
The first researchers who have dealt with the pain measurement were von Fray, Hardy.
Pain is being considered a subjective and emotional experience, with or without lesions,
which emits stimuli, presenting differences in the objective quantification (the temporo-spatial
quality, the intensity).
More subjective methods are used (scale) and objectives.

Simple scales (for the acute pain)

1. The visual analogic scale: is represented by a certain dimension chosen previously (for
example 0-10), which is read from left to right. On this line the patient marks a sign which
represents the intensity of his pain measured in cm.
2. The numeric scale: a set of numbers is chosen, for example from 0 to 101, out of which the
patient choses a number which could represent the intensity of his pain.
3. The numeric scale with boxes/houses: some numbers are grouped in a box. The patient
underlines one of the boxes, corresponding to his pain.
4. The verbal descriptive scale: a number of adjectives are chosen which describe the
intensity of the pain (absent, light, medium, strong, very strong). The patient choses the
most suitable adjective for describing his pain.
Combined scales
1. The analog visual scale with 4 orientations is used by Aun and colab. For the population
with vertical writing, and also from right to the left.
2. The combined scale with numbers and adjectives, published by Borg 1982, uses numbers
from 1 to 10 and suitable adjectives “without pain” to “maximum pain”.
For the systems of behaviour evaluation there are many scales:
1. The simple behaviour scale: measures the intensity of the pain by 6 points of
appreciation:
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 - No pain
- Present pain which can be ignored
- Present pain which can’t be ignored, but which doesn’t affect the regular activity
- Present pain, can’t be ignored, affects the process of focus
- Present pain, can’t be ignored, which affects the general state and all the activities
with the exception of washing up and eating.
- Present pain, can’t be ignored, the patient can’t get used to it
2. The scale of social reintegration: tests the family conscience, the marriage, occupation,
economy, group relations, education, religion, health, etc., data which in the end give a
stress index.

The clinic image of the pain

In order to give an exact diagnostic for the pain symptoms we must keep in mind some
factors:
 Rhythm of expansion of the pain
 Localization
 Factors which start it
 Periodicity
 Projections of the pain which take to the interpretation of the pain through:
1. Excess of nociception – when the painful stimulus is intense and prolonged
(the acute pains) intact nervous system (inflammatory pain, post traumatism)
2. Excessive stimulation of the sympathetic nervous system (cutaneous disorders,
trophic = causalgia, algodystrophy), perspirations, etc.
3. Neuropathic (burns, torsion, painful cold sensation, spontaneous or provoked
electric discharge, tingles, itches, numbness, pricks)
4. Psychogenic – the emotional state is predominant
5. Mixed – possible association

The pain treatment

Before deciding the pain therapy it is necessary to make the global evaluation of the pain by
knowing:
 The aetiology and the pain mechanism through:
- the therapy of the aetiology on first plan
- the therapy of the pain symptom
 Auto-evaluation of the pain through the analysis of the pain intensity which is
made through the diagnosis of the:
-acute pain (the one-dimensional scale of the pain: visual analogical (VAS), simple
numeric (SNS) or simple verbal (SVS)

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 -chronic pain (the multidimensional scale, of behaviour, psychological aspect,
economic, social)
1. Non-opioid
a. Paracetamol – analgesic and antipyretic with great bioavailability, with peak of
efficiency between 30-90 minutes after the oral administration, has a risk of
hepatic cytolysis and intoxication for doses › 10g. Administration: 1g/intake,
maximum 4g/day
b. Anti-inflammatory non-steroidal
 Central and peripheral action, antalgic, antipyretic, anti-
inflammatory, anti-plachetar through the CoX inhibition
 Side effects: nephrotoxicity, gastritis, bleeding
 Aspirin – antalgic effect, anti-aggregate plachetar, anti-inflammatory
through the inhibition of the cyclooxygenase (COX), antipyretic. Oral
administration 1g/intake, maximum 3g/day
2. Central antalgics and light opioids
a. Codeine – light opioid, good efficiency, light respiratory depressor with side
effects, dyspeptic syndrome with nausea, vomiting, constipation, vertigo, light
somnolence
b. Tramadol (contramal, Zamudol) – is an agonist µ and inhibition of the
receptors of the nor-adrenaline and serotonin. It is administered orally and i.v.
Side effects: somnolence, dyspeptic syndrome with nausea and vomiting,
cephalagia, vertigo. It is not associated with IMAO. It is not administered in hepatic
or renal insufficiency.
c. Dextropropoxyphene – weak opioid derived of the methadone. Administered
only per bone.
Side effects = dyspeptic syndrome, cardio toxic, respiratory depressor.
Combinations: - 500mg paracetamol + 30 mg codeine
- 400mg paracetamol+30 mg dextropropoxyphene
- Paracetamol + tramadol
d. Nephropan (Acupan) – analgesic non-morphine. Administered per bone or i.v..
Side effects: dyspeptic syndrome, atropine reaction, sweat.
Contraindications: glaucoma, convulsive syndrome.
3. Strong opioids
- morphine in vials of 10, 20, 50, 100 mg
- morphine drinkable vial 10, 20 mg
- actiskenan gel 5, 10, 20, 30 mg
- sophidone (hydromorphon) gel 4, 16, 24 mg
- temgesic (buprenorphine) cp 0,2 mg
- durogesic (fentanyl) plaster 25, 50, 100 µg/h
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 Agonists of pure morphine type:
- Morphine: administered per bone, s.c., i.v., peridural, intrathecal, in the
discontinuous or continuous administration, analgesia programmed controlled by
the patient (PCA)
- Skenan and Moscontin – administered per bone 1-2 intakes/day
- Hydromorphon
- Fentanyl and the derivatives (Durogesic) transdermic plaster
Partial agonists:
- Buprenorphina (Tengesic). Administered orally.
Agonists-antagonists
- Nalbuphyn (Nubain) i.v. recommended in the postoperative analgesia for the children.
Side effects: respiratory depressor, sedation, dependence, renal insufficiency in high
doses, dyspeptic syndrome, constipation, urine retention.
The medication or the analgesic method depends on the doctor's instructions depending on the
intensity and location of pain, etiology, triggering mechanism, environment, race, religion,
cause analysis and of the failure, etc.
The analgesics can be administered also in combination with other drugs: sedatives,
antiemetics, muscle relaxants.
4. The co-analgesics
There is a very intense pain and also difficult to treat such as the neuropathic pain. Therefore
co-analgesics are used in the pain therapy in combination with the antalgics.
- The tricyclic anti-depressives with effect over the state of mind by inhibiting the
reception of the nor-adrenaline and serotonin (Laraxyl)
- The anti-epileptics – in neuropathic pains (Rivotril, Tegretol, Lyrica)
- Psychotropic-anxiolytics when the psychical component predominates
5. Other antalgic treatments – are used when there are rebel pains to the analgesics.
- Spino-thalamic cordotomy
- Thermo-coagulation of the sensitive fibers of the trigeminal nerve
- Posterior radiculotomy
- Thermotherapy
- Neurosurgical stimulation through medullar electrode posterior or profound
thalassemia
- Cryotherapy
- Thermotherapy
- Acupuncture
- Vibrotherapy
- Hypnoses
- Sophrology

15
The therapist doctor will choose the most appropriate technique that is necessary certainly
with the consent of the patient.
It consists in analgesic medication (major and minor analgesics) administered per bone, i.v.
and i.m., techniques of anaesthetics: general anaesthesia, contact anaesthesia, infiltrations,
nervous blocks and spinal anaesthesia, acupuncture, epidural catheter, laser analgesia,
hypnosis.
Any administration of analgesic produces unwanted side effects.
Currently the complete parameters of the pain are in study, a series of researches in
algotherapy in order to suppress the pain in all pathological conditions, by informational
means.

Chapter I – Anaesthesia

I.1. DEZIDERATES
The anaesthesia which has been a necessity in the human development comes from ancient
times as being a medical specialty that includes all the techniques used in soothing pain of any
kinds.
The anaesthesia is a medical specialty of interdisciplinary type that includes: the techniques
which assure the analgesia during surgeries and in various painful conditions, maintaining in
normal limits the vital functions during the surgery act, cardio respiratory resuscitation and
specific techniques of the inhaling treatment.

Short history
With the emergence of the living matter pain appeared which would be the expression of a
cellular suffering. The pain is present in the whole living plant and animal world, but its
manifestation is different.
The opium, belladonna, hashish and alcoholic beverages were the first substances used in
anaesthesia.
There are records about a “knife” torture in the early stages of surgery when all the
interventions were made on conscious patients.
From the Greeks the words “algos”, “Algena” and “algesis” were sent that left in the Indo-
European language the root “ALG” found in many medical words from our times, from which
we quote: algia (pain) neuralgia (pain irradiated on the path of a nerve), hyperalgesia (very

16
high pain) hypoalgesia (mild pain), analgesia (pain absence), analgesic (pain medication that
suppresses the pain), Algocalmin (Romanian analgesic).
In time, after using the magical methods, substances with analgesic effect were discovered for
pain suppression.
The anaesthesia appears since ancient times for suppressing pain.
In the year 350 BCE Hilaire said: "The soul must be passed to sleep with drugs which
overcome the pain."
The pain is “an unpleasant sensory and emotional experience, given by the tissue aggression
real or potential or a description of the terms that refer to such injuries” (IAPS - Seattle).
There is a series of elements that have an essential role in producing pain; the pain memory,
pain causative agents the potential producers, elements of personality and the mental side of
the individual.
The pain must be treated. Therefore, in time after using the magic methods there were
discovered that substances with analgesic effect, of pain suppression. The surgeon of the great
Napoleon Bonaparte performed amputations through cryotherapy, Hippocrates used of
belladonna and opium. In the year 1774-1776 Priestley discovers the oxygen and the azote
protoxide (irritant gas) the last one producing insensitivity to pain. Faraday in 1818 revealed
the inhibitory effects of ether. In 1842 Crawford performed anaesthesia with ether and in 1846
W.T.G. Morton makes the first public demonstration of an ether anaesthesia which he calls
“eterisation”. Joung Simpson performed in 1847 the chloroform anaesthesia. The general
anaesthesia is improved over the years by the introduction of the anaesthesia apparatus, by the
oro-tracheal intubation in 1901 made by Fritz Kuhn carried out by introducing the curare and
by all the methods to prevent operatory shock.
Along with the general anaesthesia is profiled also the local anaesthesia through the discovery
of the cocaine in 1855 by Goedecke and used as a local anesthetic by Koller in 1844. The
conduction anaesthesia starts in 1885 by performing the peridural by Corning and the
rachianaesthesia by Bier in 1898. The first general anaesthesia with ether was carried out in
our country in 1847 in Timisoara and the first general anaesthesia with oro-tracheal intubation
at Bucharest in 1951 by Prof. Univ. Dr. Litarczec George, the first professor of anaesthesia
from Romania.
The ATI specialty, in Romania was recognized in the year 1957 and enacted in 1972, and as
discipline of higher education, in the year 1992.
The anaesthesia is the method that removes the pain, provides relaxation of the patient by still
maintaining his vital functions in physiological conditions, allowing the surgeon to perform
safely long and laborious surgical interventions.

In the last years the equipment and drugs were codified and diversified, so that today we can
speak of advanced techniques of anaesthesia, with the monitoring of the vital physiological

17
parameters, in greater safety through computerization. In this way there were possible great
achievements of the modern medicine: laborious interventions and organs transplant.
The anesthetist specialist has the duty to prevent and relieve pain, to maintain the body
homeostasis in conditions of surgical aggression or of other causes, being an indispensable
member of a surgical team.

I.2. DEFINITION AND OBJECTIVES

Anaesthesia covers a range of pharmacological and technical means aimed to suppress pain,
fear and anxiety, providing shock protection, comfort the patient and the surgical team
Anaesthesia gives:
- Safety of the patient during the surgery
- Removes pain
- Supports the vital functions of the patient
- Ensures the patient’s safety by permanently monitoring the vital parameters
Anaesthesia has 2 branches:
The therapeutic anaesthesia has as an objective the treatment of the acute and chronic pain,
using different methods.
The surgical anaesthesia has as an objective the suppression of the pain which is consecutive
to the surgical intervention from all the surgical specialties.
In exercising this specialty, although it is a safe specialty, sometimes with great difficulties,
there are many risks, anaesthesia becoming a science.
The specialty unites many fields: anatomy, physiology, pharmacology and therapeutics,
biochemistry, medical physics, clinical neurology, traumatology, obstetrics, haematology,
toxicology and more.
The greatest responsibility in medicine nowadays belongs to the anaesthesia. Like this the
anaesthetist doctor takes a series of major responsibilities for the patient:
- Pre-anaesthetic examination and preparation of the patient for anaesthesia establishes the
most appropriate anaesthetic technique for the patient
- Monitors vital parameters and restores the homeostasis in the pre, intra and post-operative
period of the patients and of those critically ill or traumatized
- Establishes the diagnosis and the treatment of the painful syndromes
- Establishes the pre- and postoperative treatment
- Determines the clinical treatment and the cardio- respiratory-cerebral resuscitation
- Assesses the respiratory function and the application of the respiratory therapy
- Assesses and monitors heart functions

18
- Establishes, evaluates and supervises the performance of medical and paramedical staff in
anaesthesia and intensive care
- Establishes complex treatment schemes
- Cooperates with all the medical and surgical specialties
- gets involved in the administrative work of the section, hospital, medical school, outpatient
and emergency service
The labour activity of the anaesthetist doctor aims, for the sick persons since the first day of
life (neonatal) and the last day of life (elders).
The general anaesthesia affects three fundamental functions of the central nervous system:
- The function of de sleep-vigilance
- The function of de memory
- The affective function
To not be confused the general anaesthesia, narcosis and sleep.
The general anaesthesia means general insensitivity that does not involve sleep, and it may be
general vigil anaesthesia.
The narcosis is a reversible inhibition of the neuron.
For an anaesthesia to be complete, correct and effective, it must meet four goals:
Analgesia – soothing the pain through the absence of perceiving the memorizing process and
the pain diffusion is made with major analgesics.
Hypnosis, by administrating sedatives, psychological disconnection, the patient is protected
by not participating at the surgical acts and the stressing microclimate from the surgery room
and is made with hypnotic medication and sedatives.
The muscular relaxation, which assures the optimal conditions of execution of the surgical
intervention, through the relaxation of the musculature. It is made with the help of the curare.
The neuro-vegetative protection (homeostasis) or anti-shock by maintaining the vital
functions (respiration, circulation, excretion, metabolisms) in the limits of the homeostasis.
The circulation during the anaesthesia is maintained through crystalloid solutions and colloid
solutions, making a balance between the contribution and loss. It will be monitored
throughout the whole process of the anaesthesia TA, AV, PVC, EKG, PaO2, PaCO2,
temperature.
The respiration during the anaesthesia may be:
- spontaneous
- assisted (when the spontaneous breath is helped)
- controlled (manual and mechanic)
The rational and efficient use of the drug doses is linked to the particularities of each
individual subjected to anaesthesia. The painful shock produces changes at the neuro-
vegetative level, endocrine and catecholaminic with phenomena of vasoconstriction and
reduced tissue perfusion and at cellular and metabolic level acidosis, ischemia and blockage
of the ATP through shock.
19
I.3. THE DEVICES IN ANAESTHESIA
A system or anaesthetic circuit comprises an assembly of parts through which is administered
oxygen and anaesthetics to the patient through the same system also eliminating the carbon
dioxide from the body.
The component parts of the system are:
 the intubation probe endotracheal or the facial mask
 the ways of access of the gases made out of: tubes, valves, re-inhalation balloon.
The anaesthetic system comprises 3 parts:
- source of oxygen.
- the device of eliminating the carbon dioxide
- -the device which makes the concentration of anaesthetic administered (vaporizer).
There are 4 classic systems of making the general anaesthesia:
1. the open system, where the anaesthetic is not separated from the atmosphere;
2. the semi-open system, where the gases coming from the gas machine after they were
inhaled are eliminated through the one-way valve ;
3. the closed system, where gases given by the machine in low flow 300-500 ml are re-
inhaled. This system requires sodium calcein to absorb CO2.
4. the semi-closed system, where part of the inhaled gases are re-inhaled.
The anaesthetic systems which present a higher security are those that assure the oxygen
contribution at least equal to the atmospheric concentration (21 %), the proper disposal of
CO2 and the good adjustment as constant as possible of the concentration of the anaesthetic
solution administered. Until reaching these performances over the years it has been a very
long period. The first inhaled anaesthetics were carried out on a cloth soaked with volatile
substances, were then the Schiemmelbusch mask was used (a metal frame covering the mouth
and nose which is provided with gauze soaked in ether).

The Schiemmelbusch mask

20
It then reached to the rubber mask, portable anaesthesia machines DK, EMO CHIRANA, then
to the modern ones with the absorption of CO2, evaporator, and flow meter, then monitored
devices presenting alarm and memory. A modern anaesthesia machine must be composed of:
the gas machine that is fitted with the source of O2 and N2O central source or of cylinders,
decelerators, flow meters, vaporizers, circuits with valves of inhale exhale. The modern
devices have attached a respirator that can make various ventilating curves. These are the
basic elements of a modern anaesthesia machine and on them monitors are attached,
capnographs - alarm warning systems, oximeters.

I.4. THE SUBSTANCES USED IN ANAESTHESIA

In anaesthesia is used:
A. anaesthetics with parenteral administration
B. inhaling anaesthetic substances
1.4. A. ANAESTHETICS USED IN THE PARENTERAL ADMINISTRATION
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CLASSIFICATION:
a) Barbiturates (Thiopental, Inactin, Nesdonal, Penthotal);
b) Benzodiazepines (Midazolam, Dormicum);
c) Phenols (Propofol, Recofol);
d) Derivatives of imidazole (Etomidat);
e) Phencyclines (Ketamin, Ketanest, Tekam, Calypsol);
f) Others (Propane)
g) Opioids (Fentanyl, Alfentanyl, Sufentanyl, Mialgin etc.)
h) Relaxing neuro-muscular substances.
From the group A is administered by intravenous way and rare intramuscular or as rectal
suppositories. Pure intravenous anaesthesia is rarely used in anaesthesia of short duration for
small interventions (reduction of dislocations, abortions, secto-rectomy), the
electroconvulsive therapy, sedation, eclampsia. Their administration is harder to control than
for the inhalational anaesthesia and can therefore give accidents when used by staff with a
more limited degree of training.
a. BARBITURATES
General properties
1. Hypnotic action
- Neurotransmitters which inhibit the post-synaptic transmission;
- Increase the GABA action;
- Decrease the frequency of opening of the channels of chlorine and increases the
duration of opening.
2. Decrease the consume of O2 and the cerebral debit of blood
3. In small doses are anti-analgesics
4. On the cardiovascular apparatus they produce:
- vasodilatation;
- myocardia contraction;
- reduction of the baro-reflexion.
With these properties the barbiturates cause: increase of the O2 consumption of the
myocardium, arterial hypotension and tachycardia. They are contraindicated in hypovolemic
patients, decompensated heart cardiopathy or coronary insufficiency
5. The respiratory apparatus:
- Depress the proportional respiratory center with the doses and speed of
administration, resulting initially hyperpnoea and then apnoea
6. Other effects:
- Histamine liberating;
- Decrease transiently the renal debit;
22
 - Ischemia at the intra-arterial administration (i.a.);
- Being alkaline they produce pain at administration;
- They pass the foetal-placenta barrier but they don’t give foetal depression in small
and medium doses (3-4 mg/kg body);
- Enzymatic hepatic induction;
- Trigger for the acute porphyria;
- Tissue necrosis in high doses.
Contraindications for the administration:
- Impossibility for a ventilation stand;
- Allergy;
- Acute porphyria;
- Small children under 3-4 years old;
- Bronchoscopy;
- Patients in shock, hypovolemic, anemic, uremic, adissonien, cardio-respiratory or
hepatic decompensed insufficiency.
Forms of presentation
Thiopental (Pentothal, Nesdonal), in bottles of 0, 5 g and 1 g. It is diluted in 9 % physiologic
serum, concentration of 2, 5 %. It is used only in the induction 5-7 mg/kg/body and if
necessary it is repeated 20-25% of the original dose. After a unique dose i.v. the plasma level
decreases rapidly, moving in the organs with rich circulation: brain, liver, kidney and
myocardium.

The re-distribution of the thiopental

The awakening of the patient does not signify the elimination of barbiturates but the decrease
of the cerebral concentration through redistribution.

23
The metabolisation occurs in the liver in a rhythm of 10-15 % per hour. The excretion of the
metabolites is inactive via the kidneys.
The Methohexital 500 mg bottle, dilution of 50 ml. Is administered quickly, it can cause
comitial seizures activating the epileptogenic focal points being contraindicated in epileptic
crises or for the chronic ethylic patients.
Doses:
- In induction of 1,5 mg/kg/body i.v. or intra-rectal 25 mg/kg/body for children
(solution 10 %),
- For maintaining the continuous perfusion with 100-500 µg/kgb/min
Side effects: coughs or hiccups, abnormal movements, myoclonuses.
It has a potential of 3.3 times higher than thiopental, faster wakening 3-4 minutes than the
thiopental. Solution of 1% does not cause thrombophlebitis, arterial thrombosis or tissue
necrosis.
It also produces no vomiting and nausea. It is used in sedation anaesthesia loco-regional or
continuous infusion for cerebral protection. It is incompatible with atropine sulphate, Ringer's
lactate, silicone (not stored in plastic).
Butalilon (baytinal)
- Tio-barbiturate with shorter action and weaker than the one of the biopenthal. It has
vagotonic action. It is, used in short anaesthesia in ambulatory, in stomatology
associated with N2O/O2.
b. BENZODIAZEPINES (Midazolam, Ketamin, Diazepam)
PROPERTIES:
- rapid action and short duration, myorelaxant sedative, anticonvulsilvant produces
retrograde brief anaesthesia .
The hepatic metabolization with intermediary products.
Indications: in premedication, anesthetic induction, combined anaesthesia, maintenance of the
anaesthesia, sedation in small intervals, in pain therapy.
Doses in anaesthesia:
Premedication:
- 0, 07-0,1 mg/kgb adults,
- 0, 15-0, 2 mg/kgb children i.m. 30 minutes before the induction associated with
anticholinergic drugs.
- 0, 35-0, 45 mg/kgb intra-rectal 30 minutes before surgery.
Induction:
- Patients without pre-anaesthesia: 0,2-0.6 mg/kgb
- Pre-medicated patients 0, 15-0, 35 mg/kgb and 0, 15-0, 20 mg/kgb for children.
The maintenance is made in continuous infusion in combination with Ketamine 0, 03 - 0, 1
mg/kg or opioid analgesics 0, 03 - 0, 3 mg/kg/h (at low doses for frail and elderly). If
24
administered intermittently injecting small doses of 0, 25 mg since the first dose depending on
the case.
c. PHENOLS (Propophol, Diprivan, Recophol)
Presentation: bottles of 200 mg/20 ml (l0 mg/ml)
Pharmacokinetic properties:
- Rapidly diffuse in the brain
- Is bound to plasma proteins
- No signs of accumulation not even in perfusion,
- Decreased clearance in the elderly,
- Hepatic metabolism influenced by cirrhosis and liver insufficiency.
Pharmacodynamic effects:
1. On the CNS:
- intracranial pressure decreases
- cerebral oxygen consumption decreases
- cerebral blood flow decreases
2. On the eyes:
- the intraocular pressure decreases
3. On the cardio-vascular apparatus:
- decreases the arterial pressure
- decreases the cardiac debit
- decreases the cardiac frequency
It is indicated for the coronary patients and also in urology.
Contraindications:
- hypovolemic patients
- left cardiac insufficiency
4. On the respiratory apparatus:
- Decreases the response to CO2,
- Doesn’t produce bronchoconstriction, favours the depression to morphine.
The anaesthesia doses.
Induction: 2,5 mg/kgb, elderly 1,5 mg/kgb.
Maintenance:
- Re-administration of 20-25% since the first dose (it is administered in
bolus of 25-50 mg).
- Continuous perfusion 0,1-0,2 mg/kgb and minute
Sedation: 3-4 mg/kgb and hour in perfusion.
Side effects:
- produce pain while injecting, very rare allergic effects, rare uncontrolled moves

25
d. IMIDASOLE DERIVATIVES (Etomidat, Hipnomidat)
Pharmacokinetic properties:
- produce pain while injecting
- short duration
- the duration increases for the cirrhotic patients
Pharmacodynamic effects:
1. over the CNS;
- decrease the metabolism of CNS,
- decrease the sanguine cerebral debit,
- they can activate the epileptogen focal points,
- hypnotic effect.
Is used in neurosurgery.
2. On the cardio-vascular apparatus:
- Small hemodynamic variations, being indicated in the chronic ischemic
cardiopathy, hypovolemia, low cardiac debit, cardiac tamponage.
3. On the respiratory apparatus:
- No significant depression in the normal doses
4. Other effects:
- inhibit the pseudo-cholinesterase,
- no degranulation of the mast cells,
- decrease the intraocular pressure.
Doses used in anaesthetics:
Induction: 0, 2-0, 3 mg/kgb (induces palpitations, cough, hiccup, laryngospasm).
Maintenance: in continuous perfusion or reinjection 10-20% from the initial dose from the
induction.
Side effects:
- rarely pain, thrombophlebitis,
- inhibit the cortico-suprarenal.
e. PHENICYLINS (Ketamine, Ketanest, Tekam, Calipsol)
Ketamine
Presentation: bottles of 10, 50 mg/ml. It is an analgesic which produces a strong analgesia,
hypnosis, maintenance of the pharyngeal and laryngeal reflexes. It doesn’t produce relaxation
and breathing depression, cardio-respiratory stimulation.
Pharmacokinetic effects:
- rapid distribution,
- hepatic bio-transformation,
- also intramuscular absorption.
The halothane and diazepam produce the prolonging of the Ketamine effect.
26
The pharmacodynamics effects:
- produces dissociative anaesthesia, depressing the emotional composition to the cortical area
- increases intraocular pressure causing blepharo-spasm and/or nystagmus,
- on the cardiovascular apparatus it produces an increase of the blood pressure and heart rate
when the sympathetic reaction is blocked (high peridural), or it is exhausted (shock) increases
the pulmonary vascular resistance,
- on the respiratory apparatus produces broncho-dilation (given in bronchial asthma),
depresses the ventilation,
- stimulates the secretions (so it is administered as anticholinergics), increases the skeletal
muscle tone, increases the block determined by the myorelaxants, unrelated to the
benzodiazepines produces nightmares.
Anesthetic doses: i.v. 2-3 mg/kgb; i.m. 5-10 mg/kgb.
Induction:
- indicated for the patients in shock and in cardiac insufficiency uncompensated,
spastic bronchopathy.
Maintenance:
- it is injected intermittent 25% of the initial dose to 10-15 minutes or in continuous
perfusion 50µg/kgb and minute.
- It is used for completing the loco-regional anaesthesia in small doses of 0, 2-0, 5
mg/kgb/minute.
f. OTHER ANESTHETIC SUBSTANCES
1. The sodium gama-hidroxybutirat (Gamma-OH)
Presents hypnotic properties.
Presentation:
- ampule of 2g
- bottles of 10 ml
Doses: 60 - 80mg/kgb i.v. the effect is installed in 5-10 minutes and it lasts 90 minutes. The
dose 2 is ½ of the initial dose or in perfusion l5 mg/kgb/h.
Sedative: 70 mg/kgb/h then i.v. 0,5 mg/kgb/h.
Gamma-OH produces the penetration of the K in the cell.
2. The propane (Epontol)
It is an old anaesthetic that causes myocardial depression, being also histamine-liberating. It is
often used in short-term interventions (in obstetrics, traumatology). Currently no longer used
because of its negative side effects.
g. OPIOIDES
Drugs which bind to the opioid receptors which are divided in:
- agonists,
- agonists-antagonists,
27
 - antagonists.

 AGONISTS
Morphine
Action over the CNS: analgesic (predominant), sedative and hypnotic (the excitation
decreases), euphoria, meiosis.
Action on the respiration: depresses the respiratory center by lowering the rate and depth of
breathing, volume/low minute, decreases the action of the effect of the cilia in the bronchial
mucosa.
Action on the digestive tract: it contracts the sphincters (Oddi, pyloric), producing spasm by
increasing the contractility of the smooth musculature, reduces peristalsis, induces nausea and
vomiting.
Action on the cardiovascular system: produces vasodilation, slightly decreases the blood
pressure and ventricular allure.
The metabolism is hepatic. It has a prolonged and slow action.
Presentation: bottles of 20 mg.
Doses:
- 0.05 - 0,2 mg/kgb in analgesia preparatory,
- 0,2 - 0,3 mg/kgb initial dose in general anaesthesia,
- 2 mg/kgb dose of induction for the patients needing prolonged ventilation (cardiac
surgery).
The time of installation is of 30 minutes. The time of redistribution is of 8-10 minutes, and of
reducing to half and elimination of 3-4, 5 hours. Good tolerance to morphine present: the
children, the sick neoplastic patients with myocardial infarction and cardiac asthma. Patients
with low tolerance have: hypothyroidism, asthma, the elderly, the emphysematous patients,
those with decompensated chronic pulmonary heart.
The morphine has a hepatic metabolism.
Myalgin (petidin, docontral)
- Analgesic and spasmolytic action,
- Analgesic effect especially pain associated with muscle spasm, lasting 2-4 hours
- Depressed the respiratory center after 15 minutes after the injection i.m.
- Antispasmodic effect on the smooth muscles of the intestine, ureters, bronchi and arteries,
- Cardiovascular depression,
- Oliguria,
- Addiction (addictive)
- Muscle stiffness,
- Cholinergic effects (bradycardia, bronchospasm, secretions),
- Dyspepsia with nausea, vomiting, vertigo,
28
- Dissociates in time the analgesia, of respiratory depression,
- Psycholeptic effect.
Presentation: bottles of 100 mg.
Doses:
- 0,5-1 mg in perfusion,
- 1-2 mg in induction.

Meperidina
Its effect is installed faster than the one of the morphine. It has higher liposolubility. Presents
hepatic metabolism.
Doses:
- 0, 5-2, 0 mg/kgb for the preparatory analgesia,
- 3 mg/kg initial dose of general anesthetic.
Time of installation 15 minutes. The time for reduction to half, of redistribution is of 7-17
minutes, and the time of elimination is of 3-4 hours.
Fentanyl
- is an analgesic 100 times stronger than the Myalgin,
- has action over the thalamus and hypothalamus,
- produces analgesia and sedation,
- is cholinergic bradycardisant and a powerful respiratory depressant,
- analgesic action in 2-3 minutes after i.v.,
- short duration of action 20-30 minutes after injection,
- it is very fat-soluble,
- through the redeployment from the CNS to other tissues high doses or repeated may saturate
the receptors in the inactive tissues and transform fentanyl in opioid with prolonged action.
Presentation: bottle of 0, 5 mg.
Doses:
- children 1-2 μg/kg
- induction i.v. 5-30 µg/kg
- infusion 0,05-0,2 µg/kg h
- analgesia i.v./i.m. 0,7-2 µg/kg
- spinal 0,1-0,4 µg/kg
- epidural 1-2 µg/kg
The time of installation is of 5-7 minutes. The time of redistribution is 13 minutes and the
time for reducing to half and elimination is 4-7 hours.
Sufentanyl
- the strongest opioid, 5-10 times stronger than the fentanyl,
- its action installs very fast and has a short duration.

29
Doses:
- induction i.v. 2-10 µg/kg
- infusion 0,01-0,05 µg/kg/ min
- analgesia i.v.0,2-0,6 µg/kg
- spinal 0,02-0,08 µg/kg
- epidural 0,2-0,6 µg/kg
The time of installation of the action is 3-4 minutes. The time for the redistribution is of 10-13
minutes, and the time for reducing of half and elimination is of 2-5 hours.
Alfentanyl
- it is a strong analgesic
- quick installation action,
- without risk of accumulation,
- it is good for continuous perfusion.
Doses: in function of the duration of the intervention.
- induction i.v. 50-150 µg/kg
- infusion 0,1-3 µg/kg/min
- analgesia i.v./i.m. 10-25 µg/kg
- epidural bolus l0-20 µg/kg
- infusion 100 -250 µg/h

 AGONISTS – ANTAGONISTS
Pentazocyn (Fortral)
- for analgesic effect occupies the Kappa receptors,
- depresses less the respiration and the hemodynamics.
- doesn’t give addiction,
Presentation: bottles of 30 mg.
The average dose for an adult is 20-40 mg i.m.
Sintalgon (Methazocyn, Butalgin)
- strong analgesic action,
- used for completing the spinal or regional anaesthesia and in the postoperative
analgesia.
Nalbuphina
- antagonist µ and agonist Kappa,
- assures a good analgesia and it fights against the ventilator depression determined
by the agonists.
 ANTAGONISTS
- produce respiratory depression,
30
 - produce light analgesia,
- combat the effects of the agonists
Nalorphines
- opioid antidote through the competitive antagonism.
Presentation: bottles 1 ml = 5 mg.
Doses: i.v. 5-10 mg titrate.
Naloxone (Narcan)
- rapid effect in 1-2 minutes and it lasts 2-4 h
- pure antagonist of the opium and pentazocyn derivatives,
- doesn’t produce respiratory depression,
- psychomimetic effect.
Presentation: BOTTLES 1 ml=0,4 mg.
Doses:
- i.v. 0,1-2 mg titrate
- children 5-10 µg/kg
Naltrexone
- administered per bone.
h. ATARACTICS
Actione:
- anxiolytic
- antihistaminic
- antiadrenergic
- anti-spastic
- antiemetic
- anticonvulsant
Diazepam (Valium)
Presentation: bottles 2 mI =10 mg and compressed/tablets 2 mg or 10 mg.
The average dose is in premedication of 0, 1-0, 2 mg/kg.
Induction i.v. 0, 3-0, 5 mg/kg
Anticonvulsant i.v. 0, 1-0, 2 mg/kg 10-15 min
Napoton
Presentation: compressed/tablet of 10 mg.
The average dose in premedication is of 10 mg.
Mepobamat (Carbaxim, Equantin)
Presentation: tablets of 400mg
The average dose is of 400 mg (premedication).
31
Hydroxyzine (Neurolax, Atarax)
Presentation: bottles 2,5 ml = 100mg, drop 25 mg.
The average dose in premedication is of 25-50 mg.
i. MAJOR NEUROLEPTICS
Action:
- sedative
- hypnotic,
- potentiate the major anaesthetics,
- antihistaminic,
- tranquilizing,
- antiadrenergic,
- hypotermisant,
- produces extrapyramidal disorders,
- produces hypotension,
- cardiac effects of chinidinic type.
Chlorpromazine (Clordelazin, Largatil)
- used in premedication,
- effect over the hypotension and tachycardia.
Presentation: tablets of 25 mg.
Dose: 25-50 mg.

Haloperidol
- sedative effect,
- antiemetic effect.
Presentation: bottle of 10 ml (2mg/ml) and bottles of 1 ml (5mg).
Doses:
- i.m. 2-5 mg at 4 h
- premedication: 2,5-5 mg/dose
- children 2-5 mg/dose
Dehydrobenzperidol (Droperidol)
- strong neuroleptic
- produces sedation,
- antiarythmic effect,
- antiemetic effect,
- hypotension effect, rapid and intense action.
Presentation: bottle of 10 ml (5 mg/ml)
Doses:
- antiemetic i.v. 0,65-2,5 mg
32
 - premedication i.v./i.m. 2, 5 - 10 mg (NLA)
- i.v. 0,2 mg/kg with fentanyl 4 µg/kg
Levomepromazyn (Nozinan)
- action weakly analgesic used together
- antihistaminic effect,
- sensibilises the myocardium at catecholamines.
Presentation: tablets of 25 mg and 2 mg; bottles of 1 ml (25 mg). The average dose is of 15
mg; 25-50 mg/min at 200-300 mg/day i.m.
j. ANTIHISTAMINICS AND ANTIMASTOCYTAR
Promethazine (Romergan)
- antihistaminic action,
- antiemetic action,
- sedative, hypnotic action ,
- hypotensive action,
- hypotermisant action,
- simpaticolytic action,
- parasympaticolytic action.
Presentation: drops of 30mg, bottles of 2ml (50 mg); syrup for children of 125 mg.
Dose:
- adults: 30 mg/dose,
- premedication 50 mg i.m.,
- for children the dose is depending on the age:
 1-5 years ½-1 teaspoon/day
 5-10 years 1-2 teaspoon/day
Indicated for the allergic patient, the ones with hydatid cyst, bronchial asthma.
Ketotifen (Zaditen)
- antihistaminic specific and antimastocytar effect.
- anti-anaphylactic effect.
Presentation: tablets of 1 mg; syrup l ml = 0, 2 mg.
Dose: 1-2 mg/day.
k. ANTICHOLINERGICS
- substances that are used in premedication, as they have the following effects; anticholinergic
- they suppress the vagal effects over the heart in the maneuvers that are performed in
anaesthesia (oro-tracheal intubation, use of gases in the maintenance of the anaesthesia,
traction on the mesenteries during surgery)
- partially they counteract the depressant action on the respiration produced by the central
analgesics,
33
- reduce the bronchial secretions and from the digestive tract,
- reduce the salivary secretions,
- produce mild sedation and amnesia,
- reduce the regurgitation.

Less favourable effects:

- their administration dries the bronchial secretions, they become viscous and sticky, making
their elimination difficult and delayed,
- tahicardisants, causing abnormal disorders of heart rhythm (not used in cardiac surgery)
- hyper-thermic effects,
- anti-sweating effects,
- they cause dryness of the mouth,
- increase metabolism,
- stimulate the nervous system
- influence the papillary reactions
Atropine
It is a substance that antagonizes the muscarinic effects, but not the nicotinic ones of the
acetylcholine.
Presentation: bottles of 1 mg.
Doses:
- 0,01 mg/kgb or 0,1 mg/10 kg
- for the broncho-dilatation 0,025 mg/kg at 4-6 h
- children 0,01-0,02 mg/kg i.v./i.m.
Scopolamine
- vagolitic action stronger than the atropine, but with tahicardic lower action.
For the older persons is produces delirium and disorientation.
- sedative and amnesia action

l. RELAXANT NEURO-MUSCULAR SUBSTANCES

They are substances with action at the neuro-muscular junction and they block the
transmission of the neuro-muscular influx in two ways, depending on the type of the curare.
- non-depolarizing curative that is competitive with the acetylcholine resulting the
nedepolariant block (of d- tubocurarine, vecuronium gallamine, pavulon, mivacurium).
- depolarizing curative, secured on the acetylcholine nicotinic receptors favoring as the fast
and powerful acetylcholine the depolarization of the muscle cell, followed by a short period of
muscle relaxation (succinylcholine) resulting the depolarizing block. This produces a neuro-
muscular blocking at different levels.
The acetylcholine synthesis
34
Ac-ch

Deposit Ac-ch Activation of the receptors. Change of the

in synaptic vesicles Absorbs Ac-ch permeability of the
at the basal membrane muscular membrane

impulse ionic transport

nervous
Potential of action
Liberation of Ac-ch division of Ac-ch and contraction of the muscular fiber

There are four types of neuromuscular blocks:

Non-depolarizing neuromuscular acting as blocker by competing with the acetylcholine, case
in which the curare occupies the cholinergic receptors (thorough tetanus after the progressive
decreasing of the muscle contraction in a subsequent stimulus it appears the muscular secusa).
Depolarizing neuromuscular block, uncompetitive, with phenomenon of production like the
acetylcholine depolarizing the neuromuscular plate.

Neuromuscular blockade dual or through the desensitizing when the continuing of the
depolarization causes a gradual repolarization of the motor plates, the block receiving the
character of non-depolarizing block.
Mixed non-depolarizing neuromuscular block, then polarizing, when administered various
types of curare.
Non-DEPOLAR1ZING CURARE (COMPETITIVE)
D -Tubocurarina
The dose for induction 0, 45-0, 55 mg/kgb.
The dose for reinjection 0, 075 mg/kgb for Halothane ; 0, 075 mg/kgb for Isofluran and
Enfluran.
The average paralyzing dose is of 18 mg.
Its action begins in the first 2-3 minutes and it lasts 30-40 minutes. The substance is
redistributed then in different tissues.
- cholinergic action: block the pre-ganglionic sympathetic fibers,
- hypotensive action with ganglioplegic effect and muscular relaxation,
- liberates the histamines so it is not administered to allergic persons.
Presentations: bottles of 1, 5 ml with 15 mg of D-tubocurarin.
Gallamin (Flaxedil)
Intubation dose of 2, 2 – 2, 4 mg/kgb.
35
The variable dose of 60 – 120 mg with duration of 20 minutes.
The doses for reinjection is 0,356 mg/kgb for the Halothane şi 0,025 mg/kgb for Isofluran
and Enfluran.
It is a synthetic competitive miyorelaxant. Its action happens rapidly after 1 -2 minutes and it
lasts 20 minutes.
Action: vagolitic, atropinic only on the heart.
Elimination through the kidneys.
Presentation: bottles of 2 ml = 20 mg.
Pancuronium (Pavulon)
Dose for intubation: 0, 6-0, 8 mg/kgb.
Dose for reinjection: 0, 015 mg/kgb for halothane and 0, 010 mg/kgb for isofluran and
enfluran.
It is a bicuaternar aminoandrostan. The action installs rapidly, within 90 seconds and lasts 30-
40 minutes. It doesn’t cause histamine elimination it does not cause bronchospasm,
hypotension, does not produce any ganglion block. It is widely used for the oro-tracheal
intubation. The depth of the relaxation with pancuronium is potentiated by the halothane.
Presentation: bottle of 2 ml = 4 mg.
Alcuronium (Diallyl-Nortoxiferina)
Dose for intubation: 0, 25-0, 35 mg/kgb.
Dose for reinjection is 0,035 mg/kgb for the halothane and 0, 025 mg/kgb for the isofluran
and enfluran.
It is a synthetic product of the aloferin. The action installs 15 seconds after the injection i.v.
and it lasts 20-30 minutes.
Presentation: bottles of 1 ml = 5 mg.

Vecuronium (Norcuron)
Dose of intubation is 0, 07-0, 1 mg/kgb.
Dose of reinjection 0, 015 mg/kgb for the halothane and 0, 010 mg/kgb for the isofluran and
enfluran.
The action installs rapidly and it lasts 20-30 minutes. Has reduced vagolitic action and it
doesn’t produce ganglionic blockage.
Presentation: bottle with liophylisate powder containing vecuronium bromide 4 mg and 1
bottle of 1 ml solvent.

Atracurium (Tracrium)
Dose of intubation 0, 4-0, 6 mg/kgb.

36
Dose of reinjection 0, 075 mg/kgb for the halothane and 0, 050 mg/kgb for isofluran and
enfluran.
The action installs rapidly 1, 5-1 minute and it lasts 15-35 minutes.
Presentation: bottle of 2, 5 ml or 5 ml solution 1 % antracurium besilate.
Mivacurium (Di-ester bicuaternar)
Neuromuscular blocking agent of non-depolarizing type, with action of short duration 15–20
minutes.
Dose ED95 0, 07 – 0, 08 mg/kgb.
Dose of intubation 0, 15 – 0, 2 mg/kgb.
Its usage is indicated in continuous perfusion with a rate of 5–10 mh/kg/minute.
In clinical doses it doesn’t present cardiovascular effects.

Esmeron 10 mg/ml (rocuroniu bromure)

The usual dose is 0, 6 mg/kg, and its effect lasts for 30-40 minutes. During surgery, the effect
of Rocuronium Kabi is controlled continuously.

The use in children and adolescents: for the new-borns (0-28 days), the sucklings and toddlers
(28 days-2 years), children (2-11 years) and adolescents ( 12-17 years) the recommended
doses are similar to those for adults, except the rate of the continue infusion in children (2-11
years old), which can be higher than in adults. The anaesthetist will adjust the infusion rate
accordingly. The use of rocuronium bromide in a particular type of anaesthesia technique
called rapid sequence induction anaesthesia, in children and adolescents is not recommended.
Therefore, the rocuronium bromide is not recommended for this purpose, in children and
adolescents.

DEPOLARIZATING CURARE
Succinylcholine
Dose of intubation: 1-1, 5 mg/kgb i.v..
The action installs after 20-40 seconds and lasts for 3-5 minutes. Is administered in perfusion
in solution of 1‰ but it presents the risk of dual block. It is used in the oro-tracheal
intubation.
After the administration presents negative effects:
- post-surgery causes muscular pains,
- increases the arterial pressure (effect nicotinic),
- after repeated doses causes bradycardia,
- for digitize patients causes cardiac arrhythmias,
37
 - does not pass the placental barrier,
- higher sensitivity in new-born and premature
- increases the intraocular pressure,
- prolonged action in malnourished patients
- favors the vomiting and regurgitation by increasing intra-gastric pressure,
- it is destroyed (split) of serum pseudocholinesterase
- releases potassium (K) cells giving ventricular arrhythmias or cardiac arrest,
- no medicine antagonists.
Presentation: bottles of 5 ml = 100 mg.

m. ANTAGONIST SUBSTANCES (of the competitive relaxants)

Neostigmine (Myostin, Prostigmina)
It is a synthetic anticholineslerasic.
- inhibits the true cholinesterase (acetylcholinesterase)
- stimulant of the striated musculature and decurarisant.
- stimulant of the gastrointestinal smooth musculature and of the bladder by inhibiting
anticholinesterasic action,
- it is the most effective antidote of the competitive relaxants,
- it has nicotinic effects on the vegetative ganglions and muscarinic effects
(blocked by atropines): increased salivation, bronchospasm, increased bronchial
secretions, spastic contraction of the intestinal muscles, bladder, meiosis, atrio-
ventricular conduction block, bradycardia.
Doses of administration: l-2, 5mg up to 5 mg i.v. lent, associated with the atropine in rapport
of 1/3.
Presentation: bottle of 1 ml = 0, 5 mg and bottle of 2, 5 ml = 2, 5 mg.
Edrofonium (Tensilon)
Dose: 5-15 mg; but with short action. There is the risk of recurarisation, this is why it is used
more in purpose of diagnostic.

Bridion (Sugammadex)
- the reversion of the neuromuscular block induced by rocuronium or vecuronium in adults.
- for the pediatric population: children and adolescents aged 2 to 17 years sugammadex is
only recommended for routine reversal from the neuromuscular block induced by rocuronium.
- sugammadex should only be administered by an anesthesiologist or under supervision.
- it is recommend the use of appropriate techniques for assessing neuromuscular monitoring
through the evaluation of the neuromuscular block
Doses:

38
- the use of a dose of sugammadex of 4 mg/kg if recovery has reached at least 1-2 post-tetanus
contraction (CPT) after the block induced by rocuronium or vecuronium.
- the median until the recovery of the T4 / T1 to the value of 0, 9 is around 3 minutes. If the
spontaneous recovery has progressed up to at least the reappearance of T2 after the block
induced by vecuronium is recommended the use of a dose of sugammadex of 2 mg/kg. The
median time until the recovery of the T4/T1 ratio to the value 0, 9 is around 2 minutes
- When using Doses recommended for routine reversal of the block, the median time to
recovery of the T4 / T1 ratio to 0, 9 will be slightly reduced if neuromuscular block induced
by rocuronium compared to that induced by vecuronium
- If the recommended doses are used for the routine reversion of the block, the
median time until the comeback of the rapport T4/T1 at the value of 0,9 will be less
reduced in case of the neuromuscular block induced by rocuronium, comparative to
the one induced by the vecuronium
The immediate reversion from the neuromuscular block induced by rocuronium:
In the case when the reversion is necessary immediately after the administration of
rocuronium, it is recommended the use of a dose of sugammadex of 16 mg/kg. after the
administration of 16 mg/kg sugammadex at 3 minutes a dose of rocuronium bromure 1,2
mg/kg administrated in bolus, we can anticipate a median time until the comeback of the
rapport T4/T1 at the value of 0,9 of approx. 1, 5 minutes.
There are no data to sustain the administration of sugammadex for the immediate reversion
from the induced block of vecuronium.
The re-administration of sugammadex:
In the exceptional case of postoperative recurrence ofthe neuromuscular block after an initial
dose of sugammadex 2 mg/kg or 4 mg/kg is recommended to repeat the doses of
sugammadex. After the second administration of sugammadex, the patient should be closely
monitored to ascertain the return of the neuromuscular function

1.4.B. THE INHALANT ANECTHETICS

They are substances used frequently in anaesthetics.
General characteristics:
- they are substances ranging from very strong potentiality (methoxyfluran) to weak (azote
peroxide) ;
- some are metabolized in the body in small amounts (12% for fluotan) others not, therefore
the lung ventilation has a great role in their elimination and absorption ;
- they have slight controllability, they are easier to control; the minimum anaesthetic alveolar
concentration (MAC) required to prevent muscular reaction to pain stimuli is influenced by
preanesthetic medication, age and metabolism;
- the diffusion of the inhalant anaesthetics through the alveolar wall depends on: their
concentration, their solubility in blood, pulmonary blood flow;
39
- depresses the respiration depending on dose;
- the muscle relaxation is weak and occurs only in deep anaesthesia ;
- effects on liver function by reducing splanchnic blood flow .

GASEOUS ANECTHETICS
Azote protoxide
It is a general inhalator anaesthetic with the following properties:
- anaesthesia with weak analgesia;
- weak muscle relaxation;
- gas without colour and odour;
- at a concentration of 50 % with O2 produces analgesia and amnesia used as an adjuvant to
anaesthesia in concentrations of up to 66 %;
- potentiates the effect of other analgesics;
- is an inert gas which is not metabolized;
- performs the diffusion hypoxia (Fink phenomenon);
- it is eliminated unchanged from the lungs;
- at a concentration of 80 % N2O causes cardiac depression by decreasing the contractile
force;
- depresses the cortical functions

In the anaesthesia with N2O there are 4 phases:

Phase I. Analgesia
Phase II. Loss of consciousness with the exaggeration of the reflexes
Phase III. Surgical anaesthesia with 3 degrees
- superficial
- normal
- profound
Phase IV. Bulbar paralysis with breath seizure
- not supplemented N2O can reach maximum the degree of the 3rd degree.,
- administered in semi closed and semi opened circuit,
- it can be administered through the mask also,
- is usually associated with barbiturates, opiates, volatile anaesthetics, tranquilizers,
myorelaxants, neuroleptics, etc.,
It is to be avoided the anaesthesia with N2O is the hypoxia.
For the calculation of the concentration of O2 for the patient connected to closed circuit semi-
closed it is used the Foldes formula,
ml O 2 in debitmeter  300
Concentration O2 = X 100
ml total gas flux  300
40
The minimum admitted concentration in the mixture of inspiration is of 20% O2.
The advantages of using N2O:
- it can associate well with other anaesthetics,
- it is easily inhaled,
- it is non-explosive,
- no major toxic effects,
- if the hypoxia is avoided it has a relatively good security,
- induction and rapid awakening,
- does not post-anaesthetic disorders.
Disadvantages:
- risk of hypoxia during anaesthesia
- requires compact equipment
- not administered to cardiac patients, hyperthyroidism anaemic, alcoholics, children under 4
years old, liver diseases, brain interventions
The cyclopropan, is a strong gaseous mixture explodable and expensive, not used anymore.

HALOGENATED DERIVATES
Halothane (Fluotan)
It is a non-explosive liquid, colourless, nonflammable. It has an irritating odor, powerful
anaesthetic with induction and rapid awakening. The administration produces hypnosis,
analgesia and low bronchodilation. The substance is currently used in anaesthesia, but the last
5 years his place was taken by isoflurane and sevoflurane.
Once inhaled, the halothane is absorbed from the alveoli into the circulatory current. The
blood circulates through it in the body towards to the site of the main action, the brain. Here
the halothane produces a central nervous system depression, starting with the higher centers
(cerebral cortex) and then moving towards the vital medullary centers. This depression is
reversible. Its mode of action as of other anaesthetics is unknown. Low blood has a low
sensitivity in blood and therefore the concentrations in the alveoli/blood are balanced rather
quickly. The decrease under as triexponential of the concentration in blood after the
interruption of the administration would represent the tricomartimental distribution in the
richly vascularized group (brain, heart, liver), musculature and adipose tissue.
Approximately 80% of the inhaled halothane is eliminated in unchanged form through the
lungs, the rest of 20% is metabolized at the level of the liver through oxidative mechanisms
and in the conditions of hypoxia through reductive mechanisms. The maximum concentration
of the metabolites is obtained in 24 h post operatory and they are eliminated by the excretion
during one week. It has advantages and disadvantages compared to other inhalator
anaesthetics.
The action on the cardio-vascular apparatus:

41
- it is a depressant of the cardio vascular apparatus, decreasing myocardial contractile force
and heart rate
- it lowers blood pressure by direct suppression of smooth muscle in peripheral circulation ,
ganglioblocantă action,
- suppresses the noradrenalitic effect,
- diminishes or inhibits the of central vegetative activity,
- potentiates the hypotensive effect of the curare,
- favors the stasis in the latch area,
- produces bradycardia
- produces ventricular premature beats of ventricular tachycardia and the increase of the
excitability of the myocardium may even produce ventricular fibrillation .
Action on the breathing apparatus:
- depresses the respiration,
- it is a bronchodilatator,
- decreases the bronchial and salivary secretions,
- depresses the pharyngeal and laryngeal reflexes.
Action on the liver:
- toxic hepatic for the sick people with existent hepatic affections,
- it can induce halothane hepatitis in repeated administrations.
Action on the CNS:
- induces a hypnosis, weak analgesia and light myorelaxation,
- offers a light vegetative protection.
Presentation: bottles of 150 g Halothane. Doses: concentration 0, 8 - 1, 5%.

Pentran (Metoxyfluran)
- volatile strong analgesic,
- the maximum dose of analgesic required is 0, 35 % and for deeper anaesthesia 0, 5-1, 5 %
- depresses the cardio-vascular apparatus, sensitizing the heart to catecholamine, induces
arrhythmia (bradycardia)
- is bronchodilator depresses breathing, decreases the respiratory rate and the current volume,
- it is a powerful muscle relaxant,
- non-toxic for the liver
- depresses the liver function
Sevofluran
- An inhalation anaesthetic administered in the form of vapour for inhaling.
- It is used for induction and maintenance of general anaesthesia in adults and children.

42
- Induction is performed in combination with oxygen or oxygen mixtures/nitrous oxide
(inspired concentrations of up to 8% sevoflurane surgical anaesthesia in less than two minutes
in adults and children).
- Maintenance: the necessary anaesthesia is maintained with sevoflurane 0, 5-3 %, with or
without the concomitant use of nitrous oxide.
- The recovery from anaesthesia: the wake-up time is generally short. The old patients MAC
decreases with age.
- The average concentration of sevoflurane to achieve MAC at age 80 years is 50 % of that
required for the age of 20 years
- Effective and well- supported by patients with hepatic insufficiency from the classes Child-
Plugh A and B.
- Tt does not cause further deterioration of the renal function.
- Prudence in the renal failure and in cases of intracranial hypertension.
- Cardiorespiratory depression according to the dose.
- Nausea and vomiting,
- Cough,
- Arterial hypertension, tachycardia or bradycardia,
- Restlessness, drowsiness, chills, dizziness, salivation,
- Respiratory disorders, laryngeal spasms,
- Fever
- Transient increases in blood glucose and white blood cell number.
-Transient increase in plasmatic levels of inorganic fluoride during and after the anaesthesia
with sevoflurane.
- Transient changes in liver function tests, rare cases of postoperative hepatitis.
- Dystonic motor disturbances of spontaneous recovery in children.
- Malignant hyperthermia.

Enfluran
- It is a fluorinated ether, nonflammable, non-explosive, pleasant smell,
- It is a powerful anesthetic, giving strong analgesia,
- Shows rapid induction and awakening,
- Ensures a good hypnosis,
- It is a cardiac depressor high concentrations,
- Muscle relaxant effects,
- Provides a stable heart rhythm
- It doesn’t sensitize the heart to catecholamine.

Isofluran
43
- It is a powerful inhalation anaesthetic malodorous, nonflammable, non-inflammable,
- It is an effective muscle relaxant,
- Has good amnesia,
- It is compatible with the adrenaline.
Doses: the applied concentration (%) depends on the association with the other anesthetic
gases.
Desfluran and Sevofluran – have the same effects as the Isofluran.
The minimum alveolar concentration (M.A.C.) in vol.% is the concentration of an anesthetic
to which 50% of the sick people do not react to pain.

Physical properties of the inhaling anaesthetics

Solvability
Pressure of Concentration
Boiling point coefficient
Substance vaporization of saturation M.A.C./ vol.
(°C) Blood/gas/
Torr vol.%
fat/gas

AZOTE
PROTOXYDE
18752 89,5 - 0,47 1,4 101

ENFLURAN 175 56,5 24 1,78 9S.5 1,68

HALOTHANE 243 50,2 12 2,3 224 0,77
I SOFLURAN 250 48,5 - 1,41 99 1,3
C1CLOPROPAN 4800 82,8 - 0,4-0,6 11,8 9,2
D1ETILETER 442 35 5S 65 1,92
METOX1FLURAN 24 104 3 12,0 970 0,16

The diethyl ether

- It was used among the first complex anaesthetics, being used as substance mono-anesthetic
substance,
- Muscle relaxation is satisfactory,
- Appears as a colorless, strong-smelling, flammable liquid (cannot be used in the presence of
the cautery)
- Produces agitation, hyper-secretion, vomiting, laryngospasm, hypotension and cyanosis,
- In postoperative headache, dyspepsia, acidosis.
The concentrations used for maintaining the anaesthesia are between 1 – 3 – 5 %.
Action on the cardio-vascular apparatus:

44
 - cardiac depressor, produces arrhythmia, increase of the cardiac rhythm by the
liberation of adrenaline,
- the cardiac debit increases in the beginning of the anaesthesia and then it decreases
when the anaesthesia is deeper,
- produces arterial hypotension,
- coronary-dilatator.
Action on the respiratory apparatus:
- Initially the bronchial mucosa is irritated and stimulates the respiratory center leading to
increased ventilation,
- Relaxes the bronchial mucosa,
- being an irritating gas the ether vapors stimulate the cough, laryngeal spasm - > apnea reflex
(if the induction was rapid )
- Favors increase of the salivary secretions,
- Bronchodilator, decreases the activity of vibrating cilia - atelectasis (higher doses).
Action on the nervous vegetative system:
- produces photo reactive midriasis,
Action on the nervous sympathetic system:
- Increased catecholamine stimulation → in central tachycardia, hyperglycemia →
glycogenolysis,
- Splenocontraction,
- Expansion of the intestine, decreased peristalsis - > atonia,
Action on the digestive apparatus:
- Depresses the liver functions, but reversible,
- Intestinal hypotonia,
- Dyspepsia with vomiting.
Action on the renal apparatus:
- vasoconstriction —> oliguria,
Action on the metabolism:
- metabolic acidosis (increases the lactation and piruvations),
- respiratory acidosis (hypercarbia).
Action on the skeletal muscles:
- produces relaxation.
It is not administered to diabetics, to patients with pulmonary infections and when in the
surgery room are used inflammable or electro-cautery.

45
I.5. TYPES OF ANAESTHESIA
The anaesthesia has 3 types of anaesthesia;
1. The general anaesthesia
2. The conduction anaesthesia
- the spinal anaesthesia (rachi-anaesthesia)
- epidural anaesthesia (epidural)
3. The regional anaesthesia

I.5.1. THE GENERAL ANAESTHESIA

General data:
The anaesthesiologist performing this technique must be competent, to be equipped with
equipment and drugs adequate to the technique. The general anaesthesia is performed in team,
ensuring the safety of the patient and for the complications that arise from this technique to be
cropped as quickly and efficiently as possible. During the anaesthesia the patient's life
depends on who manages this technique until the patient recovers completely.
The anaesthesia happens in the surgery room or in medical cabinets with specific equipment
and adequate medication.
The general anaesthesia is a method through which is modified reversibly the function of the
CNS meaning:
- The function of wake-sleep,
- The affective function,
- The function of relation with the environment.
The general anaesthesia creates a protection against the nociceptive stimuli, creating security
conditions for the patients adequate for performing the surgery.
The obligatory equipment for the general anaesthesia is:
- device for anaesthesia + aspirator,
- laryngoscope with different blades,
- oropharyngeal pipes,
- intubation probes of different sizes and traheocstom canula,
- laryngeal probes,
- mandren,
- probe adaptors,
- masks,
- local diffuser with anesthetic,
- tensiometer,
- monitor EKG, EEG,
- capnograph,
- pulsoximeter,
46
 - defibrillator.

All of them are checked if they are in working order before each anaesthesia. The anaesthesia
apparatus is installed and checked for tightness, motion of the valves, and the presence of gas
in cylinders and of the liquids required from the vaporizers. The intubation probes need to be
sterile and they are not reusable. Like the masks of ventilation assistance they are disposable
or they have to be sterilized in ethylene oxide. The way that contact is made with the patient
who will undergo the surgical act and anaesthesia must be adequate in the sense that he or she
will have to understand how the anaesthesia and wakening process will take place, having the
verbal warranty of the success of the established technology. In this way the patient earns
confidence in the anesthetist, increases his calm and composure and eases the induction. On
the operating table the patient is placed in a most comfortable position for him and the
anesthesiologist, with a small pillow under his neck, the hair is covered. Any modification of
the patient's position (lying on the side, lordosis, ventral decubitus) will be made after the
patient was anesthetized. Then the "last" overall assessment of patient’s condition happens,
inquiring about how the last 6 hours before anaesthesia went, if the patient ingested liquid or
solid food if he slept well, if he was conducted through preoperative preparation, indications.
However, all this information is noted in the anaesthesia sheet. Then it passes to the
monitoring and measurement of the BP, installation of the EKG monitor, pulse oximeter, and
perfusion fitting the cannula to have venous access if necessary. The intra-anaesthesia
permanent monitoring of the ECG gives no direct indications of the contractile force of the
heart or about hemodynamic changes but allows the highlighting of some types of
arrhythmias:

- tachycardia (over 150 beatings/minute),

- bradycardia (under 50 beatings/minute).
- ventricular extrasystola,
- bigeminate pulse,
- branch block,
- changes of the ST segment,
- agonic heart.
During the anaesthesia the patient is monitored permanently having a global analysis
meaning:
- the color and temperature of their skin,
- eyeballs (meiosis and mydriasis during anaesthesia and during awakening)
- vascular bed,
- minimum and maximum blood pressure,
- oxygen saturation,
- continuous monitoring of ECG tracing, heart and lung auscultation,
47
- amplitude of breath,
- airway resistance.
Using the equipment it is monitored permanently:
- the gas flow,
- tightness and freedom of the anesthetic circuit pipes,
- opening of the vaporizers
- movement valves,
- pressures from the gauge,
- loss of gas
- color of the soda lime,
- infusion rate.
Simultaneously with the monitoring of the patient and the equipment they work with, the
anaesthesiologist will follow permanently also the way the surgical act happens: surgical time,
the depth of the anaesthesia of offering comfort to the patient and surgeon, the intensity of the
trauma, muscle relaxation, difficulty in the operative technique, and duration of surgery. To
be effective it has to meet general anaesthesia anaesthetic quadrangle: hypnosis, analgesia,
muscle relaxation and neuro-vegetative protection by maintaining the homeostasis.
The hypnosis will be provided by one or more types of drugs or by several groups of drugs:
a. Hypnotics:
- barbiturates: (tio-barbiturates, oxy-barbiturates) thiopenthal, brietal
- non-barbiturates: propophol, diprivan, etomidate
b. Analgesics:
- opiate: natural (morphine), synthetics (Fentanyl, Sufentanyl, Alfentanyl)
- dissociative anaesthetics: Ketamina, (Ketanest)
c. Tranquilizers:
- benzodiazepines (diazepam, midazolam, flunitrazepam).
d. Volatile substances (ether, halothane, sevofluran, izofluran)
the analgesia is obtain by:
a. Opiate analgesics: Morphine, Petidina, Pentazocina, Fentanyl, Sufentanyl, Afentanyl,
b. Gaseous agents: N2O,
c. Volatile agents: ether, izofluran, halothane, sevofluran, etc.
The muscular relaxation is obtained by using the 2 types of curare:
depolarizing (succinilcolin) and non-depolarizing (D-tubocurara; rocuronium, gallamina,
pancuronium, alcuronium, norcuronium, mivacurium).
The vegetative protection with the maintenance of the homeostasis is made by using each
drug adequate to the sick patient from case to case and uses a great drug variety:
- anticholinergic vegetative medication, which decouples a series of vagal reflexes (atropine,
scopolamine)
48
- cortisol medication (hydrocortisone succinate, dexamethasone)
- the cardio-tonic medication digitalis, dopamine, izoket)
- the fluid-coagulant medication (heparin, dipyridamole, clexane, clivarin, trasylol,
cryoprecipitate, vitamin K, etc.)
- diuretic medication (furosemide)
- ganglioplegic medication (thiometaphan, hexametonin)
- antiadrenergic medication:
 alpha - blocker (Hydergin)
 beta - blockers (Propranolol)
- the antihistaminic medication (anti H1 and H2):
 H1 promethazine (Romergan)
 H2 cimetidine, ranitidine, axyde
- anti-mastocitar medication (Ketotifen)
- antiserotonin: methysergide medication,
- ddrenergic medication (epinephrine, norepinephrine, dopamine)
- calcium channel blocker medication (nifedipine, diltiazem, izoptin)
- neuroleptic medication (levomepromazyne, clordelazyn)
- benzodiazepine medication (diazepam, midazolam)
- crystalloid and colloid solutions, the blood and its derivatives
All these drugs are administered by following a strict observation of the vital parameters:
breath, circulation, excretion.
The general anaesthesia is made by using the anaesthesia device, which has evolved over the
years from the cloth to the Schiemmelbusch mask -> the rubber mask —> portable devices
DK, EMO -> modern devices with absorption of CO2 on soda lime with debitmeter and
vaporizer —> the modern devices with monitors of O2 (pulsoximeter), monitors for TA, EEG,
EKG, temperature, PVC, etc. no matter the device of anaesthesia it has the following
elements:
1. The source of O2 and N2O flowmetry
2. Sensor of O2
3. Humidifier
4. Pressure gauge
5. Vaporizer
6. Evacuation clack valve
7. Over pressure of the clack valve
8. The breathing valve and expiration connected through the Y piece
9. Balloon
10. By-pass
11. Lime soda

49
 12. Volumeter
13. Peep
14. Automate respiratory
15. The ventilation mask
The anesthetic devices present 3 types of circuit:
1. Semi-opened circuit (the gases from the anaesthetic circuit after they are inhaled are
eliminated through the unidirectional valve),
2. Semi-closed circuit (a part of the inhaled gases are re-inhaled),
3. Closed circuit (all the gases which come from the devices of small debits of 300-500 ml
are re-inhaled by the patients, this type of circuit needs obligatory absorption CO2 on lime
soda).
The general anaesthesia is a consequence of the absorption of the anaesthetic substances by
some areas of the nervous systems.
The general consists of 54 phases:
The phase I (of analgesia) lasts from the start of the anaesthesia until the loss of
consciousness, when the cerebral cortex depresses. In this phase we can observe the
modification of: the integration functions, the temporal-spatial memory and orientation. The
reaction of the patient to pain is altered but he perceives pain.
This phase has 3 degrees:
1. Pre-analgesia: sedation and pre-amnesia,
2. Partial analgesia: total amnesia,
3. Total analgesia: total amnesia, with loss of consciousness. In this phase we can perform
small surgical interventions.
Phase II of stimulation (unconsciousness) begins with the loss of consciousness until the
installation of the regulate breathing. The pupils are photosensitive and enhanced, the
breathing is irregular, and the arterial pressure and the cardiac frequency are growing. In this
phase no surgical manoeuvres are performed because incidents might appear: bronchial
aspiration, glottis spasm, coughs, vomiting, apnoea, atrial and ventricular fibrillation, rhythm
disorders and cardiac arrest. In this situation the oxygenation of the patient is made,
enhancing the analgesic amounts, barbiturates, myorelaxants.
Phase III the surgical one, of analgesia it begins by installing the regular breathing, stop of
the spontaneous breathing, with the paralysis of the breathing centre. It is divided into 4
degrees:
 Degree 1
- breathing becomes regular,
- the current volume increases,
- movements of the eyeballs,
- decreases the muscle tone of the small muscles,
50
 - loss of the vomiting reflexes, swallowing, pharyngeal, palpebral
 Degree 2
- breathing becomes superficial but regular, that is why breathing is assisted,
- the eyeballs are fixed centrally, the pupil is semi-dilated,
- the laryngeal, cough, corneal and visceral reflexes disappear,
- the abdominal muscles relax.
 Degree 3
- the intercostal muscles diminish their activity, then they stop with the abdominal
ones,
- the muscle tone disappears except the diaphragm,
- pupil dilation is moderate and does not react to light.
 Degree 4
- begins with intercostal muscle paralysis and lasts until the seizure of the spontaneous
breathing, remaining the diaphragmatic breathing with short breath. Then there is also
the diaphragm paralysis when a passive retraction of the thorax in inspiration in
produced. A thoraco-abdominal balance appears.
Phase IV, respiratory paralysis that starts with the end of breathing, with circulatory failure
and cardiac arrest. This stage is not need to be reached, this being a pre-death phase. If you
accidentally have reached this stage, anaesthesia is superficialised quickly by stopping the gas
inhaled, the stop of the parenteral administered anaesthetics, and performance of the artificial
respiration with high flow oxygen and possibly cardiac massage.
The depth of the anaesthesia can be assessed by measuring the concentration of anaesthetic
substances in the arterial blood or by analysing the electrical activity of the cerebral cortex
recorded by the EEG. The electroencephalogram reveals the cerebral anoxia by the collapse
of the cerebral circulation. In cases when there is no electronic monitoring of the vital
parameters, the depth of anaesthesia is made through continuous assessment of the clinical
signs. The assessment of the effects of anaesthesia and the supervision of the patient shall be
recorded in the record of the anaesthesia.

51
 Anaesthesia device, monitor

The medical anaesthetic act is consigned in the clinic sheet of observation as in the model
presented beneath:

52
53
54
55
56
I.5.1.a. THE TRACHEAL INTUBATION
It consists in introducing a probe in the trachea. It is performed in many purposes;
- to ensure free breathing passage,
- allows the control of the ventilation,
- separates the respiratory tract from the digestive one,
- decreases the breathing effort,
- allows the control of the respiratory airways in difficult breathing positions,
- it assists the ventilation through artificial respiration with positive pressure without the
stomach distension,
- allows the anaesthetist to depart from the surgical block,
- allows the use of relaxing substances,
- the intubation probe can aspire bronchial secretions, blood,
- the resuscitation cardio-respiratory can be performed more efficiently.
The tracheal intubation will not be used in case of laryngeal tumours, acute laryngitis,
aneurism of aortic arc.
Necessary materials:
1. The endotracheal probes:
- made of rubber: without balloon, for the naso-tracheal intubation, with balloon for the
oro-tracheal intubation (endobronchial), endobronchial probes with double lumen and
spur which stops at the bifurcation of the trachea (Carlens type) that allows the selective
ventilation of each lung of plastic material.
- probes with metal armature and balloon which allow the mobilization of the patient
during the surgical act.

The calibre of the probes is established depending on the age and weight of the sick.

Size of the probe

Age Wight (kg) Internal diameter External diameter
Premature 1,5-2,5 3-3,5 12-14
New born 2,5-3,5 4 16
1 month 3,5-5 4,5 18
6 months 7 4,5 18
1 year 10,5 5 20
2 years 13,5 5,5 22
3 years 15.5 5,5 22
4 years 17,5 6 24
5 years 20 6 24
57
 6 years 25 6,5 26
8 years 32,5 6,5 26
10 years 40 7 28
12 years 50 7 28
14 years 55 7,5 30

For children the intubation probe is calculated following the formula:

Age / 4 + 4
For the intubation in women the size of the internal diameter of the intubation probe is ≥ 7 –
7, 5 (about the size of the last phalanx of the little finger).
In men the internal diameter of the intubation probe is ≥ 8 to 8, 5. While preparing an oro-
tracheal intubation usually 2-3 probes are prepared. Some intubation probes are provided with
mandrel which can be metallic or made out of strong plastic. The mandrels are inserted in the
intubation probes with the purpose of directing the position of the probe more easily.

2. The laryngoscope – is a device used in the intubation in order to create the path to the
glottis where the intubation probe is inserted, device provided with a light source. The
laryngoscope is formed by a blade, the handle, the source of light.
There are several laryngoscope types:

- with a straight blade (Chevalier-Jackson)

- with a curved blade

58
 batteries

light source (light bulb)

The blades are made of stainless steel or plastic, they are interchangeable and they can be
sterilized.
The blades are attached through contact at the handle of the laryngoscope which includes the
light source (batteries).
3. The diffuser or syringe is a local anaesthetic with lidocaine solution 2-4%. All these
materials are checked before starting the tracheal intubation they are sterilized for each sick or
disposed in order to avoid the anaesthetic infection.
4. The Magill tuck, for directing the probe towards the trachea.
5. Mandrel
6. Plug

The technique of the tracheal intubation:

- the necessary instruments heck for the tracheal intubation are checked,
- the patient is examined, the posed difficulties: thick and short neck, narrow and deep mouth,
large mandible, protrusion of the upper incisors (rabbit teeth), difficulty opening the mouth,
cervical spondylitis, edentulous patients and with mobile prosthesis, mobile teeth, tracheal -
larynx deviation.

59
 Materials for intubation

Laryngeal mask

There is nasal-tracheal intubation when using the lubricated probe without balloon. In the
position of dorsal decubitus the probe is inserted on the widest nostril into the pharynx. With
the help of the laryngoscope which visualizes the way the probe is directed with the Magill
tuck among the vocal cords after the local anaesthesia was carried out to them. This can be
performed without the laryngoscope and it performed under local or general anaesthesia. The
probe without balloon is inserted in the widest nostril it feels the shift from the inferior cornet,
then the thyroid cartilage is taken with the left hand, and with the right hand the proximal end
of the probe is pushed through the vocal cords.

60
We must listen at the proximal end of the probe the sound respiratory that gets maximum
when the distal end of the probe reaches aditus.
The oro-tracheal intubation using the laryngoscope is done in a certain order: the most
commonly used laryngoscope blade is the curved one. It provides greater visibility. The
position of the patient is dorsal the patient's head is on a pillow of approx. 5-10 cm for the
gathering of the axes of the trachea and pharynx. The patient lies on the operating table with
the shoulders near the edge of the table, his head being at the level of the xiphoid appendix of
the anesthetist. The head of the patient is placed in hyperextension, as well as the neck and the
chin towards the zenith.

The hyperextension of the head on the neck in the atlanto-occipital joint, clamps the mouth of
the esophagus and avoids the introduction of oxygen into the stomach during
hyperventilation, which is performed before the intubation. The lips and the dental arcades are
removed using the thumb and index of the right hand and the situation of the teeth is checked.
Then we take the laryngoscope the left hand and the blade is inserted into the mouth of the
patient, through the right corner of the lips, placing it in the back of the tongue pushing it to
the left. The blade reaches the base of the tongue in the gloso-epiglotic canal. We perform a
supero-anterior lifting maneuver of lifting the laryngoscope, the base of the epiglottis is lifted
and the glottis phant is visualized or its posterior portion. The mandible and the tongue are
lifted slightly. The laryngoscope is not leaned on the upper incisors because there is danger of
being broken.

61
We spray the vocal cords with lidocaine 2-4%. If there is a risk of regurgitation the Sellik
manoeuvre will be performed, which involves performing a digital pressure on the cricoid
cartilage. With the right hand we take the intubation probe, guiding it with its upward curve,
is inserted through the right oral commissure under light control of the laryngoscope, in the
mouth and then in the glottic opening. The intubation probe is inserted into the trachea only
enough to overcome the inflatable sleeve of the balloon. In major emergencies when there is
no laryngoscope for the oro-tracheal intubation the intervention can be performed using a
pocket torch for viewing, and as blade to direct the probe a spoon with bent handle. After the
probe is inserted, we check its position by auscultation of the bilateral vesicular sound in the
sub-clavicular region, the existence of a flow of air at the exterior end of the intubation probe
by pressing on the patient's thorax, the chest distension synchronized with the discharge of the
balloon of ventilation.
Inside the balloon with air is introduced using a syringe, but only enough to prevent
the escape of the air from the lungs. The pressure from the balloon increases when anaesthesia
is superficialised or the head hyperextension is enlarged.
The degrees of difficulty in the direct laryngoscopy
The Cormack-Lehane classification:
- Degree 1 - the whole laryngeal apparatus is viewed
- Degree 2 – when it is visualized only the posterior portion of the laryngeal wall
- Degree 3 - only the epiglottis is viewed
- Degree 4 - exclusive visualization of the rough palate

In cases when the patient is moved during the surgical position (ventral position, lateral, etc.),
the intubation probe is fixed by using plaster. The intubation is performed on patients after the

62
induction was performed under general anaesthesia, the patient with intravenous anaesthesia
and muscle relaxation, without anaesthesia in newborns, comatose patients, in severe
respiratory failure, moribund patients.

THE WITHDRAWAL
Represents the removal of the intubation probe from the trachea.
It is made in the following conditions:
- after the anaesthesia was superficialised,
- when the reflexes return,
- when the spontaneous breathing resumes,
- after the oropharyngeal secretions were aspired.
- after the patient was decurarsed or the time of decurarization passes
In case the patient doesn’t retake the normal spontaneous breath, the patient remains intubated
for a longer period and he will be protected ventilator.

I.5.1.b. THE COMPLICATIONS OF THE TRACHEAL INTUBATION:

1. Complications which appear during the tracheal intubation:
a. Complications which appear through traumatisms:
- lips injuries with the appearance of hematomas, small wounds,
- tongue injury
- breaking a tooth or its removal if it is damaged,
- bleeding or the pharyngeal mucosa or of the epiglottis,
- the lesion of the epiglottis or larynx with the apparition of the local hematoma or edema,
- posterior epistaxis,
- mandible subluxation
- creating a false path through the rupture of the naso-pharyngeal mucosa,
- the piercing of the trachea with subcutaneous emphysema, mediastinal or even
mediastinitis.
b. Complications through the apparition of the reflex disorders;
- laryngospasm,
- coughs,
- prolonged apnea,
- vomiting and bronchial aspiration of the gastric content,
- arrhythmia
(bradycardia, tachycardia, ventricular extra-systole, ventricular fibrillation),
- the allergies caused by drugs after the parenteral administration which can evolve
to allergic shock,
- reflex hypotension.
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However these interfere because of the hypoxia and hypercapnia which occur due mostly to
difficult tracheal intubation that last a bit longer. In order to reduce a part of these
complications it is good besides knowing them, to also prevent them by:
- performing the local anaesthesia in the case of intubation with xylene 2 – 4 %,
- the administration of atropine in premedication in order to assure efficient vagal
protection,
- pre-oxygenation on oxygen mask 100 % for 3 minutes and passive hyperventilation
with oxygen 100 % for one minute before the intention of intubation,
- the discharge of the succinylcholine for the patients with hyperkalaemia (uremic)
for intubation and its replacement with inhalator anaesthetic or another curare.
c. Complication through the impossibility of performing the manoeuvre for intubation.
After 2 - 3 intention with no success we must try to:
- Change the technique of intubation by: changing the laryngoscope, positioning the
patient, choosing the nose as a way, changing the doctor who performs the
anaesthesia,
- Continue the anaesthesia through the mask,
- Awaken the patient and postpone the anaesthesia for 24 hours,
- Change the technique that we used if the surgical intervention allows it,
- Tracheostomy.
2. Complications which appear during the maintenance of the tracheal probe;
a. Complications caused by the position of the probe:
- the intubation of the oesophagus,
- unilateral intubation of a bronchi usually the right one, which causes hypoxia and
hypercapnia due to the lack of ventilation of the left lung→ atelectasis of the left
lung,
- the disconnection of the probe from the ventilation device,
- the probe pops out from the trachea while moving the patient in the position that
the surgery requires,
- inflating too much the small balloon of the probe—> local oedema, necrosis

b. Complications through the obstruction of the intubation probe;

- replacing the probe,
- flattening of the probe,
- obstruction of the probe due to the abundant secretions of the bronchi,
- the torsion of the probe,
- moving the probe through insufficient anaesthesia,
- dislocation of the balloon.
c. Complications due to other causes:
64
 - caught and bronchial spasm which appear during the superficial anaesthesia,
- using an intubation probe of a too small calibre,
- pulmonary oedema.
3. Complications which interfere after the removal of the tube:
- The laryngoscopy with devices is traumatising for the patient and also the
manoeuvre for performing the intubation with superficial anaesthesia produces in
most of the cases immediate complication and also late with pains at the level of
the neck which might last up to 2 - 7 days,
- Local pains due to excessive friction of the intubation probe on the pharyngeal-
laryngeal mucosa when the patient is moved several times during the same
intervention,
- Pains while massaging the pharynx in the case that the balloon is popped,
- Cough,
- Hiccup,
- Laryngitis: due to hoarseness → complete aphonia and it lasts up to 7 days under
local and general treatment,
- laryngeal obstructive oedema,
- ulcerations of the vocal chords,
- granuloma of the vocal chords (more frequent in women), which are created due to
the static local pressure of the intubation probe, caused by the accentuate extension
or flexion of the head,
- pulmonary infections after the anaesthesia,
- the aspiration of gastric content,
- tracheitis and tracheal stenosis.
The traumatic lesions which could interfere during the tracheal intubation can be avoided
through more means:
- the correct use of the muscle relaxants (myorelaxants) with the suppression of the
effects during the tracheal intubation,
- the fixation of a leucoplast on the teeth if they are in the imminence of breakage,
- using a correct technique,
- using the blind nasal-tracheal intubation when the oral-tracheal intubation does not
succeed,
- using the plastic probes lubricated which pass easily through the larynx and using
the local anaesthetic,
- the intubation probe will be manoeuvred easily and not brutal,
- using the intubation disposable probes,
- avoiding the efforts of coughing, hiccup or hyperventilation during the anaesthesia,
- using the metal armoured probes when the patient is moved,
65
 - the intubation probe is introduced 3-4 cm under the level of the vocal chords,
- after changing the position always the auscultation of both lungs must be done,
- all of the used materials, probes, oral pharyngeal pipes, blades, laryngoscope,
mandrel, must be sterile in order to avoid the intra-anaesthetic infections.
I.5.1.c. THE DIFFICULT INTUBATION
It is the intubation that is difficult to make or which cannot be performed.
The predecessors of the tracheal intubation:
1. Obesity, goiter, reduced mobility of the maxillary, cervical spondylosis, short neck,
acromegaly,
- Vicious scars, arthrosis,
- operated ORL tumours,
- dyspnoea, stridor,
- maxillofacial traumatisms,
- vicious dentition, pragmatism,
2. Distance chin - thyroidal cartilage < 6cm
- Oral opening < 35mm man,
- Oral opening < 30mm women,
- Mandibular distance – hyoid bone < 2 fingers.
3. The Mallampati Classes
4. Radiography head neck:
- the Delegue angle from the horizontal line of the superior and vertical maxillary
through the tracheal axis:
 angle < 90° → I.O.T. difficult,
 angle 90 -100° → I.O.T. prudent
0

 angle > 100° → I.O.T. without problems.

- The balance between the length of the horizontal branch of the mandibular and the
thickness of its posterior part < 3, 6 = difficult, the distance atlas-occiput < 4 cm =
difficult.
New methods used in the case of difficult intubation:
- retrograde trans-laryngeal thread for wedging the probe,
- video laryngoscope
- using the fibroscopic guide illuminated as mandrel;
- using the fibroscopic illuminated stylet.
- flexible fibroscope

66
I.5.1.d. THE PRE-ANAESTHESIA
The administration of the anaesthesia assumes both knowing and handling all of the
techniques and also being acquainted with the details about the person that we administer it.
This is why the doctor must perform a pre-anaesthetic exam which includes more objectives:
- establishes a more detailed contact of the doctor with the patient,
- the doctor can evaluate the state in which the patient is in that moment respectively
evaluating the pathologic reversible (dehydrated patient, associated affections),
- evaluates the pathologic irreversible processes which can make the technique
harder (cervical spondylosis, cardiopathy, pulmonary affections, atherosclerosis,
etc.), which can guide him while choosing the anaesthetic technique and in
administering the adequate medication for the associated disease.
- reduces the psychological stress of the patient. It is said that the visit of the
anaesthetist made to the patient before the procedure is the equivalent of 100 mg
of phenobarbital (sedative effect, anti-anxious),
- initially a general objective exam is made and then the devices and systems are
checked, establishing the degree of the different dysfunctions: cardio-vascular,
respiratory, digestive, renal, hydro-electrolytic, immunologic, fluid-coagulant,
metabolic, thermoregulatory.
- The special examination for the anaesthetist doctor is: the detailed examination of
the superior aerial ways, the mandible, teeth, throat, pharynx, larynx, the last
ingestion.
- The examination of the patient from the point of view of the personality and the
psychological state of mind (calm, agitated, anxious) the doctor discussing with the
patient, explaining the purpose of the visit, assures him that it will be a good end
and that the success of the anaesthesia and of the surgery intervention depend on
the patient also, of the way that he accepts and obeys the indications that he is
given and the way that the patient respects the advice of the anaesthetist doctor.
- The global examination of the patient: if the biological age corresponds to the
chronological one, the weight of the patient, the appetite, if some recent or older
transformations happened in his life. The stature the constitution (muscular,
underfed, obese, cachectic),
- The examination of the functional reserves of the breathing, circulation, functions
of the liver, kidneys and of the other endocrine glands. The capacity of the patient
to tolerate the undesired effects of the anaesthesia and of the operation depends on
their efficiency. In the organism none of the apparatus or systems work at their
whole functional capacity thing which in the greatest part remains as a reserve,
being activated in case of a greater need of the respective organ.

67
 - The examination of the breathing apparatus is very important because the majority
of the anaesthetic substances depress the breathing, and the pulmonary
complications that happen after the surgery are severe. Data are given about:
cough, dyspnoea, smoking, the professional toxic environment, chronic bronchial
affections (chronic bronchitis, pulmonary emphysema, fibrosis, tuberculosis), acute
infections of the superior aerial ways (pharyngitis, laryngitis, sinusitis, trachea-
bronchitis),
- Ventilator samples are taken for knowing the pulmonary capacity and its reserves.
The voluntary sample of apnoea: at the end of a profound inspiration the mouth is
closed and the nostrils are tucked with the fingers, retaining the breath as long as
possible. The minimal values for the adult are 25-30 seconds. The sample of
extinguishing the match (Snider 1959) which consists in: the patient with his mouth
wide open tries to blow out a match situated at a distance of 15 cm. a positive probe
after 3 tries shows a VEMS of over 75%.
The examination of the cardio-vascular apparatus – will evaluate the color of the extremities,
the temperature, pulse the arterial pressure will be measured, its degree of incapacity to effort
(how many steps they can climb without stopping), the existence of some cardiac affections
associated or existent in the antecedents (recent myocardia infarct, aortic stenosis, effort
pectoral angora, ischemic cardiopathy, arterial hypertension, valvulopathy). In the cardiac
affections it is not contraindicated the anaesthesia but the acute hypervolemia is avoided, the
hypotension, hypoxia, myocardial and vascular anaesthetic depression (Sechzer 1968).
The examination of the venous system for the perfusions, the spine in case that the
anaesthetist doctor will be decided for a leading anaesthesia, the mobility of the cervical spine
for the oro-tracheal intubation, the nose orifices for the oro-trachea; intubation.
In case of surgical emergency only 6 questions are made:
- If the patient ingested liquids or solid aliments in the last 4-6 ore,
- If the patient suffers of major cardiac diseases
(pectoral angora, recent myocardia infarct),
- If the dyspnoea appears and he gets tired while climbing the stairs of a floor,
- Weather he has prosthesis or removable teeth,
- If he has urinated,
- If he is allergic to medicines and what treatment he currently follows.
In the case of the programmed surgeries the anaesthetist stops the ingestion of aliments 6-12
hours before the anaesthesia. In case of full stomach he aspires the gastric content through a
naso-gastric probe. For the patients with gastric affections it is indicated an antagonist
medicine of H2 ranitidine or axid type.
Laboratory exams. Will be solicited and interpreted depending on the clinical state of the
patient. They can be classified as it follows:
- Blood exams:
68
 o Haemoglobin (hemati and/or haematocrit)
o Sanguine group, Rh factor
o Glycaemia
o Time of bleeding (the Howell time)
o Time of coagulation
- Renal function:
o Urine exam (density, albumin, glucoses, microscopic exam)
o Uro-culture (in the cases of infection)
o Sanguine urea (in the urinary infections, piuria, albuminuria),
o Urinary urea
- The cardio-respiratory functions
o EKG
o Tests of pulmonary ventilation (vital capacity, expiratory volume maxim/sec),
o Radiography or pulmonary radioscopy.
Supplementary paraclinic investigations which are asked for differentiately depending on the
affection:
Blood:
- sanguine ionogram (Na, K, Cl, Ca),
- acido-basic balance,
- sanguine volume,
- hemoleucogram, etc.

Respiration:
- spirographic tests,
- pulmonary total capacity,
- the pxyfgen consume,
- bronchoscopy,
- bronchography,
- thorax radipgraphy, sanguine gases (PaO2, PaCO2).

Cardio-vascular:
- effort EKG,
- debit cardiac,
- tele-cardio-monitoring,
- coronary angiography.
Hepatic probations:
- electrophoresis,
- bilirubinemy,

69
 - coagulation tests,
- BSP clearance.
In case that the biologic assays are modified the repetition is asked for and also the
administration of adequate medication. If the patient is diabetic the treatment must be
translated from medication to regular insulin. If the patient received during the last 3 months
more than 7 days corticoids, pre and postoperator it will be administered 100 mg
hydrocortisone hemisuccinate in perfusion of 1000 ml glucoses 5% for 8-10 hours.
I.5.1.e. THE ANAESTHETIC RISK
Any anaesthesia involves a degree of risk. The anaesthetic risk involves for the patient a
degree of risk. The anaesthetic risk represents the frequency of the mortality and morbidity
connected to the anaesthetic act, deduced as a statistical probability in a similar lot. Knowing
the anaesthetic risk it can be refused and anaesthesia which needs urgent surgery. The
anaesthetic risk does not allow the prevention steps for reducing it:
- preparatory treatment, the decrease of the ampleness of the surgical intervention,
- the temporisation of some postponed emergencies,
- chosing the anaesthetic sample by taking prophylactic measures. The appreciation
of the anaesthetic risk is made after certain scales: A.S.A. - American Society- of
Anaesthesiologists, the scale of the Bucharest Emergency Hospital.

The A.S.A. score

CLASS SPECIFICATIONS I
I Healthy patient programmed for routine surgery
:
Patient with light disorders of the function of the
II
important organs
Patient with severe disorders of the important organs
III.
which do not activate incapacity
Patient with severe disorders of the organs and
IV important functions which threaten the life of the
patient
V Moribund

VI Cerebral death (Glasgow score 3+ apnoea)

In emergency at the respective class added an U.

The Bucharest Scheme:
a. sick:
70
 - vigorous 1 point
- compensate 2 points
- decompensed 3 points
- moribund 4 points

b. intervention:
- small 1 point
- medium 2 points
- great 3 points
- precocious re-intervention 4 points

c. additional:
- of emergency 1 point
- of age (> 65 years) 1 point
Total S:
- minimum 3 = minimum risk
- maximum 10 = maximum risk.
The main data are obtained from the pre-anaesthesia exam they are consigned in the
anaesthesia paper. It is obligatory to inform the patient about the method of the anaesthesia,
the patient will be given a questionnaire, protocol that he will sign for acceptance. After the
patient was evaluated at the pre-aesthetic exam, he will be recommended the sedatives,
analgesics or barbiturates an evening before. In the morning of the surgical intervention
another pre-anaesthetic medication will be administered which consists in an analgesic,
sedative, tranquillizer, anti-allergic or anti-masocitary.
I.5.1.f. CHOICE OF THE ANAESTHESIA
Each sick person is particularity. The anaesthesia must be adapted for each sick person in
particular. In choosing the anaesthesia we must keep in mind:
- the security of the patient,
- the comfort of the surgeon,
- the comfort of the patient,
- the competence of the anaesthetist, the technic equipment.
The security of the patient: the doctor must maintain the patient alive. This is why while
choosing the anaesthesia he must keep in mind the general state of the patient, age, the
associated affections and their degree of compensation and also some interference with the
medication that the patient was using before taking contact with the anaesthetist doctor. There
are a series of extra surgical affections which can influence the choice of the anaesthesia.
Example:
- the chronic alcoholism needs higher doses of anaesthesia.
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 - Anaemia: under 8 g it needs lower doses of anaesthetic
- Low Hb %, the sick people tolerate difficultly the hypoxia and the rehabilitation is
made slower.
- Coma does not need the administration of the hypnosis only the analgesics and a
good oxygenation.
- The leading anaesthesia, especially the spinal one is not made for the persons with
low arterial pressure.
- Fibrosis needs during the anaesthesia a greater demand of oxygen.
The neoplasm under cytostatic treatment produces leukopenia, thrombocytopenia, anaemia;
this is why during the anaesthesia it might appear:
- bleedings, hydro-electrolytic disorders, hepatic-renal and cardio-respiratory.
- The pluri-anti-biotherapy implies the risk of the apparition of the mycosis
infections.
- The pulmonary emphysema and the bronchial asthma increase the risk of a post-
surgery respiratory insufficiency
- The epilepsy increases the risk of the intra-anaesthetic convulsions, this is why
extra attention is given to the anaesthesia with a more profound hypnosis, a strong
post-operatory sedation.
- The acute respiratory infections imply more complicated problems and if the
surgery allows it, it is good to make a temporisation. If it is urgent and it is
possible, a regional anaesthesia must be done.
- Septicaemia – the regional anaesthesia will be contraindicated the general one
being preferred.
- The cancer with metastasis – presents disorders of the metabolism of the serotonin
and it can lead to bronchospasm and low arterial pressure.
The anaesthetist doctor must know very well all these affections in order to choose the best
tolerated anaesthesia for the patient, and the surgical comfort must be adequate so that the
intervention to be well finalised.
The preparation of the technique for the anaesthesia:
1. The verification of the devices for anaesthesia in the case of the general anaesthesia:
- The verification of the oxygen source, eventually the N2O tank,
- The control of the pressures which can be visualised on the manometer,
- The control of the circuit, to be well air-tight,
- The verification of the by-passes of overpressure,
- The verification of the soda lime,
- The verification of the functionality of the ventilation device,
- The verification of the breathing system,
- The verification of the system for gas elimination.
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2. The verification of the monitors:
- EKG,
- EKS,
- pulsoximeter,
- temperature,
- central venous pressure (PVC),
- tensiometer,
- defibrillator,
- volumeter.
3. The verification of the device with emergency medicaments:
- digoxin,
- hydrocortisone hemisuccinate,
- adrenaline,
- atropine,
- sodium bicarbonate 8,4 %,
- beta-blockers,
- gluconic and lactate calcium,
- nitro-glycerine,
- izogroup blood, izoRh,
- sodium nitroprusiat,
- xilin,
- dopamine,
- perusable solutions,
- alupent,
- dextran,
- manitol 10 %; 20 %,
- diuretics (furosemide).

4. The preparation for the start of the anaesthesia:

- the device for the anaesthesia and aspiration is verified,
- the oro-tracheal and nasal-gastric intubation probes,
- the choice of the ventilation mask and the oro-pharyngeal,
- the preparation of the perfusion,
- preparing the anaesthetic substances (barbiturates, curare, analgesics, xilin, the
inhalator anaesthetic in the vaporiser, myosin, ketamine, propophole, etc.),
- izo-group blood, izoRH,
- the verification of the effect of the pre-anaesthesia,
- the most adequate positioning of the patient on the surgery table,
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 - the monitoring of the perfusion (the venous peripheral or central way depending on
the case),
- avoiding the vicious positions or the exaggerated extension of the hands,
- the connection to the EKG, EKS, monitors, pulsoximeter,
- the verification of the functioning of the monitors and the follow up of the values
since the start of the monitoring.
- the start of the induction.

I.5.1.g. THE INDUCTION

The anaesthetic induction is the pass from the awaken state to the surgical anaesthesia. It
corresponds with the installation of the specific anaesthetic affection. In the functions of the
organism in this period some substantial modifications interfere over the: central nervous
system (C.N.S.), breathing and haemodynamic. The induction exists in all the types of
anaesthesia but it is more obvious at the general anaesthesia (G.A.). In the G.A. the hypnosis,
analgesia and amnesia produce modifications over the sympathetic vegetative nervous system
with an increase of the catecolamines which also bring a modification of the general
metabolism, increasing the arterial tension, the pulse frequency, increase of the glycaemia,
increase of the amount of hormones, modifications of the pupils, modifications of the
peripheral circulation, mastocytar degranulation, etc. some substances used in the anaesthesia
produce bradycardia, vasodilatation, arterial hypotension (thiopental). In all of these
modifications which occur rapidly, some minor accidents might appear which can be
corrected, but they can also induce fatal accidents if the anaesthetist is not very secure on the
technique that he is using in order to counteract the accident. The most anaesthetic accidents
are experienced in the induction and awakening. For children the anaesthetic induction is
shorter than in adults. The anaesthetic substances have a directly proportional effect with their
solvability in tissues, the cardiac debit and the alveolar ventilation.
In the general anaesthesia the induction might be done on 3 ways:
1. inhalator induction (mono-anaesthetic and pluri-anaesthetic)
2. intravenous induction
3. mixed induction
1. the mono-anaesthetic inhalator induction
it is made on the mask with semi-closed circuit with oxygen for the diethyl ether, halothane,
sevofluran, isofluran, desfluran, enfluran and metoxifluran.

The technique:
For the beginning is administered oxygen 100 % with a debit of 2–4 1/minute with the
expiratory valve open. It follows the gradual introduction in higher and higher cncentrations
of the inhalator gas on a spontaneous respiration of the patient. After the patient has lost
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conscience after the lash reflux is gone (attention to the elder and vitiated persons = lower
doses), the excitation phase passes and a regular breathing starts. In continuation the
ventilation is assisted with the balloon until it is felt the decrease of the glottis resistance and
the decrease of the laryngeal reflexes, when we can pass from the tracheal intubation. In case
that during the assistance of the intubation with the balloon cough interferes, the glottis
spasm, apnoea, the amount of anaesthetic is reduced with some breaths. Then the gradual
increase of the inhalator gas is retaken. The installing of the surgical phase on this way is
made in 5 minutes for the halothane, 10 minutes for metoxifluran and 12 minute for dietylic
ether. For the anaesthetic substance to reach in the alveoli and then to get diffused in the
blood in sufficient concentrations for maintaining an efficient anaesthesia, a certain time must
pass. The induction with drops on the Schimmelbusch mask is not used currently. The
induction on an inhalator way can be rushed by using an anaesthetic with rapid action: azote
protoxid with flux 6/2 litres/minute, followed by tracheal intubation with succinylcholine.
This type of inhalator induction is used for sick persons in a difficult state, small children and
it is not used for sick people who ingested aliments.

2. The induction on intravenous way

It is the most elegant way, rapid, pleasant and easily accepted by the patients. It represents a
risk, due to the rapid depression of the haemodynamic.
The technique
After the patient has the perfusion on and he was connected to the monitors which follow the
vital parameters, hypnotic propophol is administered, Dose:0, 6mg/kg/body, thiopenthal
dose:7-8 mg/kgb and curar (not polarising or depolarising). The oxygen mask is ventilated,
the patient (hyperventilation with oxygen 100%), in order to stand easier the apnoea period
which follows during the oral-tracheal or nasal-tracheal intubation. After the intubation was
made (technique described at the tracheal intubation) the intubation probe is connected to
anaesthesia device, assuring as correctly as possible the liberty of the aerial ways. The balloon
of the intubation probe is air tightened with 4-5 ml of air introduced with the syringe in the
balloon of the probe. There is a series of schemes for the anaesthetic induction, using also
other substances:
- ketamine doses of 100-200 mg + succinylcholine 50-100 mg,
- diazepam 10-30 mg + succinylcholine 50-100 mg,
- petidine 20-50 mg + thiopental 25% 200-300mg + succinylcholine 50-100 mg,
- thiopental 25% 200-500 mg
other schemes will be described at Methods of anaesthesia.
3. The mixed induction.
It is quite often used in the anaesthesia and it consists in using an inhalator gas together with
other intravenous substances.
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Example:
- N2O/O2 with flux 6/3-10 l/min: the mask is held at few centimetres from the face
until the patient falls asleep. It is ventilated through the balloon. Intravenous is
administered succinylcholine 1, 5 mg/kg/body, it is ventilated still, followed by
intubation (O.T. or N.T.).
or:
- It is used intravenous :
 Droperidol 0, 3 mg/kg/body +
 Fentanyl 0, 01 mg/kg/body +
 Succinylcholine 1, 5 mg/kg/body followed by l. O. T.
For the shocked patients barbiturates is not administered anymore, it is administered oxygen
100% through the mask for 2-5 minutes + succinylcholine, followed by l.O.T.. the surgical
intervention will never be started without having the analgesia installed, because reactions
appear with peripheral vasoconstriction thing which males the absorption of the inhalator gas
to be slower. In the case of the hyperventilation the absorption of the inhalator gases is too
accelerated, and the balance between the arterial blood and brain is a lot slowed down due to
the cerebral vasoconstriction provoked by hipocarbia (Ngai, 1970). In this situation if the
amount of administered anaesthetic increases, it will increase also the amount of anaesthetic
in the blood which reaching in the coronarian circulation it will decrease the cardiac debit and
it accentuates the peripheral vasoconstriction. It is recommended for the induction to be
profound and followed by “Maintenance”.
I.5.1.h. THE MAINTENANCE
It represents the period of maintaining the anaesthesia between induction and awakening. In
this period is realised an equilibrium of the anaesthetic concentrations between the device of
anaesthesia-alveoli-blood. So that in this period of the anaesthesia to be well done, the
anaesthetist must know well the surgery times so that during some surgical manoeuvres the
anaesthesia to be more profound (mezous traction, vagotomy, the dilatation of the anus, etc.).
the anaesthesia must be more profound by the beginning of the intervention and it must get
superficial by the end of the surgery. The correct anaesthesia is made with the help of the
analgesics, hypnotics and curares towards the end of the surgery. The correct anaesthesia is
made with the help of the analgesics under ventilation with oxygen. The analgesic substances
depending on the technique established by the anaesthetist doctor are:
- Analgesics:
 Morphine,
 Propopjole (Diprivan),
 Petidhia (Mialgin)
 Sufentanyl,
 Fentanyl,

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  Alfentanyl,
Dose per kg/body was exposed to the presentation of each medicament.
- Hypnotics:
- Volatile agents:
o Halothane,
o Isofluran,
o Sevofluran,
o Desfluran.
- Gaseous agents: N2O (azote protoxide).
- Analgesics – hypnotics
o Ketanest (Ketalar, Ketamina, Calipsol)
- Barbiturate:
o Thiopenthal
- Benzodiazepine:
o Diazepam.
- Non-barbiturate:
o Midazolanum (Dormicum).
- Non-depolarising curare:
o Gallamin (Flaxedil), Pavulon
o Vecuronium, Alloferin.
o Esmeron
The doses of administration for each of these substances are presented in the chapter for
anaesthetic substances.
The ventilation is established in adequate parameters for the age, weight, body surface
meaning:
- Current volume (V.C.): 8 -12 ml/kg/corp.
- Breathing frequency = 12 breaths/minute.
- Inhale pressure = +20 cm H2O.
Corrections will be done depending on:
- PaO2 (the partial oxygen pressure in the arterial blood).
- PaCO2 (the partial carbon dioxide pressure in the arterial blood),
- FiO2 (the oxygen concentration in the inhaled air),
- ETCO2 (carbon dioxide by the end of the exhale).
In order to establish these parameters correctly the capnograph is used.

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The capnogram
P = breathing starts, PQ = CO2 from the great bronchi,
QR = CO2 from the alveoli, R = CO2 by the end of the exhale ETCO2,
RS = the debit of the exhale, ST = respiratory plateau.
In the spontaneous respiration the deepness of the anaesthesia can be evaluated as it follows:
a. The superficial anaesthesia:
- Movements appear at the surgery stimuli,
- The frequency of the pulse increases,
- Increases the arterial pressure,
- The breathing frequency increases
b. The sufficient anaesthesia;
- The patient remains still, does not move,
- Breathing is normal (the frequency and the amplitude),
- Stable hemodynamic,
- Tolerates the tracheal probe
c. The anaesthesia with overdose:
- The modification of the hemodynamic, the arterial pressure decreases to lower
values,
- Tachycardia,
- Pupile modifications appear.
For the controlled respiration in the G.A. the deepness of the anaesthesia is evaluated as it
follows:
The superficial anaesthesia:
- The intolerance of the tracheal probe,
- Movements of the hands and fingers,
- Movements of the eyebrow and the frown, tears.
- Sweat,
- Pallor,
- The spontaneous respiration comes back after an accumulation of CO2,
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 - Hiccup,
- Thoracic respiration, without abdominal,
- The photo-motor reflex is present,
- The reflex of deglutition is present.
Sufficient anaesthesia:
- still patient,
- the movements lack,
- tolerates the tracheal probe,
- hemodynamic stability,
- teguments and hot mucosa, well coloured,
- the manual respiration with the balloon is followed by the movements of the thorax
and abdomen,
- no modifications appear the la traction reflexes,
- the association of the myorelaxants supress the motorial reaction to pain.
Anaesthesia with overdose:
- low tolerance to the insufflation of the lungs,
- the depression of the haemodynamic, decrease of the TA, filiform pulse,
- tachycardia or the absence of the peripheral pulse
- prolonged apnoea after the end of the artificial breathing,
- cold, pale extremities.

I.5.1.i. THE AWEKENING

It is the third stage in the anaesthesia and it presents periods between the surgical anaesthesia
and the comeback of the conscience. It is realised superficial and the interruption of the
administration of the anaesthetics in the optimal time, depending on the pharmaco-dynamic of
the anaesthetic substances and their antagonisation. The antagonisation of the opiates is made
with naloxone, of the curares with myostin, (neostigmine) which is an inhibitor of the
cholinesterase, of the benzodiaseprenes with flumazenil.
The superficial anaesthesia is made through the elimination of the inhalator gases which is
rapid for N2O, halothane metoxiflurane. Another part of the administered substances
(barbiturates, competitive relaxants) are redistributed in the organism then they suffer a bio-
transformation (metabolisation). The awakening represent a more difficult moment for the
organism because they are under the cumulative influence of the operatory and surgical shock
(adrenergic reactions, the reflexes from the painful areas, hypervolemia, the residual action of
the anaesthetic substances, etc.). After the inhalator anaesthesia is rushed through:
- the maintenance of a minim level of anaesthesia compatible with the demands of
the patient

79
 - the replacement of the major anaesthetic (ex. metoxifluran) with a weaker
anaesthetic (ex. Azote protoxide),
- the anticipation of the operative manoeuvres (the anaesthesist must know the
operatory technique and injects the curare and the analgesic before the most painful
moment). The patient will hyperventilate towards the end of the anaesthesia
because it appears the hypocarbia which decreases the excitability of the breathing
centre, producing apnoea.
In case that the hyperventilation was produced there is a method of comeback of the
spontaneous respiration in a short time lapse, by increasing the PaO2 it is the limit of the
apnoea (approximately 5 - 10 min.), (Ivanov and Num 1969). It is made through
hypoventilation with a minute-volume of approximately 3 l/minute in circuit with re-
inhalation and without soda lime. The PaCO2 increases with approx. 3 mmHg/min. In case
that it was associated with miorelaxants in anaesthesia, the existence of the signs of residual
are shown through:
- hypertonia of the palpebral muscles,
- the impossibility of the patient to lift his head at demand from the surgery table
(Jobanseen, 1964),
- the hypoventilation of costal superior type after retaking the spontaneous
respiration,
- finding a thoracic resistance at the insufflation with the balloon.
The decurarisation is made for the well ventilated and oxygenated patient. There are used
substances as: atropine with tranquilising effect and the miostine (neostigmine) with
bradicardisant effect (besides the basic action). It is recommended the sequence of the
administration of the two substances as it follows, the injection of atropine with 2-3 minutes,
before the miostine. The 2 substances are administered together it is produced a slight
increase of the pulse frequency, followed by a bradycardia produced by the miostine, the
increase of the salivary secretions, the risk of unwrapping the intestinal anastomoses in the
abdominal surgery through the extraction of the peristalsis. After retaking the breathing ad
mobility, the stabilisation of the hemodynamic at the normal parameters the patient is
transported in the awakening room. The transportation of the patient is made when the
ALDRETE score is 10.
The ALDRETE score
The spontaneous motility or at command:
- moves 4 members 2
- moves 2 members 1
- immobile 0
Breathing:
- the patient breathes profoundly and coughs 2
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 - dyspnoea, superficial limited breathing 1
- apnoea 0
The state of the conscience:
- perfect 2
- awakes at command 1
- does not respond 0
The coloration:
- normal 2
- pallor, marbled, icterus, etc. 1
- cyanotic 0

I.5.1.j. THE COMPLICATIONS OF THE GENERAL ANAESTHESIA

When the anaesthetist establishes the anaesthetic technique for each patient, he must
know the advantages that the chosen technique presents against the disadvantages of another
technique. Always the advantages must prime towards the disadvantages of another
technique. Certainly each technique presents also a risk. Any technique must present a certain
security for the patient. The anaesthetist must know each complication, to prevent them and to
solve them in the most favourable way. Tough the intra and post-anaesthesia complications
interfere.
A. Breathing complications:
The obstruction of the breathing ways which can be:
- complete
- partial.
In this case the breathing effort grows, the current volume diminishes, the breathing becomes
noisy, and the extremities become cyanotic.
The breathing obstruction can be produced through:
- vomiting,
- regurgitations,
- laryngospasm,
- bronchospasm.

The regurgitation and vomiting

There are some anaesthetic factors which are predisposing:
- hypoxia,
- superficial anaesthesia,
- the oral-pharyngeal excitation through the great pipe, through the aspiration probe,
laryngoscope.
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The regurgitation
It is the passive pass of the liquids from the stomach, through the relaxed oesophageal
sphincters, in the pharynx. It is produced when the patient is sited in Trendelenburg, when the
cardia is not efficacious, when the pharyngeal reflexes are absent, when there are pharyngeal
lesions or when the stomach is full of hypertonic liquids.
The vomiting
Anaesthetic causes of producing the vomiting:
- ventilation with intermittent positive pressure before the intubation
(usually when the patient has his muscle relaxed),
- the Trendelenburg position which increases the intra-abdominal pressure.
- the accidental intubation, of the oesophagus,
- the laryngoscopy with exaggerated closing of the crico-pharyngeal muscle,
- the fasciculation after the administration of succinylcholine.
The vomiting and the regurgitations produce intra- and post-anaesthesia risks:
- hypoxia and anoxia, through the obstruction of the breathing ways or through
laryngeal spasm,
- the Mendelson syndrome (1946) or the clinical bronchoalveolitis through aspiration
of acid gastric liquid,
- post-operatory complications: pneumonia, bronchopneumonia, atelectasis,
pulmonary abscess, etc.
In order to prevent the vomiting and the regurgitation there is a series of steps:
- for the patients who have a full stomach the anaesthesia will not be performed, only
after the evacuation of the stomach (with the exception of the emergencies),
- the installation of the gastric probe before the start of the anaesthesia,
- lateral position, in post-operatory,
- the probe with balloon during the anaesthesia.
The laryngospasm: represents the partial or complete adduction of the vocal chords this can
be done through:
- foreign body at the level of the vocal chords (mucus, blood, vomitting,
laryngoscope),
- local irritating substances,
- superficial anaesthesia (reflexes through painful visceral tractions),
- hypoxia
- thiopental.
The treatment of the laryngospasm
Prophylactic:
- the local pharyngolaryngeal anaesthesia with spray or xylene 1 %,
- the decrease of the secretions with atropine in the premedication,
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 - the superficial anaesthesia must be avoided,
- correct induction,
- devices, resuscitation and intubation for any anaesthesia.
Curative:
- The elimination of the cause (if there is the case),
- Administration of halothane (broncho-dilatator),
- The thoroughness of the anaesthesia (if it interferes in the surgical time),
- Administration of oxygen on the mask (with positive pressure),
- Oral-tracheal intubation,
- Tracheostomy (in case of major emergency).
The glottis oedema
It appears in the region under the glottis favoured by the local traumatism produced by the
more difficult tracheal intubation or local infections. It can produce breathing obstruction. It
can be prevented through:
- Local pharyngeal-laryngeal-tracheal anaesthesia,
- Intubation a-traumatic soft.
It appears more frequently in children between 2-5 years.
Treatment:
- corticoid administration,
- oxygen therapy,
- in extreme cases tracheostomy.
The bronchospasm
It represents the spasm of the intrinsic muscles of the bronchioles. It is produced for sick
people who present bronchial asthma, chronic or tobacco bronchitis, allergies, superficial
anaesthesia.
The prophylaxis
- profound anaesthesia,
- anti-allergic and anti-mastocitar,
- preparatory aerosols.
Treatment:
- the exclusion of the cause,
- succinylcholine, ventilation on the mask or tracheal intubation,
- soft induction,
- the administration of hydrocortisone hemisuccinate.
- Administration of bronchodilators (Berotek, Ventolin)
The post-operatory atelectasis or post-anaesthetic

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It is the complete obstruction of the breathing ways with the distal resorption of the gases. It
presents signs of hypoxia and tachycardia, cyanosis, tachipnea, sweat, agitation, the limitation
of the movements of the thoracic box, the absence or diminution of the vesicular noises.
Radiologic: the deviation of the trachees from the colobated part, the narrowing of the
intercostal spaces. It is produced though the absence of the profound respirations with
modification in the tension of the alveolar surfaces due to the alteration of the surfactant.
Treatment:
- Oxygen-therapy,
- Artificial cough provoked,
- Intercostal infiltration with xylene,
- Tapotage of the thoracic region,
- Aerosols with bronchial dilatators,
- Treatment with antimastocitars,
- Bronchoscopy,
- Respiratory gimnasctics.
Retention of the carbon dioxide
It is based on more causes:
- hypoventilation of anaesthesia cause due to overdose of anaesthetic drugs,
- the depletion of the soda lime,
- increase of the dead space (prolonged anaesthesia on the mask for children).
The effects of the hypercapneea:
a) over the central nervous system:
- increase of the blood flow,
- somnolence,
- increases the pressure of the cephalorachidian liquid.
- over the vegetative nervous system;
- the circulate catecolamines increase, decreases the parasimpatico activity
b) over the breathing:
- produces respiratory insufficiency,
- the curve of dissociation of the oxyhemoglobin is deviated towards the right (Bohr
effect).
c) Over the haemodynamic:
- Depressing effect over the myocardium it decreases the cardiac debit,
- Cardiac arrhythmia → ventricular fibrillation,
- Vasoconstriction through central effect and vasodilatation through peripheral effect
d) Over the biochemistry:
- Breathing acidosis with the decrease of the Ph,
- metabolic alkalosis,

84
 - the K serum increases.
The hyperventilation is produced during the controlled anaesthesia. It produces hypocarbia
and the increase of the blood pH. It appears the compensatory metabolic acidose.
The effects of the hyperventilation:
a) over the central nervous system:
- it decreases the cerebral tension of the oxygen,
- produces cerebral vascular vasoconstriction, the depression of the reticulate
ascendant formation.
b) over the hemodynamic:
- decreases the pressure through increase of the intra-thoracic pressure,
- decreases the cardiac debit,
- decreases the difference between the partial pressure of the alveolar and arterial
oxygen,
- protects against the arrhythmia,
- decreases the ionising calcium.
Hyperventilation in anaesthesia presents also some advantages:
- maintains a rich oxygenation,
- produces a more secure breathing alkalosis more secure than a breathing acidosis,
- decreases the doses of anaesthetic.

Disadvantages:
- it may produce overdose of anaesthesia gas,
- arterial hypotension,
- it influences the cardiac debit and the blood flow,
- hypoxia and anoxia
It has more causes:
- the breathing obstruction,
- overdose of anaesthesia products,
- overdose of miorelaxants.
The apnoea has the following cases:
- overdose of anaesthesia products.
- it is produced in prolonged anaesthesia,
- complete breathing obstruction,
- induction with irritating inhalant anaesthetics,
- hyperventilation through central breathing,
- oxygen administration for the sick people suffering of chronic hypercapneea.
- severe anoxia,
- increase of the intracranial pressure
85
 - tachipnea (breathing over 30/minute in adult)
Causes:
- superficial anaesthesia,
- overdose of halothane or ether,
- hyperthermia,
- hypoxia,
- shock.
Treatment
- assistance of the anaesthesia,
- depth of the anaesthesia,
- administration of intravenous analgesic (actions rapidly).
B. The hiccup
It appears in the superficial anaesthesia in the case of the stimulation of the vague nerve,
hypercarbia.
Treatment
- depth of the anaesthesia,
- controlled breathing with hyperventilation,
- injection of analgesics,
- block of the phrenic nerves,
- clearing the stomach,
- the administration of curare.
C. Cardio-vascular complications
a. The arterial hypotension
It is inoffensive if it is not associated with hipovolemia and myocardial depression. When it is
associated with arterial cerebral affections or of coronation rapid therapeutic solutions.
The causes of the intra-operatory hypotension arterial:
- bleeding,
- too rich premedication,
- too profound anaesthesia,
- too high leading anaesthesia,
- deletion of the too rapid hypercarbia,
- sanguine absorption of the locale absorption of the anaesthesia,
- modification of posture of the patient,
- traction on the mezou,
- myocardia infarct,
- pulmonary and central emboli
b. Arterial hyper-tension

86
Causes:
- administration of vasopressors in excess, superficial painful anaesthesia,
hypercarbia and asphyxia,
- aggressive induction, pheochromocytoma,
- thyreotoxicosis,
- increase of the intracranial pressure.
c. Arrhythmia
Arrhythmia supra-ventricular:
- sinus tachycardia,
- sinus bradycardia,
- tachycardia paroxistic atrială şi nodulară,
- fibrillation and the atrial flutter,
- the atrio-ventricular block degree I and II,
- atrial extrasistole.
All these things are produced by hypoxia and anaesthetic overdoses.
Treatment: causal and medicaments (digital, atropine, rytmonom).
Ventricular arrhythmia:
- the atrio-ventricular complete block,
- ventricular tachycardia,
- ventricular extrasistole

Treatment:
- avoiding the overdose of anaesthesia,
- clearing the hypoxia and hypercarbia.
- antiarithmic medication (xylene, beta-blocker).
The most frequent intra-operatory arrhythmia are the tachycardia and bradycardia.
d. Tachycardia: -the frequency of the pulse is over 90 beatings/minute.
Causes:
- aggressive induction,
- lack of the analgesia,
- medicamentous substances: atropine, gallamina, ketalar,
- substantial intraoperative bleeding,
- hipo and hypercarbia,
- hyperthermia,
- arterial paroxistic tachycardia.
e. Bradycardia: decrease of the pulse frequency under 60 beatings/minute.
Causes:
- vagal sino-carotidian stimulation,

87
 - anestesices: halothane, fentanyl, sufentanyl,
- succinylcholine, neostigmine, digital,
- hypothermia,
- intra-cranial hypertension,
- anoxia and cardiac depression.
Treatment: deletion of the cause and the administration of atropine.
f. The gaseous venous emboli
Causes:
It is produce through the penetration of the intravenous air during the transfusions, perfusions,
radiographic exploration, pneumo-peritoneum. The mechanism of production is in the
formation of a bubble of air while the blood gets out from the right ventricle in the pulmonary
artery followed by cardiopulmonary arrest and the cardiac. An amount if 200 ml intravenous
air is considered as being lethal. It is not allowed this accident because the perfusions,
transfusions are followed permanently during the anaesthesia. Currently there are used some
bags of infusible solutions which by the end of the content of the bag do not allow the entry of
the air in the venous system. The installation of the gaseous emboli is announced by listening
the vesicular noise as the “mill wheel” on the precordial area, and the heart is listened with
metallic noises “like a horse galloping on a woood bridge” (Schixpuri, 1959).
Treatment:
- Sitting the patient in left lateral decubit the head being lower,
- Oxygen administration of 100 % and vasopressors,
- In the case that these are inefficient the thoracotomy is practiced and the air is
aspired from the right ventricle,
- cardiac massage and the artificial ventillation,
- catheter for measuring the central venous pressure (C.V.P.) through which the air
is aspired.
g. The ischemic phlebitis
are accidents provoked by the injections of anaesthetic substances irritant on peripheral veins.
They appear also when the endovenous catheter brannula type is kept longer without being
injected with anticoagulant substance.
Treatment:
- permanently checking the brannula,
- administration of anticoagulant substances,
- local refrigeration,
D. Neurologic complications
a. Convulsions

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They are more frequent for the people with fever, septic states. In these case the atropine will
be avoided, the high temperature from the surgery room. Their apparition is shown through
fibrillation around the eyes and mouth.
Treatment:
- oxygen-therapy,
- hypnotic thiopental type,
- myorelaxants with short action.
Psychotic disorders of post-hypoxia are more frequent for older people with generalised
atherosclerosis.
b. The post-anoxic coma
It is recognised by:
- fixe pupils, uneven and/or dilated,
- rigidity of the extensor musculature,
- thoracic anarchic contractures,
- convulsions,
- hypothermia.
Treatment
- oxygen-therapy,
- nervous tropics (Piracetam, Cerebrolizin)
- assuring a satisfying diuresis for eliminating the cerebral oedema (manitol 10%
250ml in quick perfusion 30 min.),
- hypertonic glucose 33% 250-300 ml quick perfusion 30 minutes,
- hypothermia (with ice bags on the vascular areas),
- administration of HSHC (hydrocortisone hemi-succinate).
Traumatic lesions of the peripheral nerves due to the intra-anaesthetic position or the
compression of a member.
They are rarer and they can be avoided through the positioning as physiological as possible of
the patient during the operation.
Other accidents
E. The malignant hypothermia – is the rapid and progressive increase of the temperature of
the organism (42-43°C)
It is associated with:
- hipotonia of the muscles after the administration of succinylcholine,
- mixed acidosis.
The survival depends of:
- precocious diagnosis (tachipnee, tachicardia, hyperthermia),

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 - the rapid reduction of the body temperature, hypothermia through local
refrigeration, gastric refrigeration,
- hypothermia mattresses,
- the correction of the acidosis through THAM or sodium bicarbonate 14 %o,
- the correction of the hypovolemia.

F. The anaesthesia hypothermia

The general anaesthesia depresses the thermoregulatory centres, decreases the metabolism and
it dilates the peripheral vessels. The hypothermia produces cardiac arrhythmia and prolongs
the awakening.

G. Ocular complications
- ocular trauma by applying incorrectly the ventilation mask, operatory fields,
- the exposure to air of the ayes provokes the cornea abrasion, when the orbicular
muscle is relaxed, in the same way the one of the creases, they stay separate and the
cornea dries very rapidly. This is why during the anaesthesia the eyes are kept
closed.
Treatment: the eyes are closed through ocular bandage 12-24 hours, solutions ophthalmic
ointments.
Explosions of the anaesthetic gases:
- using the inflaming gases in the presence of the electric cauter leads to the
explosion in the surgery room,
- currently the explodable gases are not used anymore.

I. 6. TECHNIQUES OF GENERAL ANAESTHESIA

I.6.1. THE GENERAL PIVOT HALOTHANE ANAESTHESIA (G.A. pivot fluothan)
Pre-anaesthesia:
12 hours (for the programmed anaesthesia) it is indicated a light nutritional regime, and 6
hours before, the stop of the ingestion of solid aliments and liquids. The patient is prepared;
bath, shaved, the hygiene of the cavities is performed, etc.
In the evening:
- sedation with phenobarbital l00mg i.m. or per bone, sedation with dormicum 15 mg
per bone 30-40 minutes before the anaesthesia.
Before:
- 40-50 minutes of starting the anaesthesia : Myalgin 50-100 mg i.m
- Atropine 0,1 mg/'kg body i.m. + Romergan 1 mg/kg body i.m. or
- Diazepam 10 mg i.m. + Atropine 0,1 mg/l0kg body or
- Droperidol (dehidrobenzperidol) 5 mg i.m. + Atropine 0, 1 mg/l0kg.

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The patient is sited on a table with the head elevated to 100.
The venous puncture is performed preferably 1/3 distal of the forearm with flexure and the
adaption to the perfusion. The checkout of the T.A., pulse, the monitoring of the (T.A., EKS,
SaO2, temperature, respiration), the non-invasive or invasive monitoring (a. radial, PVC, etc.).
Induction.
- Atropine 0,5 mg or 0,1 mg 10 kg/c:
- Flaxedil 15 mg or Pavulon 1 mg for protection and prevention of the muscular
fasciculation
- Thiopental sol. 2,5 % in a dose of 5 mg/kgb, until the clearance of the ciliary
reflex, slow injection approx. 1 minute,
- O2 100 % through the mask for desazotisation,
- Succinylcholine 100 mg or 1,5 mg/kgb,
- Ventilation O2 100% through the mask 1-2 minutes
- I.O.T. after which previously the local anaesthesia was performed for the vocal
chords,
The auscultation of the two pulmonary areas is performed with the stethoscope, the
positioning of the probe for intubation, the fixation of the probe in the holder, the air tight of
the balloon of the intubation probe.
Maintenance
- N2O + O2 50 % (2 l + 2 l) - (3 l +2 l or 4 l +2 1), (l = litres)
- Halothane 1-1, 5% for 4-6 minutes and then the concentration is decreased to 0, 7-
0, 8% depending on the arterial pressure.
The completion of the analgesia from the premedication with myalgine from the
premedication with myalgine 40-50 mg or Fentanyl 0,5 mg with re-administration of 0,1 mg.
Muscular relaxation with Galamina (Flaxedil) 1, 5-2 mg/kgb or Pavulon 0, 8 - 1 mg/10 kgb or
Alcuronium 0,2-0,4 mg/10 kgb or Vecuronium 0, 8-1 mg/10 kgb or Pipecuronium (Arduan)
0,8 - 1 mg/10 kgb.
Manually controlled ventilation (with the balloon) or mechanically with a volume of 10-12
ml/kgb, it is fixed to the frequency of 12-14 ventilations/minute and a minute volume (M.V.)
8-10 litres and is verified then the pressure in the aerial ways.
The monitoring of the T.A., A.V, the colour of the blood in the plague, the colour in the
temperature of the teguments, the expansion of the thoracic box, PVC., the pupillary diameter,
the degree of muscular relaxation, EKG, SaO2, diuresis, the position of the patient, perfusion,
the functioning of the mechanics of anaesthesia, the surgery times.
The awakening
- Is started by the end of the surgery.
- Decreases gradually the concentration of halothane 0, 8 —> 0, 5 → 0, 3 —> 0, 2
and it is interrupted when it reaches the last layer of skin.
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 - The stop of N2O at the last layer of skin and the increase of the concentration of O2.
- the calcea is removed from the circuit,
- It is ventilated normal with the balloon, with O2 100%, rarer ventilation for the
accumulation of CO2, stimulant al of the breathing centres. In the case when the
breathing is not retaken the opiaceu is antagonised with the nalorphine 0, 5 - 1 mg
or the sequence is made with the Pentazocin (the last injection of opiaceu is
replaced with the Pentazocine).
After the breathing is retaken the decurarisation with Myostin 2,5 - 3 mg + Atropine 1 mg (in
rapport 3 curare/1 myostin).
If the breathing will be retaken, the efficient ventilation is of minimum 8 ml/kgb
approximately 400 ml O2 100 %.
The aspiration of the secretions is followed by de-intubation and the aspiration of the
secretions.
After the de-intubation is administered O2 100 % for 1-2 minutes.
The reflexes are studied, questions are asked, he is invited to move the arms, to open his
mouth, to raise his head, etc.
The sick is transported in the awakening room.
The general anaesthesia I.O.T pivot sevofluran uses the same anaesthesia technique as in
the pivot general anaesthesia halothane with the change of the halothane pivot with pivot with
sevofluran with the concentration:

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I.6.2. THE HIPNOANALGESIS
The pre-operatory preparation is the same as in the G.A. pivot halothane.
Premedication
- Induction: Atropine 0,1 mg/10 kgb (it is not obligatory it can be cancelled)
- Protection: Flaxedil 10 - 15 mg, Pavulon 1mg i.v., Esmeron 0,6mg/kgbody
- Perfusion with physiologic serum 9 ‰ or glucose serum 5 % to which is added:
Fentanyl 10 micrograms/l kgb, Diazepam 0, 3 mg/kgb, Pavulon 0, 1 mg/kgb (after
which is intubated).
- The respective perfusion some minutes, while is ventilated with O2 100 %.
- Succinylcholine is administered 100 mg (in case that in the perfusion is not added
Pavulon).
- Is positioned the intubation probe, the vesicular noise is listened, the probe is set
and adapted for the anaesthesia device.
The maintenance
- N2O + O2 50 % apoi 60 %
- Pavulon 1 mg/10 kgborp + 1-2 mg re-administration la 40 minutes
- Fentanyl 0,2 mg i.v. la 30 minutes.
- Ventilation controlled manually with semi/closed circuit with a V.C.10 - 12 ml/kgb
and with a frequency of 10-14 ventilations/minute.
- The monitoring of the B.P. , V.A., EKG, SaO2, temperature, etc.
- Perfusion 500 - 700 ml/hour + the losses.
- The surgery times are followed
The awakening
- By the end of the operation is antagonised the fentanyl with naloxone (only when is
the case)
- The soda lime is removed 5 minutes before the end of the operation.
- It is closed N2O at the last thread.
- Is ventilated with O2 100% 5 1/minute.
When the breathing is efficient 8 ml/kgb the decurarisation is made.
- Is administered O2 on the mask 1 - 2 minutes,
- The patient is transported in the awakening room.
In this anaesthesia we can associate a series of anaesthetics:
- N2O + Fentanyl,
- Midazolam (Dormicum) + Alfentanyl,
- Diprivan + Alfentanyl hypnoanalgesics

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I.6.3. THE ACUPUNCTURAL HYPNOANALGESIS
This technique is performed through electro-punctured hyper-stimulation in two pairs of
points.
The effectuation of the puncture:
The acupuncture points are stimulated with 4-6 Hz and 100-1201-Hz as much as the patient
can take.
At the extremity of the plague is punctuates more with two needles with a frequency of 100-
120 Hz and with a maximum intensity.
The premedication
- Ketamine 0,3 - 0,5 mg/kgb i.m. 20 minutes before the induction.
The induction
- Diazepam 0,3 mg/kgb i.v.
- Esmeron 0,4-0,6mg/kgb, Pancuronium, Vecuronium 1 mg/l0kgb followed by
I.O.T.
- Maintenance
- The electric stimulation is increased to 30 - 70 V
- Respiration controlled with N2O +O2 60 %.
- It is injected, curare at need.
The awakening
- It is decurarised in case of need.

I.6.4. THE NEUROLEPTANALGESIS TYPE II (NLA TYPE II)

It is a combination between a neuroleptic and a strong analgesic.
The pivot of the analgesia is the Fentanyl associated in induction with the Dehidrobenzperidol
(D.H.B.P.)
The premedication
1. D.H.B.P. 5 mg (2ml) i.m.
2. Fentanyl 0, 1 mg (2ml) i.m.
The premedication is administered 30 minutes before the surgery. It follows the positioning of
the patient on the surgery table, the set of the perfusion in fast rhythm 500 ml while
monitoring the vital parameters:
- Atropine 0,1 mg/l0kgb
- Protection.
The induction
- D.H.B.P. 0, 3 - 0, 4 mg/kgb i.v. slowly.
- Fentanyl 12-15 microgrames/kgb.
- Respiration on the mask with O2 100% followed by the administration of N2O +
O2 50% or 60%.

94
 - Curare type Succinylcholine 1 - 1, 5 mg/kgb.
- It is administered N2O + O2 on the mask of assistance of the respiration which
becomes depressed.
- The local anaesthesia for the vocal chords followed by I.O.T., the fixation of the
probe, the air tight of the balloon.
The maintenance
- Is made with N2O + O2 permanent in concentration of 60 – 66 %.
- Muscular relaxation with DTC: 0, 5 mg/kgb or Pavulon 0, 1 mg/kgb.
- Re-administration of Fentanyl 0, 1 mg la 10-15 minutes followed by the curare in
need.
- The ventilation controlled with V.C. 10 - 12 ml/kgb, frequency of 10-14
ventilations/minute in semi-closed circuit, plus soda lime.
- The monitoring of the vital parameters.
- The last administration of analgesic with 15-20 minutes before the end of the
surgery.
- It is preferred Fortral 1-2 doses (30-60 mg).
The awakening
- It is interrupted the administration of N2O.
- It is made the antagonisation of the fentanyl with the nalorphyne.
- It is ventilated with O2 100% 5 l/minute.
- It is decurarised until the breathing is retaken.
- It is perfused with crystalloids: physiologic serum 9 ‰ or glucose serum 5 % with
rhythm of 500 -700 ml/hour/intervention.
N.L.A. type II can be made in two ways
A. Induction: - in bolus or rapid perfusion D.H.B.P. 0,3 mg/kgb, together with the Fentanyl
12 - 15 μg/kgb plus relaxant competitive type Succinylcholine si l.O.T.
B. Induction: - with barbiturate + droperidol, fentanyl and competitive relaxant Maintenance:
- curare + ventilation with N2O + O2
C. N.L.A. with spontaneous respiration
Premedication: fentanyl + droperidol
Induction: 100-200 mg barbiturate
Maintenance: fentanyl with pentothal or ketamine.
N.L.A. is an anaesthesia which is used a lot in the thoracic surgery, in neurosurgery,
gerontosurgery and the emergency surgery.
I.6.5. THE RELAXING SURGERY
The premedication
- Hydromorphon 0, 3 mg/kgb i.m.

95
 - Atropine 0, 3-0, 6 mg i.m.
The induction
- Esmeron 0,6mg/kgb, Pavulon 1 mg or Flaxedil 15 mg for protection.
- Propofol 2-2,5mg/kgb, Thiopental sol. 2, 5% 5 mg/kgb.
- O2 100% on mask for desasotisation.
- Myorelaxin (succinylcholine) 100 mg. l, 5mg/kgb.
- Ventilation O2 100% on the mask.
- I.O.T. with local anaesthesia.
- The auscultation of the pulmonary areas + positioning of the probe + fixation of the
probe with the air tight of the balloon.
The maintenance
1. N2O + O2 60-75%.
2. Analgesia with petidina 0,5 -lmg/kgb (is repeated in need)
3. Pavulon l, 5-2mg /10kg or Flaxedil 3-4mg/kgb (competitive relaxants in high doses,
apneisant)
The awakening
- The removal of the soda lime 5 minutes before the end of the operation.
- Closure of the N2O at the last thread.
- O2 5 1/minut.
- Decurarizare cu miostin 2/3.
- Respiraţie eficientă 8 ml/kgb
- O2 pe mască.
- Transport la sala de trezire.
I.6.6. THE ATARANALGESIS
A. With breathing assisted/controlled
The premedication
- Diazepam 0, 2-0,3 mg/kgb or
- Droperidol 2, 5-5 mg or
- Hydroxyzine 50-100 mg,
- Atropine 0, 1 mg/kgb.

The induction
- Diazepam 2,5 mg which is repeated until profound sedation,
- Ketamine in concentrated perfusion 1‰ with speed of 5 - 8 ml/minute, up to 1-1,5
mg/kgb,
- Competitive relaxant (Atracurium 0;5-0,6 mg/kgb) or Pavulon 0, 1 mg/kgb,
Esmeron 0,6mg/kgb
- O2 100%, ventilation,
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 - I.O.T., balloon probe,
- The fixation, auscultation of the vesicular noise, the position of the intubation
probe and its air tight.
The maintenance
- Diazepam 2, 5 mg which is repeated up to profound sedation
- Ketamine 0, 25-0, 50 mg/minute in perfusion.
- Competitive relaxant in need.

The awakening
Decurarisation with Miostin 1/3.

B. With spontaneous breathing

Premedication
- Atropine 0, 5-1 mg.
The induction
- Ketamine 0, 5-1, 5 mg/kgb.
- Flunitrazepam 0, 7-1, 5 mg/kgb.
The maintenance
The Ketamine, when the anaesthesia is superficialised 0, 3-1 mg/kgb or continuous perfusion
with Ketamine 20 micrograms kg/minute.
Another form of ataranalgesia with spontaneous breathing:
Premedication
- Diazepam 0,2-0,3 rng/kgb sau
- Hidroxizin 50-100 mg sau
- Droperidol 2,5-5 mg
The induction
- Diazepam 2,5 mg until profound sedation
- Ketamine up to 1-1, 5 mg/kgb.
The maintenance
- Ketamine 0, 25-0, 5 mg/minute + N2O + O2

C. With midazolam (dormicum) i.v. with spontaneous breathing

The premedication
- Atropine 0, 5 mg i.v.
The induction
- Midazolam 0:05-0, 2 mg/kgb + Ketamine 0, 5-1 mg/kgb.
The maintenance
- Ketamine 0, 3 -1 mg/kgb + Midazolam 0, 3 mg/kgb.
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D. With midazolam with assisted respiration
The induction I
- Midazolam 0,05-0,2 mg/kgb
- Ketalar 0,5-1 mg/kgb + Pavulon 1 mg/l0 kg or Esmeron 0, 6 mg/kgb
- O2 100%, ventilation.
- I.OT.
The maintenance
- Midazolam 2 - 3 mg/hour.
- Ketalar 0, 3 - 1 mg/kgb.

The induction II
- Midazolam 0, 02 mg/kgb + propofol 2 mg/kgb,
- Midazolam 0, 02 mg/kgb + thiopental 2, 5 mg/kgb,
- Midazolam 0, 02 mg/kgb + alfentnyl 0, 02 mg/kgb + propofol 1 mg/kgb.
The awakening
- The decurarisation of the competitive curare with miostin

I.6.7. THE i.v. ANAESTHESIA POTENTIATED WITH SPONTANEOUS

BREATHING
The premedication
- Phenobarbital 100 mg per bone
- Atropine 0, 1 mg/10 kg.
The induction
- Propofol 2-2,5mg/kgb, Tiopenlhal 2 mg/kgb,
- Petidine 1mg/kgb and it is repeated
It is used for the short interventions.
The i.v. anaesthesia of short duration is used in the hospital where there are anaesthesia
devices. It is practiced in the operation rooms which are equipped with devices and
medication of emergency in case of complications of the anaesthesia. It is practiced in the
surgery rooms where small interventions happen, which need general anaesthesia, the patient
wanting to have anaesthesia and to sleep (genecology cabinets, aesthetic surgery, the small
surgery, stomatology, etc.).
In any place where the G.A. is performed i.v. the anaesthetist doctor must have the emergency
case with him in order to control the ventilation, which comprises:
- The tracheal probe,
- The Magill tuck,
- The auto inflatable Rubben balloon,

98
 - laryngoscope with 2-3 blades of different sizes,
- the Guedel pipe,
- metallic or plastic mandrel,
- tuck,
- syringe,
- aspiration probes.
- portable aspirator,
- defibrillator,
- cardioscope,
- O2 cylinder,
- Kit for i.v. perfusion,
- Different sizes branula

Also in the emergency case he must have medicaments used in case of emergency:
- Adrenaline 1mg/ml, Calcium clorure lg/10 ml,
- Sodium bicarbonate 8,4 % (molar),
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 - Isuprel l mg/5ml,
- Noradrenaline 4mg/ml,
- Digoxin 0,5mg/2ml,
- Ephedrine l0mg/ml,
- Miofilin240mg/10ml,
- Hydrocortisone hemisuccinat 25 mg and l00mg,
- Dextran 10% 500ml/flacon,
- Manitol 10%, 20%,100ml, 250ml,
- Dopamine 50mg, 200mg.

I.6.8. THE GENERAL ANAESTHESIA IN THE C-SECTION

The pre-anaesthesia (Atropine, petidine)
The pivot halothane anaesthesia
In obstetrics all the parturitions, no matter the lapsed time from the last ingestion of aliments
is considered as in having a full stomach, because the labour increases the gastric secretion
and it delays the evacuation of the stomach.
- Atropine 0, 5-0, 7mg i.v. 30 minutes before the anaesthesia,
- Per bone 1 tablet of Ranitidine of 150 mg.
Induction
- Atropine 0, 5mg i.v. followed at 5 minutes by:
- Thiopental 2, 5% (Inactin, Nesdonal) 5 mg/kgb i.v
- Myorelaxin (succinylcholine) 1 -1, 5mg/kgb i.v.
- Hyperventilation on the mask l-2 min
- I.O.T., fixation of the probe
- The contact of the anaesthesia device
The maintenance
1. Manual or mechanic ventilation with O2 100% or
2. Manual or mechanic ventilation with O2 +N2O 50%
If the extraction of the foetus is made with great difficulty the N2O is intercepted in order to
not be diffused to the foetus, it is ventilated with O2 100% 4-51/minute and it is reinjected
myorelaxin 0, 5mg/'kgb.
The umbilical cord is cut and then it is injected:
- Ocytocic (Ergomet, Oxytocin),
- Sevoflurane 1-1, 5%
- Mialgin 1 mg/kgb i.v. or fentanyl 0, 2 mg,
Curare: flaxedil 1 mg/kgb or pavulon 0, 1 mg/kgb.
the awakening

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 - Atropine 0,5 mg i.v.,
- Miostin rapport 1/3,
- Detubation,
- Transport in the awakening room.
We must prevent the syndrome of compression on the cava inferior and on the aorta with
implication in the foetus-placenta circulation.
The ablactating:
- Antipirin 3 tb/day
- Bromergocriptin 3 tb/day 5 days or
- Estradiol 2 tablets of 2 mg/day.
In the last time in the C-section is applied the peridural anaesthesia and the spinal one (will be
described in the leading anaesthesia). Also the spontaneous birth was relieved in the last
years, for them assuring the analgesia through simple peridural anaesthesia or continuous with
catheter.

I.6.9. THE ANAESTHSIA FOR CHILDREN

The anaesthesia in children presents great particularities because the child is not a miniature
adult, the development of the internal organs and of the central nervous system with the
vegetative one is made in 2 age stages that we must respect. For a good anaesthesia in
children we must keep in mind some physiologic particularities which are specific for each
age. The anaesthetist who realizes the anaesthesia for the children must keep in mind the
following:
- To have an experience close with a paediatric anaesthetist,
- To have specific equipment for the age and to not male improvisations that can be
fatal,
- The doctor must use the pharmacology of the drugs that he uses in the doses
adequate to the age,
- He must be aware of the functional reserves and the gravity of the disease of the
child,
- The re-evaluation pre and post-operatory of the child is more frequent than in
adults.
The anaesthesia in children is a bigger success when the anaesthesia knows the anatomy and
physiology of the child. The temperature of the environment has a greater importance
increasing the risk of the hyperthermia and hypothermia as the age is smaller. The baby and
the new born both lose heat easily this is why they are protected in the incubator, when the
bigger child is predisposed to accumulating heat (hyperthermia).
THE BABY AND NEW BORN
Breathing apparatus and aerial ways:
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The ribs are predisposed horizontal, and the oblique position appears towards the age XI-XII,
the position of the diaphragm is high T8-T9 from where it results that its movements are more
reduced, the dyspnoea is installed more rapidly than in the adult due to the abdominal
distension. For the baby between 3-5 months in 25 % of the cases it appears the obstruction of
the nasal ways because there is a hypertrophy of the lymphoid tissue, with the increase of the
secretions and bilateral coanal atresia, macroglosia, shorter pharynx situated at the level C 3 -
C4, the epiglottis is larger, the trachea has a narrower portion subglottic (probes I.O.T. without
balloon) the length of the trachea is of 5 – 9 cm.
It results differences of IOT.

The dimensions of the trachea

Age Length (cm) Diameter (mm)

0-1 months 4 5
1-3 months 4 6,5
3-6 months 4,7 75
6-12 months 4,2 7,6

The breathing excursions are reduced in compensating exchange the frequency is high.
The breathing frequency:
- New born 40 - 90 resp./minute,
- The first months 30 - 80 resp./minute,
- 1 year 20 - 40 resp./minute.
The rapport volume current/dead space are smaller for the baby (15/5), increases the dead
space through tubes and mask,
- The functional and residual capacity is smaller, this is why the fast induction can be
performed with volatile substances,
- The existence of the anatomic connection induce hypoxia and after the apnoea of
30-40 sec.,
- The breathing centres are not completely developed in this way explaining the
prolonged post-anaesthesia apnoea, the basal metabolism is high (increases the
consumption of oxygen 8ml/kg/minute and the production of CO2 twice),
- High ventilator volume.
The cardio-vascular apparatus
- the heart is bigger,
- the frequency of the cardiac beats is higher, at 12-30 years is closer to the one of
the adult),

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 - the cardiac debit is 2-3 times higher than the one of the adult (180-
240ml/kg/minute),
- the muscular wall of the ventricle is weaker,
- the compensatory capacity of the ventricles is small (through tachycardia).
- the bradycardia decreases the cardiac debit,
- B.P. is 30 mmHg and increases up to one year to 80 - 85 mmHg,
- The blood volume is 100 – 120 ml/kg new born, 90 – 100 ml/kg for the baby,
- The frequency of the pulse 120-180 beatings/minute for the new born, 85 - 115
beats/minute for the baby.
The hydro-electrolytic balance
- the extracellular liquid is double than the adult (29% of the body weight),
- the hydric balance represent approximately ½ from the extracellular liquid (700ml),
- the dehydration appears very rapidly,
- the capacity of renal concentration is weak,
- the distribution of the drugs and the relation dose/kgb is influenced due to the high
percentage from the organism (80 %), the doses being greater with 20 – 30 % than
in the adult,
- there is the tendency of retaining the Na and Cl this is why 1/5 of the amount of
perfused liquid will be physiologic serum molar solution,
- usually is present in the hypocalcaemia.
The gastrointestinal apparatus
- the regurgitation is more frequent than in the adult, the reflux and the pulmonary
aspiration, because the cardial sphincter of the oesophagi is not functional,
- for the new born the digestive rest in pre-operatory is 2 hours,
- for the baby 1-6 months the digestive rest is 4 hours, baby of 3-6 month, 6 hours
and over 36 months 8 hours.

The liver
- for the new born the metabolisation of the drugs is low,
The endocrine system
- the children are exposed to hypoglycaemia due to the low reserves of glycogen.
The hematologic system
- the blood volume is of 80 – 100 ml/kgb;
- the haematocrit is of 46-60% at birth at it decreases by the age of 1 year to 33-40%.
Thermic regulation
- under 3 months in the presence of the cold the shiver does not appear, in the cold
the stress of cold with hyper-metabolism appears with (consumption of liquids,
increase of the catecholamine, acidosis, hypoxia, vasoconstriction, etc.).

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Anaesthesia principles in children
For the children under 18 months is not necessary a premedication. For children over 18
months a psychological contact will be established for knowing the personality of the child,
the habits, trust in the doctor, the examination of the venous capital and the set of a flexure.
The premedication in children over 18 months is of 0, 02 mg/kgb of atropine and eventually
the petidine 1 mg/kgb.
The anaesthetic circuit in children up to 10 kg will be the semi-opened circuit unidirectional.
There are standard devices for children depending the age and weight.
The laryngoscope – it is used the blade for children, the straight blade, and over 5 years the
curved one. The diameter of the probes was described in the oral-tracheal intubation.
The monitoring will comprise: the temperature, the pulse, the colour of the teguments, the
oesophageal stethoscope, EKS, pulsoximetry, capnography, urinary debit.
After the premedication it is administered 20-25 mg/kgb thiopental i.m. and the child is
brought while sleeping in the surgery room monitoring permanently the respiration. The
necrosis is made usually with inhaling anaesthetics, the most used are the halothane + N2O +
O2 or sevofluranes + N2O +O2. The induction is rapid, the maintenance is easy, the
homeostasis is slightly influenced, and the awakening is rapid. The liquid losses will be
corrected, also the ones of blood, and if it interferes the obstruction of the aerial superior ways
the obstruction must be cleared rapidly through aspiration.
The intubation O.T. in small children may be performed after the anaesthesia with inhaling
gas is made, without using curare. For bigger children the succinylcholine i.v. is injected 1
mg/kgb for I.O.T. which assures a good laryngeal relaxation. During the maintenance the
curare is injected rocuronium type 0,6 mg/kgb which by the end of the anaesthesia will be
decurarised with miostin.
The anaesthesia circuits in children are the ones without re-inhalation and the ones without
soda lime. The T tube is used, case in which it is used a debit of fresh gas of 2, 5-3 times
minute/volume to the patient. Usually it is used for the anaesthesia in the Kuhn circuit.

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 The Kuhn circuit

In the intubation there are used probes without balloon preferably. In case they are used with
balloon the air introduced for ait tightening in the balloon is small for not creating lesions at
the level of the laryngeal mucosa. The hydration is made on a venous way with solution of
glucose serum 5 %, Ringer solution lactate or physiologic serum 9 ‰ with a rhythm of 8
ml/hour.
During the anaesthesia as in the case of the adults it is performed the monitoring of the
ventricular allure (V.A.), B.P. , of the breathing, coloration of the teguments, temperature, the
capillary bed of the nails, the size of the pupil, the amount of lost liquids, the bleedings, the
O2 saturation, etc. by the end of the anaesthesia the patient is aspired with the tracheal probe
and then in the oral cavity. Then the tube is removed keeping in mind the monitoring of the
breathing and of the liberty of the oral cavity. Then the tube is removed keeping in mind a
monitoring of the breathing and of the liberty of the aerial ways. In post-operatory is assured a
good analgesia, major analgesics (petidina) or minor analgesics (algocalmin, perfalgan,
ketonal, etc.).
For the parenteral re-hydration and electrolytic equilibration there are international standards
for 24 hours meaning:

Age Liquids Na K Cl
New-Born 70 ml/kg l-2mEq/kg 2 Eq/kg 2 mEq/kg
Baby up to 10 kg 100-120 ml/kg 2-3 mEq/kg 2 Eq/kg 2 mEq'kg
Baby between 10-
80-100 ml/kg 1-3 mEq/kg 2 Eq/kg 2 mEq/kg
20kg
Baby over 20kg 60-SO ml/kg 3 mEq/kg 2 Eq/kg 2 mEq/kg

The veins used for the hydro-electrolytic re-equilibration are the ones of the forearm and the
epi-cranial ones.
The most frequent complications frequent in children are: the obstruction of the aerial ways
through secretions, mucus or subglottic oedema. Hydrocortisone hemisuccinat is
administered, O2 + halothane on the mask or aerosols with ephedrine.

I.6.10. THE ANAESTHESIA IN PATIENTS WITH HIGH RISK

The anaesthetist doctor is forced to make the pre-anaesthetic examination in order to know
better the patient, the possible complications that may appear intra and post-operator, the
affections associated with the background disease. The anaesthetist must get assured of the
security of the patient intra and post-operatory, this is why besides the technical equipment
and the theory knowledge he must also anticipate the intra- and post- anaesthetic
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complications. This is why the affections associated to the background disease must be well
known, being able to increase the operatory risk.
There is a series of affections which may increase the operatory risk.

1. The anaesthesia for the asthmatic patient

If it is well made by the doctor it does not imply special problems. The great risk is for the
patients who are in crisis of bronchial asthma and need to be operated immediately. They
must be prepared especially in pre-operatory meaning:
- Aerosols with isoproterenol 0,4 %,
- Miofilin or eufilin 200 - 300 mg/at 4 hours,
- Alupent 20 mg per bone as bronchial-dilatator,
- Corticoids (decrease the oedema and the bronchial spasm), H.S.H.C. 100 mg i.v.,
- The patient must be intubated O.T., ventilated mechanically,
- The molar solutions will be perfused, which are expectorant,
- In premedication the narcotics are to be avoided and the atropine is used, the
promethazine and the barbiturates,
- At the awakening it is to avoid the doses of miostin which produce bronchospasm,
- The election anaesthesia for the asthmatic patients is the one with pivot halothane,
induction with O2 then N2O +O2 and halothane.
The patients who present bronchial asthma and are not in crisis will receive an anaesthesia
without risk, with the condition that the induction is mild, to receive an anti-allergic
premedication, a good analgesia and to respect the quadrangle of the anaesthesia.
2. The anaesthesia in older people
A patient is considered old after the age of 65, when it happens the ossification of the last
ossification point of the stern.
There are patients in which the chronologic age does not correspond with the biological one.
Although after the age of 65, there are a series of modification less visible but existent:
- On the conjunctive tissue. The atrophy of the parenchyma, the proliferation of the
conjunctive tissue, the tissue aging, dehydration.
- On the bone tissue the atrophy of the mandibular, the osteoporosis, the edentation,
the rigidity of the thoracic box with calcifications and the ossification of the
cartilages.
- On the breathing apparatus: pulmonary emphysema, the narrowing of the
bronchioles and the dilatation of the alveoli, the diminution of the thoracic
breathing and the amplification of the abdominal breathing, decrease of the cough
reflux, the breathing insufficiency.
- Over the cardio-vascular apparatus: decrease of the blood volume, decrease of the
haemoglobin, decrease of the haematopoiesis, decrease of the cardiac debit, the
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 global cardiac dilatation, decrease of the time of circulation, the coronarian
atherosclerosis cerebral and renal.
- On the metabolism: decrease of the metabolism.
- On the digestive tube: decrease of the amount of digestive ferments, the diminution
of the intestinal peristalsis.
- On the CNS: hypoxia tolerated difficultly, the cerebral hypoxia is installed rapidly
giving confusion states and disorientation, the administration of scopolamine
produces delirium and agitation, cerebral atrophy and the increase of the cerebro-
spinal volume.
Keeping in mind all of these modifications we must keep in mind the reduction of the doses of
anaesthetics in older people (the barbiturates, anaesthetics, relaxants). The thiopental and the
halothane are well tolerated in the anaesthesia for older people. Preferably where the surgical
approach allows the loco-regional and spinal anaesthesia is preferred. In post-operatory we
must assure a good oxygenation, a precocious mobilisation, breathing gymnastics.
3. The anaesthesia for the cardiac patients
The cardiac patients need relaxation, specific medication therapy, indicated by the cardiology
doctor (cardiologic consult will be requested). In the emergency the i.v. rapid digitalisation
will be performed associated with diuretics of fast action. The patient must be monitored
permanently in order to follow the effects of the therapy and the toxicity of the digital
(bradycardia, ventricular extrasystole, atrio-ventricular block, etc.).
An adequate sedation will be made, a mild induction, a maintenance in order to not modify
the haemodynamic, an adequate ventilation. The chronic ischemic cardiopathy is frequent
associated to the background disease for many patients who are or not taking treatment do not
need a special preparation in pre-operatory. The patient will take coronarodilatators, and the
treatment of the anxiety. The hypoxia it is to avoid and the sudden increase of the arterial
tension.
The coronarian insufficiency favours the decrease of the coronarian blood flow. In the arterial
hypotension can favour the apparition of the myocardial ischemia and of the cardiac
insufficiency.
The arrhythmia
Their cause will be treated; a good oxygenation will be assured. The flutter and the atrial
fibrillation will need digitalisation. The tachycardia or the ventricular extra-systoles need
specific treatment plus xiline administration 1%.
The bradycardia needs administration of O2 and atropine.
As an example of anaesthetics used in the G.A.: the azote protoxide is the least cardio-toxic.
The induction is made with N2O/O2 in a proportion of 3/1 with miorelaxant for I.O.T., the
maintenance is made with N2O/O2, fentanyl, miorelaxant. The sevofluran and the Izofluran
are indicated as inhalator anaesthetic substance. The hypoxia will be avoided. Concentrations
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over 30 % O2 will be assured in the alveolar air for obtaining a PaO2 normal intra and post-
anaesthesia. In post-operator a good oxygenation will be assured for the patient and a
precocious mobilisation.
4. The anaesthesia for the hepatic patients
The patients with hepatic cirrhosis, with acute hepatitis, icterus, hepatic insufficiency, present
metabolic and functional troubles which can get worse during the anaesthesia and after.
The preparatory anaesthesia needs:
- The resting in bed,
- The hipoproteic diet,
- Parenteral energetic contribution (glucoses, vitamin K),
- The correction of the metabolic misbalances,
- Hepatic trophic (arginine, aspatofort),
- The correction of the anaemia, of the haemorrhagic syndromes.
The anaesthesia must be as less toxic as possible, anaesthetics with renal and not hepatic
elimination will be used, the hypotension will be avoided, hypoxia and hipercarbia. The
majority of the anaesthetics depress the hepatic blood flow direct proportional with the depth
of the anaesthesia. The halothane is incriminated as a hepatic toxic, but this if it is repeated in
more anaesthesia. The patient with difficult hepatic lesions has sensitivity to opiates and local
anaesthetics. The plegomazin is contraindicated because it produces the colestatic icterus. In
premedication it is indicated to administer barbiturates with long action and renal elimination.
The most indicated general anaesthesia for the hepatic patient is the G.A. with metoxifluran
and neurolepanalgesia in low concentrations with tracheal intubation and controlled
respiration. In the intubation the succinylcholine is used, and in the maintenance are used
miorelaxants with renal elimination galamina type (competitive relaxant) which can decrease
the amount of analgesic (fentanyl, pentran).
In post-operatory it will be performed the hepatic encefalopaty, of the acidobasic treatments
and electrolytic, renal, infectious.
5. The anaesthesia in diabetics
In diabetes there are major metabolic troubles. These patients present disorders in the glucidic
and lipidic metabolism which produce:
- metabolic acidosis with hyperventilation,
- Na loss and extracellular water,
- de-hydration with circulatory insufficiency,
- hyperglycaemia with polyuria  thirst.
There is a series of substances and techniques which influence these metabolic troubles and
accentuates them:
- metoxifluran,
- servofluran,
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 - thiopental
- neuroleptanalgesia,
- azote protoxide,
- spinal anaesthesia,
- local anaesthesia.
At the anaesthetic consult the values of the glycaemia will be monitored, and also for the
glycosuria and acetonuria. The patient will be asked if he takes insulin, what type, the dose,
the time laps. In case that the patient does not know that he has diabetes and the diabetes is in
an incipient stage, the patient will have to consult a specialist in diabetes, he will have to
follow a specific diet and the dose of insulin before starting the surgical intervention.
Pre and post-operatory he will take hydro-solvable crystalline insulin with a duration of action
4-6 hours. The glucids that are administered to the sick will be glucose i.v. 10 % tamponed
with insulin 12 U.I/500ml. it is associated insulin 1 U.I. for 2 g glucose. The insulin will not
be administered in too big amount in order to not reach hypoglycaemia, it is indicated for the
patient to have a slight hyperglycaemia. In the emergency interventions in the absence of the
cetonuria it is administered 100 g glucose with 25 U.I. insulin. For the patient with slightly
higher values of the glycaemia in pre-operatory the insulin will not be administered. In post-
operatory se the glycaemia will be repeated depending on the values doses of insulin will be
prescribed or not.
The signs of hypoglycaemia intra-operator (i.o.) there are:
- pallor,
- transpiration,
- tachycardia,
- mydriasis,
- normoton ocular bulbs.
When a modification of the glycaemia of i.o. hypoglycaemia is suspected the i.o. glycaemia
will be repeated as many times as necessary (the glycaemia is taken when the patient is
perfused with physiologic serum).
6. The anaesthesia in obese patients
The obese or overweight patient is considered a sick person. Why? Because the obesity is
associated with breathing insufficiency, with coronaropathies, with biliary affections, etc. The
anaesthetic risk for the obese person is the cardio-pulmonary one:
- decreases the residual capacity,
- pulmonary hypertension,
- hypoxia and hypercapnea appear more frequently,
- the cardiac debit increases,
- the cardiac global insufficiency,
- the myocardial insufficiency.
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If the surgical intervention is programmed, it is postponed, for a few days for a specific diet
and breathing exercises. The technique that is preferred for these persons is the simple
peridural or with a continuous catheter. The pre-anaesthesia medication will be the regular
one but with doses for an adult with medium weight of the same height. The intubation
usually is more difficult as the mask ventilation. For the anaesthesia the inhalation techniques
are used completed with intravenous anaesthetics. Curare may be used which are needed to be
decurarised. The awakening is usually slower. In post-operatory it is possible to be necessary
the assistance of the breathing.
7. The anaesthesia in hyper-thyroidal patients
The severe forms may present:
- cardiac insufficiency,
- atrial fibrillation.
- high metabolism.
The preparatory preparation.
Sedatives are administered, anti-thyroidal substances, digital in case there are phenomena of
cardiac insufficiency.
The rest in bed and the complete diet are obligatory.

The premedication:
- strong sedation with phenobarbital 100 mg, diazepam 10 mg, petidina 50 mg i.v.,
hydergin 0,03 mg 2 - 3 hours before surgery.

Anaesthesia:
- anaesthesia with pivot halothane
- anaesthesia with pivot metoxifluran
The intubation - is necessary and it avoids the breathing obstruction and the intra-operatory
hypoxia.
Post-operatory: - semi-sitting position (Flowler)
- sedation (mialgin, romergan, diazepam)
- monitoring of the TA, AV. SaO2, temperature
- analgesia (ketonal, fortral)
8. The anaesthesia in the sick rheumatic patients
the sick people with this affection present:
- ventilation anomalies (pulmonary fibrosis, prolonged cardiopathy, etc.),
- hypoplasia of the mandible, temporo-mandibular anchilosis, cervical spondilosis,
stenotic crico-aritenoidian arthritis, laryngeal destruction, dysphagia, etc.,
- cardiac lesions,
- anaemia.
The most indicated is the pivot halothane anaesthesia.
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The major anaesthetic is chosen depending on the predominant affection. In preparatory or
post-operatory it is needed to have the cortico-therapy. It will be given attention to the
position of the patient during the surgery and post-operatory. In post-operatory is indicated:
gymnastics, sedation, analgesia.

I.7. THE REGIONAL ANAESTHESIA

The regional anaesthesia comprises anaesthesia techniques which realise the reversible block
of the reception or transmission of the nociceptive stimuli through nervous fibers and which
uses the local analgesic substances (L.A.A.).
The analgesic local substances
Usual local analgesic anaesthetic substances:
1. Cocaine:
- Has an action over the CNS: it produces the central stimulation with agitation,
excitation euphoria,
- action over the cardiovascular apparatus: bradycardia through vagal stimulation,
- action over the breathing apparatus, increase the breathing rhythm in small doses,
in great doses depresses the breathing centre,
- action over the muscular system: relaxation of the smooth muscles,
- on the mucosa it produces a topic analgesia with vasoconstriction,
- applied on the ocular globe produces mydriasis.
It is used as a surface analgesic in solution of 2 %, 4 % in the eye surgery, 10 % and 20 % in
the surgery of the nose and throat. The dose is of 1, 5 mg/kgb.
2. Procaine (Novocaine) is ether. L.A.A. 4 times more toxic than the cocaine. It is
administered i.v., i.m., s.c.
The action is installed in 2-3 minutes:
- Over the CNS: at the beginning a stimulation and then an inhibition,
- Over the cardiovascular apparatus: peripheral vasodilatation, increases the heart
rhythm,
- Over the respiratory apparatus: increases the respiratory frequency with superficial
breathing,
- Over the muscular system: neuromuscular bloc through the inhibition of the
acetylcholine and it potentiates the muscular non-depolarising relaxants
- action on the mucosa: weak anaesthetic,
Use:
- for the anaesthesia through infiltration solutions through infiltration solutions 0, 25
– 0, 50 – 1, 0 %,
- for the regional block and the epidural one solutions 1%. The dose is of 10 ml for
the block of one nerve, 30ml for the block of the brachial plexus,
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 - 15 – 50 ml for the epidural and caudal block,
- For spinal anaesthesia solution 0, 5 - 1 % in dose of 0, 5 – 2 m1.
3. Xylene (Lidocaine)
The L.A.A. efficient and cheap in solution of 0, 5 %. It has a greater toxicity than the procaine
and in solution of 2 % it has a double toxicity in comparison with the procaine. It has the
same action over the apparatuses and the tissues as the procaine. The local administration
produces vasodilatation (it is associated with a vasoconstrictor). On the mucous surfaces it has
a stronger action than the procaine. Administered i.v. produces general anaesthesia. It is used
in the local anaesthesia through infiltration, for the epidural block and caudal one, the spinal
anaesthesia and less for the G.A.
Use:
- For the anaesthesia through infiltration it is used a solution of 0,5 %
- The maximum dose being 100 ml (500 mg) when associated with the adrenaline
(slows down the absorption) and 40 ml (200 mg) without adrenaline,
- For nervous blockage: for the blockage of a single nerve it is used 10 ml xiline 1%
plus adrenaline; for the blockage of the brachial plexus it is used xiline 1 % in dose
of 15 – 30 ml,
- For the surface anaesthesia (ex. cornea) the xiline is used 2%; for the pharynx,
larynx, trachea, solution of 1,5 %, 15 – 50 ml,
- For the epidural and caudal block it is used sol. Xiline 1,5 %, 15 – 50 ml,
- For the subarahnoidian anaesthesia the solution xiline 4%, in dose of 2 – 4 ml.
4. Bupivacaine (Marcaina, Carbostesin)
It has the same properties as the L. A.A. the toxicity is lower in the bupivacaine and higher in
lidocaine 5%.
Action: 3-5 hours for solution 0. 5% adrenalinised and administered epidural.
It does not present a toxic local effect for the nerves.
Use:
- Bupivacaine solution 0, 25 - 0, 50 % for infiltrations,
- Solution 0, 5 % for spinal anaesthesia.
5. The mepivacain (Carbocaine) is an L.A.A. situated between the bupivacaine and lidocaine.
The vasodilatation is not produced at the injection this is why it can be administered also
alone.
Use:
- For nervous blocking solutions of 2 %, 3 %,
- Solutions 1 % for the contact anaesthesia and through infiltration.
6. The cincocaine: is the strongest local anaesthetic but also the most toxic one. It is used in
concentration of 1:4000.

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Use:
- For local infiltrations of solution 1:1000 is dose of 120 ml; the solution
1:2000 is dose of 240 ml,
- The maximum dose for adults is of 2 ml/kgb,
- For the block of the brachial plexus the solution 1:1000 in dose of 30ml,
- For the spinal anaesthesia is used the solution 1:200 in solution 6%
- For the epidural and caudal block is used saline solution 1:600 in dose of 15 - 50
ml,
- For the contact anaesthesia is used solution of 1:1000.
All the locale anaesthetics make a block of the ionic modifications (the elimination Na from
the cell) which accompany the transmission of the nervous impulses. They stabilise the
membrane of the nervous cell, they realise the disappearance of the action potential and the
great increase of the excitability limit. The depolarisation of the cellular membrane is
prevented.
The duration, the diffusion and the intensity of a local anaesthesia depends on:
- The total dose of administered anaesthetic,
- The concentration of the used substance,
- The total intracellular vacuum.
The pre-anaesthetic preparation of the patient
The doctor will evaluate the state of the patient after a consult before the anaesthesia, in which
is comprised the anamneses the general exam on the apparatuses and the para-clinical exams.
In function of all these data it will be established the anaesthetic technique which is the most
adequate to the respective patient.
The fear, the anxiety of the patient may lead to complications intra- and post-anaesthetic this
is why it is necessary to discuss with the patient and to give him the certainty that everything
will end well and that the patient will overcome the surgery with no pains. The psychological
profile of each patient is very important, depending on this and of the data resulted from the
clinical and para-clinical exam the preparatory and the pre-anaesthesia sedation will be
performed. For a good sedation and a pre-anaesthesia they are used a series of medicament
substances meaning: barbiturates, tranquilisers and neuroleptics.
1. Barbiturate substances:
- Phenobarbital tb.l00 mg - 1 tablet in the night before sleeping,
- Ciclobarbital tb. 200 mg. 15 mg - 1 tablet in the night before sleeping and one
tablet in the morning before the operation,
- Amobarbital tb. 100 mg - 1 tablet in the night before sleeping and one tablet in the
morning before the operation,
2. Tranquilising substances (anxiolytics)

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 - Meprobamat tb. 400 mg - 1 tablet in the night before sleeping and a tablet in the
morning before the operation,
- Hidroxizin tb. 25 mg - 1 tablet in the night before sleeping and a tablet in the
morning before the operation,
- Diazepam tb. 2 mg; vial 2 ml = 10 mg 1 tablet or vial i.m. in the night before
sleeping and a tablet in the morning before the operation,
- Oxazepam tb. 10 mg. -1 tablet tablet in the night before sleeping and a tablet in the
morning before the operation,
- Napoton tb. 5 mg; tb. 10 mg, tb. 2 mg - 1 tablet in the night before sleeping and a
tablet in the morning before the operation,
3. Neuroleptic substances (major tranquilisers). It is not administered for the patients with
spinal anaesthesia.
- Clordelazin (Largactil. Plegomazin), tb. 25 mg; vial 5 ml = 25 mg - 1 tablet in the
night before sleeping and a tablet in the morning before the operation,
- Levomepromazin (Nozinan, tb 25 mg; vial l ml = 25 mg - 1tb tablet in the night
before sleeping and a tablet in the morning before the operation,
- Haloperidol flacon ~ 10 ml = 2 mg/ml; one vial = 1 ml = 5 mg, 2 mg in the night
before sleeping,
- Droperidol 1 vial =10ml =2,5mg/ml, 5mg before the surgical intervention i.m. or
i.v.
The pre-anaesthesia
It uses the following classes of substances (analgesic, anti-histaminic, anti-cholinergic).
4. Analgetice majore:
- Morfina 1fiolă = lml = 2mg; se administrează 10 mg i.m. cu 15 minute înaintea
operaţiei,
- Hidromorfon 1fiolă = 1 ml = 2 mg; 1-4 mg i.m. cu 15 minute înaintea operaţiei,
- Mialgin (Petidina) 1fiolă = 2ml = l00mg; 50 - 100 mg i.m. cu 15 minute înaintea
operaţiei,
- Metadona 1tb. = 2,5mg; 1 fiolă = l ml = 5 mg; 2,5 sau 5 mg i.m. cu 15 minute
înaintea operaţiei,
5. Antihistaminice şi antimastocitare:
- Prometazina (Romergan) 1 mg/kgb seara
- Ketotifen 1tb = 2 mg; 2 mg per os seara şi dimineaţa,
6. Anticolinergicele:
- Atropina 0,1 mg/10 kgb cu 30 minute înaintea operaţiei,
- Scopolamina cu 30 minute înaintea operaţiei.
Sedarea bolnavului în preanestezie se poate efectua în mai multe scheme cu alte substanţe:
Sedare i.v.:
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 - Midazolam 0,05 mg/kgb + Fentanyl 2 µg/kgb,
- Ketamina 0,5 mg/kgb,
- Ketamina 15 mg + Midazolam 2 mg.
- Propofol 2 mg/kg/h,

La alcoolici:
- Haloperidol sau Droperidol 2,5 - 5 mg.
La copii:
- Sedare cu substanţe inhalatorii:
- N2O,
- Halothane ,
- Izofluran.
- Sevoflurane

I.8. TECHNIQUES OF LOCOREGIONAL ANAESTHESIA

1. The contact anaesthesia, uses as local anaesthetics; cocaine, lidocaine as solutions, spray,
gel. The anaesthetic solutions are applied on the teguments, mucosa and for the
anaesthesia of the superior aerial ways (lidocaine 2- 4 %, 2-4 ml), conjunctive, nose
cavities, vagina, ureter, perineum.
2. The anaesthesia through infiltration is injected the L.A.A. on the area of the operating
field. The technique is made injecting in the area that must be operated in layers starting
with the intradermic tissue, under the skin and gradually the other layers.
3. The intra-osseous anaesthesia – is used more on the limbs. The anaesthetic is injected in
the distal epiphysis of the anesthetised limb.
4. The regional intravenous anaesthesia – is applied also on the members and it is made
through the introduction of the anaesthetics in the venous bed, after it was emptied using
a tourniquet (the Esmarch band).
5. The blockage of peripheral nerves
- The blockage of the inter-digital nerves: the anaesthetic is introduced at the base of
the fingers,
- The blockage of the cubital (ulnar) nerve: the L.A.A. is introduced on the posterior
face of the epitrochleea
- The blockage of the radial nerve; the L.A.A. is introduced between the tendon of
the biceps and the epicondyle,
- The blockage of the median nerve; the L.A.A. is introduced between the L.A.A. is
introduced between the L.A.A. is introduced in the crease of the elbow between the
tendon of the biceps and the epitrochleea

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 - The blockage of the sciatic nerve: the L.A.A. is introduced in the point situated at 3
cm caudal perpendicular on the middle of the line traced between the iliaque
postero-superior spine and trochanter.
6. The blockage of the plexus:
- The blockage of the brachial plexus is made through 2 more usual methods:
a. The supraclavicular method Kuhlenkamf which is made through the
instillation of the L.A.A. on top of the clavicle directing the needle of the
syringe with local anaesthetic down and back towards the rib I.
b. The axillar method – the tourniquet is applied on the arm, it is accentuate
through palpation the axillar artery, peri-arterial two needles are
introduced which are positioned so that they pulsate together with the
axillary artery. It is introduced the anaesthetic on a needle then the
tourniquet is opened. This anaesthesia is used at the anaesthesia for the
hand surgery.

I.8.1. THE LEADING ANAESTHESIA

I.8.1.A. THE SPINAL ANAESTHESIA SUB-ARACHNOIDIAN
(RACHIANAESTHESIA) IN UNIQUE DOSE
It is the anaesthesia obtained through the introduction of the local anaesthesia in the sub-
arachnoidian. It continues nowadays in our country to be the technique with a wide use in the
surgical practice. The sub-arachnoidian anaesthesia intercepts the centripetal ways and the
centrifuge ones at the level of the osseous marrow.
Some anatomic data
The intervertebral bodies and the intervertebral disks delimit anteriorly the medullar channel.
The vertebral arches delimit the posterior vertebral channel. The pedicles and the vertebral
blades delimit the lateral vertebral channel. In the vertebral channel are sheltered the roots of
the rachidian nerves and the marrow of the spine wrapped by its membranes. In the thoracic
region the apophasis of the vertebras have oblique orientations, in the lumbar one direction
almost horizontal (the place of election for the rachianestesia). The orifices of the apophysis
are united through the spuraspinous ligament.

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Between two apophysis it is find the intraspinos ligament which unites two adjacent
apophysis from the tip to the root and which anterior unite with the supraspinous ligament. On
the lateral part, of the vertebral arches is found the yellow ligament.
The marrow of the spine has a length of 45 cm and it is ended at the superior edge of the
lumbar vertebra L2. Between the bone landmarks and the segments of the marrow do not exist
a correspondence. In the cervical region the apophysis of the vertebra is with a lower segment
than the medullar one which corresponds. In the thoracic superior region the difference is of 2
segments, in the inferior thoracic region of 3 segments. The marrow is wrapped by 3 layers:
duramater, arachnoid and piamater. Between the yellow ligament and the duramater is found
adipose tissue, sanguine vessels and areolar tissue. Between the duramater and arahnoid is
found the subdural space (epidural). Between the arachnoid and piamater is found the
subarachnoidian space in which the cefalorachidian circulates (C.R.L.) with a pH of 7, 4 - 7, 6
(alkaline).

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The indications of the rachi-anaesthesia:
1. Diagnostic indications:
- In order to make a difference between the pain of peripheral type and the one of
central type,
- For the diagnostic of some neurologic disease.
2. Therapeutic indications:
- Anaesthesia in arterial occlusions and through spasm or thrombosis,
- Strong pains resistant to major analgesics,
- in anuria produced by immune mechanisms,
- for the sick people with pulmonary sclera-emphysema and the sick persons with
asthma, the surgical interventions in the abdominal inferior level
- the congestive cardiac insufficiency through the decrease of the peripheral
resistance.
The contraindications of the rachi-anaesthesia
- in sanguine dyscrasia,
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 - massive bleeding,
- arterial hypotension,
- pre-terminal stages,
- the altering of the blood morphology,
- in some neurologic diseases
(poliomyelitis, degenerative diseases of the nervous system),
- abdominal affections which increase the care intra-abdominal pressure
(intestinal occlusion, pregnancy, obesity, etc.),
- arthritis and spondylitis,
- the anxious patient (with a stronger medication the technique may effectuate the
technique),
- the rejection of the patient of receiving a leading anaesthesia.

The effects of the rachi-anaesthesia

The rachi-anaesthesia is made with a local anaesthetic introduced in the C.R.L.
This induces:
1. The pre-ganglionic reversible sympathectomia. The paralysis of the sympatric pre-
ganglionic fibres induce a diffuse sympathetic answer: non segmental and it extends in
rapport with the level of the spinal puncture.
2. The sensorial paralysis after having produced the sympatectomia, are paralysed the fibres
of the painful sensibility.
The order of lack of the sensibility is:
a. painful,
b. thermic (for cold, heat),
c. tactile,
d. the sensibility foe pressure,
the order of coma back is inverted.
Modifications produced by the rachi-anaesthesia on devices
The cardio-vascular apparatus
The hemodynamic is modified through the sympathetic paralysis which provokes
vasodilatation arteriolar with the diminution of the peripheral resistance —> arterial
hypotension. The veno-dilatation is produced which becomes a reserve for the deposit and
stagnation of a great amount of blood which is taken from the systemic circuit. The relaxation
of the striate musculature appears. Depending on the position of the patient and the degree of
the venous dilatation the amount of immobilised blood reaches to 800-1000 ml. In the
abdomen interventions, in this anaesthesia the abdominal pressure decreases and with it is
accentuated more the venous torsion (stasis). It is reached to a tissue ischemia and the

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decrease of the cardiac debit. For the prevention of these negative effects of the anaesthesia
this anaesthesia is avoided in hypovolemic and dehydrated patients.
In pre-anaesthesia the atropine is administered as a vagolitic in order to prevent the
bradycardia, vasopressors (ephedrine in order to stop the peripheral vasodilatation), volemic
re-balancing with crystalloid substituents, colloidal or blood. Over the myocardium appear
modifications through the decrease of the cardiac debit, bradycardia. The coronarian flux
decreases with the installation of the arterial hypotension.
Modifications over the CNS; the cerebral flux decreases.
Modifications over the respiratory apparatus
They depend of the height of the paralysis thoracic of motion. In the rachi-anaesthesia of
medium height the inspiratory capacity decreases with 20 %, the ventilation of relaxation
practically stays unmodified. The expiratory volume of reserve decreases with 40-50%.
Modifications of the digestive tube
- the sphincters relax,
- when the traction is performed on the viscera during the surgical act the nausea is
produced, vomiting, bradycardia and hypotension,
- in hypotension which is more accentuates it is produced a decrease of the arterial
irrigation of the liver with the loss of the glycogen through hypoxia.
Metabolic modifications
- the rachi-anaesthesia has a hypo-metabolising effect, with the decrease of the
necessity of oxygen of the organism.
Modifications of the renal apparatus
- they appear only when the arterial pressure decreases under 70 mmHg, when
filtration modifications are produced,
- the peristalsis of the uterus decreases.
In rachi-anaesthesia the intensity of the anaesthesia depends on the volume of the anaesthetic
which determines the metametric extension and the concentration of the anaesthetic which
determines the quality of the anaesthesia. The local anaesthetic is eliminated through urine.
The pre-anaesthesia exam.
Is made in the same way for each anaesthesia.
The premedication and the pre-operatory preparation:
- psychological preparation,
- the breathing gymnastics,
- the consent of the patient,
- explaining the type of anaesthesia,
- the seizure of consuming solid aliments, allowing the liquid ones, and 6 hours
before the surgery all type of alimentary ingestion is prohibited,
- the clearance of the digestive tube and of the urinary bladder before the operation,

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 - the administration of a sedative (phenobarbital l00mg per bone, plus the
promethazine 50 mg),
- the sedative will be repeated in the morning, and if the patient is psychologically
labile a major analgesic may be used, such as the petidine type 50 - 100 mg i.m.,
- the administration of atropine for stopping the bradycardia and vomiting,
- the administration of an antiemetic metoclopramide type i.v. or i.m.
The preparation of the anaesthesia type
The instruments:
The standard case with the following content:
- syringe of 5 ml,
- syringe of 10 ml,
- syringe of tuberculin or insulin,
- intradermic needles for the local anaesthesia,
- needles for the aspiration of the anaesthetic substance,
- Pitkin neddles usually for the rachidian puncture have a diameter of 0, 80 mm and
length of 80 mm.
- 4 surgical fields:,
- the port-tampon tuck and compresses for the local disinfection of the teguments,
- anaesthetic substances
Anaesthetics used:
- xiline 4 – 5 % 2 ml,
- xiline 1 % for the local anaesthesia,
- procaine 8 – 10 %,
- tetracaine 1 % + glucose 10 % = solution 0,5 %,
- glucose 7,5-10% or dextran 70 (for the preparation of the hyperbaric solution),
- distilled water – for the preparation of the hypobaric solution,
- adrenaline 1:200000.
In order to prolong the action of the anaesthetic substances and in order to prevent the
anaphylactic shock in case that the testing of the local anaesthetic wasn’t performedthe
epinephrine is used (adrenaline) solution 1:200000.
For the local anaesthesia of the tegument and of the adipose tissue the xiline is used in
solution 1 % in dose of 2-5 ml.
The steps for asepsis and antisepsis will be strictly respected:
- washing hands just like the surgeon,
- the sterile clothes,
- mask, sterile gloves, (in case there is talc on the gloves he will clear it out with
alcohol, in contrary case, there is the risk of septic meningitis).
The technique of the rachi-anaesthesia
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The patient is positioned. There are two positions: sited and in lateral decubitus. The sited
position when the patient is cooperative. This position shows better the interspinous spaces.
The patient sitting of the edge of the table, with his feet on the chair or free, with his head
extended on his chest, and with the arms crossed in front (right hand of the left shoulder and
the left hand on the right shoulder), and the vertebral kyphosis spine.

The technique of the rachi-anaesthesia

Poziţia bolnavului

From the moment the patient is sited on the table, he is assisted by the medical assistant in
order to not fall from the table. If the sick person gives signs of dizziness he will be
immediately sited on dorsal position. This position is indicated for obese people, pregnant
women, intratrochanterian fractures. The position of lateral decubitus right or left consists in
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the strong flexion of the knees on the abdomen and the head on the chest; the assistant
sustains the patient by the back of the head and the popliteal spaces. The arm under creates a
straight angle with the body and the one above is stretched on the chest. The position of
ventral decubitus is rarely used. For this position the surgery table must be well fixed for the
legs and head of the patient to be left hanging.
The space for the puncture must be established in order to satisfy the demands imposed by the
surgery:
- the spinous apophysis of the cervical vertebra C 7,
- the line which unites the tip of the shoulder blades passing through the body of the
vertebras T 7
- the rib Xll-a next to the T12,
- the line which unites the iliac peaks which cross the L4 vertebra and the lumbar
space 4
Then we count from the skull towards the caudal, the intervertebral space which interests us.
The place of the rachidian puncture is chosen depending on the area of the surgical
intervention meaning:
- for the surgical interventions in the region in the perineal region in the space L3 - L4
- for the inferior abdomen region on the inferior limbs the space L1- L2,
- for the surgical interventions in the abdominal inferior and medium region the
space T12 – L1,
- for the surgical interventions in the abdominal superior region the space T9 - T10,
- for the surgical interventions in the medium thoracic region the space T5- T6.
Before performing the puncture the following manoeuvres will be performed:
- the control of the arterial tension,
- setting a flexure and the adaptation to a perfusion with crystalloid solution (usually
physiologic serum),
- preparing a pillow for the head (approx. 10°).
The spinal puncture
- the spinal needle is used19-27 G with unique use, sterile field,
- the anaesthetist doctor after washing his hands wears sterile gloves, robe and mask,
- performs the asepsis of the skin with alcohol and betadine,
- the intradermic anaesthesia is performed using 0,5 - 1 ml xilin 1% ,
- the puncture needle is introduced (19 - 27 G) perpendicular on the teguments being
held by the doctor between the medius and index and the thumb must be on the
head of the mandrel.

The layers that the needle passes through:

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 L.C.R Space
Subarachnoidian

1 2 3 4 5 6 7 8 9

1. skin
2. subcutaneous cellular tissue
3. supraspinous ligament
4. yellow ligament
5. peridural space
6. dura mater
7. subdural space
8. arachnoid
9. subarachnoidian space
10. piamater

The puncture needle will oppose 3 obstacles: supraspinous ligament, the yellow ligament and
the duramater. The yellow ligament is the easiest to be identifies through the resistance that it
opposes giving the sensation of greater and greater resistance. Piercing the duramater is
accompanied by a feeling of popping, followed by a low resistance when the needle pierces
easily. It follows the slow retraction of the mandrel from the needle, and when the needle is
inserted the C.R.L. flows. The distance that the needle follows from the tegument to the
C.R.L. is of 4 cm in the lumbar region, 7 - 8 cm for obese people and 2 cm in children.
There are situations when the lumen of the needle is blocked by the duramater or by the root
of the spinal nerve and in these conditions after the mandrel was removed the liquid does not
flow. In these situations the needle is rotated with approximately 180° without mandrel. When
the needle is in the peridural space the needle will be slowly pushed without the mandrel until
the liquid flows.
There are situations in the puncture a bony obstacles are met. In these situations the needle is
withdrawn and it is directed a few mm caudal.
Other situations which induce the prolongation of the anaesthesia technique happen when the
needle tip takes a piece of the duramater like this being obstructed the C.R.L. does not flow
through it. The needle is removed, it is checked by inserting the mandrel which was
maintained sterile and the puncture is repeated. After the puncture the C.R.L. flows freely. If
the liquid is slightly sanguineous also if after 3, 4 drops is does not get clear, the puncture is

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repeated for another level. If at this level the liquid is again of the same bloody colour, the
puncture must be aborted and another technique will be used.
The tip of the needle can be directed cranial or caudal as we wish to direct the local
anaesthetic. The local anaesthetic is introduced (in injected) after having eliminated an
amount of cephalorachidian liquid approximately equal with the amount of anaesthetic that
we introduce. The rhythm of the injection is of 0, 5-1 ml per second. By the end of the
injection the anaesthetic absorbs 0, 3 - 0, 5 ml of liquid that he injects, confirming the correct
position of the needle. The injection will be stopped if the patient accuses great local pains.
After finishing the anaesthesia technique the needle is withdrawn and the patient is sited in the
necessary position in order to obtain the wanted analgesia. The B.P. will be monitored
permanently. After the anaesthesia the installation of the spinal block will be checked by
stinging or pinching. The spinal block is installed after 5-20 minutes from the introduction of
the anaesthetic depending on the used substance. The spinal block after 20 minutes cannot
extend in height. In case that after 30 minutes the block is not installed the technique can be
repeated but only with 1/3 or ½ from the initial dose in order to not produce the accumulation
of substances. During the anaesthesia intermittent it will be administered at 10 minutes O2 or
continuously because any type of block leads to the stagnation of the blood through
vasodilatation so it produces hypoxia. Permanently the T.A., will be monitored, also the pulse,
colour of the teguments, the respiration, SaO2. Through this spinal anaesthesia the motor and
sensitive bloc is produced with a specific duration for each local anaesthetic substances used.
The installation of the spinal block depends on the used substance. Example: for lidocaine the
installation of the motor and sensitive block is produced at 5-7 minutes, for the bupivacain at
8 -10 minutes.
For 20 minutes a verbal contact will be maintained with the patient who will be able to speak
about the states that he finds himself in.
The leading anaesthesia when it is incomplete or it is necessary a consult discussion among
colleagues or the patient wishes to sleep can be completed with diazepam 10 mg i.v.,
thiopental 50-150 mg, midazolam 5-10 mg in perfusion until the sick sleeps. The completion
of the anaesthesia may be performed also with a major analgesic petidine type 50-60 mg,
fentanyl 0, 1mg. The leading subarachnoidian anaesthesia may be completed also with
general anaesthesia superficial for abolishing the toxic reflexes through the block of the vague
and phrenic nerves.

The risk of the spinal puncture

Many times an anaesthetist who has experience from thousands of cases, does not succeed to
execute the technique due to numerous reasons:
- Wrong indications (deformations of the spine, ossifications, vicious positions, non-
experimented help, etc.).

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 - Agitated patient who does not collaborate with the ones who perform the
technique.
- If the intervertebral space cannot be reached on the medial line the doctor tries to
reach with the needle on the lateral side of the spine at approximately 1, 5 - 2 cm
from the medial line, with the tip of the needle oriented towards the medial which
passes on the vertebral lamina,
- If after 3 tries he doesn’t succeed, the action is aborted and another technique is
used at the moment (usually the general anaesthesia),
- There are some persons for who the anaesthesia was well done but it is inefficient
and the surgery can’t be performed. These are refractor persons to this type of
anaesthesia. And in this case the anaesthesia will be completed with general
anaesthesia.

I.8.1.B. THE SUBARACHNOIDIAN CONTINUOUS ANAESTESIA

It is obtain through the continuous or intermittent injection on the catheter of the local
anaesthetic in the subarachnoidian space. It is used for the long lasting anaesthesia, needing
reinjection of substance.
It has the same indications as the one with unique injection. Currently is used less, due to the
fact that there are local anaesthetics with a longer duration and the majority of the
interventions from this floor are fitted in the time of the effect of the anaesthetic. It depends of
the surgical intervention but also of the surgeon who performs the intervention.
The technique
Instruments
The same as for the subarachnoidian anaesthesia in unique dose. Extra:
- 1 catheter made of plastic material marked at 14 - 15 cm at the distal end,
- 1 mandrel made of wire which is introduced in the catheter,
- 1 filter with an orifice to which is adapted the syringe in which the anaesthetic is
introduced.
Currently there are complete cases for the rachidian anaesthesia of single use.
Used anaesthetics:
- Tetracaine in dose of 40 mg = 4 ml from sol. tetracaine 1 % diluted in 6 ml sol.
glucose 10 (hypertonic solution),
- novocaine {Procaine Dose of 300 mg diluted in 10 ml distilled water (hypobaric).
The technique
The position of the patient is the same as in the simple rachianaesthesia: lateral decubitus and
siting position. The preparation of before the surgery and the pre-anaesthesia is the same as in
the simple rachianaesthesia, the same as in the local disinfection, the preparation of the doctor
who makes the puncture, the local anaesthesia.
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Differences:
- the Tuohy needle of 18 G,
Execution
The anaesthetist takes the needle in the hand so that the big finger presses the mandrel, and
the spindle to be sustained between the index and medius so that they prevent the movement
of the mandrel. The anaesthetist leaves the last two fingers on the back of the patient and the
index and medius of the free hand, delimitate the intervertebral space in which the needle is
placed. The puncture needle must be permanent to stay parallel with the spineous apophysis
and perpendicular on the transverse ones. The Touhy needle is introduced in the skin with the
orifice of the bizou in up, approximately on the distance 2 - 5 cm to the yellow ligament. The
needle is pushed passing through the peridural space, then duramater and it reaches in the
subarachnoidian space. When withdrawing the mandrel an amount of C.R.L. leaks. The
rhythm of leaking is important being a landmark of the tip of the needle. If the C.R.L. flows
slowly it means that the needle entered partially. If the C.R.L. flows rapidly, the tip of the
needle is inserted completely in the subarachnoidian space. If the orifice of the needle entered
partially we can still push about 0, 15 cm, very slowly. If we are convinced that we are in the
subarachnoidian space we reintroduce the mandrel in the needle. We orientate the orifice of
the cranial needle. The wire mandrel is withdrawn on a distance of 1, 5 cm from the end, the
mandrel of the needle is withdrawn and the plastic catheter is inserted on the Touhy needle,
then removing the complete catheter.
All along this manoeuvre the Touhy needle will be held steady with the left hand. Along the
needle is forwarded the plastic catheter until its mark reaches in front of the racord of the
needle. The catheter goes forward on the needle and it reaches in the subarachnoidian space
after it passed the tip of the needle. Then it is withdrawn slowly the Touhy needle from the
back of the patient taking with the fingers of the right hand at a distance of 1 - 2 cm from the
external end of the needle, the plastic tube, and the needle will be taken with the left hand and
pulled out slowly. In this time the right hand will not be moved in order to move the position
of the catheter from the subarahnoidian space. After the needle is out, with the left hand we
fix the catheter at the entrance in the skin. At the external end of the catheter is fixed a filter
with a record on which is injected and re-injected the anaesthesia substance. The position of
the catheter is checked and some drops of C.R.L. are released placing the catheter down. If
the C.R.L. doesn’t flow through the catheter the patient is placed in Fowler position for
increasing the pressure of the C.R.L. . If the L.C.R does not flow in this way either, we aspire
the C.R.L. with the syringe at the end of the catheter. The catheter can be withdrawn 2 -3 cm
in the last instance if the liquid is not obtained on the catheter. If on this way we did not
obtain liquid, it means that we must withdraw the catheter and we repeat the technique.
In the case of succeeding the catheter will be fixed on the back of the patient with an adhesive
band. The anaesthetic substance is inserted. The patient is sited in the established position for
the surgical intervention. The anaesthetic substance is introduced. Usually the lidocaine is
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used in 2 %. It is aspired in the syringe 5 vials of lidocaine 2% (200 mg solution) which is
introduced on the catheter and the catheter is filled: 0, 7 cm3. The first dose which is
administered is of 80 mg = 2 vials which are injected slowly in 8-10 seconds. The re-
administration of lidocaine is made before the apparition of the pain during the time destined
for the intervention. On the amount of anaesthetic that remains in the syringe the C.R.L. is
aspired until we reach at 10 ml (initial volume). This is made with the purpose of reducing the
dose of anaesthesia at the reinjection. The first dose of reinjection is of ¾ from the initial
dose. In the syringe through this dilution we have 12 mg of anaesthesia, so we inject 5 ml
from the solution in the injection. At the reinjection on the surgery table must be in
Trendelenburg position. AT the end of the surgery the catheter may be withdrawn or is left on
the spot for 12 - 24 hours in order to make the post-surgery anaesthesia. If the headache is
involved at the end of the surgery the catheter is withdrawn and checked if it did not break.
The catheter is never introduced in the subarachnoidian space for more than 5 cm.
I.8.1.C. THE PERIDURAL ANAESTHESIA (EPIDURAL) IN UNIQUE DOSE
It is the anaesthesia obtained by introducing the anaesthetic in the peridural space. This space
is found between the spinal duramater and the wall of the vertebral canal from the occipital
hole to the inferior extremity of the sacral channel. The peridural space contains celulo
adipose tissue, the roots of the spinal nerves, arteries, veins and lymphatics. In the peridural
space there is a negative pressure (from - 0, 25 to - 12 mmHg) (Jansen, 1926). The indications
of the peridural are broader than the ones of the rachianaesthesia.
A. General indications:
- discharges of the abdominal wall,
- submesocolic abdominal surgery,
- urology,
- genecology,
- orthopaedics,
- plastic surgery,
- vascular surgery.
The peridural anaesthesia is considered superior to the general anaesthesia due to the reduced
toxicity, assures good analgesia, moderated relaxation, minimum bleeding, the doses of
anaesthetics are smaller. The peridural anaesthesia has advantages over the rachianaesthesia
in the sense that is does not produce headache after the anaesthesia, assures analgesia without
motorial paralysis and analgesia after the surgery.
On the abdominal superior floor is less indicated because the accidents connect to the
technique may occur, the execution needing a higher level.
B. Particular indications
- in obstetrics:
- analgesia at birth,
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 - in the C-section,
- eclampsia,
- indications connected to the age:
- it is used seldom in children,
- in older people it doesn’t need the surgical intervention at a too high level,
- obesity,
- breathing insufficiency.
C. Therapeutic indications
- analgesia for the arteritis patients,
- analgesia for the neoplastic patients
- analgesia for the poliomyelitis patients,
- analgesia for the radicular neuralgia,
- analgesia for traumatic lesions of the inferior limbs,
- analgesia in the multiple rib fractures.
D. Diagnosis indications
- For differentiating an organic lesion from a functional one
Contraindications:
- extreme ages,
- rejection of the patient,
- scoliosis,
- spondylarthroses,
- allergies to the anaesthetic substances,
- sanguine dyscrasia, the patients with high blood pressure of the atherosclerotic ones
who do not react good to the tensional breakdown,
- affections of the spine marrow,
- neurologic disease.
In the peridural anaesthesia the diffusion of the substance is very important. For the analgesia
of a pair of rachidian nerves it is necessary 1½-2 ml of anaesthetic substance. For the older
people, atherosclerotic patients the amount of anaesthetic is reduced because the rachidian
channel is reduced. The anaesthesia is produced on the mixed rachidian nerve, after the union
of the two roots.
The preparation of the patient for the anaesthesia is made in the same way as it is for the
rahianestesia.
The pre-anaesthesia
It is identical with the one of the rachianaesthesia. We must keep in mind also the time of the
surgical intervention and the substances with hypotension effect will be avoided.

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Phenobarbital will be administered 100 mg or Diazepam 10 mg in the evening and 30 minutes
before the intervention. It is performed the test of the local anaesthetic.
Instruments
The case of rachianaestesia completed with a puncture needle thicker than the one from the
rachianaesthesia with short bisou. They are special needles (Tuohy, Crawford). The puncture
needle has a diameter of 0, 3 mm.
- venous puncture, the monitoring of the perfusion.
- Measurement of the arterial pressure.
Always the anaesthesia device will be prepared and verified for some incidents and accidents
which can interfere.
Used substances:
- lidocaine l%, 1,5%, 2%,
- mepivacaine (Carbocaina) 1,0 – 2,00%,
- bupivacaine (Marcaina) 0,1 - 0,25%,
- tetracaine (Pantocaina) 0,1 - 0,25%,
- etidocaine. (Duranest) 0,5 – 1,00%,
- petidine, Fentanyl
Technique:
Usually this technique is made more in a lumbar level or thoracic inferior, because here the
space is larger (4-5mm) and the risk of perforation of the duramater is lower.
The position of the patient is the same at in the rachianaesthesia, siting and lateral decubitus
lateral.
After performing the pre/anaesthesia the patient is sited in specific position, the case for the
peridural is prepared (of single use), then the measurement of the B.P. is performed, followed
by the assurance of a free venous way, after which:
- asepsis of the skin is made
- the sterile fields are applied,
- the local anaesthesia is made (button) intradermal and intramuscular,
- the puncture is then performed with the Tuohy needle,
- the intraspinous ligament is pierced—>supraspinous→the yellow ligament  the
peridural space (epidural)
The peridural space is identified through the Dogliotti method (loss of resistance):
- slowly, we go forward with the needle attached to the syringe with physiologic
serum or air (5-6 ml), pressing on the piston of the syringe, trying to inject the
physiologic serum or air.
- After a distance of 4 cm from the skin the yellow ligament is reached. After
reaching here no liquid or air can be injected easily finding a greater resistance,
- From here the needle is pushed other 2-3 mm permanent pressing on the piston of
the syringe,
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 - After passing the yellow ligament the resistance disappears suddenly and the liquid
or air is injected easily in the peridural space, then the syringe is disconnected from
the needle,
- It is the moment when on the needle liquid must not flow,
- In case that the liquid is flowing, we must check if there is any liquid injected by us
or C.R.L. (C.R.L. has an increasing flow rhythm when the liquid that we introduce
is decreasing), L.C:R. is warm, the liquid that we introduce is cold (the test of the
forearm drop),
- In the case when C.R.L. flows the technique will be repeated of the
rachianaesthesia is used as second option
- In case that we are in the peridural space, it is injected 5 ml from the anaesthetic
solution prepared and we wait for 5 minutes, if the rachianaestesia is not installed
the rest of the substance is injected
- It is well to not overcome 20 - 40 ml of anaesthesia with rhythm of injection of
1ml/sec.
- For old people or vitiated the dose is lowered up to 16 ml.
Doses of anaesthetic substances
- lidocaine 2 % 400-500mg adrenalized 1:200000; the duration of action 1- 2 hours,
- bupivacaine (marcaine) 0.25 % up to 200 – 225 mg adrenalized1:200000 15-24 ml;
duration of 3 - 3½ hours,
- tetracaine (pentocaine) 0,1-0,25 % in dose up to 75mg with the duration of 2 hours,
- mepivacaine (carbocaine) 1- 2 % in dose up to 500 mg; the duration of action 2
hours.
The peridural block is prolonged if in the local analgesic is added morphine 2 mg or petidine
50 mg or fentanyl 0, 05 - 0, l mg.
The analgesic injected peridural produces analgesia for the metameres ontop and under the
puncture in equal number. There is a calculation formula for the minimum of local anaesthetic
on the number of segments which have to be anesthetised:
1. depending only on the age:
- at 20 years = 1,5 ml/metamer
- at 60 years = 1ml/metamer.
2. Depending only on the height;
- at 160 cm = 14 ml,
- at l70 cm = 16ml.
The action of the peridural anaesthesia is installed between 15-25 minutes. The B.P. will be
monitored every 10 to 10 minutes until it is stable, the saturation in oxygen, the pulse, the
coloration of the teguments, the breathing. In the case, in which the hypotension appears it
will be corrected with vasopressors (ephedrine, dopamine, norartrinal). The bradycardia will

131
be corrected through atropine, the nausea and vomiting, with metoclopramide. The oxygen
will be administered continuously.

The incidents and accidents of the technique

- not finding the peridural space due to not recognising the anatomic landmarks, the
lack of experience or disorders of the spine,
- the total rachianaestesia when the amount of anaesthetic is injected in the
subarachnoidian space
(the patient will be intubated and ventilated with oxygen, vasopressors),
- insufficient anaesthesia due to various reasons: insufficient amount of local
anaesthetic local, incorrect technique. In this case it is continued with general
anaesthesia,
- the anaesthesia at an inadequate level the respective metamers do not comprise the
viscera or the surgery field
- local infections or lack of anaesthesia.
The advantages of the peridural anaesthesia
- segmental anaesthesia may be obtained,
- it does not produce post-surgery head ache,
- the duration of the anaesthesia is greater than in the rachianaesthesia,
- the haemodynamics is less influenced than in rachianaesthesia
- the patient can be mobilised faster,
- the post-surgery care does not need special activities, than the ones of routine,
- at smaller concentration of analgesics (1%) when the musculature is not
intercepted, the mobilisation is made immediately,
- the tardive nervous complications are rarer the risk of lesion being more less prone
to appear
- the analgesia after the surgery or the reduction of the dose of analgesic
The disadvantages of the peridural anaesthesia
- the anaesthesia technique is more difficult and needs a greater experience from the
anaesthetist doctor,
- the muscular relaxation is weaker than in the rachianaesthesia,
- the amount of local anaesthetic is too high, and the risk of toxicity increases and it
may influence the lesion of a blood vessel from the peridural space.
I.8.1.D. THE CONTINUOUS PERIDURAL ANAESTHESIA
It consists in introducing in the peridural space a catheter, that it is injected an analgesic local
or intermittent. The technique is used when the intervention is appreciated to last longer and
for an analgesia of long duration in different affections.
Indications
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 - spontaneous birth,
- C-section,
- for the post-surgery pain,
- for diminishing the pain in the vascular disease,
- in acute pancreatitis,
- in the dissequant aorta aneurism,
- in lombosciatic,
- for the neoplastic patients,
- in the thorax traumatisms.
The disadvantages are the same as in the peridural in smaller dose. The pre-anaesthesia is
identical with the peridural in smaller dose.
Material and instruments
The peridural case is completed by a catheter of plastic material, marked, at the end having a
filter and an opening for injection, the catheter has also a metal mandrel. There are standard
cases which have the whole kit of instruments and the necessary fields, sterile, of single use.
Substances that are used
More frequently are used substances with rapid effect, but also the local anaesthetics may be
used. The most used local anaesthetics are:
- lidocaine (xiline) l % - 2 % in dose of 5 -15 ml adrenalinisant 1:1000 or not. The
anaesthesia is installed in 10-20 minutes since the injection and it lasts 1½ - 2
hours. Reinjections are made before the apparition of the pain.
- bupivacaine 0,25 % adrenalinisant 1 :200.000. the anaesthesia is installed also at 20
- 25 minutes and it lasts 3 - 4 hours.
The technique
- the position of the patient is in lateral or siting decubitus,
- the puncture with Tuohy needle usually is made in the intervertebral L4 space
which has the greatest antero-posterior diameter 0, 6 cm, space which allows more
easily the introduction of the Tuohy needle 18 G and of the catheter (the Tuohy
needle has a diameter of 0, 3 mm),
- the doctor who washed his hands dresses the sterile clothes, and puts on the sterile
gloves
- the sterile fields are set,
- the local anaesthesia is made with xiline 1 % intradermic,
- the Tuohy needle is introduced with a mandrel through the same anaesthetic
technique as in the peridural and with unique injection,
- the identification of the peridural space is made through two methods: the loss of
resistance and the method of the negative pressure,

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 - after the needle reaches the peridural space the aspiration test is made in 4 plans,
rotating the needle each 90°,
- if by aspiration is obtained blood or C.R.L. the place is good, meaning that we
reached the peridural space and we continue the technique,
- the rebound test is retaken. Syringe of 5 ml is aspired 2 ml serum and then is
attached to the puncture needle and it is injected in the peridural space, rapidly.
When the injection is ready the piston is left free. In case that its position is in the
peridural space in the syringe 0, l - 0, 2 cm from the serum that we introduce, come
back. If the tip of the needle is in the ligament the amount of air which comes out is
of 0, 5–1 cm.
- the porition of the needle in the peridural space may be verified also through the
technique of the air tight. After reaching in the peridural space is aspired 3–4 cm air
from the peridural space in which is void, pulling the piston of the syringe left free
in downwards position (empty syringe). This aspiration may be repeated 2 - 3
times,
- then is verified the opening of the bisou and the needle is oriented in up. The
accord of the needle is held with the right hand and the catheter is introduced,
- the catheter is introduced on the Touhy needle, and after it passes by the needle’s
tip is introduced 5-6 cm in the peridural space, then the needle is retired from the
end of the catheter.
- It is checked again, the gradation on the catheter,
- At the end of the catheter is set a filter or an air tight needle to which the syringe
will be set with a content which will be injected continuously or intermittent
depending on the duration of the local and of the surgery.
Accidents
- The perforation of the duramater and the catheter may penetrate in the
subarachnoidian space. In this case the anaesthesia is continued with continuous
subarachnoidian anaesthesia or general anaesthesia,
- If on the catheter it appears blood we give up on the place of the puncture and we
chose another intervertebral space by repeating the puncture or we continue with
general anaesthesia,
In the case that there are no accidents and the space was identified, the peridural catheter was
placed in space 5-6cm. we pass to injecting the local anaesthetic on the catheter. We inject
test doses of 2 ml of solution of local anaesthetic after which we detach the syringe and the tip
is obstructed from the catheter. We wait for 5 minutes in order to be sure that the
rachianaesthesia is not installed while we monitor the patient through psychological
monitoring, B.P. , pulse, movements of the inferior arms. In case that the rachianaesthesia is
installed we leave the catheter on the spot and we re-inject if necessary respecting the
anaesthesia technique for the continuous rachidian anaesthesia. In the case that the continuous
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peridural anaesthesia succeeded, after we injected the total amount of local anaesthetic, we set
the catheter in a part of the spinous processes with a leucoplast tape after we put a sterile
compress on the skin at the entrance of the catheter.
The catheter is brought in a position which allows the re-injections of anaesthetic (usually
supraclavicularly). Because the patient may move his limbs during the surgery it is necessary
to be mobilised through the special belts from the surgery table.
The rhythm of administering the anaesthetic is of 1 ml to 5 seconds, and the doses vary from 5
- 15 ml. in this calculation we do not take in mind the test doses.
Some examples which show the level of the peridural puncture, the position of the catether
and the necessary dose of anaesthetic:
- For the superior abdomen: the puncture is made at the L2 position, the position of
the catheter L1, anaesthetic dose 12-16 ml, Trendelemburg position 10°,
- Fir the inferior abdomen: the puncture is made at the level L2, the position of the
catheter L1-L2 anaesthetic doses 8-12-16 ml, horizontal position,
- For the inferior limbs: the puncture is made at the level L4, the position of the
catether L3 the dose of the anaesthetic 10-14 ml, Fowler position 10°,
- For the vaginal birth: the puncture is made at level L3, the position of the catheter
L2, doses of anaesthetic 5-7 ml, horizontal position.
The re-injections of anaesthetic will be quantitatively equal with the first dose. They are made
before the patient accuses pains depending on the duration of the anaesthetic. After finishing
the surgery the catheter may be removed, but it may also remain in place 1-3 days for the
post-surgery analgesia.
In case that the catheter was installed for a long duration anaesthesia it can be kept for a
longer while (from my experience the catheter was kept for 1, 8 years), since the first signs of
meningeal irritation, headache, local irritation the catheter will be removed. When removing
the catheter it is measured in order to be sure that a part of it did not remain in the peridural
space. Some clinicians perform even a bacteriologic exam intern of the catheter in order to be
sure that it did not induce an infection.
Currently there are radiopaque catheters which may be visualised radiologic. In this case the
placement in the wanted space is easier (these catheters have a higher price) because they be
visualised.
Complications.
- The penetration in a blood vessel and its lesions,
- The twist of the catheter around the axel and the obstruction of the lumen.
- The exit through a intervertebral orifice,
- The inefficacity after a longer period when the organism was used to the respective
anaesthetic. In this case the dose of anaesthetic is increased or the anaesthetic is
changed,
- The infection of the catheter during the re-injections,
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 - The breakage of the catheter in longer while if the instrument is older,
- The modification of its position through a superficial fixation
.

I.8.1.E. THE CAUDAL ANAESTHESIA IN UNIQUE DOSE

Is made through the administration of a single dose of anaesthetic in the peridural space,
through the sacral hiatus and the caudal channel. Made in the year 1901 by Sicard and
Cathelin. This anaesthesia with local anaesthetic takes the lumbosacral and coccidian plexus.
Indications
- obstetrical: uterine col dystocia, eclampsia,
- in the eye surgery,
- in the surgery of the rectum,
- in the prostate surgery and of the urinary bladder
- vascular and peripheral disease as treatment method by clearing the spasm,
- reducing the pain in the diabetic neuropathies
- in the decrease of the essential arterial pressure (increases the inferior vascular
bed),
- in the hypertension of renal origin when other therapeutic means were depleted,
- in the reflex anuria (action of relaxation),
- in the treatment of the ureters of the calculosis assuring the clearance of the pain
and the relaxation of the musculature of the ureteral wall allowing even the
elimination of the lime,
- assures a differential diagnostic between the vascular affections of the inferior
limbs of functional nature through spasm and organic lesions that cannot influence
them
Technique
The pre-anaesthesia exam, the preparation of the patient, the necessary materials are the same
as in the rachianaesthesia.
The patient is sited in ventral position with a pillow under the iliaque bones in order to lift the
sacral bone in order to give a 35° inclination with the plan of the surgery table. The thighs of
the patient will be distanced with the heels also distanced towards the exterior. For the
pregnant woman for the analgesia at birth the position will be genupectoral in order to not
deform the plans, the ventral position is difficult due to the volume of the pregnancy. The
sacral horns are palpated which are marked each with a cross. In case that they cannot be
found the tip of the coccyx is palpated (the sacred bone is found at a distance of
approximately 5 cm from the tip of the coccyx). Then the iliaque postero-superior spines are
palpated, by them being able to find the second sacral orifice, it being at 15 cm medial and
caudal from the spine.

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It is drawn a circle of the two orifices and they are united through a straight line. The puncture
needle will have a length of 7-9 cm. the teguments are disinfected, the sterile fields are set and
then the local anaesthesia is made in layers. The puncture needle is introduced, long of 7, 5
cm with a mandrel, its bar to be sustained between the thumb and medius and the index to
press on the edge of the mandrel. The bisou of the needle must be oriented cranial with an
angle of 70-80° of skin and we push until the tip touches the sacrum. The needle is introduced
in the caudal channel but it must not pass from the second sacral orificethe needle is
introduced in the caudal channel but it must not pass the second sacral orifice. The needle is
retired a little and its angle is reduced then it is pushed again until it meets the sacrococcygian
membrane which is found at 0, 5-3, 5 cm from the skin. The needle is twisted so that the bisou
will be oriented posterior. Then the needle is lined at an angle of 20° from the surface of the
skin in men and at 35-40° for women. By pushing the sacrococcigian ligament the needle
reaches in the caudal channel on a distance of 4 cm. Then the mandrel is withdrawn and we
set it on the skin along the sacrum in order to control the distance that the needle made. The
orifice of the needle must overcome the line that was traced between the two sacral orifices.
The syringe is set for the puncture needle and it is aspired. If in the syringe we have the
C.R.L. we practice the rahianaestesia. If on the syringe we have blood, the needle is pushed
more with about ½ cm in order to get out from the vessel. The mansrel is introduced in order
to not coagulate the blood on the vessel. If we still have blood on the needle we use another
type of anaesthesia. If the needle is free and nothing leaks on it we inject 5 cm 3 of air and we
monitor if the tissues become turgescent, and at palpation we have crepitation. The patient
will feel a different sensation in the inferior limbs. It is introduced a test dose of 3-5 ml of
local anaesthetic, which is injected rapidly. After it was injected the pressure is not made on
the piston of the syringe. If the needle is found in the caudal channel in the syringe it cranks 0,
5 - l ml liquid. In this case the needle is retracted and it is reintroduced. We wait for 5
minutes, while we monitor the AT and AV. If after 5 minutes we find out that there is an
area of analgesics (abdomen, inferior limbs, perineum) it means that the test dose made
asubarachnoidian anaesthesia and in this way the caudal block will be interrupted. In the case
of success we administer 15-30 ml local anaesthesia. We will monitor as for the other
techniques of leading the vital parameters, the dialog with the patient will be maintained. The
block may be repeated at intervals of 45 minutes, in case that the surgery is prolonged.
As in any other anaesthesia technique there are also complications:
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 - a total rachianaesthesia,
- neurologic complications,
- hipotension,
- allergic reactions,
- urinary retention,
- infections,
- high rahianaestesia.
Contraindications
- difficulty of technique for the obese persons,
- disease of the central nervous system
(marrow tumours, CNS syphilis, epilepsy, hysteria),
- presence of the local infections,
- birth which needs internal version,
- placenta praevia
I.8.1.F. THE CAUDAL CONTINUOUS ANAESTHESIA
It is made by the continuous or intermittent injecting of anaesthetic substances on the catheter
introduced in the caudal channel through the sacral hiatus. It is usually used at birth. This
anaesthesia doesn’t affect the labour. It is made when we suppose that it will be a longer
labour. The pre-anaesthetic exam and the pre-surgical preparation is the same as in any other
leading anaesthesia. The necessary materials are the same as in the peridural continuous. In
plus we add a needle of spinal puncture of 7,5 cm, mandrened, a catheter made out of plastic
presenting a wire mandrel, the catheter being marked at a distance of 20 cm from the end
where it is introduced in the caudal channel, flexible needles of 5; 6,5; 7,5 cm with mandrel.
Technique
After the infiltration in the subcutaneous tissue around and on top of the sacral hiatus together
with the periost from around it through the dermic papula it is introduced a tutor needle which
will form the trajectory for the puncture needle.
There are two methods of introducing the catheter. One consists in introducing the catheter on
the flexible needle measure 19 G, and the other usual method for setting the catheter with the
help of the spinal needle of 7,5 cm. the puncture is usual for both of the methods. No matter
the needle. It must present a mandrel. The needle is taken in hand so that the bar will be
between the thumb and medius, and the index must press on the head of the madrel. The
introduction of the needle starts at the skin with a needle of 70° with the horizontal plan and
with the bosou in up, we push until the tip touches the sacrum. Then the needle is retracted,
the angle is reduced and then it is pushed again up to the sacrococcigian membrane. The
needle is twisted so that the bisou reaches to be oriented posterior then it is lined posterior
with an angle of 20° with the surface of the skin for men and an angle of 30 - 40° for women.

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After it penetrated the sacrococigian ligament the needle reaches in the caudal channel and it
is pushed here approximately 4 cm. the mandrel is removed, is measured at the skin in order
to control the distance of the needle in order to not overcome the line marked between the two
sacral openings. The syringe is attached to the needle of puncture and it is aspired 2 or 3
times. If there is C.R.L. we give up to this technique and we make subarachnoidian
anaesthesia. Is performed also the second test using 3 - 5 cm3 serum. If the crepitations appear
the needle is removed and the puncture is repeated. If the puncture was performed correctly
and the spinal needle is in the caudal channel on the lumen of the needle is introduced the
catheter with mandrel on a length of 10-15 cm reaching up to L5. Then it is removed carefully
along the catheter. The external end of the needle is taken with the left hand and is pulled little
by little, and with the right hand we hold the catheter at a distance of 2 cm from the needle.
When the needle is out completely it is removed carefully from the catheter, the catheter is
fixed with the left hand. Then the catheter is pulled. The catheter is fixed on the skin with a
leucoplast after having applied a sterile compress. At the end of the catheter is fixed a filter
for injecting the local anaesthetic substance that we want. Then on the catheter is injected
local anaesthetic 3 – 5 ml, in 5-10 minutes. We wait for 5 minutes. If in all this time nothing
happens we verify the sensitivities for more levels, in order to see at which level the
anaesthesia reached. If the anaesthesia was extended up to a thoracic level it means that the
duramater was punctured and the surgery may start with this type of anaesthesia without re-
injecting the substance and we go on if it is necessary with general anaesthesia. In this case
the anaesthesia is accompanied also by modification of the hemodynamic constants
(hypotension).
If the catheter was well placed after 5 minutes is injected 12 – 20 ml of local anaesthetic
depending on the height of the patient. The doses of re-injection are usually smaller than the
ones of injecting and they are repeated depending on the needs and duration of the used
anaesthetics. The anaesthesia is installed after 20 minutes from the injection.

Complications
The complications of this technique are the same as in any other leading anaesthesia, but there
are also some particularities:
- the introduction of the needle anteriorly from the sacral bone, when the rectum may
get perforated, or for the pregnant the head of the foetus
(the rectal touch will be performed after introducing the needle),
- the gaseous emboli, when a vessel was perforated and it appears usually at the
retraction of the mandrel.

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I.8.1.G. THE COMBINED ANAESTHESIA: THE RACHIANAESTHESIA AND THE
PERIDURAL WITH A SINGLE SPINAL NEEDLE
It is a technique made for the first time at the Arad County Hospital, from the year 1998
(Olariu T.). It consists in making the two anaesthesia techniques together, with a single spinal
needle.
The pre-anaesthesia exam and the pre-operatory preparation is made as for the other leading
anaesthesia. It is practiced more in the patients who have multiple vices, the asthmatic, with
cardiac and breathing insufficiency, etc.
Necessary materials
- materials for local disinfection,
- a syringe of 10 ml,
- a syringe of 20 ml,
- a syringe of 5 ml for the local anaesthesia.
- Needle for the local infiltration
- spinal needle of 19 G, 20 G
- sterile fields.
Technique
After the local disinfection, we pass on to the skin and tissue infiltration with lidocaine
(xiline) 1 %. The spinal needle of 19 G with mandrel in the right hand and we penetrate
crossing all the layers as in the subarachnoidian anaesthesia. The moment we reached the
subarachnoidian space we remove the mandrel and we let 1-1, 5 ml of C.R.L. to flow. We put
the syringe to the needle of 10 ml and we inject 2-4 ml of local anaesthetic. In this moment
we made the subarachnoidian anaesthesia. After the syringe was emptied of anaesthetic we
withdraw the spinal needle which remains attached to the syringe (the syringe having the
piston lowered, empty). During the withdrawal of the needle we feel a resistance which is
caused by the yellow ligament. We withdraw slowly until the resistance of the needle
disappears. In this time the piston of the syringe will be pulled in up. The moment when the
tip of the needle reached in the peridural space a void is created and at the withdrawal of the
piston it will be pulled down by the void. The manoeuvre is repeated 2 -3 times and if the
void still remains (the void will aspire by itself the piston of the syringe downwards), we have
the certainty that we are in the peridural space. We attach the 20 ml syringe with anaesthetic
solution of local anaesthetic of 10 - 14 ml depending on the weight and height of the patient
(1-1, 2 ml) are injected in the peridural space with a speed of 1 ml/sec. doses of local
anaesthetic at the injection will be 2/3 or 1/2 of the dose of the obtained regular peridural
anaesthesia.
For the older people and for the sick people with multiple vices the dose of local anaesthetic
will be reduced to 1/2.

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The position of the patient will be siting or in lateral decubitus. After injecting the anaesthetic
solution the patient is held 1 minute in the position in which the anaesthesia was performed,
then he is sited in the position for the surgery. Rapidly we pass on to the correction of the
haemodynamic parameters. In case of hemodynamic modifications we interfere with
vasopressors (ephedrine), anticholinergic (atropine), crystalloid solutions in perfusion
(physiologic serum 9 ‰, glucose serum 5 %,), antiemetic (metoclopramide). If the patient is
anxious the sedative is added (midazolam), oxygen-therapy. We will monitor permanently
until the stabilisation of the hemodynamic parameters, AT, pulse, respiration, coloration of
the extremities, the saturation in oxygen, from now and then a dialog will be kept with the
patient asking about the general state. This type of anaesthesia installs rapidly in 5 - 8
minutes. The level of the puncture is L2 - L3, reaching to maximum up to the level T12.
On this type of spinal block we can perform surgical interventions on the superior and inferior
abdomen, perineum and inferior limbs.
Complications
These are the same for both anaesthetic techniques, meaning the complications of the
anaesthesia subarachnoidian anaesthesia and the ones of the epidural. The breathing
depression in the first 5-10 minutes is more frequent than in making one of them separately
and this is why it needs in some cases of vicious patients ventilation on the mask, after which
the spontaneous breathing is retaken efficiently.
Complications:
- the high rachianaestesia, the patient will be intubated oro-tracheal immediately and
ventilated until he eliminates the anaesthetic
- the total rachianaestesia
- the failure of the anaesthetic technique (the anaesthetic technique changes)
- the respiratory insufficiency (symptomatic treatment, oxygen-therapy),
- cardiac arrhythmias (anti-arrhythmias treatment, oxygeno-therapy)
- insufficient analgesia: the analgesia will be supplemented with analgesic
administered parenteral, or the continuation of the operation with general
anaesthesia,
- the local infections when the conditions of local asepsis were not respected,
- meningeal reactions, headaches,
- dyspeptic – antiemetic syndrome,
Advantages
- the anaesthesia installs rapidly,
- good analgesia and relaxation,
- for an experimented anaesthetist the technique happens rapidly,
- uses a single puncture needle
- does not need special materials.
- the two anaesthesia power themselves and they have a longer duration,
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 - the analgesia continues also after the surgery, some sick people do not need
analgesia, and for some are sufficient 1-2 minor analgesics in order to cald the pain
down.
- the anaesthesia doses are lowered
Disadvantages
- the patient stays a few hours without moving,
- the technique need a good experience for the two anaesthesia techniques from the
anaesthetist doctor,
- a lot of doctors refuse this technique accusing the technique difficulty
- a technique administered incorrectly may give neurologic complications.

I.9. THE ANAESTHESIA IN THE SURGICAL EMERGENCIES

We are referring to the anaesthesia which is administered for the sick people who are
traumatised or multi traumatised for who there is no time of preparing before the surgery, but
we need emergency surgical measures, otherwise the life may be geopartised. The sick is not
investigated, and the risk of the anaesthesia is high. For this type of patients we need to keep
in mind a series of risks:
- the patient may be in traumatic shock, hypovolemic shock (dehydrated),
haemorrhagic shock, etc.
- the patient may have a full stomach (risk of broncho-pulmonary aspiration),
- the patient does not have the routine investigations (biologic assessments,
imagistics, etc).

However, these patients must be operated and must have an expert anaesthesia that the
anaesthetist who knows many methods of anaesthesia and the risk that a patient presents must
take quick decision to choose the most appropriate anaesthesia. There is a preoperative
preparation minimal, brief the anaesthesiologist is required to take at least some data from the
patient or caregiver, data with evaluating the state in which the patient is, which helps him to
make a decision as correct as possible for the patient. In this respect the doctor will make the
following evaluation:
- general data about the patient,
- the general state in which the patient was,
- the nutrition state,
- the hydration state,
- the evaluation of the cardio-vascular device
- the evaluation of the respiratory apparatus,
- the evaluation of the renal apparatus,
- the evaluation of the CNS (conscious or unconscious)
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 - the mobility of the temporo-mandibular articulation,
- the mobility of the spine,
- if the patient presented some antecedents in disease, treatments, if he consumed
hypotensive drugs (doses, if possible, cortisone, tonicardiacs, sedatives,
tranquilisers, IMAO which might interfere with one of the anaesthesia techniques,
- the consumption of alcohol, tobacco
- known allergies,
- the lesions will be well studied, if they influenced the vital organs.
All this will be recorded in the clinical record. It will notify the family that presents
anaesthetic risk patients explaining the terms possible elevated risk for not impatient family or
carers.
Emergency steps before the surgery
- the catheterisation of a vein and eventually the hydroelectrolytic recovery, with the
reconstruction of the volemic mass (eventually 2 veins, catheter, jugular internal
vein, etc),
- the urgent effectuation of a biologic review,
- sanguine group and eventually blood transfusion,
- evacuation of the full stomach in case of ingestion of aliments under 4 hours by
setting a gastric probe, gastric wash if it is imposed,
- warming the patient if it is necessary in case of hypothermic shock
- the compensation as much as possible of the insufficiencies of the vital organs,
- in case the patient is in imminence of cardiac harass the resuscitation measures are
applied for the cardio-respiratory resuscitation,
- establishing the dominant priority which can worsen the state of the patient and the
reanimation in first emergency (ex. cardiac tamponad),
- the cardio-respiratory equilibration through urgent measures of resuscitation: the
control of the abundant bleeding, the discharge of the breathing ways, artificial
respiration, garotabil haemostasis or the non-garotabil through rapid surgical
intervention of stopping the bleeding, the rebuilt of the sanguine mass and oxygen
administration,
- the monitoring of the AT, the decrease means the start of the cardio-vascular de-
compensation, the pulse monitoring, of the diuresis,
- the regain of the blood flow of the capillary blood with a liquid solution which is
handy,
- the rebuilt of the electrolytic disequilibrium depending on the sanguine ionogram,
- the prevention of the acidosis or installed alkalosis,
- the steps which were started before the surgery will be continued after the surgery
depending on the necessities which are imposed.

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Pre-anaesthesia
In the severe multi-traumatisms, which need emergency surgical intervention the pre-
anaesthesia is minimum or is:
- atropine 0, 5 - 0, 7 mg,
- petidine 10 – 20 mg through exploration it can be repeated,
- fentanyl 0, 05 - 0, l mg,
- Droperidol 2, 5 – 5 mg (attention to arterial hypotension)
- Midazolam 5 mg.
Anaesthesia techniques
1. In intervention of small surgeries the local anaesthesia or the loco-regional one is chosen.
2. In poly-traumatisms which need surgical investigations which are more laborious the
general anaesthesia is preferred, which allows the control of the respiration with the
correction of the hypoxia from before the surgery, which assures surgical comfort with
adequate muscular relaxation, it is manageable, assures maximum security for the patient.
Attention to the hypovolemic patient for who is supplemented the oxygen dose and are
reduced to minimum dose the anaesthesia substances.
3. For the patients with haemorrhagic shock with the breakdown of the tension when it is
necessary to make a rapid surgery, in induction the oxygen is used, succinylcholine and
isogroup blood, izoRh.
The anaesthesia with Ketamine-succinylcholine-pavulon with I.O.T. and assisted ventilation
is the successful anaesthesia for the poly-traumatised patients who arrived in emergency.
The scheme of administration of the anaesthesia for the poly-traumatised patient with arterial
hypotension:
- Ketamine 0, 5-2 mg/kgborp i.v.,
- I.O.T.
- ventilation N2O + O2,
- maintenance pavulon 0, 5 mg/10 kg + Ketalar in small and repeated doses (0, 2-0,
5 mg/kgbody)
It is used a lot the scheme "Passe partout" (Slieglitz), it is a variant, of the neuroleptanalgesia:
- oxygen on the mask,
- 0, 1 mg fentanyl in 3 doses ± droperiol 2 mg in an interval of 5 minutes:
- Local anaesthesia of the glottis with xiline spray,
- 0, l mg fentanyl,
- 4 mg pavulon,
- I.O.T.
- ventilation with N2O+O2.

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The keeping of the anaesthesia is made in repeated doses of fentanyl, pavulon. The poly-
trauma patient is compensated and altered volemic, the type of anaesthesia can be neurolep-
analgesia with volatile pivot (narcotan, sevofluoran).
4. In the case of the cranial trauma associated with thoracic and abdominal trauma we are
respecting the priority of solving the respiratory function and haemostasis then, by simple
means: pleurotomia in haemopneuraotorax simple or with valve, reducing the viscera
herniate into the chest, diaphragm suturing, suction or drainage thorax, mechanical
ventilation with or without PEEP in coastal vouchers. The respiratory function is
particularly important, not solving it leads to the fact that any type of anaesthesia is
compromised.
5. In the abdominal and cranial-cerebral lesions, the assurance of the vital functions:
respiratory and cardio-circulatory is the main objective. When it is associated also with
the trauma of the vertebral spine, we need a great caution when we transport the patient
and we sit him on the surgery table. Great attention to the hyperextension of the head
when the I.O.T. is made in order to not create medullar lesions when they do not exist.
6. In the thoracic trauma, the nasal-pharyngeal trauma, laryngeal, tracheal it is assured the
liberty of the superior aerial ways through I.O.T. or tracheostomy, pleural aspirate
draining, with or without mechanical ventilation. When the I.O.T. is difficult or
impossible to perform we use the tracheostomy or cricotirotomy after a precursory
oxygenation with a thick needle introduced through the cricotiroidian membrane
(transtraheal oxygenation). The nasal-tracheal intubation is performed which may be
performed on a sober or sedated patient with 0, l mg/kgb diazepam i.v. initially is
performed the anaesthesia of the nasal mucosa with xiline 4 % combined with a
vasoconstrictor of the nasal and oropharyngeal mucosa. At the oral pharyngeal intubation
which is made in emergencies it is recommended protection with galamine 20 mg or
pavulon 1 mg, which avoids the fasciculations, which take to the increase of the intra-
gastric pressure and they favour the regurgitation on atracurium 0, 5 mg/kgb. Also in
order to prevent the gastric regurgitation (through bronchopulmonary aspiration, the
Mendelson syndrome is produces) also the Sellick manoeuvre is produced, which consists
in compression on the cricoid for the obstruction of the oesophagus at the level C6. In the
fractures of the cervical spine the oral tracheal intubation is made with the help of the
endo-tracheal fibroscope.
7. The cardiac traumatic tamponade needs rapid evacuator puncture. In the cranial
traumatisms with cerebral oedema the anaesthesia may create cerebral oedema if the
patient is not ventilated sufficiently, determining hypercapnia with cerebral
vasodilatation. The increase of the intracranial pressure is also produced also through the
fasciculation after succinylcholine, and the cough as a sign of intolerance to the intubation
probe usually leads to the increase of the intracranial pressure. The intracranial pressure

145
 may also increase through hyper-hydration or through the incorrect positioning of the
head of the patient when the vein torsion is stopped.
8. The acute abdomen, the peritonitis, the pancreatitis, the intestinal occlusion may start in
the induction of the anaesthesia aspiration pneumonia in which 50 % of the cases are
deadly. Depending on the aspired content there are two forms of respiratory insufficiency:
obstructive acute with cyanosis and cardiac harass or breathing insufficiency of ARDS
type. The prevention of the aspiration is made:
- The clearance of the stomach through a gastric probe,
- The administration of anti H2 = axid,
- The administration of antiemetics: metoclopramide,
- Protection with pavulon 0,01 mg/kgbody in induction, or 1 mg,
- Pre-oxygenation,
- The lift of the brainstem on the surgery table with the larynx upper with 40 cm on
top of the cardia,
- Rapid induction (crash induction),
- The respiration on the mask is not assisted,
- Compression on the cricoid, the Sellick manoeuvre).
In case that the aspiration was produced immediately safety measurements are taken:
- Tracheal aspration,
- Oxygeno-therapy with oxygen 100%,
- The lain of the head and the positioning to the left,
- The administration of glucocorticoids (metilprednisolon 1 g.then 0, 5 g 2-3 days),
- Bronchial lavage,
- Antibiotherapy (after the antibiogram),
- The correction of the metabolic acidosis,
- The deletion of the bronchospasm with miofilin 240 mg i.v. diluted in 250 ml
glucose 5 %.
9. The coma or the encephalitis with respiratory insufficiency need oro-tracheal intubation
in order to separate the two ways: respiratory from the digestive one in order to prevent
the hypoxia.
10. The patients in haemorrhagic shock with blood losses over 50 % will receive an
anaesthesia in small doses until the bleeding is stopped and the volemic mass is rebuilt.
For these patients the induction is more difficult and it is usually performed with:
- Ketamina 1, 2 mg/kg body i.v.
- Propofol l - l, 2 mg/kg body i.v. in continuous perfusion.
Restoring the volemic mass is done with crystalloid saline solutions (Ringer lactate solution,
physiologic serum) on one of the veins and on another vein is administered whole blood
izogrup izoRh or its components with colloids or plasma expanders (hydroxyethyl starch -

146
HAES). During this time it will monitor the BP, pulse, PVC, PCWP, capnogram,
pulseoximetry, temperature ASTRUP parameters, tegument colour, diuresis, urinary flow.
The major problem of anesthesia is the digestive bleeding from the cirrhosis with portal
hypertension, which if history had jaundice or ascites and oedema in the legs, atrophic liver,
such cases are contraindications for the surgery. It is noted that the surgical emergencies
usually administered general anaesthesia, anaesthesia which creates a certain hemodynamic
stability, proper breathing, proper medication for a sufficient time to conduct the surgery and
surgical comfort. Spinal anaesthesia is contraindicated.
11. The anaesthesia in burned patient also poses problems because this patient lacks of
volemic mass - and plasma mass, loses heat easily and quickly, have great pain, difficult
venous access, difficult monitoring. In these patients, the administration of
succinylcholine is made with caution, because it mobilizes the K from the cell that can
lead to heart rhythm disorders. It is better to avoid as possible the administration of
succinylcholine and replacing it with pavulon.
We conclude that the general anaesthesia well run is the most appropriate surgical
emergencies if the anaesthetist is not experienced, not superficial carried out the
examination correctly appliances, analyses all the injuries, sets the priorities right where it
should intervene in chronological order
The post-surgical period
It is as important as the anaesthetic period. In this time the organ insufficiencies may be
accentuated. This is why after the surgery we will make:
- The prophylaxis and the treatment for the respiratory insufficiencies, cardiac, renal,
- The hydro-electrolytic re-balancing, acido-basic,
- Energetic balance,
- The prosthesis in post-operator of the ventilation for exhausted patients, infected or
in shock,
- The correct treatment of the fond disease and also the prophylaxis of the breathing
infections and of the general infections,
- Periodical biologic balance.

I.10. THE ANAESTHESIA AND THE ANALGESIA IN OBSTETRICS

The guides used for anaesthesia and analgesia have as a purpose the increase of the qualities
of anaesthetic cares for the obstetrical patients, in order to enhance the certainty of the
patients by reducing the incidence and severity of the complications connected to the
anaesthesia and of increasing the satisfaction of the patients.
These guides have as focus the anaesthetic activities and analgesic made during the labour,
vaginal deliverance, C-section, the extraction of the placenta retained and the tube connection
postpartum. (95)

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We could not say that in obstetrics there is a certain anaesthetic technique. It is certain that the
anaesthesia in obstetrics must respect some rules:
- have less toxicity on the foetus,
- not influence the labour,
- to not be a mixture or more substances,
- to be compatible with the oxytocic.
It is assumed that all the anaesthetic cross the placenta barrier, but their effect is not equal on
the mother and foetus.
Premedication
It is administered only 1-2 hours before the birth and in small doses. From the antalgics we
can administer:
- petidine 50-70 mg i.m. which may be repeated at 3-4 hours,
- fentanyl 0,05 mg i.m.,
- romergan 25-50 mg i.m.,
- atropine 0, 5-0, 7 mg i.m.20 minutes before the C-section.
The psychological preparation of the parturition is valuable for both mother and foetus.
It follows the gastric emptying in order to prevent vomiting.
This training is made in all the deliverances regardless of the anaesthetic technique, for both
the general anaesthesia and the leading anaesthesia.

1. In case of general anaesthesia:

Induction:
- thiopental 4-5 mg/kgbody,
- oxygen on the mask,
- succinylcholine l-l,5 mg/kgbody,
- oxygen on the mask: it is ventilated 2-3 minutes carefully in order to not introduce
air in the stomach,
- I.O.T. the probe with balloon.
The maintenance:
- The continuous relaxation until the discharge of the foetus with small doses of
succinylcholine which is re-injected 40-50 mg (half of the initial dose),
- After the discharge of the foetus in the usual doses obtained major analgesic,
petidine or fentanyl on inhalator pivot: halothane e or metoxiflurane. The relaxation
is made with competitive myorelaxant (pavulon) in doses as in any other
anaesthesia. The doses are reduced in case that the woman loses too much blood.
The awakening:
- Miostine is administered when the woman begins to breathe, the closure of the
inhalator gas vaporiser, oxygen.

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In the last time the analgesia at birth is used more and more in order to create a comfort for
the mother and in order to not be afraid anymore.
At the physiological birth there are 3 types of pain:
- The pain that appears at the contraction of the uterus with origin T11-T12,
- Expulsion pain through cervical dilatation with origin S2, S3, S4,
- Pain when the foetus descends, transmitted through the nerves with origin S1, S3, S4
The innervation of the uterus has an origin in the T6. Keeping in mind this topography of the
pain the regional analgesia is indicated in order to reduce the pain at birth.
2. The most used anaesthesia is peridural simple and continuous with catheter. For the
pregnant women the epidural space is reduced due to increased intra-abdominal pressure
and congestion of space vessels and therefore the anaesthetic dose must be reduced. The
anaesthesia technique of the peridural was described.
Used substances:
- Xiline 2 %, (lidocaine)
- Bupivacaine 0, 5 %.
- Naropine
The initial dose is of 12-15 ml, for the continuous one it may be repeated ½ of the dose. The
analgesic effect appears after 15 minutes and it lasts 2-2 1/2 hours for xiline and 3 - 4 hours
for bupivacaine.
The advantages of this anaesthesia are:
- very good analgesia,
- ameliorates the uterine activity,
- increases the blood flow,
- in eclampsia the BP decreases,
- for obese persons and with respiratory insufficiency the expulsion muscular labour
decreases,
- in case the surgery is needed the patient has anaesthesia,
- the woman may communicate with the persons around and also collaborate she can
see the foetus.
Disadvantages:
- the risk of the arterial hypotension,
- it is not applied for placenta praevia,
- it is not applied when a rushed birth takes place,
- it is recommended to be done only by the anaesthetist doctors,
- it is not performed on anaemic pregnant women.
3. The anaesthesia for the pudental nerves is made trans-vaginal usually for the premature
birth, technique performed seldom.

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4. Analgesia by inhalation. More and more patients request the analgesia at birth. The
inhalation method is one of the most efficient and most comfortable. The election
anaesthetic for the birth is the metoxifluran (pentran). There are portative devices out of
which through intermittent installation we may obtain a good analgesia, without
interfering with the uterine dynamics, without influencing the foetus.
The analgesia takes 3-4 minutes to install and provides cardiovascular stability. The patient
keeps by herself the portable device inhaling the pentran and when the analgesia is installed,
the inhalation stops, the patient letting loose the device from her hand. The concentration in
achieving the anaesthesia is 0. 3 - 0. 5 %. The pentran is compatible with the oxytocic.
There is a mixture of N2O + O2 in concentration 50% which also gives analgesia (the woman
can still communicate with the doctor).
The analgesia at birth can also be administered by: Mialgin (pethidine) not depressant for the
mother or foetus (not to exceed 200 mg) and atarax and romergan for sedation.
The decision to use a certain anaesthetic technique should be individualized according to the
risk factors, anaesthetic, obstetric, foetus and the patient’s preferences and judgment of the
anaesthetist. For most of the parturient through caesarean, the neuraxial techniques are
preferred instead of the general anaesthesia.
The epidural catheter already placed can provide an onset of anaesthesia equivalent with the
spinal anaesthesia for initiating the delivery through emergency caesarean.
If you are choosing the spinal anaesthesia, the spinal needles should be used, pencil point. The
general anaesthesia may be the most appropriate option in certain situations (eg. severe foetal
bradycardia, uterine rupture, severe placental detachment).
The volemic intravenous prerepletion may be used in order to reduce the incidence of the
maternal hypotension after the spinal anaesthesia.
Ephedrine and phenylephrine administered intravenously are both drugs acceptable for the
treatment of the hypotension during the neuraxial anaesthesia. In the absence of the maternal
bradycardia, the phenylephrine may be preferred because of foetal acid-base status best in the
uncomplicated deliveries. (95)

I.11. THE POSTANAESTHESIC PERIOD

The post-anaesthetic immediate period is a critical period when the consequences may occur
residual effects of anaesthesia and surgery, situations that could involve a major risk for the
patient. During post-anaesthetic immediate patient management includes assessment and
monitoring of vital functions and surgical wound (hemorrhage), postoperative treatment of
symptoms (pain, nausea, vomiting, chills) and treatment antagonizing residual effects of
anaesthesia.
Post-anaesthetic supervision is carried out in a specially designed surveillance salon called
post-anaesthetic, which ensures the management of patients with postoperative
evolution/post-anaesthetic normal for a limited period of time (hours).
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The purposes of the recommendations concerning the post anaesthetic surveillance:
 The assurance of a minimum standard of monitoring of the vital functions and
treatment/prophylaxis of the associated symptoms constant to the post-
anaesthetic/post-operatory period
 The uniformity of the practice at national level concerning the post-anaesthesia
surveillance
 Assuring a minimum standard of organisation and equipment of the spaces for this
purpose (94)
In this period it is necessary an adequate tissue oxygenation. We will follow especially the
functionality;
- Of the lung,
- Of the heart,
- The capacity of the blood of transporting the oxygen.
Therefore, we will monitor the haemoglobin saturation, PaO2 in oxygen (95-98%). If the
haemoglobin saturation in O2 decreases from 90 to 75% the signs of hypoxia show, which is
mqnifested through: cyanosis, dyspnoea, tachypnea, tachycardia, arrhythmia, restlessness,
headache, changes in personality, bradycardia and hypotension.
The oxygen therapy indications are based on the average value of PaO2 and decrease with
age:
- at 25 years 95 mmHg,
- at 35 years 90 mmHg,
- at 55 years 80 mmHg,
- at 75 years 70 mmHg.
The oxygen administered in overdose is toxic and it can cause chest pain, dyspnoea, cough,
muscle aches, tracheobronchial, respiratory depression, coma. The fair administration of
oxygen, is made through spontaneous breathing and on the mask or ventilator.
Also during post-anaesthetic period is ensured also the postoperative analgesia. This occurs
when the patient waking from G. A. or the end of the effect of the local anaesthetics or
substances from the leading anaesthesia. The degree of pain depends on each person and on
the patient’s response to pain.
There are more types of pain:
- superficial pain, at the level of the skin is sudden and intense,
- the profound somatic pain described through cramps.
Pain intensity is directly proportional to the magnitude of surgery (surgery is very painful
crippling), the period (longer laborious operation is more painful), and place of the
intervention (richly vascularized and innervated areas are more painful).
Postoperative pain can be combined with muscle contracture, which emphasizes pain and can
even combine different organ failure. There are patients who manifest their postoperative pain

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by psychomotor restlessness: alcoholics, elders, advanced atherosclerosis, patients with
cortical depression, patients with cerebral hypoxia.
Treatment of postoperative pain management is done by:
- major analgesics: petidine 20-30mg, fentanyl 0,1 mg, droperidol 2,5-5mg or
combined fentanyl + droperidol 1/50, pentazocine 50mg, smaller doses which may
be repeated at need (by experimenting),
- minor analgesics: algocalmin, ketonal, analgin,
- anti-inflammatory: tador, ketoprofen.
- others (paracetamol, tramadol, local anaesthetics, etc.)

The ways of administration of analgesics are parenterally (intravenously, intramuscularly,

subcutaneously), the loco-regional catheter (epidural, nerve plexuses jam), transdermal,
sublingual, rectal, etc. We recommend using multi-modal analgesia by associating analgesics
from various classes and on various routes. If the patient controlled analgesia use, the nurse
must be familiar with the use of devices / equipment specific. (94)
Sleep therapy analgesia can be combined with the administration of:
diazepam, phenobarbital, DORMICUM, but they add surveillance after 30-60 minutes after
administration major analgesic. Achieve effective analgesia and jams made by infiltration
paraspinal nerve; intercostal.
In the operations performed in epidural anaesthesia the catheter has a very good analgesia
postoperatively by reinjection of the local anaesthetic substance at predetermined intervals or
at the request of the patient.
The period after the anaesthesia is particularly important. Now a number of complications can
occur. Therefore the patient will be permanently supervised and monitored vital parameters:
BP, pulse, respiratory freedom, oxygen saturation, respiration, skin color, position in bed,
infusions, diuresis, temperature, permeability drainage tubes, local dressing. Also we will
respect the general nursing measures that will be conducted by the nurse.

In case the patient does not breathe spontaneously he needs artificial ventilation. The
parameters which are established on the ventilation device are:
- current volume (C.V. -) 10-15ml/kg,
- frequency 10-15/minutes
- the rapport inhale/exhale (I:E) =1:2,
- the speed of the inhaled debit in order to reach to I:E = 1:2,
- the trigger effort - 2 cm H2O,
- the suspiration volume l,5 x V.C. at each 5-10 minutes (when the PEEP is used).
After the device stopped:
- oxygen 100 % (FiO2 = 1,9) for 1 - 2 hours,
- the sanguine gases after few minutes,
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 (it is repeated until it reaches normal values)
- the monitoring of the dynamic compliance (dynC), normal dynC = 50 - 100 ml
H2O.
I.12. THE INTRAVENOUS THERAPY IN ANAESTHESIA AND INTENSIVE CARE
The therapy on venous way in the only modality of correcting the hydric misbalances,
electrolytic, energetic and acido-basic. As in the intensive care also in the anaesthesia the
essential objective is the maintenance of the general homeostasis assuring the surgery which
depends on:
- avoiding the dehydration or hyper-hydration, maintaining a strict hydric balance
adequate to the patient
- the maintenance of an osmotic constant pressure (isotonic),
- the maintenance of the normal concentrations of the ions of H+ (isohydria),
- assuring the caloric contribution,
- contribution of the oxygen transportations.
The hydric balance:
It is calculated based on the inputs and outputs of fluid per 24 hours that water intake equals
water loss. When this balance is altered intervene pathologies: minus (dehydration when
intake is lower than the losses), or hyper-hydration (when intake is greater than the losses).
Etalon take a 70 kg adult.
Outgoings: in 24 hours;
a) urine – 1300 – 1500 ml; 20 ml/h; min. diuresis 500 ml,
b) perspiration 1000 ml
(15ml/kgbody/24h to which is added 500 ml to each °C over 37°C),
c) the water from the ejections 100 – 200 ml,
d) other losses (vomiting, diarrhoea, puncture, fistula)
Entries: the hydric contribution for an adult is of 30-40 ml/kgbody/24h; total entries 25-120
ml/kgbody/24 h which result from the coverings (a + b + c + d).
The minimum necessary of water which is of 800 ml/24 h.
The necessary of hydric basis for an adult is of 25 – 40 ml/kgbody/24 h.
The necessary of hydric base for children is of 100-120ml/kgbody/24 h.
The electrolytic necessary (which is "the chemical skeleton" of the water):
- Na+ 1-4 mmol/kg/24 h (100 mEq/24 h adult),
- K+ 0, 7-3 mmol/kg/24 h (50-80 mEq/24 h adult),
- C1+ 1, 3-4 mmol/kg/24 h (100 mEq/24 h adult),
- Mg++ 0, 1-0, 4 mmol/kg/24 h (10-20 mEq/24 h adult),
- Ca++ 0, 1-0, 4 mmol/kg/24 h (10-20 mEq/24 h adult).
The repartition is: K, Mg intracellular, and the Na and Cl in the extracellular space. The
bicarbonate space is found in both space.

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Isotonic: osmotic pressure is given by the number of particles per unit volume. For the
extracellular space Na ion is most important, giving 9/10 of the osmotic pressure of plasma.
Space for intracellular K + generates largely osmotic pressure. In the intravascular space is in
addition coloidosmotic pressure (oncotic) given by proteins that keep water in the circulatory
tree.
Replacement of electrolyte losses in surgical patient must be accurate qualitative and
quantitative both not to cause electrolyte imbalances with involvement homeostasis.
Colloid and crystalloid solutions used in anaesthesia and intensive care
Taking these solutions restore circulating blood volume when it is in deficit.
A fluid deficit of 1.5 l triggers thirst, is a sensor that announces the lack of fluid volume. This
volume of fluid can be replaced with crystalloid (9 ‰ NaCl or Ringer's lactate) or colloidal
solution (Dextran 70, 40, HES derivatives of gelatine).
The amount of crystalloid volume expansion required to be 2-4 times higher than in the case
of colloidal solutions.
In contrast to the 1.5 liter blood loss (haemorrhagic shock), correction fluids administered
must include blood or red blood cell.
The management of these solutions is based on the loss discerning and pathological situation
created. The administration of large amounts of colloids (over 1.5 l) or crystalloid risk of
dilution coagulopathy by diluting the plasma coagulation factors, accompanied by
thrombocytopenia dilution.
Instead crystalloid administration without colloids cause edema (lung, brain).

Colloidal solutions

They are used as plasmexpanders and replacing the blood or blood derivatives. Keep at room
temperature.
Dextrans - the most commonly used colloids which have ideal properties for filling the
vascular bed.
There are a mixture of glucose polymers with molecular weight of 40 KD or 70 KD.
Dextran 70 is used for the recovery of hypovolemia and create a plasma expanding effect for
6 hours. The half-life is 24 hours. Increase red blood cell aggregation.
Dextran 40 has a large plasma expansion 130-200% but short-lived and rapidly eliminated
through the kidneys. Dextran 40 reolgic effect and prevents red blood cell aggregation in the
microcirculation.
Both dextran antiplatelet effect, are therefore useful in the prophylaxis of deep vein
thrombosis. The administration does not exceed 1-1.5 it because they cause increased risk of
bleeding and allergic reactions.
Hydroxyethyl starch (starch Hidroxyethyl = HES)

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Synthetic colloid composed of branched chains of amylopectin substituted hydroxyethyl
groups that slow enzymatic degradation in serum amylase act.
The effect of volume expansion is good, between 100-120%.
Less commonly used preparation HES 450 which has adverse side effects and allergic
reactions to clotting.
Do not use in patients with renal impairment because it affects renal function. There
preparations (HES 200, 130 HES) Low substituted and reduced side effects which are used
more frequently.
Crystalloid solutions
The glucose solutions: are administered for energetic layer and water contribution. They are
very various with glucose 5 % hypotonic and continuing with concentrations from 10 % up to
60% hypertonic solutions with a ph 4, 5-5.
In states using cellular dehydration isotonic with plasma, 5%, which is distributed evenly to
all parts of the body including intracellular.
10-60% hypertonic solutions are administered for the purpose of calories
(1 g glucose = 4.1 kcal).
Hypertonic glucose solutions are irritating vascular and therefore are administered on the
central and not peripheral veins.
In surgery, poly-trauma, etc., indicate buffering glucose with insulin: 1 IU insulin 5g glucose
and insulin in diabetics 1 IU to 2 g glucose.
Care should be taken that the pace of feeding glucose metabolism does not exceed the
capacity of the organism 0.5 g glucose / kgbody / h.
Not to fluid resuscitation indicated in plasma volume as it changes very little. If administered
glucose with electrolytes in excess there is a danger of cerebral oedema and hyponatremia.
The fructose solution (5%, 10%, 20%, 40%) have a metabolism insulin independent and it is
administered in post-aggressive states.
Sorbitol is a hexaalcool which is transformed by liver, in fructose.
Xilite solution 5 % is a penta-alcohol the same with a metabolism insulin-dependent which
increases the tolerance to glucose and it has an effect of protein spare for the cachexia sick.
The solution NaCl 0, 9 % or 9 ‰ it is also called physiologic serum and it contains 9 g NaCl/l
(3, 5gNa/l).
1 g NaCl contains 16mEqNa + 16 mEqCl.
Solution NaCl 0, 9% represents 154 mEqNa and 154 mEqCl/l with osmolality of 308
mOsm/l.
It is isotone with plasma and it has a pH = 6, it is distributed after perfusion in the plasma and
the interstitial liquid without the misplacement of the water in the intra and extracellular
space.

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When we put in the perfusion more than 100 ml NaCl 0, 9 % an expansion is produced for the
plasmatic volume with 180 ml.
It is indicated in the states of dehydration isotone and hypotonic (burns, intestinal occlusion,
diabetic coma etc.).
The Ringer lactate solution is a complex solution and it contains:
- 130 mEqNa (6g)
- 3 mEqCa
- 4 mEqK for 1 litre of solution
- 109 mEqCl
- 28 mEq lactate

pH = 5,1 and osmolality 273 mOsm/l

It is administered for the hypovolemic patient.
The solution of Na bicarbonate (concentrations 1, 4 %, isotone, 4, 2 % semi-molar, 8, 4 %
molar)
It is used for the metabolic acidosis and for the alkalinisation of the urine.
The THAM solution (trishidroximethylaminometan) as the sodium bicarbonate, it is used in
the treatment of the metabolic acidosis.
Secondary effect – respiratory depression.
The saline hypertonic solutions (5, 85% molar, 10 %)
It is administered in the hydric equilibration of the burned patients.
The KCl solution 7, 45 % molar or 10 %, it is administered for K contribution.
1 g KCl contains 12 mEqK + 12 mEqCl.
The manitole solution 10 %, 20 %, is a polyalcohol derivate from manosis and which
penetrates the hematoencephalic barrier and it creates an osmotic gradient for this level.
It is used in the treatment of the cerebral oedema. It is filtrated in the renal glomeruli and it is
not reabsorbed at tissue level, determining an osmotic diuresis, reason for which it is used in
the treatment of the acute renal insufficiency.
mg
mEq  x valence
Gr.atm
Gr. atm. = atomic weight
Isohydria = the maintenance of a normal concentrations of H ions.
PH = the concentration of the H ions, pH = 7, 36 - 7, 44.
Normal values of the acido-basic equilibrium:
- PH = 7, 4 (7, 36 -7, 44),
- PCO2 34 - 46 mmHg
The actual bicarbonate 22 - 26 mEq/1,
The standard bicarbonate 22 - 26 mEq/1,

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 - Excess of bases 0 ± 2,5 mEq/I,
- CO2 total 23-27 mEq/1.
The increase or decrease of the standard bicarbonate shows that we are speaking about a
metabolic disorder, and the modifications PaCO2 are produces by respiratory disorders.
There are 4 types of disorders:
1. Respiratory acidosis: it appears through hypoventilation CO2 increases over 40-60mmHg,
2. Respiratory alkalosis: through the decrease of the pCO2 under the normal values (in
hyperventilation),
3. Metabolic acidosis: it appears when the standard bicarbonate decreases and it is
accompanied by the decrease of the catecholamine in the blood, the decrease of the
cardiac debit,
4. Metabolic alkalosis: it appears when the standard bicarbonate increases.

The caloric contribution

The necessary in calories at the adult: 30-40 Kcal/kg/24 h; 0, 15 g N/Kg/24 h.
The rapport N/calories is 1/150-1/300.
This is realised and it is distributed as it follows:
- proteins (aminoacids, plasma, blood) 30% from the total of calories,
- glucides (glucose, fructose) 50% from the total of calories,
- lipids (intralipids, lipofundin) 20% of the total of calories.
The digestive way is the most indicated for the alimentation because the liver is not short
circuited as for the parenteral alimentation.

Contribution of oxygen transporter

For the oxygen to reach the tissues it is necessary a Hb concentration above 10g., otherwise
the blood transfusion is made. The transfusion is indicated when H (haematocrit) falls below
30%, and Hb (haemoglobin) under 10 g per 100 ml blood.

I.13. THE ENTERAL ALIMENTATION OF THE CRITIC PATIENT

The alimentation, or nutrition, enteral is useful for the patients for who the intakes are
impossible, insufficient or ineffective orally, but whose intestine remains functional.
The enteral nutrition is given to any patient who cannot achieve nutritional and caloric
needs only through oral food intake and no contraindications to this type of food.

Technique

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 Enteral feeding is performed using a probe, generally nasogastric (inserted through the
nose to the stomach), but which can be inserted through a gastrostomy or jejunostomy
(through an opening in the throat, stomach or jejunum). The administration of nutrients,
continuous or discontinuous, is controlled by a pump with adjustable flow rate, fixed or
portable, possibly equipped with a stirring and cooling (nutri-pump).
The modalities of assuring the nutrition of the critic patient are:
1. Enteral alimentation
2. Parenteral alimentation
3. Mixed alimentation, partial parenteral + partial enteral
4. Mixed alimentation, partial parenteral + minim enteral

Nutritional requirements are calculated based on the energy requirements rest of surplus
energy consumption linked to disease and nutritional status of the patient.
Refers to the nutritional requirements:
Should consume 25 kcal / kgborp x factor correction (stress index) (99) (100). This ensures
the carbohydrate and fat as energy substrate (99), the lipids may provide 30-50% of input,
depending on the pathology.
Protein requirements between 0.8 to 1.5 g / dl in most patients (less than in renal and hepatic
more against losses by plasmoragie, proteinuria, etc.)
The nutritional intake consists in the macronutrients and from micronutrients. The
macronutrients are: ƒ
 proteins – in the mentioned doses ƒ
 glucids – up to 5g/kgbody/day ƒ
 lipids – 1- 1,5 g/kgbody, the water is the transporter of all the used aliments in the
enteral nutrition and in total it must be administered in an amount of 30 – 40 ml
/kgbody or after the hydric balance (101)
 minerals: Na+ 90-150 mEq, K+ 60-90mEq, Ca ++ 1000 mg, Mg ++ 350 mg, P 1000
mg – in the enteral contribution (102)
Micronutrients: vitamins and trace elements - Mg, Zn, Co, I, M, Nb, Se, Cu, Mn.
Vitamins and trace elements are present in the pharmaceutical composition of nutritional
products.
Correction factors (stress): the patient is at rest but not basal conditions. He has an energy
consumption at rest EER (energy expenditure-rest) to be taken into account in determining the
nutritional plan. (101)
Its current energy consumption is higher than basal and can be approximated by multiplying
its value by the correction factor.
Losses of Nitrogen - N may also be used to calculate calories (grams of N x lost 100-150 kcal
/ day) (101)
The state of nutrition is appreciated depending on:
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Clinic criteria: ƒ
 the weight of the patient in rapport with the ideal one and the index of body mass
(G/Î in square meters ) ƒ
 the adipose crease under the skin ƒ
 circumference of the arm
Biologic criteria: through the laboratory assessments: ƒ
 total proteins: 5.6 – 8.4 g/dl ƒ
 albuminuria: 42± 2g/l ( 8) ƒ
 pre-albumin (transtiretine TTR) 310 ± 35 mg/l ƒ
 transferinemia 2,8 ± 0,3 g/l ( 8) ƒ
 retinol binding protein RBP 62 ± 7 mg/l
The enteral alimentation
The name comes from the Greek enteral nutrition: enteron = intestines, thus enteral
nutrition is any form of diet that uses the gastrointestinal tract.
Indications: - any time when there is a functional digestive tube
Contraindications: - after recent interventions on the digestive tube
- massive digestive bleedings
- in the absence of the intestinal transit.

It may be performed on the following ways:

- the gastric probe: nasogastric, orogastric
- the nasoduodenal probe
- the nasojejunal probe (placed intra-operator)
- the surgical jejunostoma
Even seldom:
- pharyngostom
- esophagostom
- surgical gastrostoma
- P.E.G. (gastrostoma endoscopic percutaned)
Through this method of alimentation (enteral) may be administered through 2 categories
of products:
- pharmaceutical products
- officinal products (kitchen)
Pharmaceutical products for enteral nutrition commonly used polymeric formulations
consist manageable version The probe gastric duodenal jejunal. Osmolarity of 300 mOsm
version DG / l, 1 contains 1.5 kcal Or / ml, g N and 5-7-9 1000ml.
Example: Fresubin®, ENSURE®, Survimed®, Pulmocare® etc.

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 These products contain all the nutrients necessary for a person namely: protein,
carbohydrates, fat, fibre, and electrolytes, vitamins and trace elements. Officinal products
(kitchen) used version enteral nutrition products are represented milled AND WATER
dissolved or suspended for a notification to be given a bath by relatively thin diameter of
2 - 3 mm.
Contains: - proteins: from milk, egg white, minced meat, peas
- lipids: olive oils, soy, sun flower, maize, egg yolk
- glucids: amylum, saccharine, lactose, fructose Products: chaudeau, soup.
Checking of the digestive toleration
After setting the gastric probe, followed by the evacuation of the gastric residue we check
the digestive tolerance through the constant infusion (on the infusomat) of tea with 10
ml/h in the first hour, then increasing the rhythm to 10ml/h la each hour, without
depassing the amount of 2000 ml/24h. We check the gastric residue in an interval of 4 h
and the amount of residue must not overcome150 ml.
We can use its Gesole - electrolyte solution well tolerated. (99)
After tolerance test patient can feed a steady pace infusomat provided by a 24 hours/day.
In one patient are stable at least 2 interruptions per day for a period of one to 30 minutes,
depending on the gastric residue (104). To a patient in critical we need 4 to 6 breaks / day
every 30 minutes with measurement of gastric residue. It lowers the risk of aspiration.
Breaks synchronize with other manoeuvres care (mobilization, hygiene) (104). It is
imperative to check the volume and appearance of gastric residue 4-6 times / day. The
amount of gastric residue should not exceed 150ml.
Advantages: ƒ
 the digestive tolerance is of ƒ
 reduced risk of diarrhoea ƒ
 allows the exact information about the caloric content of the macro and
micronutrients ƒ
 better absorption of the nutrients
Disadvantages: ƒ
 it is an expensive method ƒ
 it is more difficult to make due to the glycaemia for the diabetic patients
 is achieved with an increased consumption of materials and medical technology Note:
If enteral feeding continuous glucose monitoring is needed especially in diabetic
patients.

Enteral nutrition in boluses can be achieved by using a syringe or Guyon nutripompe

slowly ensuring maximum 20 ml / min to avoid sudden distension of the stomach and
vomit default. Precisely to avoid this amount of food brought to the table should be

160
 reported to the patient's weight (usually not more than 400 ml in an adult - after ROSPEN
300 ml). After carrying food probe should be washed with 30-40 ml of water.
Starting in boluses of enteral nutrition is gradual:
Example (adult 70 kg) (104):
Day 1: 6x 50-70ml
Day 2: 6x100 ml
Day 3: 6x 200ml
Day 4: 6x300 ml
Advantages: ƒ
 it is a cheap method of alimentation ƒ
 it may be realised simple and without specialised devices (with the syringe)
 allows the help of the family in the recovery process ƒ
 for the diabetics it may continue the scheme of isulino-therapy intermitent under
the skin ƒ
 better use of the under layer (intra-gastric digestion) (104)
 the decrease of the bacteria colonisation through the stimulation of the acid gastric
secretion (104)
Disadvantages: ƒ
 it is not possible to know the exact amount of calories, and of the macro and
micronutrients (for the oficinal preparations) ƒ
 high risk of complications in comparison to the continuous enteral alimentation
(diarrhoea, vomiting, constipation) ƒ
 it may be used only on gastric way
The enteral intermittent alimentation (cyclical) (104) consists in the administration of the
nutrients 16 ore/h continuous with the help of a nutripump, interrupted by 8 h pause (ex.:
nocturnal rest).
Advantages: ƒ
 better use of the under layer ƒ
 decrease of the risk of colonisation of the digestive tube through the apparition of
some moments with low pH
The administered amounts, pauses, the check of residue is consigned.

The monitor of the enteral alimentation

Clinic: - the verification of the way of administration before each administration meaning:
 the position of the probe
 the permeability of the probe

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 - it is checked the amount of gastric residue before each lunch in the case of the
alimentation in boluses and at the interval of 6 h in case of the continuous
alimentation.
- the verification of the quality of the products which will be administered meaning:
 Validity in the case of the pharmaceutical products
 aspect and scent in the case of the oficinal products (cooked)
 It is respected the amount and rhythm of administration consigned by the
doctor in the report of alimentation of the patient.
 The eventual signs are consigned of digestive intolerance: nausea and (or)
vomiting, abdominal pains with or without muscular defence, diarrhoea,
hiccup
 The first signs of allergic reaction are noticed
Laboratory findings: Serum albumin has a half-life of 20 days, and is less effective in
monitoring nutrition. Prealbumina or transthyretin (TTR) protein is most convenient for
evaluating nutritional support; more important than the absolute values are its variations over
time. It is recommended that at every 3days. (103) Blood glucose levels are measured daily or
several times daily to the diabetic. Ionogram serum Na, K, Ca, Mg and phosphate outside the
parameters whose prosecution is necessary and useful. Urinary urea, nitrogen balance that
serve to adapt to the caloric intake and protein. (110).

I.14. THE PHARMACOLOGY OF THE VEGETATIVE NERVOUS SYSTEM (VNS)

IN ANAESTHESIA

The autonomic nervous system includes all parties central and peripheral nerve innervating
organs provided with autonomic function (maintenance) of the body.
The sector provides autonomic self-regulation of business and adapt to the viscera, local or
general reactions neuroreflex.
He is closely related to spinal segment that provides somatic motility. The autonomic nervous
system (ANS) establishes links between organs of the same body, and the system performs
somatic mutual interrelationships between body and environment.
Vegetative structures are scattered visceral territory, thoraco-abdominal and in the somatic
(skin, sense organs, musculoskeletal system).
VNS has two parts: the sympathetic and parasympathetic placed back injury situated cranio-
sacral.
The main function of VNS is:
- The auto-regulation of the efector activity contractile and secretory, involved in
the maintenance of the normal biological constants

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 - The adaptation of the organism to the variable conditions imposed by the
environment
Autoregulation organo-vegetative functions neuroreflex is achieved through participation of
the two components of VNS.
Although they come from different territories of cerebro-spinal axis, simpatico-related centres
and ways parasympathetic innervation provides dual antagonist of most viscera to maintain
the dynamic balance of motor or secretory activity.
Parasympathetic innervation has simpatico-visceral action on the smooth muscles, endocrine
and exocrine glands, through the adrenergic and cholinergic mediator substances.
Sympathetic stimulation effects are opposite to those produced by the parasympathetic
arousal. Where is the mediator adrenergic stimulator, it is the cholinergic inhibitor.
Humoral regulation complements and extends the effects of nerve regulation. It is achieved by
means of vasoconstrictor and vasodilator substances that are chemical mediators of the
sympathetic-parasympathetic. Vasoconstrictor substances of category include:
- noradrenaline
- adrenaline
- serotonine
- angiotensine
- vasopresine
From the category of the vasodilator substances we have:
- acetylcholine
- histamine
- plasmakinin
- acid catabolites
There is a homeostatic balance between adrenergic sympathetic nervous system and
parasympathetic nervous system-SNS-SNP.
The autonomic nervous system (ANS) has the most central location in the hypothalamus
(center for controlling blood pressure, stress, temperature), the bulb and deck.
VNS peripheral - there preganglionic neurons originate in the CNS that make synapses in the
autonomic ganglia. Postganglionic autonomic ganglia neurons start and then distribute the
effector organs.
There are 22 pairs paraspinal ganglia SNS. SNP nodes are located near the effector organ.
The heart has innervation sympathetic and parasympathetic rich in fiber. Likewise the
peripheral circulation is under the control of SNS (vasoconstriction and vasodilation). Blood
volume is contained in the venous system is a large tank (80%).
The impulses are transmitted along the junction terminal and depend on the release of
neurotransmitters that are acetylcholine and norepinephrine.

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Acetylcholine is a neurotransmitter nerve endings of SNS preganglionic and postganglionic
nerve endings of the SNP and SNP.
The noradrenaline is the neurotransmitter of the nerve endings postganglionic of the SNS,
with the exception of the salivary glands.
In the medulo-suprarenal there are the chromatic cells which replace the post-ganglionic
simpatico neurons which liberate in the sanguine flux the acetylcholine and the noradrenaline.
In the cellular membrane the receptors (macromolecules) when they are activated by the
agonist the noradrenaline or acetylcholine, provoke an answer of the effector cells.
The antagonist is the substance that interferes with at eliciting an agonist of the receptor.
There muscarinic cholinergic receptor and. Cholinergic muscarinic receptors comprising
(postganglionic endings) and nicotinic receptors (autonomic ganglia). Cholinergic
neurotransmitter acetylcholine is. The substance is a muscarinic receptor antagonist atropine.
Adrenergic receptors are divided into alpha, beta, and dopamine.
Neurotransmitter receptors alpha and beta is norepinephrine and dopamine receptor is
dopamine. Adrenergic receptor number is inversely proportional to the concentration of the
catecholamine. The receptors are the first link in a series of reactions that lead to the cellular
responses.

The influence of the anaesthesia over the vegetative reflexes

In the carotid sinus and aortic arch there are arterial bioreceptors. SNS inhibits increased
blood pressure through baroreceptor. The result is an increase in vagal tone, with vasodilation,
decrease heart rate and decrease blood pressure.
Volatile anesthetises interfere with the baroreceptor function.
The clinical pharmacology of the VNS
Any answer which that a drug provokes depends on the:
- number and affinity of the occupied receptors
- the plasmatic concentration of the drug
- the adaptation to the effects of the drug

ANTICHOLINESTERASE SUBSTANCES
Inhibit the activity of acetylcholinesterase hydrolyzes acetylcholine to normal. Usually
resulting accumulation of acetylcholine muscarinic and nicotinic receptors. Anticholinesterase
Reversible cholinesterase inhibitors are neostigmine (miostin), pyridostigmine and
edrophonium. If taken simultaneously anticholinergic drugs (atropine), the patient is protected
from unwanted muscarinic effects (bradycardia, bronchospasm, increased salivation,
bronchial secretions and increase gastrointestinal hypermotility) without blocking the effects
of nicotine.
The organo-phosphoric compounds and the insecticides produce acetylcholinic toxicity. This
is why the atropine is an antidote.
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The ganglionic blockers (ganglioplegics)
The trimetaphan produces nodal blocking by competing with acetylcholine. It produces acute
hypotension by ganglionic blocking, by competing with the acetylcholine receptors node with
direct vasodilatation and release of histamine. The trimetaphan serum is destroyed by the
pseudocholinesterase
The anticholinergic substances block the muscarinic actions of the acetylcholine with direct
vasodilatation and with release of histamine. Trimetaphan serum is destroyed by
pseudocholinesterase.
The anticholinergic medication
The anticholinergic muscarinic substances block the muscarinic actions of the acetylcholine
through a competitive inhibition of the anticholinergic postganglionic endings.
Anticholinergic drugs are atropine, scopolamine, glicopiruvat.
Adrenergic antagonist substances
They have pressure effects (sympathomimetic) and inotropic (catecholamines). Activate the
alpha receptor and beta with certain prevalence depending on the dose. They hemodynamic
effect by changing heart rate (cromotropism), cardiac output (inotropism), conduction
velocity (dromotropism), heart rate and vascular resistance.
The antagonist adrenergic drugs are: phenylephrine, metoxamine and clonidine,
noradrenaline, adrenaline, ephedrine, dopamine, dobutamine and izoprenaline.
The vasoconstrictor substances being alpha antagonists -1 selective or antagonist alpha-2
selective.
The adrenaline is produced – by the adrenal gland, being an endogenous hormone, secreted as
an answer to stress.
Its hemodynamic effects are determined by the dose. In small doses from 0.005 to 0.002
µg/kgbody/min stimulate beta adrenergic receptors producing more peripheral vasodilatation,
increases the heart rate and contractility.
The clinical effect is reflected by a decrease of the general vascular and pulmonay resistance
and in an increase of the systolic volume and of the cardiac debit. In the case that it increases
the infusion rate there are more alpha adrenergic effects and resulting an increase in te
vascular resistance and blood pressure.
Over the respiratory system the adrenaline has effects as bronchodilator, activating the beta-2-
adrenergic effects of the bronchial muscles and inhibits other degranulation of the mast cells.
On the renal system the adrenaline decreases the kidney renal blood flow and urine output
through renal arterial vasoconstriction.
Adrenaline lowers plasmatic potassium through beta-2 adrenergic mechanism.
The indications of the adrenaline:
- severe allergic reactions (stings of wasps, beeps), 0,2-0,5 mg under the skin
- anaphylactic shock – 5-10 ml from the solution 1 at 10.000
- the acute bronchial asthma – 0,3-0,5 s.c. la 15 - 20 min.
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 - cardiac harass 0,01 mg/kgbody or 5 µg/kgbody
- in the maintenance of the homeostasis sol. 1/200.000 or 5µg/ml
- in the prolongation of the general anaesthesia – 0,2 mg which are added in solution
of anaesthetic for the rachi-anaesthesia and the peridural block.
The toxic effects
- pulsatile headache
- tachycardia
- tahiarythmia
- psycho-motor agitation
- arterial hypertension with cerebral bleeding
- pectoral angina
The volatile anaesthetics sensitize the myocardium to the catecholamine and adrenaline and
produce an excess of beta-stimulation, so the anaesthesia with volatile anaesthetics doses of
adrenaline is 1 mg / µg/kgbody.
The mefentermine - is a substance with vasopressor effects that has similar hemodynamic
effects of ephedrine.
The isoprenaline – is a beta-agonist non-specific and has no alpha-adrenergic effects.
The volatile anaesthetics sensitive the myocardium to catecholamine and the adrenaline
produces an excess of beta-stimulation, this is why in the anaesthesia with volatile anaesthesia
the dose of adrenaline is 1.
Action:
- increases the cardiac frequency
- increases the cardiac debit
- increases the contractility of the myocardium
- decreases the peripheral resistance
Produces myocardial ischemia and tachycardia
In the treatment of the cardiac congestive insufficiency it is used 1-5 µg/min, in cardiac
complete block it actions like a cardiac pace-maker.
Dopamine and dobutamine – vasoconstrictors with the exception of the renal circulation when
it actions as vasodilators.
Doses of administration: Dopamine 2 - 10 µg/kgbody/min
Dobutamine 2 - 30 µg/kgbody/min
The sympathomimetic nonadrenergic drugs: aminophylline, glucagon and digoxin.
Aminophylline
Action:
- bronchodilator
- increases the cardiac debit
- in the halothane anaesthesia produces cardiac arrhythmias
- inhibits the phosphordiesterase
166
It is administered i.v. in dose of 0, 5-1 mg/kgbody/h

Glucagon
Action:
- positive inotrope
- antagonises the inotrope effect of the beta blockers
It is used in the refractory electro-mechanic dissociation to other therapies.
The doses 5-10 µg/kgbody i.v., then a continuous perfusion with glucagon in dose of 5
mg/kgbody/min.
Digoxin
It is used in the treatment of the congestive cardiac insufficiency and in supraventricular
dysrhythmias (atrial fibrillation and atrial flutter).
Action:
- inhibits the sodium pump
- ameliorates the contractility of the myocardia fibres
- increases the concentration of intracellular calcium
- stimulates the vagal activity
The doses of administration are 0, 75 mg slowly, in 5 minutes.
It is eliminated renal.
The toxic effects in sick people:
- old people
- with decreased cardiac debit
- in states of hypokalaemia and hypomagnesaemia
- hypothyroidism
- renal insufficiency
The contraindications of the digoxin:
- atrio-ventricular block
- hypokalaemia or severe hypomagnesaemia
- hypertrophic cardiomyopathy
- syndrome Wolff-Parkinson -White
Alpha-antagonist drugs
These are drugs which produce orthostatic hypotension, tachycardia and meiosis.
Phenylamine – alpha antagonist – 1 and alpha - 2 non selective.
The doses of administration 2 - 5 mg i.v.
Prazosin –alpha antagonist 1 postsynaptic selective.
It is used in the preparation for surgical intervention of the sick persons with
pheochromocytoma.
Beta-antagonists (beta blocking substances)

167
Propranolol – non-selective beta antagonist.
Doses of 0, 1 - 0, 5 mg.

Action:
- decreases the cardiac frequency
- inotrope and chronotrope negative with the inhalator and intravenous anaesthetics
Esmolol – beta-1 antagonist, cardio-selective.
The doses of administration 1mg/kgbody i.v.
Action:
- decreases the cardiac frequency
- decreases the arterial pressure
- used in the anaesthetic induction in order to reduce the cardiovascular radiations.
The mixed antagonists:
Lobetolol: - selective antagonist alfa-1 and non-selective beta.
Indications:
- controls the blood pressure and the cardiac frequency during the anaesthesia
Doses of administration 0,005-0,15 mg/kgbody
Calcium blocking drugs
Influence the movement of the calcium in the cell through the ionic channels, specific, slow
Indications:
- the treatment of the supraventricular tachycardia
- the treatment of the coronary spasm
- depressing effects when it actions with volatile anaesthetics
Verapamil
- vasodilator
- decreases the vascular peripheral resistance
Diltiasem
Action
- dilates the coronary arteries and the peripheral vessels
- it modifies easily the cardiac debit
- bradycardie (moderated)
Nifedipin
Action (rapid)
- peripheral vasodilator
- negative inotrope
- increases the coronary flux in the ischemic myocardium
- stimulates (slightly) the atrio-ventricular nodule
168
THE SYMPATICOLITICS
These are drugs with antihypertensive effect, through the block of the central transmission of
the SNS or through the liberation of presynaptic noradrenaline.
Alfa-methyldopa: is a metabolite liberated at the level of the presynaptic vesicles and it
inhibits the liberation of noradrenaline, stimulating the receptors alfa-2-presinaptic.
Clonidin – stimulates the receptors alpha-2 central inclusively of the vasomotor centres from
the bulb, so that the activity of the SNS decreases.
Action:
- analgesic effects
- slight sedation
- bradycardia
- dry mouth
The sympathetic system

The action of some antihypertensive drugs to different levels from the CNS and the peripheral
(modified after Hickler R B and Vandam I D 1970)

169
Vasodilators – they have a hypotensive effect, auctioning over the vascular smooth muscle,
independent from the alpha or beta.
Action – increase the cardiac frequency (through reflex action over the baroreceptors)
Sodium nitroprusiate
Action:
- vascular vasodilator on the smooth arterial and venous musculature
- vascular vasodilator se administrează cu seringa automată
- doses of administration 0, 25-0, 50 μg/kgbody/min i.v.
- they have a cumulative effect with the volatile hypotensive anaesthetics
- the light deactivates a part of the action this is why it is covered with a black paper
Nitro-glycerine
- vasodilator, administrated i.v. or s.l.
- administration doses 0, 23-3 μg/kgbody/min
- major effect on the venous circulation

THE ACTION OF THE ANAESTHETIC SUBSTANCES OVER THE CNS

The halogenate products (Halothane, Isofluran)
Action:
- depresses the laryngeal reflexes
- broncho-relaxation through the direct effect over the smooth bronchial musculature
- hypotension arterial
- over the heart:
 action over the chronotropic function giving synusal bradycardia
 action over the dromotropic function provoking variable degrees of
functional block
 action over the batmotropic function decreasing the excitability of the
ventricular musculature.
- Sensitives the myocardium to the action of the catecholamine
 action over the inotrope function, decreasing the contraction force of
the myocardium, but also the consume of O2 of the heart
Barbiturates (Thiopental, Pentothal, Inactin)
Action:
- stops the blood at the periphery
- decrease the sympathetic tonus
- increase the cardiac frequency
- inotrope negative effect
- increase the coronarian flux
- decrease the muscular tonus of the capacity vessels (pooling) peripheral
170
 - decrease the pressure for filling of the left ventricle
- arterial hepatic vasoconstriction
- respiratory depressor
- cerebral vasoconstriction
Benzodiazepines (Diazepam, Midazolam)
Action:
- reduce the neuronal liberation of noradrenaline and the plasmatic concentration of
noradrenaline
- anticonvulsant effect
- anxiolytic effect
- produce sedation and hypnosis
- produce muscular relaxation (legere)
- give retrograde amnesia
- decrease the liberation of acetylcholine
- decrease the cholinergic central transmission
- in high doses produce respiratory depression
Phenols (Propofol)
Action:
- decrease the intra-cranial pressure
- decrease the intra ocular pressure
- decrease the arterial tension
- decrease the cardiac debit and the cardiac frequency
- decrease the consume of O2 cerebral
- decrease the cerebral blood volume
Derivatives of imidazole (Etomidate)
Action:
- hypnotic effect
- decrease the central nervous metabolism
- decrease the cerebral blood volume
Phenciclines (Ketamine, Calipsole)
Action:
- depresses the transmission of the emotional component of the pain towards the
cortical areas
- increase the intraocular pressure, taking to ocular movements, nistagmus and
blefarospasm
- increase the arterial pressure and the cardiac frequency through sympathetic
stimulation
- myocardial depression with arterial hypo-pressure when the sympathetic reaction
is blocked (high peridural anaesthesia), or it is exhausted (in shock)
171
 - increases the vascular pulmonary resistance
- produce broncho-dilatation (recommended in the bronchial asthma)
- depresses the breathing and the pharyngo-laryngeal effects
- stimulates the secretions (anticholinergic drugs will be used)
- increase the determined block of myorelaxants
- increase the skeletal muscular tone muscular
Opioids (morphine, petidine, meperidine, fentanyl, sufentanyl)
Action:
- strong analgesics
- produce respiratory depression, the suppression of the cough
- decrease the intestinal movability and produce nausea and vomiting
- induce the urine retention
- parasympathetic effects through bradycardia and arterial hypotension
- sympathetic effects: tachycardia (petidine, morphin), at the increase of the doses
through adrenergic stimulation
- hypothermia produce
- produce hallucinations
- inhibit the secretion of catecholamine started by the pain
- induce the sedation
- produce bronchial spasm (liberation of histamine), spasm of the smooth
musculature of the colon, spasm of the biliary ways (the Oddi Sphincter)
The neuromuscular relaxants non-depolarising (detubocurarine, alcuronium, pancuronium,
vecuronium, mivacurium)
Action:
- produce bronchospasm with eliberation of histamine through cholinergic
mechanism
- it binds to the cholinergic nicotinic receptors post-synaptic from the level of the
neuromuscular junction that it blocks, and the muscarinic receptors from the
nervous ganglions activate them
The pancuronium and gallamine, blocking muscarinic receptors myocardial causing
tachycardia, d-tubocurarine blocks cute and lymph parasympathetic (block vagal),
pancuronium increases blood pressure by increasing the heart rate effect vagolytic and effect
sympathomimetic indirectly by blocking the reuptake of norepinephrine in the sympathetic
nerve endings intramyocardial
- increases the cardiac debit (moderate)
- the vecuronium produces bradycardia with the decrease of the cardiac debit
Neuromuscular depolarising relaxants (succinylcholine)
Action:

172
 - provokes the depolarisation of the cholinergic nicotinic postsynaptic receptor
- it fixates on the nicotinic receptors and it determines like the acetylcholine the
depolarisation of the muscular cells, stretched and rapid, followed by a short perios
of muscular relaxation

Decurarisants – (neostigmine)
Action:
- anticholinesterasic, destroys the cholinesterase and it remains the acetylcholine not
divided in great amount and it competes with the remaining curare in the receptors,
coming back to the muscular activity.
Local anaesthetic substances:

It links to internal end intracellular sodium channel voltage-dependent and prevents the nerve
impulse leadership in excitable tissues, such as the peripheral nerves and spinal roots.
Local anaesthetics
Action:
- CNS: analgesia, hypnosis (sometimes)
- NS peripheral: muscular paralysis lax of variable degree
- NS vegetative: pre-ganglionic sympathectomy
- Cardio-vascular apparatus: arterial hypotension, cardiac debit decreases,
bradycardia, cardiac depression
- Breathing apparatus: reflexe broncho-dilatation
- Digestive apparatus: contraction of the digestive tube
Bupivacaine:
Action:
- action over the peripheral vessels through dilatation or constriction depending on
the dose
- the sympathetic tonus increases and the vasoconstriction appears
- myocardia inotropism decreases proportionally with the increase of the dose
- ventricular arrhythmia, electro-mechanic dissociation, refractor asystole (for great
toxic doses)
- decreases the speed of intra-cardiac conduction
- through sympathetic mechanism induces ventricular dysrhythmia, in reduced doses
increase the convulsive limit and have an anticonvulsant effect, in high doses it is
pro-convulsing
- high concentrations of bupivacaine have a bactericide effect (4,4-26mM), over the
teguments and it inhibits the increase of the viruses
Lidocaine:
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Action:
- in toxic doses induces arterial hypotension and sinusal bradycardia
- it attenuates the inflammatory answer in the pulmonary injury
- increases the micro vascular permeability
- anti-arythmic effect in acute myocardial failure, through anti-inflammatory effect
manifested in the infarcted areas
- antiinflamatory answer in the pulmonary injury, through the amelioration of the
pulmonary function, through the increase of the partial pressure of the oxygen, the
increase of the compliance and the reduction of the pulmonary resistance
- protective role in the case of the plasmatic exsudation in burns, through the
inhibition of the migration PMN (polymorphonucleares) in the endothelium and the
reduction of the formation of free oxygen radicals
- modifies the liberation of the pro-inflammatory agents
- produces moderate decreases of the glomerular filtration and of the renal plasmatic
flux
- supresses the secretion of some hormones
- increases the susceptibility to infections
- in small concentrations it is anticoagulant
- for small concentrations it stimulates the myotonic spontaneous concentrations
producing vasoconstriction, and in high concentrations inhibits the myogenic
activity producing vasodilatation.

Chapter II
EMERGENCIES IN INTENSIVE CARE

II.1.GENERAL OBLIGATORY DATA FOR THE PRACTICE OF THE

EMERGENCY MEDICINE
Objectives
1. the set of the endovenous catheter
a. Peripheral veins
 The Basilic vein or the Cephalic vein (preferably the basilica one)
 Place of puncture: the crease of the elbow
Technique:
 Branula are used (flexures) of different calibres, of single use
 Local disinfection
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  Local anaesthesia (emla)
 Tourniquet
 The fixation of the vein with the thumb of the left hand
 The puncture of the vein in an angle of 45°, until seeing the blood in the branula
 The retraction of the catheter
 The complete positioning of the branula in the vein
b. Central veins
 The internal jugular vein – the puncture of the jugular internal vein: lower from
the visible spot in the crossing of the jugular vein with the sternocleidomastoid
muscle and at approximately 1 cm lateral from the palpable artery
Technique
- We palpate the carotid artery (postero medial from the jugular)
- The internal jugular vein is situated at a depth of 3-4cm
- The puncture needle is introduced attached to the syringe trans-muscular aspiring,
under an angle approximately 30° to the skin
- Venous blood is aspired
- The plastic needle is introduced, extracting the puncture mandrel
- The catheter is introduced
- It is connected to the system of perfusion

Source: internet

 The subclavian vein

 It crosses the first rib posterior in front of the 1/3 medial of
the clavicle
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 Approach: the arm of the patient in abduction and external rotation
- The puncture of the vein on the medioclavicular line at the inferior edge of the
clavicle
- Local anaesthesia 1- 2 ml lidocaine 1 % in the periost of the clavicle and 3-4 ml in
the surrounding tissues
- The puncture needle is held between the fingers 2 and 3 of the hand which doesn’t
perform the puncture, then with the other hand the needle is forwarded pushing the
piston of the syringe of which it is attached the needle (syringe of 10 ml). In the
syringe we put physiologic serum 9 ‰.
- We sting the skin, nearly perpendicular after which the needle follows the posterior
face of the clavicle.
- The needle is introduced horizontal under the clavicle keeping the whole time the
contact with it, in the direction of the superior edge of the sternocleidomastoidial
articulation, in angle with the thoracic wall of 30°.
- After overcoming the resistance of the costoclavicular ligament, we reach after a
distance of 4-5 cm to the subclavian vein
- We aspira the blood in the syringe for the control
- It is introduced in the lumen of the lumen of the vein the catheter of synthetic
material after having removed the needle (mandrel) metallic of puncture
- The catheter is introduced 10-15 cm in the right and 15-20 cm in the left
- If we find resistance we do not introduce the catheter
2. The monitoring of the vital perimeters
- B.P. (blood pressure)
- VA (ventricular allure)
- EKG (electrocardiogram)
- PVC (venous central pressure)
- SaO2 (arterial oxygen saturation)
- PaCO2 (carbon bioxyde saturation)
- Circulation (central and peripheral)
- Respiration
- Excretion
- Temperature
- State of consciousness
3. OT Intubation (orotracheal) or NZ (naso-tracheal)
- Role of separating the breathing way from the digestive one
- Assures a better pulmonary ventilation
- Allows the more efficient control of the breathing
Necessary materials:

176
 - Laryngoscope (with curved and straight blades)
- Endotracheal probes of different sizes
- Tongue tuck
4. Tracheostomy = horizontalised incision of 2-4 cm, in front of the tracheal cartilage 2,
under the cricoid or medial incision. The dissection on the medial line of the
subthyroidal muscles.
5. Cricotomy = small incision, horizontal between the thyroid and cricoid. The
membrane is perforated with the tip of the bistoury.
6. Assisted respiration – after introducing the Guedel pipe, in order to fixate the base of
the tongue, the ventilation mask is applied connected to the Rubenn balloon and the
ventilation device.
7. The mechanic respiration – after the patient is intubated orotracheal (OT) or naso-
tracheal, it is connected to the respiratory device, then we establish the ventilation
parameters which are:
- The current volume (C.V.): 10 -12 ml/kg
- The respiratory frequency: 10 -15 respirations/min
- Rapport inhale/exhale (I:E): 1: 2
- The speed of the adjusted inspiratory debit, which must reach to the rapport
I:E.= 1/2
- Trigger (the trigger effort): 2 cm H2O
- The suspire volume 1,5 x V.C, for each 5-10 min.

8. Oxygeno-therapy
- normobar
- hyperbar
9. the respiratory normal parameters
- the respiratory frequency (F): 12-20 resp./min
- the current volume (C.V.) = 10-12 cc/kg = 350-600 cm³
- (the calculation formula Gx10-12 ml)
- the vital capacity (V.C.) = 70 cc/kg
- the inspiratory force (I.F.) = 20 cmH2O
- the total pulmonary capacity (T.P.C.) = 4500-6500 cm³
- the residual capacity (FRC) = 40% din CPT = 100-1400cm³
- the reserve inspiratory volume (RIV) = 1500-200 cm³ = 35-40 % din VC
- the reserve expiratory volume (REV) = 800-1500 cm³ = 20-25 % din VC
- the maximum expiratory volume /sec (MEVS) = 80 % from the VC/sec =
2800-4000 cm³
- ventilator volume (ventilation)= 6-8 l/min

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 - alveolar ventillation = 3,5-5 l/min
- the physiologic dead space (DS) = 130-200 cm³
- oxygen consume = 180-230 cm³/min
- the discharge of CO2 = 145-230 cm³/min
10. Normal cardio-circulatory parameters
- Cardiac debit (CD) = 7,17±0,49 l/min
- Debit beating (DB) = 50-70ml
- Blood pressure (BP) = 120/80 mmHg
- The consume of O2 of the heart = 200-250 ml/min
- The systolic arterial pressure (SAP) = 100 mmHg x age
- The diastolic arterial pressure (DAT) = SAP/2 x 100 mmHg
- Central venous pressure (CCP) = 5-8 cmHg
11. Normal values of the ASTRUP parameters
- actual Ph = 7,35-7,45
- pCO2 actual = 5,07-5,60 kPa (38-42 mmHg)
- actual bicarbonate = 23-27 mmol/l (mEq)
- standard bicarbonate = 23-27 mmol/l (mEq)
- tampon bases = 46-52 mEq/l
- excess bases = (-2) – (+2) mEq/l
- CO2 total = 24-28 mmol/l

12. The urinary normal parameters

- Amount = 1-1, 5l/24 ore
- Osmolarity = 500-800 mosmol/l
- Albumin = 1, 4 mmol/l
- Glucose = 0, 11 - 0, 83 mg/l
- Vanylmandelic acid = 1, 8-8, 4 mg/24 h
13. Normal values of coagulation
- Bleeding time (BT) = 1-4 min (Duke)
- Bleeding time (BT) = 1-6 min (Ivy)
- Coagulation time (CT) = 6-17 min (Lee-White)
- Partial time of prothrombin (PTP) = 35-45 sec
- Quik time (QT) = 70-100 %
- Howel time (HT) = 50 sec-1 min şi 20 sec.
- Protrombin time (PT) = 15 sec
- Fibrinogen (F) = 200-450 mg%

14. The sanguine ionogram: mmol/l

178
 Specification New born Suckling Children Adults Obs.
Na+ 131-165 135-144 132-150 132-148
K+ 3,7-5,4 3,8-5,4 3,6-5,5 3,6-5,0

9-11 mg/1oo,
Ca2+ 1,9-3,5 2,29-2,9 2,5-2,9 2,4-2,8
4,5-5,5mEq/l

Cl- 94-109 100-108 97-109 97-107

0,66-0,9 1,5-2,4 g%
Mg2+ 0,68-0,91 0,66-0,95 0,78-0,99
1,5mEq/l 1,3mmol/l
0,8-1,5
p.anorg 1,3-2,6 1,3-2,1 1,0-1,7 2-4,5mg%
1-1,4 mmol/l
Women/ Women/ 80-120µg/100ml (14-21,5µmol/l)
Fe
men men 90-140µg/100ml (16-25µmol/l)

15. The passive and active movement of the patients

16. Drainages
17. Punctures
18. The hydric equilibration:
The hydric contribution: 30-40 ml/kg/24ore
19. Electrolytic equilibration:
Intake: NaCl 6-8 g/24 h or 100 mEq/kgb/24 h
KCl 3-4 g/24 h or 50 mEq/kgb/24 h

20. The caloric necessary:

30-40 kcal / kgb/24 h (Elwyn)
0, 15 Ng / kgb/24 h
Rapport: N/calories = 1/150 – 1/300
Proteins: solutions of aminoacids, plasma, blood-30 % from the total of calories
1gN = 6, 25 g dry proteins = 30 g humid proteins
21. Correction of the anemia
- Blood transfusions
22. Correction of the A-B equilibrium
- Sodium Bicarbonate 8,4 % or 14 ‰
ml bic. of Na 8,4 % = BE x 0, 3 x Gr
- THAM ml 0,3 % = BE x Gr
The excessive administration of bicarbonate determines:
- Alcalemia
- Liberation of O2 from the Hb↓
- Ventricular tachycardia → F.V (ventricular fibrillation)
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 - Myocardial strong contraction
- Hyperosmolarity through hypernatremia
- Hypokalaemia (Ke-Ki) (Ke=K extracellular;
Ki=K intracellular)
23. The treatment specific for the disease:
- Medical
- Surgical
Necessary solutions and obligatory in the Emergency Medicine
- NaCl 9 ‰
- NaCl 5,8 %, from which 1ml = 1 mEqNa
- Ringer
- Lactate ringer
- Cl NH4 1 ‰
- KCl 7,4 %, from which 1ml = 1mEqK+
- Na Bicarbonate 8, 4%, din care 1 ml =1mEg
- Glucose 5 %, 10 %, 20 %, 30 %, 40 %
- Fructose 10 %
- Manitole 10 %, 20 %
- Blood gr: 0(I), A(II), B(III), AB(IV)
- Sol. Aminoacids
- Sol. Dextran 40; 60

To retain:
1 g Cl Na contains: 16 mEg Na
16 mEg Cl

1 g K Cl contains: 12 mEg K
12 mEg Cl
25. The receptors from the bronchial wall:
 Cholinergic = broncho-constrictor
 α1 adrenergic = broncho-constrictor
(predominate in bronchial asthma)
 β2 adrenergic = broncho-dilatator
26. The set of the naso-gastric Einhorn probe or of the Fauche probe
27. Punctures (paracentesis, pleural puncture, pericardia)
28. The minimum of emergency drugs:
- atropine

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 - adrenaline
- alupent
- molar sodium bicarbonate 14 ‰
- gluconic calcium, chlorate 10 %
- dopamine
- dobutamine
- ephedrine
- gordox (trasylol)
- HSHC
- beta blockers (propranolol, atenolol)
- sodium nitroprusiate, nitro-glycerine
- broncho-dilators (aminophylline)
- heparin fractioned and non-fractioned (heparin, fraxiparina, clexan, inohep)
- protamine sulphate
- hypotensives (hydergin, captopril, nifedipin)
- diuretics (furosemide)
- cardiotonic (digital)
- antiarythmic (ritmonom)
- Ca blockers (verapamil)
- perfusable solutions (crystalloid and colloidal solutions)
- lidocaine

29. The hydric balance

- urine 1500 ml (the minimum diuresis is 500 ml/24 h) = 20 ml/kg/24 h
- perspiration 1000 ml – 2000 ml (15 ml/24 h + 500 ml, for each °C over 37°C)
- the water from the dejections 100 ml
- other losses:
 entrances in 24 h: 25-120 ml/kg/24 h,
 300 ml metabolic water + (a+b+c+d).
 Necessary minimum of water = 800 ml/24h
30. The basic necessary for the adult, in 24 h:
- water 25-100 ml/kg/24 h - adult
- water 100-120 ml/kg/24 ore - child
- proteins 1-2 g/kg
- aminoacids 0, 07-3, 5 g/kg
- glucids 2-7 g/kg:
 glucose 0,75 g/kg
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  fructose 0,50 g/kg
 sorbitol 0,25 g/kg
 xilite 0,25g/k g/kg
- fats 0-2 g/kg
- the necessary of calories 25-40 Kcal/day
 lg N, is obtained from 6, 25 g of dry proteins or 30 g humid proteins
31. The resuscitation case
- Guedel pipe
- Aspirator of bronchial secretions
- Rubenn balloon
- Laryngoscope (with straight and curved blade)
- Tuck for foreign bodies
- The intubation probe, of different calibres + mandrel
- Magyl tuck
- Tracheostom Cannula
- Tube of O2
- Defibrillator
- EKG Monitor
- Medicament (drugs) for resuscitation
- Leucoplast
- Syringes of 2, 5, 10, 20 ml
- Sterile gloves
- Perfuser
- Transfuser
- Naso-gastric probe
- The Foley urinary probe
- Rubber gloves
- Trocar

II.2. THE MONITORING OF THE PATIENT IN THE MEDICO-SURGICAL

EMERGENCIES
The critical patient, needs special and permanent cares, extensive evaluation and permanent
monitoring.
The main indication when the patient is hospitalised in severe form in the INSTABILITY OF
THE VITAL FUNCTIONS.
The clinic appreciation of the patients hospitalised in emergency is based on the methods
which determine the severity of the disease and prognosis methods.

182
Monitoring critical inpatient medical and surgical emergencies Vitale version covers
monitoring functions, and all are operating parameters Follow Through care patient
behaviour, evolution of disease prognosis and care of a former Internat.
All data regarding the state of the patient during hospitalization are collected by the doctor
and nurses, consigned version of the observation foil (OF) of the patient, through graphical
representation version timeline and arranging daily progress.
The vital parameters which are being followed for the critical patient are:
1. Blood pressure
2. Pulse (the ventricular allure, VA)
3. Respiration
4. Diuresis
5. State of conscience
6. Colour and aspect of the teguments
7. Pathologic manifestations
8. Temperature
9. PaO2
10. PaCO2
11. EKG
12. Vomiting
13. Expectoration
14. Venous approach
15. Body weight
16. Dejections
17. Pathologic discharges of the genital feminine organs
18. Complications which appear during the hospitalisation
19. Para-clinic exams
20. Monitoring of the behaviour of the patient

1. The blood pressure (BP)

Factors that alter BP values are: cardio-vascular, renal, humoral, endocrine, neurovegetative,
haematology, neuro, menopause, electrolyte imbalances, shock, etc.
Blood pressure is monitored using devices: sphygmomanometers classical, electronic blood
pressure monitors.
2. The pulse (VA) – reflects the functional state of the heart and the arteries, giving clues
over the anatomic state of the arterial tree and of the heart.
In the infectious acute diseases the pulse reflects the gravity of the infection. The modification
of the character of the pulse determines the therapeutic behaviour in some cases. The
frequency of the pulse varies depending on the sex, age, body height, effort, emotions,
position of the body, physiologic states and pathologic states.
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Depending on the age the normal values of the pulse frequency, vary in the following way:
 New born 130-140 b/min
 Small child 100-120 b/min
 At 10 years 90-100 b/min
 At 20 years 60-80 b/min
 Over 60 years 72-84 b/min
Physiologically pulse accelerates in case of physical and mental stress, emotions, digestion
and pulse rate drops during sleep.
Pulse tachycardia is caused by heart disease and extra-cardiac and fever. For each degree of
temperature increase heart rate 8-10 beats / min.
Tachycardia occurs as a mechanism to compensate the deficit oxygenation of tissues
(myocarditis, endocarditis, valvular lesions, circulatory collapse, severe anaemia, profuse
bleeding, some poisoning, cardiac disorders of nervous or endocrine nature.
The Bradycardic Pulse - all caused by cardiac or extra-cardiac (acute myocarditis,
myxoedema, jaundice, digital poisoning, mercury, cerebral haemorrhage, intracranial
tumours, meningitis, starvation, impaired driving excite-conductor system, etc.).
Rhythmic or arrhythmic pulse can be. Arrhythmias may be the result of central nervous
system ailments, spinal or sympathetic.
In the appreciation of the pulse we monitor:
 The rhythmicity of the pulse (rhythmic, arhythmic)
 Amplitude of the pulse (higher or lower)
 Tension of the pulse (hard or soft)
 Speed of the pulse (tachycardia, bradycardia)
 Celerity of the pulse (celer or tard)
3. Respiration
The elements that are followed for the monitoring of the respiration are:
 the respiratory type: costal superior in women, costal inferior in men, abdominal for
older people and children
 symmetry of the respiratory movements
 amplitude of the respiratory movements
 frequency of the respiratory movements: depending the sex, age, position, muscular
activity, temperature, state of wake or sleep.
- men 16 R/min
- women 18-20 R/min
Dyspnoea
a. tachypnoea or polypnoea
b. bradypnoea
c. dyspnoea with rhythmic and periodic perturbation of the breathing
184
  Cheyne-Stokes dyspnoea is characterised by a cyclic succession of some
periods of accelerated breathing interrupted by short periods of apnoea
 Kussmal dyspnoea is characterised by a period of very accentuated
bradypnoea, with a profound inspiration and also noisy followed by a long
period and then by an exhale as long as the inhale
 Biot dyspneoea is characterised through rhythmic breathing movements, of
normal amplitude but separated by longer breaks than 10-30 seconds
 Bouchut dyspnoea is characterised by the inversion of the time of the normal
breath, in the sense of prolonging the inspiration towards the greatly shortened
breath
 Disordered dyspnoea – when the breathing doesn’t present any rhythmicity (of
effort, of decubitus, paroxistic, accidental)

4. Diuresis
We will follow:
a. The disorders of urinary emission
b. Amount of urine per day
c. The qualitative characters of the urine
The troubles of urinary emission
 polakiuria
 ischiuria or urine retention
 dysuria
 urinary incontinence
The amount of urine/day
 pathologic variations of the diuresis
 polyuria
 oliguria
 anuria
The qualitative characters of the urine
 colour (light yellow)
 aspect (clear, transparent)
 scent (resembling the one of the tomato paste)
 reaction (Ph = 6,5; acid reaction)
 density (determined immediately 1015 – 1020 )
5. The state of consciousness
 patient conscious oriented in time and space
 confuse
 somnolent
185
  psycho-motor agitated
 convulsions
 coma (different degrees)
6. The colour and aspect of the teguments
Colour:
 pallor (anaemia, insufficient irrigation of the skin)
 cyanosis (haematosis disorders with Hb reduced in blood)
 intense redness (pneumonia, fever)
 icteric (icterus)
Aspect:
a. oedema
 of white colour if the creases and the of the genital organs = renal affections
 blue oedema (cyanosis) situated in the lower parts of the body = the venous
stasis (thrombosis, tumours)
 cachexia oedema = neoplasms, tumours
 inflammatory oedema = inflammatory processes
 angioneurotic oedema = allergies, anaphylactic chock
b. desquamation (infectious diseases)
 furfuraceous
 lamellar
 flaps
c. skin eruptions (infectious diseases, allergic reactions, toxic action)
d. skin hemoragies (septic states, bleeding states)
7. Pathologic manifestations
a. paresis and paralysis (movement disorders)
b. involuntary movements
 tremblings (rhythmic muscular oscillations = diseases of the CNS)
 myoclonuses (muscular contractions which appear suddenly = sufferings of the CNS)
 coreea (ample involuntary moves but conscious disordered without logic =
encephalitis, tuberculosis meningitis)
 atetosic moves (as coreic, sudden involuntaru = CNS pathology)
 tics (involuntary contractions of some muscular groups which repeat in stereotype)
 carphology (not coordinated movements of defence, twist = severe infectious disease,
wandering)
 convulsions (infectious diseases, disease of the CNS, pregnancy toxicities, fever)
c. Pains
 headaches

186
  thoracic pains (discomfort, pressure, dagger stabs, twinge, constriction = pneumonia,
myocardia infarct, pulmonary emboli, etc.)
 abdominal pains (cramps, ruptures, burns, tearing, torsion, tenesma = intestinal
occlusion, organ perforation, acute abdomen)
 lumbar pains (painful violent crisis unilateral with irradiation in the genital organs =
renal colic)
 pains in the extremities (acute rheumatism, vascular disease)
d. perspirations (continue and periodic)
8. Temperature
Normal: 36- 37 ˚ C.
The production and loss of heat are in balance.
The measurement of the body temperature is made with:
a. maximal thermometer regular which determines the temperature in:
 arm pit (for 10 minutes)
 the inguinal crease (weak patients, children and suckling)
 the oral cavity (5 minutes)
 rectum (5 minutes, the patient in lateral decubitus with the inferior limbs in
semi-flexion)
 vagina
b. thermoelectric thermometer (thermoelectric effect which is made from a system of two
different metals welded together)
c. thermometer with resistance (platinum artery comprised in a flexible wrapping of 20
cm length and 3 mm thickness)
d. thermistors - electronic thermometer based on thermistor
Depending on the degree of hyperthermia measured in the armpit, the febrile reaction os
divided in the following categories:
 normal temperature 36-37˚ C
 under feverish temperature 37- 38˚ C
 moderated fever 38-39˚ C
 high fever 39- 41˚ C
 hyperpyrexia 41- 42˚ C
9. PaO2(SO2) = saturation of O2 (for youngsters 96-100 % mmHg)
 hypoxemia when PaO2<60 mmHg
 PaO2 sub 45mmHg = measures of respiratory reanimation
 PaO2 sub 35mmHg = lethal risk
10. PaCO2 = partial pressure CO2 in blood N = 35-45 mmHg
 PaCO2 = 46-70mmHg = slight hypercapnia
 PaCO2 = 70mmHg = severe hypercapnia
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11. EKG (electrocardiogram)
 Indication over the electric activity of the heart. The electrocardiography is performed
in more derivations.
12. Vomiting – we will follow:
 Frequency
 Schedule of the vomiting
- In the morning
- Postprandial
- Tardive
 Amount
 Smell
 Content of the vomiting – alimentary
- mucosa, watery
- biliary
- from dejections
- purulent
- bloody or pure blood
13. Expectoration (the elimination of the sputa from the breathing ways)
We will follow:
a. the amount
b. aspect – mucosa (white grey/ashen)
- purulent (yellowish greenish)
- serous (transparent, slightly pinked)
- pseudomembranous (exudate with fibrin as white membranes)
- haemoptysis (blood)
- muco-purulent (mucus mixed with pus)
- sero-muco-purulent (pus and mucus in a serous mass)
- bloody (mucous, purulent or serous mixed with blood)
c. colour
d. smell
14. The venous approach
- peripheral or central
- it is monitored the rhythm of the perfusion
- the amount of perfused liquids (the hydric and electrolytic balance)
- complications
15. The body weight appreciates:
- the state of nutrition of the patient
- the therapeutic dose of medicines

188
 - the caloric necessary
- the evolution of the patient
16. The dejections (the intestinal transit is monitored)
- the frequency of the dejections (diarrhoea, constipation)
- schedule
- amount
- consistency
- form
- colour
- smell
- pathologic aspect
 mucous–grained dejections
 liquid and semi-liquid dejections
 mucous dejections
 mucous-purulent dejections
 mucous-bloody dejections
17. Pathologic discharges of the feminine genitals – pathological leucorrhoea
We will follow: - amount
- colour
- aspect
- rhythm of the discharges
18. The complications which appear during hospitalisation
- we will follow the complications of the background disease, with the
associated diseases
- the complications which appear after the treatment with medicines
- accidents, incidents
19. The para-clinical exams
- for the biologic parameters we can repeat it daily and follow the evolution
21. The monitoring of the behaviour of the patient
- The vicious position in the bed depending the affection
- The expression of the face
- The psychological state
- Appetite
- Sleep

II.3. THE CARDIO-RESPIRATORY-CEREBRAL RESUSCITATION (R.C.R.C)

The natural death, cardiac causes which is produced by the sudden loss of consciousness,
less than an hour when the symptoms started, we call it sudden death.
189
Respiratory arrest (stopping breathing), and cardiac arrest (cardiac arrest) means the cessation
of cardiac and respiratory function corresponding clinical death.
Stopping breathing without stopping the heart, so the presence of carotid artery pulse, leave
an interval of 3-10 minutes or 12 minutes, to be able to make effective respiratory
resuscitation successfully. Instead cardiac arrest is invariably followed by respiratory arrest in
20 to 30 seconds.
So there are respiratory resuscitation with heart massage but no cardiac massage without
artificial respiration.
Debuts with clinical death which causes cardiac arrest and stopping cerebral circulation and
lasts 3-4 minutes.
If a victim with clinical death benefit of a cardiopulmonary resuscitation (CRR) effective and
timely manner, it can completely return to normal life.
Conversely if there is a delay over 4 minutes or CRR inefficient, lack of oxygen to the brain
leads to nerve cell death biological or final, irreversible damage.
Aetiology: 95% of the disease which produce sudden death have a cardio-vascular aetiology:
 Coronary,
 Left ventricular hypertrophy,
 Myocardial disease,
 Inflammatory disease,
 Degenerative disease,
 Neoplastic disease,
 Congenital disease,
 Neuroumoral instability,
 Pulmonary emboli,
 Anti-arrhythmic medicines,
 Hydro-electrolytic disorders,
 pericardial tamponade,
 Aorta disequant aneurism,
 The maxim effort etc.
The cardiorespiratory harass is an event which interferes suddenly, anywhere and anyhow
with high mortality.
The clinic diagnosis of the cardiac harass would be sustained by:
- The disappearance of the pulse in the great arteries (carotid and femoral),
- The stop of the breath which is preceded by gasp (gasping),
- The loss of the state of conscience,
- Bilateral areactive midriasis (uncertain sign),
- Complete relaxation of the musculature and sphincters,

190
 - Deformed QRS complexes (electro-mechanic dissociation = inefficient hear
with present EKG trajectory),
- Isoelectric line (asystole = stop of the heart in diastole or systole)
- Atonia or contracture.
Cardio-respiratory resuscitation, is expressed by supportive care and should ensure
oxygenation CNS, myocardium and all vital organs until full establishment plan intensive
care.
Resuscitation measures are carried out to resume spontaneous activity of the myocardium.
The success rate of resuscitation is to perform resuscitation therapy is mandatory to carry out
a maximum of 4 minutes of cardiac arrest and the establishment of definitive therapy in 8
minutes.
After apnoea, the heart continues to pump blood for a few minutes and the reserves of O2 in
the blood and lung are sufficient only for a few minutes.
Occurs in cardiac arrest to stop blood flow, blood oxygen cannot be released to the tissues and
vital organs present in the O2 is sufficient for only a few seconds.
Stopping myocardium is accompanied by ventricular fibrillation, ventricular tachycardia,
asystole and electromechanical dissociation.
Cardio-respiratory resuscitation involves techniques which covers medical staff (BASIC LIFE
SUPPORT) and untrained public and definitive management techniques of cardiac arrest,
with endotracheal intubation, defibrillation electrical and pharmacological intervention
(ADVANCES CARDIAC LIFE SUPPORT).
CRR aims to reduce disability and death avoidance.
Terminal condition requires acute decompensating of vital functions leading to loss of blood
pressure, consciousness, movement and breathing (P Safar and Negovschi). Terminal
condition continued clinical death manifested by absence of large arteries pulse, no breathing
(apnea), coma, cadaver skin. Shortly appears that brain death is manifested by the irreversible
necrosis of the brain, particularly the neocortex, but not to the bulb.
Fatal brain death (coma exceeded) is necrosis whole brain and brainstem.

Necessary materials for CRR:

1. Guedel pipe

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2. Intubation probes (all sizes) of a calibre adequate for the age of the patient, adequate
connector, with the verification of the integrity of the air tightening of the balloon.

3. Laryngeal masks.

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4. Ventilation masks (all sizes)

5. Probe for tracheostomy

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6. Mandrel, (if it is considered necessary)

7. Rubben balloon, with mask of adequate sizes

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8. laryngoscope, with more blades and adequate dimensions for the patient

9. secretion vacuum
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10. sanitary materials (syringes, branula, perfuser) for injecting medicament substances

11. Emergency medicaments

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12. Defibrillator (permanently charged)

13. Monitor for showing: TA, AV, SO2, EKG trajectory, temperature

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14. Devices of mechanical ventilation

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15. Dispositive for fixation of the endotracheal probe.

16. Solutions for perfusion

17. Emergency case for resuscitation

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18. Magill tuck

Necessary liquids in CRR

All the liquids will be administered only intravenous (i.v.)
The necessity of the administration consists in:
- Re-establishing the circulatory blood volume
- Compensates after the vasodilatation, the venous stasis and the capillary losses,
after the cardiac harass
- corrects the composition of the blood
- the replacement of some special needs: osmo-therapy, artificial alimentation
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 - they maintain the hydration and the renal flux
- assure the hydro-electrolytic balance
- assures the caloric contribution
necessary solutions:
- physiologic serum 9 ‰
- Ringer solution
- natrium bicarbonate 14 ‰
- glucose 5 % ; 10 %
- dextran 40 saline solution 6 %
- dextran 70 saline solution 6 %
- human albumin
- plasma
- integral blood and derivatives of blood
in comparison to Safar’s formula, the new guides of CRR present more modifications and the
most important are mentioned lower:
1. The immediate recognition about the state of the patient – cardio-respiratory harass –
through the fact that the patient does not respond to the stimuli and not by searching the pulse.
2. the cardiac external massage (ECM) initiated rapidly, maintained continuously, 100/min, in
the middle of the sternum, with a rapport compressions/respirations 30:2 – essential element
in the CRR, more important than the artificial ventilation.
3. Defibrillation:
• in FV or ventricular tachycardia (VT) without pulse: as precocious as possible;
• 360 J from the start to the uni-polar defibrillators;
• a single shock.
4. Drugs:
• Giving up to adrenaline in high doses
• Amiodaron antiarhythmic of first intention in the case of FV
refraction at 3 electrical shocks
5. Moderated post-resuscitation hypothermia (65)

The phases of the cardio-respiratory resuscitation

In CRR se 3 phases follow one after the other:
1. the emergency therapy (basis resuscitation): BASIC LIFE SUPPORT, it is the phase that
comprises the basic oxygenation.
2. the advanced resuscitation: ADVANCED LIFE SUPPORT, it is the phase of establishing
the general situation.
3. the prolonged resuscitation: POST RESUSCITATIVE LIFE SUPPORT, it is the phase
after resuscitation which comprises the cerebral recovery.
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All these 3 phases are categorised alphabetically, from A to I.
1. The emergency therapy.
The elementary measures of resuscitation, BASIC LIFE SUPPORT (BLS) comprise:
A. AIR WAY = assurance of the liberty of the air ways.
The patient is placed on a solid surface, supine upside extension, with open mouth.
If secretions, vomiting, foreign bodies, remove your mouth with your finger (gloved) or
pharyngeal aspiration is, pharynx-laryngoscopy with special instruments (forceps Kelly,
Magil or vacuum).
Obstruction by foreign body airway causes rapid death in young children and adults airway
obstruction is encountered during the meal, with food or after accidents.
It then moves to stem mounting Guedel, followed by tracheal intubation, insufflation or jet
cricotirotomy trans-laryngeal.

Tracheal intubation is the most effective method, because separates the airway of the
digestive keep airways free, and facilitates lung ventilation removes gastric aspiration.
In people aware, intubation, cardiac arrest is maintained in the following cases: absence of
laryngeal reflexes, shallow breathing, respiratory failure, insufficient cleaning secretions
trachea-bronchial.
Instead, the comatose patient intubation remains long time to resume spontaneous breathing
efficiency.

B. BREATHING = assuring the pulmonary ventilation.

The person who performs the resuscitation must determine that the patient has respiratory
efficiency, observe expansions of the chest.
Assessing the effectiveness of breath should not last more than 10 seconds. It quickly switch
to artificial respiration mouth to mouth or mouth to nose (in this case you need a double
current volume of one who breathes air).
Respiration is the process by which air enters lungs filled with air with oxygen and remove
carbon dioxide.
Artificial respiration technique is done after the release of the upper airways, the following
technique:
Hyperextension of the head: passing a hand under the victim's neck and neck rises, and the
second hand, placed his forehead, push the head back then insert a roll improvised a coat or
blanket under the victim's shoulders. It then moves the jaw luxation by pressing the outer
angles of the jaw with the four fingers of both hands and thumb on his chin; projecting lower
jaw forward so that the lower dental arch to exceed that upper. In infants and young children

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head hyperextension will aggravate the obstruction; in these cases we will only support the
mandible and we will sprain anteriorly, with hyperextension of the head.
The nose clamped with the thumb of both hands.
After this training, reanimate insufflates a deep breath, holds his breath in deep inspiration,
then apply quickly, his mouth wide open, his lips parted lips over the victim and blow air
down the victim's lungs airways.
Re-animator circumference lip should cover the victim's lips to prevent air leakage in corners
of the mouth. This sequence is repeated breathing 14-16 times per minute in order to be
effective. Adults should we must forcibly insufflate and for children it is easier and even more
easily in infants with special care not to break the alveoli.
If we have equipment on hand to perform ventilation mask balloon Rubben and 100% O2,
with assisted ventilation V = 10-15 ml / kg / body.
The respiratory frequency (R.F.) = 12 – 14 resp./min and O2 100 % for the intubated patients.
If the artificial respiration must be maintained for a longer while we use the mechanical
ventilation, on ventilating support.
The one who performed the mouth to mouth respiration (nose) is in danger of contamination
with the hepatic viruses, Koch bacillus, HIV virus, which are transmitted through saliva.
This is why it is necessary the protection with a clear textile material, applied on the mouth
and nose of the patient. It is recommended to use Ambu Life Key

C. CIRCULATION = assuring the blood circulation through thoracic compression.

External cardiac massage

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Checking the pulse was published in the first resuscitation guidelines in 1968 and was signed
"gold standard" in this existence or absence of mechanical activity of the heart (I Cristea).
Thus no pulse indicates cardiac arrest and need for external cardiac massage.
External cardiac massage is performed by compression of the heart.
Rhythmic chest compressions are applications, serial pressure on the lower half of the
sternum that produce blood flow by increasing intra-thoracic pressure or directly compressing
the heart.

Rhythmic chest compressions are applications, serial pressure on the lower half of the
sternum that produce blood flow by increasing intra-thoracic pressure or directly compressing
the heart.
The bloodstream through the lungs by heart massage, with ventilators executed correctly,
constitutes an adequate intake for the brain and vital organs until early defibrillation. It is
necessary for optimum oxygen flux, which is produced by a number of> 80 / compressions /
min.
During CRR, coronary perfusion pressure gradually increases performance by cardiac
massage sequences.
External chest compression produces increased intra-thoracic pressure is transmitted equally
in all intra-thoracic vascular formations. Aortic blood pressure in the arteries is transmitted
entirely extra-thoracic. In contrast in the venous vascular collapse is achieved (external
compression). The result is an arterio-venous pressure gradient which causes the mobilization
of blood extra-thoracic.
External cardiac massage (MEC), is made by applying the palm of the left (the right-handed),
the lower half of the sternum and the other hand over his left hand, so that your forearms are
parallel, the parallel shaft elbow joint. It is necessary that the shaft arms to be placed
perpendicular to the axis of the sternum.
Fingers can be reached or crossed, but does not touch the chest. Shoulders must be positioned
above the hands. There will never appendicitis xifoid table. Elbow joint will never be the
extension and flexion.
During the massage it is necessary to completely release the pressure on the chest to allow
blood flow in the heart and lungs.
Coronary and cerebral perfusion is effective when 50% of the cycle compression -
decompression phase is allocated 50% of compression and relaxation phase.
To be able to maintain proper hand position during a cycle of compressions, hands on chest
does not rise.
External cardiac massage (ECM) initiated rapidly, maintained continuously 100compresiuni /
min in the middle of the sternum with a report compressions / breaths 30: 2 - essential in
CRR, more important than artificial ventilation.

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At the beginning of reanimation will apply chest compression cycle 30 without the two
insufflation. Performing cardiac massage is more important than achieving ventilation.
However massage association with ventilation is the most effective cardio respiratory
resuscitation success. (65)
If the patient is intubated endotracheal for one Reanimator recommended synchronization
technique (simultaneity), namely: simultaneous chest compression inspiration, so in this way
obtain a greater blood flow and increased thoracic pressure increase.
Currently, based on the ideas recommended a new technique for cardiac resuscitation:
compression of the chest with a frequency of 60-80 compressions / minute, with a duration of
60% of cycle respiratory ventilation simultaneous compression of the chest and achieving
pressure in the ways overhead 60-110 cm H2O.
Children under 1 year, chest compression is 2-3 finger or thumb applied to the sternum hand
applied to the sternum and the other 4 fingers inter-scapular applied. The frequency of 80-100
compressions/min, amplitude 3. 2 cm.
For children between 1 and 8 years old, chest compression is 3 fingers with an amplitude of 3-
4 cm, chest compressions frequency / ventilation 80 / min.

We never make for children abdominal compression because the risk of rupture of the liver.
2. The advanced resuscitation, ADVANCED LIVE SUPPORT, (ACLS) follows the
reestablishment of the circulation, for this being necessary a medicament treatment and
electric defibrillation.
We pass rapidly for inserting a venous catheter (branula) peripheral or central. In case this
manoeuvre can’t be performed the medicines can be administered also endotracheal on the
intubation probe, but also in double amount, comparatively with the i.v. administration.
D. DRUGS = medicines.
1. Adrenaline (f 1mg/ml)
• 1 mg la 3-5 min i.v.
2. Amiodaron (f 150 mg)
• indications: FV or TV without pulse refraction at 3 shocks
• Doses: 300 mg i.v. (diluted in glucoses 5% up to 20 ml) → ±
repetition 150 mg → perfusion 900 mg/24h
• adverse reactions: bradycardia, hypotension
3. Atropine (f 1mg/ml)
More recent studies HAVE NOT succeeded to show the benefit of the atropine administered in
the case of the cardiac harass from the hospital or outside of it and, this is why, the routine use in the
asystole or DEM – IT IS NOT recommended!
• Doses: 3 mg i.v.
4. Lidocaine (f 2% - 20 mg/ml, 4% - 40 mg/ml)
• Indications: FV şi TV refraction (second line after amiodarone)
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• Doses: 1-1, 5 mg/kg ±50 mg (maximum 3 mg/kg first hour)
5. Magnesium sulphate (f 50 %, 20%)(43-47)
• indications:
a.FV refractor with hipoMg
b.Ventricular tachiarrhythmia + hipoMg
c.Tip trorsad
d.Digitalic toxicity
• Doses: 2g i.v. (4ml sol. 50%) in 1-2 min ± repetition at 10-15
min
6. Na Bicarbonate (sol. 8, 4%-1mEq/ml)
• indications:
a. SCR with hyper-potassemia
b. Intoxication with tricyclic anti-depressives
c. ± pH ≤ 7, 1
• Doses: 50 ml sol. 8, 4% p.e.v.
7. Calcium (sol. 10%)
• indications:
- EAWP cu – hyper-potassemy (65)
- hypocalcaemia
- overdose of Ca blockants
- Doses: 10 ml i.v. +/-repeated (65)
In situations where there is no hypocalcaemia or hyperkalaemia we can administer Ca clorure 10
% (CaCl2), 10 ml i.v. slowly. Doses for babies are 0, 3 ml/kg/body and for small children 0, 25
ml/kg/body.
E. ELECTROCARDIOGRAM = we set rapidly an EKG monitor (in 2 derivations) to show
the electric trajectory of the myocardium, the arterial tension, the saturation in O2 (SpO2), the
ventricular allure (AV) and the temperature (T), we pass to the identification of the
arrhythmia and their treatment.
EKG – for the diagnosis of form for the cardiac harass
- ventricular fibrillation
- inefficient heart
- asystolia
F. FIBRILATION TREATMENT = manoeuvres of electrical therapy, defibrillation and
electro-stimulation.
This manoeuvre is made rapidly, immediately after the diagnosis was made of ventricular
fibrillation (VF) or when the patient is in cardiac harass of over 2 minutes.
The defibrillation is made after minimum 2 minute of ventilation and thoracic compressions
and the cardiac activity weren’t retaken.

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The defibrillation FV or the ventricular tachycardia (TV) without pulse must be initiated as
soon as possible. It starts with 360 J from the start to the unipolar defibrillators (65).
It begins with an initial dose of 200 – 300 J, in this time it is perfused adrenaline, it is made in
2 shocks and if there are inefficient we increase to doses of 360 J.
The external defibrillation is made with 3 J/kg for the adult and 2 J/kg for children.
If after 1minute the fibrillation was not remitted, the defibrillation is retaken 2 - 3 times with 3
– 5 J /kgb
The internal defibrillation is made with 0, 5 J/kgb.
The repetition of the defibrillator shock, is imposed in alternation with the defibrillator with
R/ECM.
The electric shock defibrillator produces a simultaneous depolarisation of all the myocardial
fibers, after which the heart may not begin spontaneous contractions in conditions of good
oxygenation and without state of acidosis. The duration of an electrical shock is of 0, 01 sec.
It is preferable the immediate defibrillation, before starting the ABC – in CRR, when it is
possible. If it stays inefficient after 60 seconds we begin the CRR.

Instead the duration of cardiac arrest is not known, it takes 2 minutes of emergency treatment
(basic life support). They are used for defibrillation, external defibrillators, external
electrodes, portable, automatic or semi-automatic downloading shocks.
It also uses the pacing cardiac emergency can be manually (pacing fist) or electrically
maintain the heartbeat and stimulates the heart (70 b / min) with a low voltage, in cases of
severe bradycardia dissociation eletromagnetic or asystole. A peace - maker (internal) can
have a fixed frequency for atrio-ventricular gr III.
Each minute that passes after cardiac arrest patient survival decreases by 10% without
defibrillation. Therefore it is better for medical staff to be trained in performing such
manoeuvres.
The shock rhythms
For the adult the most common rhythm disorder is for the patients with SCR is VF, which
may be preceded by an episode of VT or even supraventricular tachycardia (68).
1. Once confirmed the cardiac harass:
• shout for help
• ask for a defibrillator
• start immediately the manoeuvres for the cardio-pulmonary resuscitation (CPR) with the
rapport between the ECM and VM of 30:2
2. Once you have received the defibrillator:
• diagnose the rhythm applying the paddles
• if VF or VT is confirmed, charge the defibrillator and administer one shock (150—200J
biphasic or 360-J monophasic).

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• without re-evaluating the rhythm or the pulse retake CPR (30:2) for 2 minutes. Even if the
defibrillation was successful, seldom the pulse is palpable immediately (69), then the delay
given to the palpation of the pulse could compromise the heart (70).
3. The CPR is continued for 2 minutes then we re-evaluate.
• if the patient is in VF/VT we will administer the second shock (150—300J biphasic or 360J
monophasic)
• CPR is continued.
4. after 2 minutes the rhythm is re-evaluated:
• if in continuation the patient id in VF/VT we administer one vial of adrenaline
• we administer the second shock
• the CPR is retaken
5. After 2 minutes of CPR we re-evaluate the rhythm. If we still have the VF: (65)
• a bolus of amiodaron is administered (300 mg i.v.)
• if we don’t find an organised rhythm we continue the CPR.
The re-evaluations of the cardiac rhythm must be short, and the pulse must be re-evaluated
only if it is evidenced an organised rhythm during the ECM the ECM is paused for the re-
evaluation of the pulse only if the patient presents signs of a successful resuscitation. Ifthere
are some doubts concerning the presence of the pulse, in the presence of an organised rhythm,
the resuscitation manoeuvres are retaken.
The analysis of FV waves showed that the likelihood of successful defibrillation is all the
greater as the period between ECM and management of patients with EAWP is very small if
the underlying disease is not identified or cannot be treated.
If the initial rate is EAWP or asystole, start resuscitation with chest compressions and the
ratio of mechanical ventilators
30: 2.
The asystole can be exacerbated or precipitated by vagal hypertonia and theoretically it can be
reversible if given a drug vagolytic; so despite the fact that there is still no evidence that
routine administration of atropine for asystole would increase survival, atropine is
administered at a dose of 3 mg (Dose that ensure maximum blocking vague).
The airways must be secured as quickly as possible to enable the ECM without interrupting
mechanical ventilation. After 3 minutes of CPR re-evaluated heartbeat. If no rhythm is
present, or there is no change to its resume CPR. If present an organized attempt to palpate the
pulse rate.
When the diagnosis of asystole, must be measured carefully ECG waves "P" because this type
of asystole may respond to cardiac pacing. VF is small and difficult to distinguish from
asystole unresponsive to shocks. Continuing CPR may improve the amplitude and frequency
of the waves and could increase the chances of successful defibrillation. (65)
If during resuscitation or asystole rhythm EAWP switch FV, have followed the protocol
resuscitation of FV. (65) is less shock.
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Regardless of the heart rate (able to receive shock or not) it is administered epinephrine (1
mg) every 3-5 minutes until resuscitation is successful.
The non-shock rhythms
They are: the electric activity without pulse and asystole.
The patients with electrical activity without pulse (EAWP) (also called electro-mechanic
dissociation, EMD) often present myocardial contractions, but they are too weak for
producing a pulse wave which can be detected.
EAWP is often caused by reversible affections and it may be treated if these affections are
identified and treated correctly.
3. Steps taken after the resuscitation comprise POST RESUSCITATIVE LIVE SUPPORT
(PRLS) – it is the resuscitation phase which comprises thecerebral recovery in case that the
cardiac harass was resuscitated.
G. GAUGE = the evaluation of the general state of the patient during the CRR.
In this phase is performed to further assess indication CRR and find the cause that caused
cardiac arrest. All vital parameters are evaluated: TA, AV, respiration, cardiac activity, SaO2,
diuresis.
If CRR manoeuvres are not effective after 60 minutes interrupt.
H. HUMAN MENTATION = the resuscitation of the central nervous system (CNS) with
the assurance of the protection of the neuronal rebuilding. Trophic medicines are administered
for the nervous cell: Pyracetam, Cerebrolizin, Pyramen, etc
4 probes are set: (the intubation probe, gastric, vesical, brannula) EKG, O2, artificial
ventilation.
Sedation with barbiturates 30 – 90 mg/day; ½ from the dose initially, then the rest
Liquids and electrolitites.
For the maintenance of the AT – Dopamine.
Osmotherapy – Manitole 20 %; 0, 5-1 mg/kg/24 h.
Corticotherapy: - Dexametazon; 1- 6 mg/kg, in the first 2-3 days.
Controlled hyperventilation at PaCO2 of 25 -35 mmHg = hyperbaric therapy.
Moderated external hypothermia.
I. INTENSIVE CARE = the continuation of the intensive care, for the confirmation of the
efficiency of the CRR and the recovery of the sick. In the case when the cardiac harass was
resuscitated, we pass to the effectuation of a scheme of intensive care.
Urgently we take the biologic samples and we monitor the vital parameters, connecting to all
the pathologic parameters.
We will institute specific therapies based on the analysis of the EKG trajectory made during
the resuscitation manoeuvres.
We will make general and special intensive cares of consolidation and recovery.
We will perform the treatment of the resuscitation complications (flap etc.)
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The disfunction treatment (respiratory, circulatory, cerebral, renal, metabolic)
Adjuvant medication.
Brethylium: 5 mg/kg i.v.
Nifedipin, verapamil
Volemic solutions (crystalloid and colloidal)
Propranolol 1 mg/70 kg, up to the maximum dose of 5 mg
Nitro-glycerine 50 mg at 500 ml (5 – 10 μg/min)
Opioid in micro-doses
Diuretic - furosemide 0, 2 – 2 mg/kg.
Bronchodilators – miofilin 5 – 10 ml i.v. very slowly.
Intra-tracheal administration of medication is allowed for adrenaline, atropine, lidocaine in
i.v. doses diluted in 10 ml sterile water.
If cardiac arrest occurs on an open chest cardiac massage is practiced internally.
This resuscitation is more effective offering a better chance to sustain the cerebral and
myocardial viability and restore general circulation. This happens to sick during the surgical
act or on an open chest.
The technique for this type of cardiac resuscitation is to: intermittent positive pressure
ventilation with PEEP (patient endotracheal intubation)
An incision of skin and muscle above 4 or 5 intercostal space, followed by perforation blind
with scissors or scalpel handle for opening intercostal space by introducing a pull on and far
from the coast. Is taken in the hand and compresses the heart (without opening the
pericardium), at a rate of 60 b / min. Reanimatorul patient stands on the left rear left hand and
place the thumb over the left ventricle and right ventricle previously fingers over 2-5. Avoid
compressions atria. With his right hand trying compressing the descending aorta.
It can perform the simplest technique to compress the heart against the sternum or using both
hands. If ineffective, can open and pericardium.
The internal cardiac massage adrenaline is injected into the left ventricular cavity. Internal
defibrillation electrodes begins with shock 0.5 joules / kg / body, which increases if they are
ineffective.
In any case of stopping resuscitation cardiopulmonary resuscitation is done after 30-60
minutes in case the patient remains in asystole or agonizing pace, after correct endotracheal
intubation and it is not sensitive to the medication.
If the resuscitation was ineffective and the heart has not resumed the activity we pass on to
confirm brain death. The stop of the brain function consists in the lack of responsiveness and
lack of response (patient does not respond to verbal or painful stimuli) and the absence of the
specific brain reflexes (pupillary response, cornea, oro-pharyngeal and absence of the
respiratory responses).
The decision to stop the CRR, is set by the doctor.

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Always the medical personnel should consider the patient's condition and the circumstances in
which the arrest took place, and the factors of prognostic importance for resuscitation.
It is very important to assess the length of time, that passed until the start of the resuscitation,
time to defibrillation, the stress before the cardiac arrest and the comorbidity.
The persistence for the brain death must be within a well-established time, namely:
- 6 h with the confirmation of the isoelectric aspect EEG,
- 12 h, without the confirmation of the isoelectric aspect of the EEG,
- 24 h for anoxic cerebral lesion, without the confirmation of the isoelectric aspect
of the EEG.
It is well that, the simple notions of algorithm of the CRR (BLS), to be known by each person
starting with the age of 14 years, even if it is not a sanitary cadre, in order to give the first aid
in those minutes, in which the fight with death must be won.
Particularities of the guides of CRR for children
The new guides of CRR for children has tried to simplify the protocol of resuscitation in order
to disappear the situations in which children are resuscitated due to the fear of getting sick.
This fear was alimented by the fact that these protocols were different from the ones of the
adult.
After the studies, it was shown that the survival is considerably higher if the CRR is practiced
no matter the applied protocol.
(adult or child), towards the situation in which it is not resuscitated but it is awaited for a
specialised team (71-73).
The rapport compressions/ventilations
It is recommended that in the situation in which there is a single saviour to practice a CRR
with a rapport 30:2 (as for the adult). In the case in which there are two or more saviours the
CRR will be practiced with a rapport of 15:2 (74-76).
The external cardiac massage
For the small baby the ECM is practiced with two fingers in the case that we have a single
saviour and if there are two it is practiced using both thumbs (77-78). For the childe older
than one year old the ECM is practiced using one or both hands.
The automatic electric defibrillation
Recent studies showed that the electric defibrillators are capable to evaluate correctly the
cardia rhythm to children and extremely seldom they show that they could recommend
incorrectly the administration of a shock. According to the new guides of resuscitation it is
recommended the administration of the shocks to children older than one year old (65)
(4J/kgb) (79). For the administration of the shocks it is recommended the use of the paediatric
paddles in the case of the children between 1 and 8 years (we can use also the paddles for
adults in the case that they are not available for children).
In the case of the children older than 8 years old it is used the protocol for the adults.

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Ways of administration of the medicines
The intra-venous way
The drugs may be administered in the peripheral venous system and also on the central
catheter. Even if the plasmatic peaks are obtained more rapidly in the case of the
administration on the central catheter (80), in order to set the catheter the CPR should be
interrupted thing which is not correct. The drugs that were administered in the peripheral
venous system should be followed by the administration of at least 20 ml of fluid and the lift
of the extremities.
Ways of alternative administration
They are used when the intravenous way is not accessible.
The intra-bone way is more often used in children and it may be used for adults also (81). The
drugs administered inside the bone reach an efficient plasmatic concentration in a time
comparable with the administration on central venous catheter.
The tracheal way is used when the intravenous or the intra-bone ways are not available.
During the CPR the equipotent dose of adrenaline administered intra-tracheal is of 3-10 times
higher than the administered dose i.v. (82-83). If we administer it intra-tracheal, the
adrenaline (3mg) must be diluted in at least 10 ml of distilled water (the distilled water is
preferred to the serum because it assures a better absorption).

The incidents and complications connected to the CRR manoeuvres

1. The incidents connected to the external cardiac massage (ECM)
 Costal ruptures (31,6% of the cases-study on 705 cases) (1) – unilateral or
bilateral
 Fracture-sternal disjunction (21, 1%)
 Rupture of parenchymatous organ (hepatic or splenic) (30, 8%)
 Pneumothorax (13%) unilateral or bilateral
 Hemothorax
 Hemomediastinum (18, 3%)
 Hemopericard, heart lesions (< 5%)
 Foamy blood in the heart
 The late application of the ECM (example: waiting for a team of resuscitators
in the saloon, cabinet, corridor, etc., without initiating the ECM).
The cardiac internal massage involves problems of indication, surgery moment, technique,
results.
2. Incidents connected to the respiratory resuscitation:
 The inopportune manoeuvre of the head (possible fracture of vertebral spine,
excessive hyperextension of the head, temporal-mandibular luxation)
 Excoriations, abrasions face, neck

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  Inopportune aspiration, bleeding
 Brutal tries of oro-tracheal intubation: broken teeth, pharyngo-laringeal fractures
(20,4%), hyoid fracture
 I.O.T. failed, unrecognised oesophageal intubation
 Hyperinflation or the gastric perforation
 Blocked laryngeal mask
 Pulmonary aspiration
 Cricotirotomy tentatives, hypoxemiant tracheostomy, bleeding, compressive
hematoma, subcutaneous emphysema
 The Heimlich manoeuvre with stomach rupture
 Emboli of bone marrow
3. Incidents connected to the drug administration:
 Adrenaline administered in the myocardium, lung (pneumothorax), unadequate
dilution (adults and children)
 Venous approach: - para-venous administration
- central approach: intrapleural, mediastinum, pneumothorax, catheter
knot in the right ventricle, hemothorax, sub-clavicle bilateral approach, catheter
rupture, lost catheter, faulty positioning of the catheter (catheter towards the cephalic
extremity, catheter in the heart), extraction of the catheter after the death (incorrect
medico-legally).
4. Incidents connected to the equipment
- faulty devices, not checked previously : labile connections – disconnections from the tubes;
broken balloon; electrodes for monitoring that are dry, tangled;
- uncertain use of the devices: delay, imprecise press of buttons
- defibrillation, burns –Jouli doses different for adults and children
5. Incidents connected to the methodology, tactic:
- deficiencies in the continuous medical education
- insufficient theoretical and practical preparation: incompetence, ignorance, non-prevision,
imprudence, temerity, neglect, easiness, inadvertence, not applying some measurements of
prophylaxis, all may lead to culpabilities.
- location: surgery room (disconnected alarms, leaving the room); salon (without the
minimum equipment for CRR); WC – not monitored; street; vehicle (bus, tram); factory
- attitude: promptitude (+,- ) in applying the guide; certainty in applying the CRR guide;
applying the cardiac massage for the victim with present pulse, collapse, respiratory
depression; mouth to mouth respiration, balloon, for the victim with respiratory moves (there
are guides which give up to this manoeuvre); applying the CRR manoeuvres for the deceased
victim of over 15-20 minutes – yes or no?
- the data taken from testimonies are always imprecise, subjective, emotional

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- it is usually accused the declaration of the death without taking any action for resuscitation
- fix mydriasis – criterion of abstention from the CRR ?!
- checking the pulse (carotid, femoral, humeral, radial) it is excluded from the guide – loss of
time (40% of the others do not detect the pulse, 10% do not discern the absence of the pulse)

II. 4. DIAGNOSTIC CRITERIA FOR THE DONOR IN CEREBRAL DEATH

The Conference of the Medical Regal College from Great Britain of 1976 stipulates the
following: „if the brainstem is dead, then the brain is dead, and if the brain is dead, then also
the person is dead” (64).
The donor is the individual who gives in cells (DEX 98).
The diagnostic criteria of the cerebral death, 1995 (modified after the American Academy of
Neurology Practice Parameters for Determining Brain Death in Adults.)
The diagnostic criteria of the cerebral death
• state of coma
• known ethiology of the coma
• exclusion of the reversible causes of coma: hypothermia, medicines, toxics, disorders
hydro-electrolytic, endocrine disorders
• the absence of the reflexes of the brainstem
• absence of the motor answer
• apnoea
• the evaluation of the patient must be repeated every 6 h, with the maintenance of the
diagnostic
• the additional para-clinic tests are necessary only when the clinical examination is not fully
cogent
For the success of the transformation of a potential organ donor in an effective donor we must
follow a series of steps, which follow one after the other in the form of a protocol:
A. The identification of the potential donor
B. The diagnosis of the cerebral death
C. The declaration of the diagnosis of cerebral death
D. Announcement of the coordinator doctor for the transplant, about the permission of the
family
E. The monitoring and maintenance of the potential donor in intensive care
F. The monitoring and maintenance of the potential donor during the take up
The absolute contraindications of the organ transplant: the prolonged hypotension, the
apparition of the signs of organic suffering, sepsis sever, syndrome of multiple organic
dysfunction, pre-existent or acquired lesions of the organ which will be transplanted,
neoplasies (with the exception of the primitive cerebral tumours, skin carcinoma, neoplasms
of uterine col in situ), infections: HIV infection (excepting the transplant from a positive HIV
recipient), TBC incompletely treated, infections of the CNS (acute bacterial and viral
214
meningitis, encephalitis, cerebral or subdural abscess, infections of the CNS with slow
viruses, degenerative diseases of the CNS with possible viral ethiology), age > 55 years only
for the heart and pancreas transplant cord (there is no other age limit for other types of
transplant), systemic with repercussions over the organs that will be transplanted
(collagenases, vasculitis) and the refuse of the family.
The relative contraindications of the organ transplant are: individual habits of the donor that
compromise the function of various organs (chronic alcoholism, drugs, or nephrotoxic drugs
hepato, prostitution etc.), hypertension treated without repercussions visceral recently
installed diabetes without systemic effects, increased Doses of vasoactive substances used to
maintain donor , resuscitated cardiac arrest, without being able to identify the correct protocol
resuscitation, infectious diseases: STDs, depending on the stage, hepatitis virus a, B, C, D
(excluding liver donation, but
with the possibility of donating organs to recipients other positive), herpes infection,
cytomegalovirus, Epstein-Barr virus (transplant recipients only possible positive) chronic
medication with possible organ damage.

The specific criteria for exclusion are taking heart endocarditis, severe coronary artery
disease, impaired ventricular function.
Body "ideal" should come from a young person between 18 and 40 years with no history of
disease, brain death, serious cranio-cerebral trauma row. Unfortunately these conditions are
found in less than one third of cases (66).
The diagnosis of cerebral death
The diagnosis of cerebral death includes compulsorily three elements: the diagnosis of lesion,
the clinic diagnosis and the para-clinic one.
The diagnostic of lesion
• the cause of cerebral lesion must be known and irreversible or
• the cause of the cerebral lesion is unknown, but sufficient time passed for the elimination of
the reversible causes (hypothermia, hypotension, intoxications etc.)
The clinic diagnosis
• profound coma, lax, areactive
• absence of the spontaneous ventilation
•the absence of all the reflexes of brainstem (ciliary, cornean, photo-motor, occulocephalogir,
oculovestibulary, coughs, deglutition, vomiting, absence of blinking, absence of the ocular
moves spontaneous or provoked, pupils in intermediary position or midriatic)
• absence of the spontaneous moves

The para-clinic diagnostic

a. The apnoea test investigates the presence of respiration when the patient is
disconnected from the ventilator. The test is performed after discontinuation analgosedării at a
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variable interval depending on the materials used (mean 6 hours), if therapist prior to the
occurrence of clinical brain death. Bodily patient temperature must be above 35˚C. It is
considered diagnostic for brain death when there is no spontaneous ventilation increases in
PaCO2 above 60 mm Hg.
b. Electroencephalogram (EEG) It is diagnostic of brain death if the route is flat in all
derivations, attesting to the absence of cortical electro-genesis. Because the investigation is
diagnostic must remove all potentially reversible causes of depression EEG or possible causes
of artefactar route. EEG is repeated at least 2 times at an interval of at least 6 hours.
c. Angiography must visualise the 4 vascular axes carotidal and vertebral; for the patients in
cerebral death it is seen the absence of the cerebral blood flow (is the most specific element of
diagnostic).
d. Echo Doppler the trans-cranial and cerebral scintigraphy also attest the absence of the
cerebral blood flow.
e. The visual potentials evoked, additive or somato-sensitive show the absence of the
specific waves for the patients in cerebral death.
f. The dosage of the lactic acid in LCR and the measurement of the cerebral oxygen
consume are sophisticated tests, used in general for research, which show the absence of the
cerebral metabolism.
To these are added a series of tests for the diagnosis of lesion and exclude potentially
reversible causes of coma (cerebral CT, toxicological tests etc.).
Complete neurological exam, certifying the absence of brain activity and brain stem, together
with positive tests cerebral death is repeated at intervals of at least 6 hours. When you receive
the second set of positive tests is considered the time of death. It is recorded in the
observation sheet and the statement of declaration of brain death.
The monitoring of the patient with cerebral death
1. Determination of blood group and Rh
2. Laboratory tests made in dynamics: complete hemo-leucogram, blood gases, serum and
urinary ionogram, serum lactate, urea, serum and urinary creatinine, bilirubin, transaminases,
(GTP, proteins, albumins, glycaemia, coagulation tests, amilasemia (serum lipase is more
specific for the functionality of the pancreas)
3. Screening bacteriologic samples: tracheal secretions, uro-culture, hemoculture (initially and
then repeated at 24h). The biochemical tests are repeated as much as necessary (the ones
necessary for the conduction of the maintenance therapy and the ones which attest the
functionality of the organs that will be transplanted).
4. Tests for virus: HIV, AgHBs, Ac-anti HVC, CMV (citomegalovirus), VDRL, toxoplasma,
herpes simplex (important for the criteria of inclusion, exclusion)
5. Cross match tests: for the compatibility donor – recipient
6. The non-invasive monitoring: EKG, arterial tension, pulsoximetry, temperature, hourly
diuresis, gastric aspiration, capnography, ecocardiography trans-oesophageal
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7. The invasive monitoring of the medium arterial pressure, central venous pressure, of the
saturation in the central venous blood, of the pressure in the pulmonary artery (optional, in
selected cases)
The indications of the monitoring of the pressure in the pulmonary artery are (67, 68):
• the fraction of ejection of the left ventricle under 40% (to the bi-dimensional
echocardiography)
• high necessary of inotrope substances (> 10 μg/kg/min for dopamine, dobutamin)
• doses progressively high of vasopressor substance (see the algorithm from figure 1)
8. The coronary angiography has the following indications (67):
• for the potential donors of over 55 years old for men or over 60 years old for women
• the age over 40 years and the presence of risk factors for coronary disease
• the presence of more than 2 risk factors for coronary disease, no matter the age
• the history of cocaine abuse
The angiography must be made with contrast agents with reduced risk (non-ionic or
isoosmolar), using the minim necessary amount, eventually without ventriculogram.
It is recommended the administration of N-acetylcysteine prophylaxis once anticipated
performing angiography. N-acetyl cysteine may be administered enterally, - 600-1000 mg,
two times a day, or parenterally - 150 mg / kg in 500 mL saline, 30 minutes prior to
administration of contrast substance, then further 50 mg / KGB in the following 4 hours (67).
The angiography must be completed by an angiogram whenever this is possible technically.
There is a threshold limit for the degree of coronary obstruction. The decision must be taken
in conjunction with other factors: status container functionality myocardium possibility of a
coronary bypass surgery or stenting. The absence angiography should not contraindicate
transplantation. The heart must be taken if the ejection fraction is over 40%, can provide
hemodynamic stability. Obviously play an essential role direct surgical evaluation.
9. The hepatic biopsy is made only in the selected cases
The indications of the liver biopsy are: older than 70 years (60 years in those with diabetes),
body mass index over 32, medical history suggestive of liver disease, alcoholism, positive
serology for hepatitis, imaging features suggestive of fatty liver infiltration. Canadian guide
management of organ donors (67) is much narrower criteria for liver biopsy. It is
recommended that liver biopsy guided by ultrasound in obese patients infected with hepatitis
viruses or only when the liver was transplanted in another centre and the surgeon cannot make
a prior evaluation of it.
Simplified protocol for the maintenance of the donor situated in cerebral death
A. Standard monitoring
 Vital signs – at each hour
 pulsoximetry; EKG in 3 derivations
 central venous pressure (central venous catheter)
 medium arterial pressure (arterial catheter)
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  the pressure in the pulmonary artery (catheter type Swan-Ganz) – optional, in some
circumstances
 hourly diuresis – hourly hydra balance
B. Laboratory investigations
 ionogram, analisis of the blood vessels, glycaemia – at each 4 h or even more often,
hemoleukogram, urea, creatinine – at each 8h or more often , AST,
ALT, bilirubin and fractions, coagulation tests – at each 8h or even more often,
Serum lactate – at each 4 h or more often
C. volemic resuscitation: crystalloid solutions, semimolar solutions, colloids
Purposes:
 ventricular allure: 60-100 /min
 sinusal rhythm
 systolic arterial tension ≥ 100 mmHg
 medium arterial tension ≥ 70 mmHg
 central venous pressure 6-10 mmHg
 saturation in the venous central blood ≥ 60%

D. vasoactive substances
 noradrenalin ≤ 0,5μg/kg/min
 dopamine ≤ 10 μg/kg/min
 dobutamine ≤ 10 μg/kg/min
 vasopresine ≤ 4U/h
 adrenalin ≤ 0.10 μg/kg
Indications of catheterisation of the pulmonary artery:
 the function of ejection of the left ventricle < 40% or dopamine necessary >10
μg/kg/min
E. The insipid diabetes
Diagnostic criteria: urinary debit > 4 ml/kgb/h associated with natremia ≥ 150
mmoli/l and/or plasmatic osmolarity ≥ 300 mosm/l and/or urinary osmolarity ≤ 200 mosm/l20
Treatment (doses titrate as diuresis < 3ml/kg/h): vasopressin in continuous infusion,
desmopresin intermittent
F. Fluids and electrolytes
 natremy 130-150 mmoli/l
 normal values for the potasemy, calcemia, magnezemia, phosphatemy
 diuresis 0. 5 – 3 ml/kg/h
G. Therapy of hormonal substitution (controverted)

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Indications: the ejection function of the left ventricle < 40%, hemodynamic instability,
(persistent hypotension, shock insoite of the volemic repletion adequate and of the vasoactive
support)
Substances:
 T3 - 4 μg iv bolus, then 3 μg/h continuous perfusion,
 T4 - 20 μg iv bolus, then 10 μg/h continuous perfusion
 Vasopressin - 1U bolus or 0. 5-4U/h in continuous perfusion
 Metilprednisolone - 15 mg/kg iv at each 24h
I. The nutritional support and the glycaemia
Enteral nutrition (in bolus repeated or continuous, depending on the tolerance,
on nasogastric or jejunal probe)
 20-25 kcal/kg/day
 standard enteral formula
 insulin minimum 1U/h in continuous perfusion as the glycaemia < 150mg/dl
J. Blood and derivate
The optimal level of the haemoglobin: 9-10 g/dl; minim amount acceptable 7 g/dl
 Specific therapy in the case of the coagulation disorders INR < 2, thrombocytes
>80000/mm3

K. Screening bacteriologic
Assay:
 uroculture
 tracheal secretions
 hemoculture (initially, then at each 24h)
 targeted antibioteraphy if there are some clinical signs of infection (85)

II.5. CARDIAC EMERGENCIES

The cardiac emergencies occupy the first place in mortality.
From the cardiac emergencies, the most frequent and with a greater potential of death are:
 the myocardial infarct
 the cardiac insufficiency
 the rhythm disorders
 arterial hypertension (AHT)

II.5.a. THE ACUTE MYOCARDIAL INFARCT (A. M. I.)

A.M.I. is by far, the main cause of death of the patients with the diagnostic of ischemic
cardiopathy. The risk of death is maximum in the first two hours from the start of the disease.

219
Because of this reason, the majority of the deaths happen before the patient reaches to the
hospital. (87)
It is the obstruction of a coronary artery, with myocardial consecutive necrosis, in the
respective irrigated area.
Aetiology
 the emboli of the coronary arteries (infectious endocarditis, valve prosthesis, thrombi)
 inflammatory processes (collagenases, articular rheumatism, lues, rheumatoid
polyarthritis)
 no accord between the demands and the contribution of O2 to the myocardium: (aortic
insufficiency, intoxications with CO2, tireo-toxicosis, prolonged hypotension)
 congenital anomalies of the coronary arteries (left coronary artery, coronary artery
aneurism)
Pathology
There are 2 phases of the disease:
1. the phase from the first 6 hours since the start, when biochemical and metabolic
changes are produced. It is the phase when the cellular membrane is altered through
irreversible lesions, thing which determined the liberation from the myocardial cell
protheolytic enzymes. This is why we can give the enzymatic diagnosis of the AMI,
through CPK (phosphokreatinkinase) and also through the troponines T and I.
2. the phase after the first hours since the start I.M, when the hemodynamic
consequences appear:
 the alteration of the systolic function is produced for the left ventricle, which
produces 4 types of abnormal contractions (disincronism, hipochinesy,
achinesy and diskinesy)
 the ischemia alters also the diastolic function of the left ventricle. The diastolic
function of the left ventricle precedes the systolic one.
In AMI, it is produced an anatomic and functional obstruction, in the vascular coronary bed
→ regional myocardial ischemia, which if the ischemia continues → myocardia infarct.
If the extension of the infarct is greater, it depresses the ventricular function, and the filling
pressure rises, reducing the pressure of coronary perfusion.
It follows the ventricular re-shaping, which lasts from the start of the MI, months or years,
with the consequences on the ventricular performance. MI, appears after a difficult physical
activity, on a background of tiredness and emotional stress, but it may appear also in other
situations (after surgical procedures, rest, sleep, traumatisms).
The majority of the MI, interfere around 9 o’clock in the morning, and the deaths, around 8
o’clock in the morning (hours associated with the increase of the plasmatic catecholamine, of
the cortisone and of the increase of the thrombocitary aggregation).
Symptomatology

220
  IM, it may appear in full apparent health, in 50 % of the cases, without premonitory
signs
 At 20 % of the patients there are prodromal symptoms:
- Angina precordial pain
- Fatigability
- Dyspnoea
- Anxiety
- Sensation of general sick
- Palpitations
- Cold sweat
- Nausea
- Feeling of imminent collapse
- Nausea, vomiting
The pain, is the main symptom, variable in intensity, from case to case, with the following
characteristics:
 Unbearable
 Prolonged (with a duration of over 30 minutes up to few hours)
 Atrocious
 Ravishing
 Stabbing characteristics
 Strong pressure
Location and the irradiation of the pain:
 precordial, retrosternal, in the shoulders, inter-scapular, epigastru, irradiate in the
arms, in the shoulders, in the jaws, on the cubital edge of the left superior member,
up to the last fingers of the left hand, in the region of the back of the head,
occipital, right hemithorax, thorax.
 it doesn’t give in to nitro-glycerine (important for the diagnostic)
 it gives in to opiates (morphine, mialgin)

The clinic image

 the patient is anxious, with cold and humid teguments, tachycardia, arterial
hypotension, cold sweats, vomiting, diarrhoea, sock.
Objective exam
The exam of the cardio-vascular apparatus
 the cardiac frequency may be oscillatory, from bradycardia to tachycardia, extra-
systole ventricular, rhythm of gallop (the noise III or IV)
 AT, many be normal, hypo or arterial hypertension

221
  the carotid pulse, shows the modifications of the debit beating, of the left ventricle,
a low pulse = the reduction of the systolic volume
 the cardiac noises which are deafen, the noise I, very weak, it appears the noise III
and IV
 the systolic breaths appear which are transitory or persistent
 pericardia friction at 10-20 % of the myocardial infarcts

The exam of the respiratory apparatus

 the high frequency of the breaths
 dyspnoea with Cheyne-Stokes breath
 humid rales, crepitant and subcrepitant
The exam of the digestive apparatus
 epigastric pain
 nausea, vomiting
 abdominal meteorism
 inappetence
 hepatomegaly
 hepato-jugular reflux
The exam of the nervous system
 emotional modification
 anxiety
 depression
 negativism
In order to establish exactly the diagnostic of MI, OMS (The World Health Organisation)
imposed to be present at least 2 from the 3 criteria:
1. typical retrosternal pain
2. EKG modifications in dynamics
3. Increase and decrease of the serum cardiac markers

The para-clinic exam

1. kreatinphosphokinase (CPK)
- increases in the first hours
- the maxim level of the CPK = 80 -110 UI/l
2. myoglobin – protein released in the circulation, in the start of the infarct
3. specific troponins – troponin I and T
4. lacticodehydrogenase (LDH), (N = 5O U/l)
5. transaminase glutamicoxalacetic (GOT), or the aspartaminotransferase (ASAT)
6. hyperglycaemia
222
 7. hyperleucocytosis
8. high VSH
9. high fibrinogen, up to 8-10 g/l
10. Astrup modified parameters
11. modified hemoleucogram (HLG)
12. alkaline reserve (RA)
13. electrocardiogram – the most important element of diagnostic, shows:
 subepicardiac lesion transmural (supra denivelation of the segment ST and the
wave T with convexity in up)
 necrosis (the wave Q pathologic)
 ischemia subepicardic (the wave T negative symmetrical)
Diagnostic of localisation EKG:
 anterior: the wave Q present in the V3, V4
 antero-septal: waves Q present in V1-V4
 anterolateral: waves Q present in I, aVL and V3-V6
 lateral : waves Q present in I, aVL and V6
 lateral high: waves Q present in I, aVL
 inferior: waves Q present in II, III, Avf
 posterior: waves R high in V1 or V2
Imagistics
1. Thoracic radiography – shows indirect signs of IM
(signs of left ventricular insufficiency, cardiomegaly)
2. Cardiac echography:
- Explores the walls of the left ventricle in longitudinal and transversal plan
- Anomalies of motility
- Performance of the left ventricle
(the echo Doppler, appreciates the mitral tricuspid regurgitation)
- Rupture of the inter-ventricular septum
- Presence the thrombi in the ventricle
Bi-dimensional echocardiography (2 D)
- Evidences images in longitudinal and transversal plan of the left ventricle
and a greater portion from the wall of the left ventricle which include also
significative portions from the anterior areas, septal inferior and posterior
of the wall of the left ventricle.
Echocardiography – M
- Evidences the motility of the wall of the left ventricle
The echo Doppler

223
 - Appreciates the mitral and tricuspid regurgitation, rupture of the inter-
ventricular septum and the presence of the thrombi in the ventricle
3. The isotopic exploration:
- Evidences the positive diagnosis of the acute myocardial necrosis with the
help of the radioactive trasors with tropism for the necrotic tissue
- diagnostic of some complications
- the evaluation of the ventricular performance
4. The computer tomography shows:
- The dimension of the cavities
- The thickness of the wall

5. The magnetic resonance

- The size of the infarct
- Collateral circulation
- Function of the left ventricle
Treatment
The pre-hospital phase, is extremely important, decisive for the survival:
- The ambulance is called, with the anti-shock team
- The patient is sited in leisure position
- The patient is transported in the emergency service UPU (emergency
receiving), where the emergency treatment is made depending on the
algorithm.

224
 Patient with discomfort of type
ischemic
The rapid triage in the emergency
room Term of 10 minutes
Aspirin 160 – 325 mg
Determination of the serum level of
the cardiac markers
Initial test of ECG in 12
deriaţii

Supra-nivelation ECG suspect for ischemia ECG non

of ST (sub-unevenness ST, concluding
wave T inverted)

The thrombolysis The evaluation is

is contraindicated Hospitalisation continued in DU

Initiates the strategy The monitoring of

or repeating the The ant-ischemic
the serum level of
perfusion treatment is the cardiac
initiated markers

The Eco 2D is
performed

Obvious signs of
ischemia/infarc ?

Yes No
Investigations of laboratory
and of routine are
performed
A complete laboratory Hospitalisation Discharge
balance is made Purpose = 8-
12 h

Strategies for repeating the

perfusion are made if it develops
supranivelation

The algorithm for the treatment of the patients with suspicion of AMI, in the emergency
department.
(after Antman E.M. and Braunwald E, 1997)

225
The patients with MI, are hospitalised in the coronary units.
At the hospital it is administered:
- aspirin 160-325 mg per bone or sublingual (s.l.),
(blocks the formation of the thromboxane A2 in the thrombocytes), and/or
clopidogrel (Plavix) (87)
- analgesia:
analgesics:
 Meperidina
 Pentazocina 50 mg
 Morphine 10-20 mg
 Mialgin 50-100 mg
 Phentanyl 1-5µg/kgb i.v.
- nitrates (increase the coronary blood flow through coronary vasodilatation)
- nitro-glycerine s.l., spray or i.v with the monitoring of the At
- blockers βeta-adrenergics
•the metoprolol is administered in 3 boluses, of 5 mg i.v. slowly, then per
bone
- oxygeno-therapy: oxygen 4-6l/min
- the coronary thrombolysis with streptokinase, in the first 6 h (it is practiced at the
house, ambulance, means of transport). It is administered in perfusions i.v. 1, 5
million U.I, for 60 minutes, under the control of the prothrombine.
It is followed by HEPARINOTHERAPY: 7500 UI heparin s.c. at the interval of 12 h under
control T. Howel, after the streptokinase is administered.
The urochinase, as tissue activator of the plasminogen.
- The surgical perfusion = By-pass-aorto-coronary
- Coronary stent
The general treatment:
• the elimination of the anxiety: diazepam, hydroxyzine
• the elimination of the agitation state: haloperidol 2-10 mg
- Re-equilibration H-E, depending on the blood ionogram (administration K and Mg)
- the Ca antagonists: Verapamil (in flutter, atrial fibrillation, 5-10 mg i.v), diltiazem
when the βeta-adrenergics are inefficient
- sedation: diazepam 5-10 mg i.v. slowly
- the elimination of the hypotension with bradycardia: atropine 0,5-1 mg i.v
- cardiac arrhythmia (extra-systole): Amiodarone 300 mg S.A/30 minutes (87)
- arterial hypertension with acute pulmonary oedema: sublingual nifedipine
- ventricular tachycardia: Amiodarone 300mg S.A /30 minutes, and if it doesn’t give
in => synchronic cardioversia
226
 - conduction diorders: atrio-ventricular blocks
o Degree I: without treatment
o Degree II: QRS condensed < 0,1 sec. and frequency > 50/min, without
treatment
The complications M.I
1. Arterial hypotension, complicated with rhythm complications
2. Left ventricular insufficiency
Treatment:
- Perfusions with crystalloid liquids, depending on the blood ionogram
(slowly)
- Oxygeno-therapy
- bronchodilators
3. The cardiogen shock, characterised by:
- persistent and marked hypotension
- marked reduction of the cardiac index
- pressure of high left ventricular filling
Treatment:
- O2 (2-6 l/min)
- nitro-glycerine
- correction of the acidosis
- re-equilibration of the H-E, depending on the blood ionogram
- analgesics (petidine 50 mg)
- vasopressors: dopamine 2 μg/kg/min, dobutamine 2-20 μg/kg/min,
- nitro-glycerine 1,2 -3,6 mg/h, isosorbid 5-20 mg/h
- digital (it is not administered in I.M with cardiac insufficiency)
- diuretics: furosemide 1-2 vials
- cure of the rhythm disorders
- ventricular arrhythmias: mexiletine
- paroxistic tachycardia and flutter: sino-carotidian pressure, electric shock
- atrial tachycardia: propranolol, izoptin (verapamil) 5-10 mg i.v
- ventricular tachycardia: amiodarona 800-1600 mg/day doses of charge, and
maintenance doses 300 mg/day
- pacemaker in bloc atrio-ventricular
4. the disorders of cardiac rhythm
- the atrio-ventricular blocks
- ventricular extra-systole
- ventricular tachycardia
- ventricular fibrillation

227
 - sinusal bradycardia
- supraventricular bradycardia
- atrial flutter
- HTA

II. 5. b. THE ARTERIAL HYPERTENSION (HTA)

It represents the increase of the systolic and diastolic AT, over the normal values.
The increase of the systolic AT, 130 mmHg → produces acute vascular lesions, which need
rapid treatment under one hour.
Aetiology
Affections:
1. Cerebro-vascular:
- Cerebral infarct
- Intracranial bleeding
- Hypertensive encephalopathy
2. Cardiac:
- M.I.
- Aorto-coronary by pass
- left ventricular insufficiency
3. Renal:
- acute glomerulonephritis
- collagen disease
- renal transplant
4. Excess catecholamine:
- pheochromocytoma
- Stress
- medicament interactions
- the use of the simpatico mimetic drugs
5. Surgical:
- post-operatory hypertension
6. Eclampsia
7. Severe burns
8. Severe epistaxis
Clinic image
- arterial diastolic pressure > 140 mmHg
- the modifications of the eye bottom (FO), bleeding, oedema, exudate
- neurologic disorders: headaches, loss of sight, somnolence, confusion, epileptic
crisis, coma
228
 - renal modifications: oliguria, haematuria, azotaemia, proteinuria
- gastro-intestinal disorders:
- nausea, vomiting
- haemolytic anaemia
- hyperaldosteronism
Treatment
- niphedipin s.l. 10 mg, which is repeated at 30 min.
- when the diastolic pressure > 140 mmHg, the treatment is made rapidly with:
 sodium nitroprusiate 0, 25-10 µg/min in perfusion i.v.
 nitro-glycerine 5-10 µg/min, in perfusion i.v.
 enalapril 1, 25-5 mg la 6 h, 15 min
 regitin (phentolamin) 5-15 mg i.v.
 esmolol 500 µg/kg/min i.v.
 metoprolol 50 mg at 12 h
 furosemide 20 mg/24 h

II.5.c. CARDIAC INSUFFICIENCE

It is the incapacity of the heart, of furbishing the peripheral circulation, a sufficient blood
volume.
The acute heart failure may present one of the following distinct clinical conditions:
A.The acute insufficiency decompensated heart failure (ICAD) (`de novo`` or
decompensation of an ICC) with signs and symptoms of acute heart failure mild
Hypertensive b. ICA: signs and symptoms ICA + HBP + + radiography preserved ventricular
function compatible with EPA
The acute cardiac insufficiency may present in one of the following distinct clinic conditions:
a. The acute cardiac insufficiency decompensed (ICAD) (``de novo`` or as a decompensation
of a ICC) with signs and symptoms of acute cardiac insufficiency of medium intensity
b.ICA hypertensive: signs and symptoms ICA+HTA+ventricular preserved function
+radiography compatible with EPA
c. Pulmonary oedema: EPA(radiologic objectivised)+severe respiratory insufficiency
d. cardiogen shock (CS): tissue hypo perfusion of cardiac cause after the correction of the
precharge.
e. the insufficiency with high cardiac debit (DC): CD high, tachycardia, warm
periphery, pulmonary congestion and/or AT decreased (similar to the sepsis)
f. right cardiac insufficiency (ICdr): low cardiac debit + signs of jugular
congestion+ hepatosplenomegaly+hypotension. (84)

Mechanisms of production
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 - the volume debit/beat is reduced
- it increases the tonus of the sympathetic nervous system, with the purpose of
maintaining the AT
- a peripheral vasoconstriction is started and also a tachycardia, which
distributes a part of the intra-thoracic blood volume. This blood volume
distributed in the thorax, if it meets a ventilator dysfunction → E.P.A.
Aetiology
 deficit of O2 at the level of the myocardia muscle (coronary disease, anaemia,
disorders of ventilation-perfusion).
 the over-solicitation of the pressure for the left ventricle (HTA, aortic stenosis).
 tachycardia, bradycardia, arrhythmia.
 myocardial necrosis (I.M, aneurism of cardiac wall)
 mechanic causes (hemopericardia, cardiac tumours)
 aortic insufficiency, mitral, shunts
There are 4 stages of the cardiac insufficiency (CI)
I. Without subjective accuses to normal efforts = cardiac affection without insufficiency
II. Light accuses, at normal efforts, the capacity for effort is reduced.
III. The accentuated reduction, of the effort capacity at regular efforts.
IV. Dyspnoea of rest, incapacity of having a daily activity.

The clinic image

 the insufficiency of the right heart: oedema of the descending parts

(perimaleolar, gambier, anasarc), stasis in the veins of the neck, cyanosis,
hepato-jugular reflux, stasis liver, hepatosplenomegaly, stasis gastritis,
proteinuria, nicturia, pleural gushing.
 The insufficiency of the left heart: dyspnoea of rest and effort, orthopnoea
(most of all nocturnal), cyanosis, when there is E.P.A, dyspnoea of rest,
imitative cough, hemoptoic sputa, humid rales at the pulmonary bases,
tachycardia, rhythm disorders, gallop rhythm.
Treatment
Objectives:

 Increase of the contractility

 The reduction of the precharge (diuretics, nitrates, vaso-dilators).
 The reduction of the postcharge (diuretics, vasodilators).
 General measures:
- Low salt regime
- Reduction of the liquid intake
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 - Rest in bed
- Prophylaxis of the thrombosis
- O2
1. Diuretics:
 Thiazide: hidroclortiazida 25-75 mg/day, (daily hydro-electrolytic
balance)
 furosemide 20-40 mg i.v.(in the morning)
 spironolactone
2. Human albumin
3. Rebalancing H-E, after the blood ionogram
4. Digital glycosides: digoxin 0, 25-0, 375 mg/day
5. Vasodilators (nitrates) Isosorbid dinitrate = izocket 4x10-20
mg/day
6. Inhibitors ACE (84)
Hypotensors
 captoprile 6, 25-12,5 mg
 enalaprile 2, 5-5 mg
Sedative
 hydroxyzine 25 mg
Nursing measures, in the cardio-vascular affections

The severe heart disease, are hospitalized in the intensive care department, coronary polling.
Medical treatment, prescribe doctor and nurse will care for the sick, all measures of nursing. For
these patients there are specificities cares that the nurse must know and apply. Coronary wards
are located in isolated places in the hospital. Lounges to large, permanent airy, bright, heated to
19-20 ° C, isolated from noise and disinfected daily. Bedding, to be specific, adaptable position
that the patient wants (preferably those with bedsteads, which can turn into an armchair and
fitted with castors, signaling device, folding table)
The devices. The medical assistant, has the obligations of preparing and checking, the
emergency devices, the instruments (defibrillators, the emergency case for the oral/tracheal
intubation, ventilation devices, monitors, pacemaker, syringes, needles, emergency
medicaments).
The position of the cardiac patient in the bed, must not be imposed, the patient choses it, as
he wishes:
- horizontal position, without pillow
- semi-sitting
- sitting
- sited on the edge of the bed, with the legs hanging

231
The personal hygiene:
- permanently kept
- the skin is fragile, due to the circulation disorders, presents oedema with
vulnerable teguments to escares.
- The patient compensed cardiac, has the permission to bathe, but under surveillance, the
bath, must not depass 20 min, and water, to not be hot
- The temperature of the water, to be 34-36 °C, for the bath in bathtub, and
the thorax, to be on top of the water.
- The decompensed patients, will be hygienised, la pat, on body segments, dressed
carefully, without being traumatised verbal or physically.
Kinetotherapy:
The medical assistance, will perform passive and active gymnastics, monitoring the respiration,
AT, the pulse and the state of consciousness, partial or general massage, as indicated.
The monitoring of the cardiac patients:
It will monitored, permanently by the medical assistance:
- AT
- pulse
- colour of the teguments
- diuresis
- respiration
- expectoration
- cyanosis
- extremities
- oedema
- the pulsations of the jugular vein
- the central venous pressure
- complications
- the psychological state
- the emergency devices
- the complications which appear after the treatment
The alimentation of the cardiac patient:
- comprises all the main alimentary compounds, plus vitamins and minerals.
- low salt regime.
- potasium contribution (banana, tomatoes for the digitalised patients).
- often and meals reduced in consistency.
- the aliments which produce abdominal distension are not administered
The para-clinic examinations:
232
The medical assistant, will accompany the patient, and in the case of those immobilised in
bed, the investigations, are performed at the bed of the patient. The medical assistant will
prepare the patient, for the para-clinic exams.
The administration of the medicaments: medicaments: the medication will be prescribed by
the doctor.
We must respect the schedule of the administration of the medicaments.
From self-initiative, at the apparition of a complication, until the medic arrives, the medical
assistant, will administer only O2 and NTG.
The medication of emergency.
The medical assistant, is forced to verify and to complete permanently, the emergency
cupboard, with the medicaments for emergencies.
The sanitary education.
At the exit from the hospital, the medical assistant, will instruct the patient, how to administer
the medicaments.

II.6. THE ACUTE RESPIRATORY INSUFFICIENCY (ARI)

Definition:
The respiratory failure is the inability of the lungs to cope respiratory gas exchange alveolo-
capillary membrane.
In these conditions the respiratory system is unable to maintain its primary function of venous
blood oxygenation and removal of carbon dioxide (CO2).
There is a lack of oxygen which is expressed by lowering the O2 partial pressure (PaO 2) in
the blood and ventilator insufficiency that CO2 is not normally removed so PaCO2 rises
above normal.
Production mechanism
- in the blood plasma the arterial pressure of the O2 decreases under 60 mmHg
(PaO2)
- the partial pressure of CO2 from the plasma increases over 50 mmHg
PaO2 (SO2) = the saturation of O2, for the young people of 96-100 mmHg
PaO2 (SO2) = the saturation of O2, for the older people is of 79-83 mmHg
It is considered:
- hypoxia when the PaO2 decreases under 60 mmHg
 at PaO2 under 45 mmHg = measures of respiratory reanimation
 at PaO2 under 35 mmHg = lethal risk
The normal values of the PaCO2 in the arterial blood is of 35-45 mmHg
- at 46-70 mmHg, PaCO2 = light HIPERCAPNIE
- at 70 mmHg PaCO2 = severe HIPERCAPNIA with risk of respiratory insufficiency
or respiratory encephalopathy
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 - when PaO2 decreases, and PaCO2 increases is produces HIPOXEMIA
- when PaO2 decreases, and PaCO2 is normal is produced NORMOCAPNIA
The global respiratory insufficiency = HIPOXEMIA+ HIPERCAPNIA
ARI which is produced through the alteration of the hemostasis for the blood gases through
the troubles of the function of the lungs is called pulmonary insufficiency (PI) or respiratory
pulmonary insufficiency (RPI).
The manifest ARI may be:
 Compensed when all the alteration of the homeostasis (hypoxia, gaseous acidosis
compensed metabolic) are produced at effort. PaO2 + PaCO2 is kept a long period
 Decompensed: with all the disorders of the sanguine gases with severe consequences
on the other organs and systems. PaO2 + PaCO2 are altered progressively and rapidly.
Ethiopathogeny
There are 4 mechanisms which compete to the apparition of ARI:
1. Alveolar global hypoventilation
2. Alterations of the pulmonary diffusion
3. Alteration of the rapport ventilation/perfusion
4. The development of the intra-pulmonary shunt right left

1. The global alveolar hypoventilation is produced through the increase of the PaCO2
over 50 mmHg, as a consequence of the decrease of the alveolar ventilation, of the
increased production of CO2 or due to the increase of the ventilation of dead space.
The causes of the global alveolar hypoventilation are:
 The absence of the aerial superior ways:
 Mouth tumours, pharyngeal abscess, foreign bodies, tongue hypertonia
 Spasm at the level of the larynx, paralysis, oedema, tumours
 At the level of the trachea and bronchi: foreign bodies, tumours,
tracheomalakia, compressive goitre, abscesses, spasm, hematoma
 The pathology of the superior respiratory centres:
 tumours, traumatisms, intoxications with barbiturates and opioids, anaesthesia
with overdose of anaesthesia
 the paralysis of the respiratory muscles: curarisation, the leading anaesthesia (high
rachi and peridural), myasthenia, poliomyelitis
 pathology of the integrity of the thoracic box: costal flap, costal multiple fractures,
thoraco-plasty
 the stop of the thoracic expansion: pneumothorax, massive pleurisies, hematoma,
abdominal voluminous tumours, ascites in high amount
 the reduction of the pulmonary parenchyma: pneumonia, cysts, tumours, atelectasis
affections of the vertebral spine: cipho-scoliosis
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In these forms of M.A.I. there is an increase in the arterial and venous blood of the content of
CO2 and of the partial pressure of the CO2 (PaCO2).
The oxygenation decreases also the hypercarpnia is associated with the hypoxemia.
The gradient P (A-a) O2 which represents the difference between the partial pressure of the
O2 in the alveoli (PAO2) and the partial pressure from the arterial blood (PaO2), remains
normal (5-15 mmHg).
2. The alteration of the pulmonary pressure
The blood gases pass from the alveoli in blood and vice-versa through the alveolar-capillary
membrane. If alveolar-capillary membrane diffusion is impaired blood gas is changed.
There are many factors that can change the alveolar-capillary membrane this:
- The thickness of the membrane
- The difference of partial pressure of the gas in the two surfaces of the membrane
- The coefficient of diffusion of the gas
There are many causes pathological alveolar-capillary membrane thickening produce edema,
hemorrhage, fibrosis.
Carbon dioxide diffuses through the membrane 20 times easier than O2 and alveolar-capillary
membrane thickening has among the consequences hypoxemia. During the pulmonary
capillary cross Hematite is second and the diffusion of oxygen is in 0.3-0.4 seconds.
3. The alteration of the rapport ventilation/perfusion (V/P)
To carry out gas exchange in the lung areas must be ventilated and well perfused and vice
versa. Normally it is slightly superior ventilation perfusion ratio V / P being 0.8-1.
Pulmonary ventilation is 4l / minute, and perfusion close 5l / minute. The socket ratio V / P is
different between alveoli and ranges from zero (non-ventilated alveoli) and infinity
(neperfuzată socket). When changing the ratio V / P of a large number of wafers, it causes gas
exchange alterations which produce hypoxemia.
If the number of ventilated alveoli but neperfuzate (V / P> 0.8-1) increases, there is increasing
dead space (hypovolemic shock, asthma attack, pulmonary embolism, pulmonary
emphysema, extensive capillary damage from sepsis, burns, ARDS) . If a patient
hiperventilează and manages to reduce the dead space through an increased effort ventilator,
blood gases begin to normalize.
Instead if hipoventilate and normal alveoli are perfused (V / P <0.8-1) blood perfused alveoli
that oxygen is insufficient, PO2 decreases.
4. The development of the pulmonary shunt left right
It is a form of I.P. severe enough when the rapport V/P is altered very rapidly. In this situation
completely non-ventilated alveoli crossing venous blood and mixed with arterial blood,
decreasing its saturation O2 and PO2 (atelectasis, aspiration pneumonia, ARDS). It follows a
hypoxemia that is refractory to 100% O2.

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The pulmonary insufficiency through hypoxemia and hipercapnia will influence the
metabolism of all the tissues from the organism:
- Effects over the brain.
 The state of the contribution of the O2, even for a little while,
provokes over the nervous cell irreversible lesions
Clinic: dysarthria, anxiety, sight disorders, confusions, delirium, coma.

- Effects over the heart and circulation:

 at low hypoxemia is produced coronary vasodilatation
 at more pronounced hypoxemia it appears the myocardial
suffering
 at old people there are signs of myocardial ischemia and rhythm
troubles
- Effects over the pulmonary circulation:
 hypoxemia produces arterial pulmonary vasoconstriction and
pulmonary hypertension → chronic pulmonary heart
- Effects over the haematogenous marrow:
 The chronic hypoxia, stimulates the secretion of erythropoietin,
from where it results poly-globulia
- Effects over the control of the ventilation:
 hypoxemia stimulates the respiratory centre from the bulb, only
when the PaO2 decreases beneath 60 mmHg. Normally, the
hypercapneea stimulates the respiratory centre from the bulb. In
case of chronic hypercapneea, the hypoxemia remains the
unique stimulant
 the chronic hipercapneea provokes the depression of the
regulatory centres of the breath, giving somnolence, flapping,
tremor, papillary oedema and coma (when the PaCO2 is over 80
mmHg)
- Effects over the kidney:
 The kidneys interfere compensatory and they resorb the ions of
Na and of bicarbonate and they eliminates the ions of H
- Effects over the systemic circulation
 The hypercapneea produces vasodilatation or vasoconstriction
depending on the individual
The clinic image
1. Respiratory signs

236
 - Rest dyspnoea
- Orthopnoea
- Coughs
- Expectoration
- Pain (at thoracic level)
- Tachipneea or bradypneea
(the breathing frequency over 30 or under 12 breaths/min.)
- Modification of the respiratory rhythm
Breathing pauses, Cheyne-Stokes breath, Kussmaul)
- Prolonged expiration, with the contracture of the abdominal muscles
- Inspiratory dyspnoea (triage, cornaje, beatings of the nose wings)
- apnoea (absence of the respiratory moves)
- paradox abdominal-thoracic breath
2. Hemodynamic signs
a. Signs of hypoxemia and hypercapnia
- cyanosis (when PaO2 decreases under 80% and the patient is anaemic,
Hb<5g/100ml)
- disorders of cardiac rhythm
- arterial hypertension (associated with the neurologic signs of anxiety,
disorientation)
- profound sweat
- facies vultuos
- palmar erythrosis
- the disorder of the state of consciousness
b. Hemodynamic signs:
- tachycardia (120b/min) or bradycardia (sub 12 resp./min)
- disorders of cardiac rhythm (extra-systole, atrial fibrillation)
- arterial hypertension followed by arterial hypotension
- paradox pulse
- fusiform pulse
- cold teguments and cold mucosa, cyanotic and marmorates
- alteration of the state of conscience (confuse, coma, cardio-respiratory stop)
c. Neurologic signs
- irritability
- euphoria
- psycho-motorial agitation and somnolence
- aggression
- insomnia

237
 - muscular secuses
- disorientation in time and spaces
- the alteration of the memory
- convulsions
- coma
The para-clinic exams
- the functional respiratory samples which make the diagnosis of obstructive
dysfunction, restrictive or mixed
- the sanguine gases (repeated measurement of the PaO2 and of the PaCO2)
- the determination of the A-B balance
- the radiologic thoracic exam
- tomography
- bronchoscopy
- EKG (indirect information)
- blood ionagram
- monitoring of the renal function (urea, creatinine)
- glycaemia
- HLG
- R.A.
- The exam of the sputa
Treatment
The treatment is mainly addressed to support pulmonary ventilation, improve oxygenation by
increasing the concentration of inspired O2.
main measures.

1. The clearance and permeability of the breathing ways.

The clearance of the superior aerial ways (supra-glottis) are performed rapidly, the
sustainability of the tongue, the position of the patient in decline position for the drainage of
the secretions.
The clearance of the aerial oral-nasopharyngeal ways is made:
- hyperextension of the head back with the sustenance of the mandibular bone
- opening and clearance of the mouth (manual aspiration or mechanical), oro-
tracheal intubation
- the introduction of the Guedel pipe
- the placement of the laryngeal mask
- the tracheal intubation on oral or nasal way
- cricotiroidotomy
- tracheostomy
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 - aspiration of the tracheobronchic secretions on oral way, nasal, on the
intubation probe or on the cannula of tracheostoma
- the evacuation of the bronchial secretions may be performed through the
periodic instillation in the trachea of physiologic serum 0, 9 ‰ and then the
aspiration
The clearance of the aerial ways includes the introduction of the pharmacologic medication:
- bronchodilatators simpaticomimetics (adrenaline, salbutanol, phenoterol)
- bronchodilatators parasympaticolitics (ipratropium bromure)
- bronchodilatators musculotrope (aminophylline, diprofilin)
- fluidificants of the bronchial secreton through mucolytic agents: N-acetil
cisteine
- hydric rebalancing
- corticoids (dexametazon, methyl-prednisolon) as anti-inflammatory and
inhibitors of the bronchoconstrictor prostaglandins
The administration of the pharmacologic medication must respect the aetiology and the
clinical situation of the patient.
We administer:
- in laryngospasm
o postextubation: succinylcholine 20 mg i.v.
o hypocalcaemia: calcium clorure 10 % 10ml i.v. slowly
- in glottis oedema, subglottis postextubation, anaphylaxis: adrenaline 1:10.000,
1-10 ml very slowly i.v.; hydrocortisone hemisuccinate 100 mg i.v.
dexamethasone 4 mg i.v.
- retropharyngeal abscess: antibiotics, drainage
- tracheobraonchic secretions: atropine
- the artificial ventilation with internal action through pulmonary insufflation
which can be performed through normal inhale of the resuscitator or with the
help of the ventilation devices automatic or not.
2. Oxygeno-therapy
It presupposes the increase of the concentration of the oxygen in the inspired air. The increase
of the tissue needs of oxygen will activate the compensatory sympathico-adrenergic
mechanisms.
In physiologic conditions it is maintained a balance between the amount of oxygen given to
the tissues in the time unit (DO2) and the tissue consume of oxygen (VO2).
The value DO2 it is reduced when it decreases the amount of Hb, or the degree of saturation
dependent on the partial pressure of the O2 in the arterial blood (PaO2). The saturation is
maximum at values of the PaO2 of 100 mmHg. The decrease of PaO2 determines the
reduction of the SaO2 after a sigmoidal curve which is the curve of dissociation of the oxy-

239
haemoglobin. The knee of the curve corresponds at values of 90% SaO2 and respectively
60mmHg PaO2.

The curve of dissociation of the oxy-haemoglobin

Ways of administration of the oxygen

- on nasal cannula
- on the oxygen cort
- mechanical ventilation
- systems which don’t allow the re-inhalation
 dispositive with low flux and variable performance which
assure a debit of O2 which does not cover the necessary
volume of air for the patient and in completion is used the
atmospheric air
 dispositive with high flux and fixed performance, when the
concentration O2 is fixed, indifferent of the factors which
depend on the patient. Through this method it is assured the
whole air volume (O2+air) necessary for covering the needs
of the patient
3. The evacuation of the pleural collections
It is made through thoracocentesis or thoracotomy.
The thoracocentesis is the method for evacuating the pleural secretion, with a needle
introduced through the tegument and the thoracic wall (the described techniques for the
objectives)

240
The thoracotomy – the method through which is realised a communication between the
pleural amount and the athmospheric air, for the evacuation of the pleural gaseous or liquid
collections.
The thoracotomy is performed through two methods:
- Through a tube introduced intercostal minimum pleurotomy
- Through catheter introduced with the help of the needle/cannula of
thoracocentesis
4. The correction of the acidosis with sodium bicarbonate after the formula
Sodium bicarbonate (mEq/l) = base deficit (BE) x G x 0,3
5. Antibiotherapy: as prophylactic treatment or if there is an infectious process
- Doxycycline 200 mg/24 h
- Fortum 1 g at 8 h
- Medocef 2 g at 12 h
- Cefozon 1 g at 8 h
6. Kinetotherapy
- Through directed respiratory moves, with medical gymnastics, is stimulated
and it potentiates the respiratory musculature.

Particular forms of acute respiratory insufficiency

The thoracic traumatisms with thoracic flap
In the thoracic traumatism the acute respiratory insufficiency is due to hypoventilation
produced through the alteration of the mechanics of the thoracic wall through pain, costal
fractures, costal flap.
Also the inadequate expansion of the lungs through pleural and mediastina collections
In this situation both vital organs are affected: lings and heart.
Treatment:
- Rebalance of the respiratory functions
- Assuring the liberty of the respiratory ways
- Control of the ventilation
- Evacuation of the secretions
- Re-establishing the normal dynamics of the thoracic wall
- Consistency of the flap through external compression
- Osteosynthesis of the fractured ribs
- Mechanical ventilation with positive intermittent pressure
- External stabilisation of the flap stabilizarea externă a flapului
- Pain killing: novocaine infiltrations, lidocaine sol 1 %; central analgesics -
fortral 50 mg at 4 h; ketoprofen, ketonal, tador; peridural catheter T4 - T6 with
injection of lidocaine 1 %; interpleural analgesia – the introduction of a
catheter in the pleural space at the level of the V intercostal space on the
241
 medio-axillary line and it is injected 20 ml bupivacaine 0,5 % with
1/2000.000 adrenaline
1. The crisis of bronchial asthma
It is produced through spasm, inflammatory oedema of the bronchial mucosa, mucus
accumulation on a field with high bronchial reactivity.
Due to the resistance from the aerial ways seen in the exhale and of the shortening of the
exhale caused by the tachipneea, the patient is not capable to complete the respiration. This
produces captive air with the increase of the reserve residual volume and of the functional
residual capacity.
Clinic image:
- severe dyspnoea with highly prolonged exhale (wheezing)
- tachipnoea (30respiraţii/min)
- obnubilation
- tachycardia
- paradox pulse
- arterial hypotension
- congestioned facies
- transpirations
- contractions of the sternocleidomastoid muscles, of the scalen
Para-clinic exam:
- VEMS < 20%
- The reduction of the rate of the exhaling flux under 100l/min
- The decrease of the PaO2
- hypocapnia with normocapnia, then hypercapnia
- bronchospasm
- bronchial hypersecretion
Emergency treatment
a. Oxygenotherapy (up to SaO2 96%)
b. Bronchodilatators
- agonist beta-2 adrenergic: adrenaline 0,3-0,5mg subcutan and repeated at 15-
30 min
- beta-adrenergic: salbutamol, phenoterol
- beta-adrenergic: aminophylline
- anticholinergic: ipratropium bromure
c. Cortisone – as membrane stabiliser, anti-inflammatory and reduction of the mucus
secretions
d. Ketamine i.v. for preventing the bronchospasm resistant to treatment
e. During the anaesthesia: halothane, eufluran
f. Mechanical ventilation
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2. The syndrome of respiratory distress (ARDS)
It is characterized by interstitial and alveolar infiltrates changes that stretch throughout the
lung and causes IRA with hypoxemia and hypocapnia.
Here is present right shunt - left and hemoglobin saturation with O2 is insufficient.
Ethiopathogeny
- Sepsis
- Shock
- Traumatisms
- Aspiration of the gastric content
- Chocking
- Inhalation of toxic gas
- Administration of a long time of the O2
- Massive transfusions
- Gaseous emboli
- Eclampsia
- CID
Clinic image
- dyspnoea + tachipnoea
- thoracic radiography: image of honey comb in; micro-opacities at bases
- submatity altering with state of hypersonority
- atelectasis
- bronchiolar obstruction
- decrease PaO2
- agitation psycho-motorial
- teguments and pale mucosa
Treatment
Measures of maintenance:
- the correction of the arterial hypoxia through administration of O2 until the
realisation of a concentration in O2 of 50-60 %
- orotracheal intubation with mechanical ventilation with PEEP between 5-15 cm
H2O until we obtain PaO2 over 60 mmHg
- the position of the patient ventilated in ventral decubitus and the inhalation of nitric
oxide (NO)
- administration of the liquids for the hydric rebalancing to be in negative balance
(administrating prudently and in lower amount). It is recommended maximum 1500
ml liquids/24 h
- administration of diuretics: furosemide
- administration of human albumin at the hypoproteinemic patients
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 (it is forbidden to administer it to the normoproteic patients)
- in anaemia, blood transfusion, integral blood, izogroup, izoRh, pluse crystalloid
solutions
- mucolytic
- expectorant
- aspiration
- antibiotics with large spectrum (antibiogram from bronchial secretions)
- administration of the corticosteroids
- adequate alimentation with high contribution of calories and proteins, alimentation
mixed parenteral and on gastric probe
Measures of CLINIC NURSING in the pulmonary affections
Chronic lung disease, may receive care at home or in hospitals chronic lung disease worsens
and if hospitalization is needed.
These patients require special care.
The position in bed:
- semisitting
- establishes it by himself, depending on the necessities
- permanent mobility, in order to avoid the hypostatic complications, which lead to
complications (paresis, escars, supra-infections)
- repaus absolut la unele afecţiuni (embolia pulmonară, hemoptizia), poziţie dorsală,
cu trunchiul şi capul ridicat
The nurse will assist the patient to establish position in bed, will provide annexes (blankets,
pillows) and will help to mobilize. Personal hygiene - the hospitalized patient, all medical
personnel will do. The patient will be protected from cold drafts. Sweating will be removed
by wash with soap and water will help clear skin, then pat with alcohol mint (patient's skin
is fragile and vulnerable to infections and bedsores).
The hospitalisation
- in separate rooms, from other affections
- the furniture will be reduced and with shiny surfaces, smooth, in order to be
cleaned easily.
- the bed of the patient, will have wheels, in order to be able to move the patient with
the bed, for different investigations of for the air therapy
- the windows of the room, headed north, for the room to have a good light.
- the temperature from the room, adequate, 18-19° C and humidified with aerosols.
- the ventilation system must be permanent.
- the room, must be equipped with emergency devices, with closed orifices
for spitting and disinfected permanently.
- the bacteriologic exams, are performed at the bed of the patient.
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 - The permanent monitoring of the vital functions (through monitors or manually).
- The consignation of all the data, in the observation sheet.
- The emergency instruments must always be sterile.
- Kinetotherapy and medical gymnastics will be performed permanently.
- The emergency device with medicaments completed up to date.
The alimentation of the pulmonary patient
- Must be synchronised with the period of evolution of the disease
- in fever, we administer more liquids and semi-liquids, rich in vitamin A and C (fruits,
vegetables).
- after a feverish period, the alimentation will be mixed, hypercaloric, easy to digest.
- Permanently, we will make the hydric and caloric balance.
Preparation of the sick person for investigations
- The doctor will make an investigation and treatment plan that the assistant will respect.
II.7. THE BRONCHIAL ASTHMA
Is a chronic, inflammatory airways that land in people with predisposing causes diffuse
obstruction of the airways and causes an increase in air reactivity to a range of stimuli.
Etiopathogeny
- There is a bronchial hyperactivity with bronchoconstrictor effect to a series of
allergens (chemical substances, cellular mediators, infections, etc.)
- The atopic transfer + external factors.
1. The allergic asthma – the trigger is an allergen, which produces asthma, through an
immunologic mechanism immunologic type I, mediated by IgE.
2. The non-allergic asthma – in which the role of starting it is of the neurogenous
mechanisms (intrinsic asthma)
The asthmatic crisis may be started by:
a) Allergic factors
- Spores of mould
- Pollen
- Dust from the rooms
b) Infectious factors
- Bacteria
- Virus
- Mycoplasma pneumonia
c) Medicaments
- Aspirin

245
d) Aliments (strawberries, peaches, mushrooms, some proteins from the cheese, conserves,
cold meats etc.)
e) Occupational factors
- Dyers
- House painters
- Sampler
- Miller
- The personal from the emergency services
f) Physical effort
g) Psychological factors
h) Other factors
- Meteorological factors
- The atmosphere pollution

The diagnosis of the bronchial asthma in crisis:

- Anamneses
- The environment for living and working
- Contact with the allergens
- The crisis appears suddenly or it is preceded by an aura with
exploratory dyspnoea with wheezing
- Dry cough, pearled mucous expectoration
- Polyuria by the end of the crisis
- The crisis are more frequent during the night, and they are accompanied by
cyanosis, anxiety.
The objective exam:

Inspection:
- Patient agitated psiho-motor, cyanotic, dyspnoeic
- The thorax is emphysematous, diminished respiratory amplitude
Palpation:
- Horizontal ribs
- Reduced amplitude
- diminished pectoral commotion
- Percussion: pulmonary hyper-sonority
Auscultation: bronchial rales, sibilant, ronflant and subcrepitant (columbary noise)
Paraclinic exam:
1. Hemoleucogram:

246
 - Eosinophily
- In the infectious forms, increase of the polymorphonuclears (PMN)
2. The exam of the sputa:
- Macroscopic: - pearled white sputa
- Microscopic: - Curshman spirals
- Antibiogram: shows the sensitivity to the necessary antibiotic, after evidencing the
germ which provoked the asthma
3. The exam of the blood gases – show the indication for the assisted respiration:
- PaO2 < 55 mm Hg (N = 95 mm Hg)
- PaCO2 > 70 mm Hg (N > 40 mm Hg)
- pH < 7,30 (N = 7,38-7,42 )
- SO2 < 80% (N > 95%
4. The functional respiratory samples show:
- Obstructive ventilator dysfunction
- Low VEMS
- Low vital capacity
- The residual volume increases
- CPT increases
5. The radiologic exam
- pseudo emphysematous thorax
6. Electrocardiogram
- in crisis = sinus tachycardia (if there are no other affections)
in advanced asthma = chronic pulmonary heart (CPC)
7. The alergologic exam
- Evidences or not the allergen which started the disease
8. Tests of provocation
- The test of provocation with acetylcholine or histamine, show the bronchial
hyper-reactivity.
The differential diagnosis:
1. The cardiac asthma:
- inspiratory dyspnoea
- tachycardia
- tachiarrhythmia
- HAT
- electrocardiographic modifications
- cardiac breaths
2. The obstruction of the superior aerial ways (tumours, foreign bodies, compressions, etc)
3. Spontaneous pneumothorax
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4. The pulmonary thromboembolism
5. The chronic obstructive bronchitis degenerated in acute

Complications:
- Spontaneous pneumothorax
- Subcutaneous emphysema
- Mediastina emphysema
- Hemoptisies
- chronic pulmonary heart
- Supra-infections
- Acute and chronic respiratory insufficiency
- Bronchiectasis
Treatment:
1. The etiologic treatment
- Elimination of the exposure to allergens
- The change of the place of work
- Avoiding the factors which increase the bronchial ventilation (fog, smoke,
cigarette smoke)
2. The anti-allergic treatment
- Ketotifen 2x1 cp/day (1 cp = 1 mg)
- The disodic chromo-glicate (Intal, Lomudal), stabilises the mastocitary membrane
: 1 cp la 6 h. 1capsule = 20 mg
- Sodic Nedocromil (Tilade), inhibits the eliberation of thebasofiles given by the IgE: 4 mg
inhalator.
3. The specific hyposensitivity is administered s.c. small doses of allergen, for the formation
of blocker antibodies (IgG)
4. The treatment of the broncho-dilatators:
A. Medicaments with effect ß adrenergic
- Adrenaline (Epinephrine), - unselective
- Izoprenalina (Izupren, Audrin) Dose 1 x 4 cp/day, 1 capsule = 10 mg –
semiselective
- Orciprenalina (Asmopent) Dose 1 x 4 cp/day, 1 capsule = 20 mg (semiselective)
- Salbutamol (Ventolin) Dose 1 x 4 cap/day or spray 1 capsule = 2 mg (selective)
- Fenoterol (Berotec) spray
- Terbutalina (Briconyl) Dose 1 x 3 cap/day 1 capsule = 2, 5 mg
B. Methylamines – also with bronchodilator effect
248
 - Teophylina
- Aminophylline (Miofilin) Dose 13 mg/kg/day, in 3 reprises, per bone and 5
mg/kg/day i.v.
1 tb = 100 mg; 1 f = 240 mg

C. Anticholinergic medication
- Atropine, Dose 0, 5 mg i.v. slowly, 1 f = 1 mg
D. Anti-inflammatory medication
- Corticosteroids – inhibit the prostaglandins F2, broncho-constrictors
- Hydrocortisone hemisuccinate (HHC), Dose 600-800 mg/day, 1 vial = 100 mg and
25 mg
o Triamcinolom (Volon, A and B)
o Betamethasone (Diprophos), Dose 1 vial, at 4-6 weeks.
o Dexamethasone , Dose 400-500 mg/day
o Beclometasona (Becotide), Dose 400-500 mg/day

E. Other therapies with:

- Furosemide – aerosols
- Antihistaminic (seldom)
- Methotrexate
- Niphedipine
- Verapamil
- Antibiotics:
 Cephalosporins generation III
 Quinolone
 Macrolide (Izomycin)
 Amoxicillin 2-3 mg/day
 Augmentin 3x650 mg/day
- Psychosedatives
- Expectorants and fluidificants of the bronchial secretions
- Climatotherapy
The assisted ventillation, is used when the breathing frequency is over 30 breaths/min, or
under 10 breaths/min, PaCO2 increases progressively, when the obnubilation and imminence
for a cardiac harass appear.
The treatment of the asthmatic crisis:
- O2 humidified administrated with intermittence
249
 - ß adrenergic
- Aminophylline
- HHC
- Antibiotics
- Anxiolytics
Contraindications in the asthma treatment:
- Aspirin
- Penicillin (risk of sensitivity)
- Sedatives and hypnotics
- O2 continuous therapy
- Simpaticomimetics

II.8. THE SHOCK

Definition: shock is a hemodynamic and metabolic process with acute allure, resulting from
an imbalance of intravascular fluid and vascular bed.
Shock is a pathophysiological process that characterizes the decline in the flow of oxygenated
blood tissue below the critical work processes of cellular metabolism. Hypoperfusion rapid
expansion produces cellular hypoxia. Insufficient perfusion of tissue and organs has several
causes: cardiac pump failure, decreased venous return, hypotension with increased cardiac
output produced by decreasing arterial tone, which combines with a maldistribuţie blood flow.
In the shock is inadequate oxygen consumption, reduced corespude needs no tissue hypoxia
and metabolic disorders leading to cellular dysfunction of the vital organs.

Aetiology:
 Infections
 Traumatisms
 Bleedings
 Dehydrations
 Intoxications
Clinical signs:
- Cold extremities, cyanotic, pale, humid
- absent ungheal pulse
- modifications of the AT, pulse PVC
- disorders of cardiac rhythm
- respiratory disorders (frequency, amplitude)
- conscience disorders (cerebral irrigation)
- oliguria, anuria
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 - fever (absent)
- tachycardia (when there is the lack in case of administration of beta-blockers)
- marmoration of the teguments most of all at the level of the knee articulations
- disorder of the conscience and attention (septic encephalopathy)
- polypnoea (in the case of the metabolic acidosis and of the sympathetic
stimulation)
- signs of the causal disease (crepitate rales in case of pneumonia, cardiac signs of
the right heart in case of pulmonary emboli)
Biologic signs
- cytolisis and cholestasis hematic (shock liver)
- in the distress respiratory hypoxia with the increase of the Pco2
- the increase of the creatinine and urea (renal insufficiency)
- metabolic acidosis with anionic void (theincrease of the lactacidemia)
- intravascular disseminated coagulation (coagulant factors, fibrinogen, thrombocytes,
D-dimers)
- elevation of the arterial lactatemia (and non-venous) ›1-2mmol/l

Mechanisms of production.
The aggressive agent

Hemodynamic Neuroendocrine Metabolic disorders

disorders reactions (secondary to the neuroendocrine ones)

In the hemodynamic disorders we assist to:

The catabolic phase: when it is produced a sympatheticotonia with endocrine regulation and
secretion of ADH =» liberation of catecholamines → arteriolar and venular vasoconstriction
with the centralisation of the circulation → ischemia tissues.
A series of organs are sacrificed:
The first organ that is sacrificed is the kidney, due to the decrease of the renal perfusion and it
is characterised through:
 oliguria
251
  azote retention
 acidosis
 hyper K

It follows the liver and small intestine, followed by other agencies.

Anabolic phase (recovery) with neuroendocrine regulation, when the flow improves tissue,
remove acid metabolites, protein anabolism and install the appropriate treatment rebalancing
hydroelectrolytic in a few weeks, the shock fades.
Within metabolic disorders, electrolyte metabolism modification witness retention cation
phenomenon of being affected transmineralizare sodium pump => release of proteolytic
enzymes in the cell -> autolysis cell. Report inverted pyruvate lactate = 10/1.

If action is not taken quickly to correct shock treatment, he becomes irreversible (shock
delayed), when cell death occurs - >> death.

The classification of the shock

after Broock:
- bleedings
Hypovolemic (decreases the blood V) - dehydration
- plasmorrhagies
Shock

- toxic
Normovolemic - allergic

252
 (decrease of the heart function - neurogenic
or of the vascular bed) - metabolic

Another classification:
After the case of production
- central causes – insufficiency of cardiac pump
o the cardiogenic shock
o thrombosis
o myocardial infarct
o arrhythmia
o emboli
- peripheral causes – the decrease of the venous torsion through:
o loss of liquids; hypovolemic shock
o blood losses; haemorrhagic shock
o plasmatic losses; the traumatic shock, burns
o water losses + electrolytes; hypovolemic shock
- The redistribution of the blood in the vascular bed (pooling)
o the septic shock (bacterial and viral infections)
o vasogenic shock (anaphylactic, anaesthetic)
o the neurogenic shock (pain, scare, warmth, affections of the bone marrow)

The neurogenic shock

It is produced by the sudden decrease of the arteriolar tonus → collapse → vasodilatation →
arterial hypotension → stagnation of the blood in the veins (pooling).
The sequestration of the blood → sympatheticoadrenergic reaction → vasoconstriction →
decrease of the tissue perfusion → decrease of the cerebral flux.
Clinic image:
- pallor
- cold sweats
- weakness
- dyspeptic syndrome
- AT ↓
- bradycardia
Treatment:
- Oxygenotherapy
- IOT+ ventilator support
- Trendelenburg position
253
 - isoproterenol
- hydroelectrolytic rebalancing (crystalloid and colloidal)
- inotropic (adrenaline, noradrenaline, dopamine)
The rachidian anaesthesia → neurogenic shock, through the blockage of the pre-ganglionic
fibres:
Treatment:
- Trendelenburg position
- Hydroelectrolytic rebalancing
- vasopressors (ephedrine, dopamine)
- efficient pulmonary ventilation
The cardiogenic shock
It is produces by the sudden decrease of the D.C. without a modification of the total blood
volume.
It is produced through insufficiency of cardiac pump.
Aetiology:
- I.M
- tamponament
- septal interventricular defect
- ventricular aneurysm
- pneumothorax
- severe tachycardia
- severe bradycardia

Clinical image:
- pale teguments, cold, cyanotic, marmorate
- filiform pulse, high PVC
- arterial hypotension + tachycardia
- oliguria
- conscience disorders
- PVC = N or high
- agitation or lethargy
- severe dyspnoea
- thoracic pain
Treatment:
- rebuilt of the cardiac debit
- O2
- cardiotonics

254
 - natural inotrope catecholamine (adrenaline, noradrenaline, dopamine,
dobutamine, izoprenaline)
- analgesics
- pericardial puncture (in the cardiac tamponade)
- xylene in arrhythmia
- digital in atrial arrhythmia
- pronestil in the ventricular arrhythmia
- vasoconstrictors: Isoproterenol (0, 5mg in 500 ml, gluc 5 %)
- permanent maintenance of the hemodynamic parameters
- hypotensors in the phase II for the optimisation of the post-pregnancy: sodium
nitroprusiate, nitro-glycerine (in perfusion)
- repolarising perfusion: glucose-insulin-potassium
- the correction of the metabolic acidosis
- prevention of the electrolytic imbalances
- etiologic treatment

The septic shock

It represents a tissue hypoxic suffering, caused by a circulatory failure associated with the
existence of blood pathogens and / or their toxins.
Aetiology
Severe infections: gram negative (ginecologice, urinary), gram positive (viruses, rickety)
Septic shock
- hypervolemia
- cardiac insufficiency, through toxic lesions

The production mechanism:

a. through the sequestration of liquids in the III extracellular, with hypervolemia, through
pooling and extravasation of liquid.
Clinic image:
- D.C low
- anxiety
- agitation
- tachycardia
- polypnoeea
- arterial hypotension
- cold teguments, cyanotic, pale

255
 - PVC decreases
- diuresis decreases, oliguria
- confusions
- SaO2 increases in the first phase
The catecholamine increase the peripheral vascular resistance → tissue perfusion decreases
→, decreases the consume of O2 → lactic acid ↑→ consume of the coagulation factors →
bleedings.
Treatment:
Objectives:
1. eradicate the infection
2. neutralisation of the toxins
3. inhibit the pro-inflammatory mediators
4. sustain the vital functions
1. Eradicate infectious outbreak by surgery, bacteriological examinations, samples of
pathological products

 The administration of antibiotics with a wide spectre to comprise the eradication of the
gram positive germs, negative and anaerobic.
It is eligible to use the bactericide i.v. antibiotics in maximum doses
Ex: Carbamapenem (Meropenem 1g l2 h + aminoglycosides (Gentamicin 80 mg at 8 h or
piperocilin: Tazocin), or cephalosporins the 3rd generation (Ceftazidin, Fortum, Medocef etc.)
associated with a fluorochinolon
 inotrope positive substances: dopamine 5-20 μg/kg/min, adrenaline, noradrenaline 1-2
mg/min, dobutamine + adrenalin
 Catheter Swan – Grantz – registers continuously the saturation of O2
 Oxygenotherapy + mechanical ventilation: facial mask; at PaSO2 under 80 →
mechanical ventilation
 The CPAP mask – the spontaneous ventilation with positive continuous
pressure
 Mechanical ventilation with PEEP in the aggravation of the hypoxemia (paCO2 under
50)
 The correction of the metabolic disorders
 Glucose solutions corrected with insulin
 Alkaline solutions
 Fresh frozen plasma
 Thrombocytar concentrates
 Heparin
2. The neutralisation of the microbial toxins
256
  The neutralisation of the endotoxins liberated by the infection is made with polyclonal
and monoclonal antibodies with immune serum J5
3. The anti-inflammatory therapy
- The administration of monoclonal antibodies anticytokines (TNF-a , IL-1)
- The inhibitors of cycleoxidase: ibuprofen
- pentoxifilin (experimented on animals and it follows the confirmation for humans)
- cortisone: methylprenisolon 30 mg/kg, dexamethasone 6mg/kg; small doses, the
great doses determine immunosuppression
4. The treatment of the organ insufficiencies
The anaphylactic shock

It is the sudden expansion of the vascular bed with widespread vasodilation (no longer filled
vessels). In the first stage the substance comes into contact with an allergen and hapten results
in the synthesis of immunoglobulin E (IgE), which is fixed to mast cells and basophils.

The reaction atg-atc

Interests 4 sectors:
1. derma
2. respiratory apparatus
3. the gastrointestinal tract
4. the cardio-vascular system
The clinic image:
- generalized rash + oedema
- glottis oedema + bronchial spasm
- cough + asthmatic status
- arterial hypotension + tachycardia
- loss of conscience
- midriasis
- incontinence for the urine and dejections
- convulsions
- death
- cyanotic teguments and mucosa
- nausea
- vomiting
- abdominal cramps
- diarrhoea
- cough, stridor, rheum, wheezing
- itching
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 - erythema
Treatment:
- sitting the patient in an adequate position (pseudo-trendelenburg)
- release of the superior breathing ways + O2
- adrenaline + O2 (increase of the level of AMP from the mast inhibiting the
liberation of histamine). Doses s.c. 0, 3-0, 5 mg, repeated la 10-15 min. or i.v. 1-2
mg in 100 ml physiologic serum 9 ‰. Adrenaline: equivalent of noradrenaline +
dobutamine 1mg/h i.v. on S.A.
- calcium
- romergan
- aminophylline
- alupent, ventolin
- coloids (plasma, plasmexpanderi 1-2 l rapid)
- cardio-respiratory resuscitation
- intubation O.T. and ventilator support
- corticosteroids
The hypovolemic shock
Appears it is reduced blood volume by large losses of: blood (hemorrhagic shock), plasma
(burns, trauma), liquids (overall dehydration by diarrhoea, vomiting, fistulas or fluid loss via
the kidneys), the intestinal occlusion, pancreatitis, permeability of capillaries (capillary
leakage) of fluid accumulation in the interstice or cavities.

The physiopathology of the hypovolemic shock

The hypovolemic shock is the consequence of reducing relative or absolute circulating

volume, followed by decreasing venous return and preload. To survive a person needs 70% of
the plasma volume. Reducing plasma volume by more than 30% lead to critical condition,
with low chances of survival. If volemia falls by more than 25% triggers rapid hemodynamic
compensatory mechanisms initiated by a neuroendocrine response. The first phase is catabolic
phase occurs sympathetic nervous system activation release of catecholamine excess. The
reaction is immediate and is produced by stimulating presoreceptors the carotid sinus and
aortic arch vessels Spahn and reflex receptors in the right atrium, triggered by hypovolemia.
Signs are transmitted to the upper cortex (posterior hypothalamus) that trigger a response

258
sympathetic-adrenergic, followed by a neuroendocrine
Peripheral vasoconstriction
Retention Na/water

Retention Na and H2O↑ The stimulation of the Peripheral

Cortisol ↑ nervous simpatico vasoconstriction
Adrenaline ↑ Cardiac stimulation
Noradrenaline ↑
Renin/angiotensin/aldosteron ↑

Stimulation Nervous central response

of the
hypophysis
ADH ↑
ACTH ↑
Activation of the baroreceptors
and mechanoreceptors ↑

The intravascular volume ↓

response.

The activation of the sympathetic nervous system leads to arteriolar peripheral constriction
(skin, muscle, kidney, splanchnic territory) and a redistribution of blood flow with the
centralization of the circulation, increasing contractility and heart frequency, the contraction
of the vessels of capacity (splanchnic) with increasing venous torsion, stimulating the
medulosuprarenal with release of adrenaline, activation of the renin-angiotensin system.
Under the act catecholamine cardiac output is restored in the beginning, circulating levels of
adrenaline reaches 2-4 mg / ml in terms of hypotension. Under the act sympathetic nerve and
increased levels of catecholamines constrict arterioles and venules occurs rich in alpha
adrenergic receptors in the skin, muscles and viscera. Here are mobilizing a mass of blood to
the brain and vital organs.
For rebalancing the TA in shock it intervenes also the renin-angiotensin system and the
release of arginine vasopressin. Damage, baroreceptor afferent renal arteries triggers the
release of renin which generates angiotensin I transformed to angiotensin II. They restore TA
vasomotor tone through increased mesenteric arteriolar bed and contributes to the release of
catecholamines from the adrenal medulla.
Aldosterone is released from the adrenal cortex that determine retention of Na and water.
Posterior pituitary intervenes 3rd pressor clearing system by releasing vasopressin, which
increases the resistance in the splanchnic nerve.
259
The catecholamine vasoconstriction interests the arterioles, metaarterioles and the capillary
sphincters. The precapillary vasoconstriction favours the transfer of liquids by reducing the
hydrostatic pressure vessels.
Glicogenilose is favoured by the catecholamines with release of glucose favouring the
increased volume and pressure at this level and attracting cellular water. Increased interstitial
pressure would help restore intravascular volume. In the subsequent phase compensation body
launches endocrine mechanisms. ACTH-cortisol reaction is completed and thyroid hormones
act retrohipofizari attributed to increased osmolality through sodium retention.
The stimulation of the pituitary hypothalamic osmoreceptors produce about the release of
DNA from the distal convoluted tubule, replenish the volume of extracellular fluid, and on the
other reaction ACTH stimulates the adrenal cortex leading acting on the secretion of cortisol
produces sodium and water retention.
If the therapeutic intervention is reversible phase quickly and efficiently. Otherwise,
compensatory mechanism is still inefficient and installs tissue hypoxia associated with lactic
acid, lowering energy phosphate reserves. (ATP).
If the hypoxia and the acidosis are continued, the physical metabolites are accumulated, the
response of the microcirculation to endogenous catecholamines decreases progressively, the
capillaries are opened, the pre-capillary sphincters, meta-arterioles and even the arterioles are
dilated.
A large vascular bed is opened that takes some of the circulating blood emphasizing
hypovolemia. It follows a stagnation of blood in the vascular bed, diminishes venous return
and cardiac debit is reduced further.
They interfere also other mechanisms that contribute to the decompensation of the peripheral
circulation and vasodilator prostaglandin release, reducing the sympaticotony due to ischemia,
impaired recycling process of the catecholamine followed by their depletion.
It is released also endogenous opioids which are reducing the sympathetic response from the
central nerve centres (after having reduced ≈ 1250ml / 70kg).
In advanced stages of shock increases the capillary permeability by releasing vasoactive
mediators: histamine, bradykinin, platelet activating factor and endothelial damage by oxygen
free radicals produced by xanthine oxidase system or activated polymorphonuclear.
It occurs the disseminated intravascular coagulation (DIC) by slowing blood flow, blocking
the capillaries aggregated by the activated white blood cells and platelets, decreased red cell
deformability, decreased by inhibition titre of heparin-histiocitary reticular system.
Blood pressure falls and irrigation vital organs is critical.
Capillary stasis, capillary thrombosis acid and achieved a vicious circle untreated in time lead
to irreversible lesions installation.

260
The endoplasmic reticol is oedematiated, as well as the mitochondria. The lysosomes are
broken by the release of proteolytic enzymes determining the intracellular digestion and
deposition of calcium.
Increasing cell membrane disintegrates phospholipid substrate, arachidonic acid metabolism
which path will provide leukotrienes, prostaglandins, thromboxane.
Besides the hemodynamic component the shock has also a systemic inflammatory component.
The hypoxia generates altered function of organs by inadequate production of ATP and
removal of toxic metabolic products inadequate, including lactate and carbon dioxide.
Resulting decline in organ function have a high energy consumption: heart, kidney, intestine.
The inflammatory response varies in relation to the chemical form of shock. In sepsis, a
systemic inflammatory response may even be severe due to the impact itself, on the other
hand shock can trigger an inflammatory response type as ischemia-reperfusion injuries are
followed by such a response.
In the case of the hypovolemic shock the first sacrificed organ is the kidney due to renal hypo-
perfusion produced by hypertonic sympathetic, catecholamines, angiotensin and vasopressin.
In the splanchnic territory, causes vasoconstriction suffering ischemic liver, pancreas and
gastrointestinal tract. The substances released from these bodies contribute to the
irreversibility of the shock.
The brain and heart comparatively to other organs are protected in the first part of the shock.
CNS depression occurs only if BP falls below 50 mmHg. But the association promotes
systemic inflammatory response suffering neurological installation (if traumatic shock).
The hemorrhagic shock occurs through internal or external blood loss and depends on the
amount, speed and duration of blood loss.
- Losses of 35 % = severe shock
- Losses of 45 % = irreversible shock
- Losses of over 50 % = fatal shock
Clinical signs:
- teguments and mucosa pale-marmorate, cold, humid, cyanotic with the absence of
the capillary pulse, icteric
- thirst
- tachycardia +hypotension
- PVC low
- hemodilution (from the extra-cellular space)
- polypnoeea
- oliguria
- hypothermia
- digestive bleeding
- anxieties, agitation/phase I
- apathies, somnolence/phase II
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Treatment:
- blood transfusions, blood izo group, izo Rh
- hydroelectrolytic rebalancing (on at least 2 veins with the control of the PVC), cannula
14 G in peripheral veins
- transfusions - plasma
- correction of the hypoxia and acidosis – anti-shock trousers
- dismissal of the cause – in the cardiac tamponade thoracotomy and cardiac internal massage
- surgical haemostasis
- oxygeno-therapy, IOT, ventilator support
- perfusion with crystalloid and colloidal solutions in rapport 3:1
- colloidal solution: blood, human albumin, fresh frozen plasma, dextran, gelatines
(Gelofuxin, Haemacel) and HES (hydroxietilate amidon)
- integral blood
- human albumin 5 % plasmatic proteins
- fresh frozen plasma ( with the factors of the coagulation)
- Dextran 70
- Gelatine solution 3,5 %
- crystalloid solutions: saline isotone solutions (NaCl 0, 9 %, sol. Ringer-lactate)
- cardiotonic (digoxin)
- vasoconstrictors (dopamine, noradrenaline)
- correction of the electrolytic and acido basic imbalances (spdium biccarbonate 8, 4% or 4, 2
%)
- the treatment of the organ insufficiencies
For losses of 100 - 200 ml of blood, the compensatory mechanisms interfere.
The general treatment for shock
It is addressed to:
- the primary cause
- hemodynamic disorders
- metabolic disorders
The evaluation of the lesions:
1. The hemodynamic and metabolic disorders
- the balance of the losses
- catheter of PVC (N = 5 -15 cm H2O)
- appreciation of the contraction force of the heart
- monitoring the AT.
2. The pulmonary ventillation
- amplitude
- frequency
262
 - free respiratory ways
- IOT
- tracheostomy
3. The aspect and coloration of the teguments
- humid
- pale
- warm
- plagues
- fractures
4. Urethral probe
- Monitoring of the D (1 ml/kg/h)
5. Examination of the abdomen + the global exam
- Gastric probe (ameliorates the vein torsion)
6. The laboratory exams
- Ht, Hb, pH, blood ionogram, PCO2/ SO2/ O2 = optimum at Ht = 35-40 %
The order of the treatment:
a) C-V apparatus
b) respiratory apparatus
c) renal apparatus
The team treatment.
The treatment is made in the order of the physical-pathologic disorders
1. the treatment of the hemodynamic disorders
2. the treatment of the metabolic disorders
3. the treatment of the organ insufficiencies
4. assuring the sleep, analgesia, nutrition, prevention of the escars
A. The therapy with liquids:
- the rebuilt of the blood V. + plasmatic
- assuring a normal diueresis
- the LEC maintenance
- adequate nutrition
Liquids:
a. macromolecular solutions:
- integral blood
- plasma
- albumin solution
- plasma-expanders
The integral blood, at losses over 1/3 of the plasmatic volume + electrolytic and volemic
solutions

263
 - slow losses of blood, not transfused (100 – 200 ml of blood)
- attention in older people and children
- the risk of blood administration
PLASMA - Double Or Triple = intake of frozen protein and resulting the increase of the
oncotic pressure and it can be quickly administered without stating the sanguine group (also
brings clotting factors)
Human albumin 5%
Plasma-expanders (colloidal solutions natural or synthetic)
- they produce pseudo-agglutinations, coagulation disorders
- it is not administered more than 1000 - 1500 ml
 Dextrans
- Macrodex
- Dextran 70 and 40
- Reomacrodex
 Gelatine derivate
- Oxypolygelatine
- Fluid gelatine (Plasmogel)
- Marisang
b. Crystalloid solutions
- they leave rapidly the vascular bed
- it corrects the volume intra and extracellular
There are:
- the physiologic serum 9 ‰
- the solution of glucoses of 5 %, 10 %, 20 % + insulin 1UI la 5 g glucose
- Ringer solution
- The solution of sodium bicarbonate 14 ‰
The rhythm and amount of the solutions is appreciated depending on the: TA, PVC, diuresis,
Ht.
The way of administration, is a central vein.
B. Vasotrop medication:
- Adreno-stimulents
- Adreno-blockers
- Sympatheticocholitics
The adreno-stimulents are vasopressors and they are divided into 4 groups:
1. α adrenostimulants (Vasoxil) = arteriolar vasoconstriction.
2. adrenostimulents with mixed action α and β: Noradrenaline, Ephedrine, Metaraminol (in
the cardiogenic shock)

264
3. adrenostimulents with mixed action α and β and which increase the cardiac frequency:
Adrenaline and Mefentermine
4. betaadrenostimulants: Isoproterenol = inotrope and cronotrop positive with effect α
peripheral blocker.
C. Vasodilator medication:
- it is administered after the vessel is filled with liquids
- decrease the vascular frequency and increase the venous torsion
- decrease the effort of the heart
- increase the D.C
- ameliorate the tissue perfusion
- decrease the acidosis and anoxia from the tissues
They are divided into 3 categories:
1. Neuroleptics
- DHBP (dehydrobensoperidole)
- Chlorpromazine (α blocker)
2. α adrenoblockers
- Hydergin, redergin (α blocante)
- Isoproterenol = α blocker and β stimulant, 1 mg kg/body in perfusions
- Fenoxibensamine
3. Vasodilators with direct action over the smooth musculature
- Regitine
- Nitro-glycerine 5 -10 μg/min
- Sodium nitroprusiate
D. β blocker medication
- Propranolol (Inderal) = diminishes the consume of O2 and it bradycardises
E. Cortisone medication
- small doses 150 - 200 mg/24 h (potentiate the action of the catecholamine)
- big doses 20 - 50 mg/kg body → increase the D.C. and reduce the peripheral
resistance; inhibit the atg reaction – atc neutralises the effect of the endotoxins.
F. The cardiotonic medication
- Digital
G. Medication for the prevention of the metabolic acidosis
- Sodium bicarbonate 8, 4 %, depending on the BE, pH, pCO2, B.S.
- THAM = free acceptor of H+
H. Medication for the prevention of the tissue anoxia
- O 2: 4 – 6 l/min
- Decrease of the temperature at 32° C
I. Medication for the prevention of the coagulation disorders for the CID = fresh blood.

265
 - Heparin
- Fraxiparin
- Clexane
- Clivarin
J. Medication for the prevention of the hydroelectrolytic disorders
- Hydra balance
- Blood and urine ionogram

K. Medication for the prevention of the infection.

- antibiotics depending on the antibiogram for 7 -10 days.
The treatment of the organ insufficiencies.
- The prevention of the CID = micro-infarcts in the heart, liver, lungs, kidneys
- Arterial pressure
- Haemolysis
- Dehydration

The prevention of the renal acute deficiency (I.R.A)

functional (pre-renal) when the kidney is normal,
and the composition of the blood pathologic =>
azotaemia + oliguria.
It is administered solutions rich in Na,
rebalancing H-E

organic, when there are lesions of the renal parenchyma, results N.T.A with:
- oliguria
- azotaemia
- decreases the power of concentration of the kidneys
(density under 1015, urinary urea under 14 g ‰)
The probation is made with manitole 20 %
If at 100 ml of 20% manitol the diuresis resumes 30-40 ml / hour = Functional IRA.
If the diuresis has increased by 50% in 2 hours => organic IRA and it is administered
Furosemide 20-40 mg i.v.
The IRA treatment:
- restriction of liquids
- the diminution of the protein restriction
- it is not administered K
- the correction of the acidosis
- reduction of the medication with renal administration
266
 - hemodialise when:
 N increases over 300 mg %
 K increases over 6, 5 mEq
 Acidosis: B.S. under 15 mEq

II.9 MODS – MULTIPLE ORGAN DYSFUNCTION SYNDROME

MODS – Multiple Organ Dysfunction Syndrome is a dysfunction or failure of two or more

organs or systems in a patient in critical condition, homeostasis can be maintained only by
therapeutic interventions.
MODS it is a nonspecific response of the body's inflammatory response and the activation of
inflammatory signals as a result of activation of the biological cascades of the different
causative agents (alone or in combination). The organs most commonly affected are:
respiratory, cardio vascular, renal, liver, central nervous system and digestive tract,
hematologic, metabolic, endocrine and immune.
Aetiology: sepsis, peritonitis and intra-abdominal infections, pneumonia, necrotizing soft
tissue infections; Acute pancreatitis; Extensive tissue damage: poly-trauma, burns; Tissue
ischemia caused by shock (hypovolemic, cardiogenic, obstructive, distribution); Autoimmune
diseases, rejection of a transplanted organ; Iatrogenic factors: un-removable devitalized tissue,
multiple transfusions, mechanical ventilation, extracorporeal circulation, surgery laborious;
Poisoning.
In the early 1970s, multiple organ dysfunction is seen as a syndrome with severe and multiple
concomitant vital systems, using the term MSOF (multiple system organ failure). In 1991 it is
recommended to refer to MODS (multiple organ dysfunction syndrome) because by definition
are included, and biochemical organs.
MODS is characterized by generalized systemic inflammation and tissue damage. It is known
that when tissues are damaged, the body simultaneously (105) pro- and anti-inflammatory
mediators release. The balance between these facilitate tissue repair and healing. But when
imbalance appears exaggerated inflammatory response is manifested by lesions endothelial
microvascular dysfunction, impaired tissue oxygenation and multiorgan injuries.
The consequences of exaggerated inflammatory response are anergy and immunosuppression
with infections and / or septic syndrome (106). MODS is actually a "continuum", a syndrome
dynamic, constantly changing, which includes SIRS (systemic inflammatory response
syndrome), and CARS (compensatory antiinflamatory response syndrome) and MARS
(mixed-antagonist response syndrome) (107).
The early twentieth century, intensive development has enabled prolong life in patients in
critical condition by using modern techniques or life support devices, thus making possible
the emergence of multiple organ dysfunction and a series of associated iatrogenic problems.
267
Regardless of MODS etiology, clinical and laboratory, pathological changes of organs
involved in systemic inflammatory syndrome are similar. Supporting the function of vital
organs (heart, lung, kidney) led to the postponement development of critical conditions and
allowed the development of other disorders, such as liver, gastrointestinal tract (bleeding,
perforation, translocation of bacteria), immunological disorders, metabolic ( " autocabalismul
"with hepatic consecutive skeletal muscle), practically all organs can reach the stage of
dysfunction. Simultaneous or sequential mode of occurrence is given the severity of primary
lesions, that develop complications, genetic antecedents and conditions of the patients (105).
On the other hand, monitoring and therapy of invasive interventions are new colonization and
infection sources contributing to the development of sepsis and multiple organ dysfunction
(108).

II.10 THE SYSTEMIC INFLAMATORY RESPONSE SYNDROME (SIRS)

Body reaction in the presence of an infectious etiology aggression or non-infectious sums,

initially, the association between an inflammatory immune reaction and one locally, that tends
to generalize later. Clinical manifestations indicating generalization that reactions have been
associated with several bio-humoral markers to outline a clinical-biological syndrome
significantly. It was originally called SIRS (systemic inflammatory response syndrome).
Systemic inflammatory response to infection called sepsis syndrome does not necessarily
indicate the presence of bacteraemia. More inflammatory response to severe infections is not
unique: similar events can also be found within non-infectious disease. (98)
In 1992, the American College of Chest Physicians (ACCP) and the Society of Critical Care
Medicine (SCCM) introduced definitions syndrome systemic inflammatory response (SIRS),
sepsis, severe sepsis, septic shock syndrome and organ dysfunction multiple (MODS). (88)
The idea was to define a nonspecific clinical response to an insult either of infectious origin or
non-infectious.
SIRS is defined as two or more of the following variables:
Fever higher than 38 ° C or less than 36 ° C
- the cardiac rhythm more than 90 beatings per minute
- The respiratory frequency higher than 20 breaths per minute or PaCO 2 less than
32 mm Hg
- The number of white cells from the blood abnormal (> 12.000/ul or <4000/ul)
SIRS is nonspecific and it may be caused by ischemia, inflammation, traumatisms, infection,
or more combined aetiologies.
The infection is defined as "a microbial phenomenon characterised by the inflammatory
response to a microorganism or the invasion of the normal sterile tissue through these
organisms."
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The microbiological infection is a phenomenon characterized by an inflammatory response
directed against an invading microorganism normally sterile tissue.
Bacteremia is defined as the presence of viable bacteria in the blood, but this condition does
not always lead to sepsis or SIRS
Sepsis Clinical signs include the presence of biological defining SIRS and demonstrated the
presence of infection (culture-bacterial, viral, fungal or parasitological) or presumed. Sepsis
severity is graded according to organ dysfunction and degree of impairment of the
hemodynamic status and with different scores organ failure (such as SOFA score - evaluation
score of the sequential organ insufficiencies).
Severe sepsis meets the above criteria and is associated with organ dysfunction,
hypoperfusion, or hypotension. The patients fulfilling the criteria for septic shock if they
hypotension and perfusion abnormalities persisting despite adequate fluid rebalancing. (98)

II.11. THE ACUTE ABDOMEN

It is characterised through an intense abdominal pain, installed rapidly, with duration of
several hours up to 2-3 days, determined by severe affections and which needs treatment of
intensive therapy (IT) or surgical intervention.
The clinic exam:
- Anamnesis
- The objective exam
The paraclinic exam:
- Taking the biologic samples (blood, urine, gastric juice, defecation)
- The imagistic explorations (radiologic exam, echography, endoscopy, computer
tomography, magnetic resonance)
The pain in the acute abdomen has certain characteristics:
1. The parietal pain is caused by noxious stimuli acting on the spinal nerves and
sensory fibers include: diseases of the spine, the spinal meninges and nerves.
2. The pain of visceral origin is determined by stimuli that act on the sensory nerve
endings vegetative: pain is dull, deep, is not precisely located. Stimuli that induce
pain and spasm are distension of hollow organs in the abdominal inflammation,
visceral and peritoneal irritation destruction neighborhood.
3. Pain of vascular origin is caused by stimuli that fall into somatic and autonomic
nerve endings. The pain is vascular occlusion gives tissue damage.
4. The central pain - stimuli acting on the CNS. Spinal marrow disorder is triggered,
the brain, such as inflammatory, vascular or tumoral.
5. The pain generated by extra-abdominal disease is about pain irradiated to other
organs within the chest or other diseases like diabetes, porphyria, collagen diseases
and so on.
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The general symptomatology in the acute abdomen
The general exam:
- Agitated psiho-motor patient (mesenteric infarct, renal colic)
- Pale teguments and mucosa, icteric, face congestion
- temperature (it is not compulsory)
- Burton gingival lizereum
- Global dehydration
- Oedema
The exam of the abdomen
Inspection: in dorsal decubitus and orthostatic
- participation of the abdomen to the respiratory moves
- collateral circulation in flancs
- vascular stars
- purpuric eruptions
- fat excess
Palpation:
- we must search the areas of muscular defence
- we search for impastation area
- the pain: localised, diffuse, with irradiation, at movement
Percution:
- meteorism (pancreatitis, intestinal occlusion)
- pain at percution
- matity
Auscultation:
- abdominal silentium
- rubbing
- suffles
The gynaecologic consult– in suspicion of gynaecologic affections
The rectal touche – the pain from the bottom of the Douglas sack
The paraclinic examination
- glycaemia
- hemoleucogram
- urea, serum creatinine
- amilasemia, amilasuria
- lipase
- blood ionogram

270
 - hepatic samples
- blood group
- time for bleeding, coagulation and indicator of prothrombine
- peritoneal puncture in Douglas
- dosage of the prophirines, plumbemia
- endoscopy
- pulmonary radiography and native abdomen
- echography abdominal
- electrocardiogram
- computer tomography
- nuclear magnetic resonance
- finally the laparotomy
The general treatment in the acute abdomen
- the patient is rapidly sent to the hospital
- absolute rest in bed
- complete alimentary rest
- venous approach (1-2 veins)
- hydro-electrolytic rebalance
- correction of the acidosis
- the set and maintenance of a gastric probe for the diagnosis and therapeutic
- the set of a bladder probe (critical patients)
- administration of antibiotics with a wide spectrum (suspect of faecal peritonitis)
- laparotomy in case of incertitude in diagnostic, when there is a suspicion of organ
perforation
- the temporisation of the laparotomy in case of myocardia infarct, saturnic colic,
cardiac insufficiency, acute porphyria.
Aetiology
Bennet believes that 90% of the etiology of acute abdomen presents six diseases: acute
appendicitis, intestinal obstruction, acute diverticulitis, peptic ulcer to flare, acute pancreatitis
and biliary colic.
1. The acute appendicitis – it appears more frequently in young children but it is not
excluded at any age.
Clinic signs
- the pain appears firstly periombilical or in the epigastrium, then after several hours
it is located in the right iliac fossa
- inappetence
- fever (differences of temperature rectum-armpit of 0, 8-10 C)
- nausea

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 - vomiting
- diarrhoea (more frequent in children)
- the Blumberg positive manoeuvre
- muscular defence (it may be absent)
- impastation of the area from the right iliac fossa (it may be absent)
Paraclinic exams:
- hyperleucocytosis
- VSH (slightly modified or normal)
- T.S and T.C (for the surgical intervention)
- hemoleucoram (HLG)
- glycaemia (for the surgical intervention)
- amylases (for the differential diagnosis)
- ECO abdominal for the differential diagnosis
- the abdominal radiography on empty stomach
Differential diagnostic:
- extra-uterine pregnancy
- renal colic
- acute anexitis
- gastro duodenal ulcer (acute outburst)
- biliary colic
- follicle rupture
- acute diverticulitis
Treatment:
- chirurgical exclusively
- rebalancing H-E
- rest in bed
2. The intestinal occlusion
It represents the stop of the intestinal transit, with all the complications which result.
The intestinal occlusion is classified in:
a. functional (dynamic ileus)
- paresis or the paralysis of the intestinal wall
- exaggeration of the intestinal muscular contractions
Ethology:
 generalised or localised peritonitis
 acute pancreatitis
 digestive haemorrhages
 renal colic
 post-operatory states
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  anti-peristaltic drugs
 shock
 basin fractures
 cranial traumatisms
 thorax diseases
 infections and retroperitoneal bleedings
 diseases of the CNS
b. mechanics through:
- complete obstruction of the intestinal lumen
- occlusion through obstruction produces hyper-peristalsis with colic and noises
(gargurisments)
- antiperistalsis with vomiting
- ischemia and parietal necrosis →shock
Aetiology:
 tumours,
 inflammatory lesions,
 congenital stenosis,
 post-operatory states,
 foreign bodies (biliary calculi, fecaloms, laxatives, ascarides, etc),
 extrinsic compressions
(intra-parietal foreign bodies, abdominal tumours, congenital brides)
- the constriction produces obstruction together with the block of the mesenteric
circulation → ischemia of the intestinal wall → intestinal perforation.
Aetiology:
 bride,
 internal and external hernia,
 volvulus,
 invagination
Symptomatology:
- abdominal colic pain with small pauses of 10-15 minutes
- continuous pain in great supraiacent distensions = ischemia + necrosis
- pain localised in the epigastrium in jejun-ileon occlusions
- pain localised in flanks with colon occlusion
- the stop of the intestinal transit for gases and faecal matters
- vomiting (rotten eggs or fecaloid)
- borborisms
- peristalsis (seen in thin persons)
- clapotage
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 - at percussion timpanism
- abdominal distension
- cardiac signs (arterial hypotension, tachycardia, filiform pulse)
- obnubilation, apathy, adynamia
- global dehydration.

Para-clinic exams:
- abdominal radiography = hydroaeric images (organ pipes or swallow nests)
- high number of leucocytes (hyperleucocytosis)
- the values of the urea and high creatinin (azote retention)
- hemo-concentration (Ht↑)
- modified blood ionogram
Differential diagnosis:
- acute pancreatitis
- acute appendicitis
- renal colic
- intestinal infarct
- diverticulitis

Treatment:
- stop of the oral alimentation
- nasogastric probe with aspiration
- set of two venous lines and the rebalance of the H-E
- conservator treatment in the paralytic ileus, rebalance H-E, stimulation of the
intestinal peristalsis (α and β blockers)
- evacuator enema
- suurgical treatment, in case of constriction, obstruction or peritonitis
- antibiotherapy
- vesicle probe
- monitoring of the vital parameters,
- treating the complications
3. Diverticulitis
It is a complication of the colon diverticulosis. It appears through the bacterial inflammation
of the diverticular wall.
Clinic signs (similar with the appendicitis):
- Pains in the left iliac fossa
- Fever
- Disorders of intestinal transit (diarrhoea, constipation, ileus)
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 - mucus or blood in the dejections (seldom)
- dysuria
- leucocytosis
- Blumberg positive sign
- defence
Para clinic exam:
- the same as in the appendicitis
- passage barium (obligatory)
Differential diagnosis:
- renal colic
- sigmoidal
- colon cancer
Treatment:
- rest in bed
- anti-spastics
- antibiotics (cephalosporin)
- stop of the alimentation
- local refrigeration
- rebalance H-E
- avoiding the enema

4. The gastro-duodenal ulcer

It is a chronic disease, localised at the level of the stomach and/or duodenum shown through
cratetiform lesions of the mucosa, sub-mucosa and mucosa muscular.

Aetiology and pathogeny:

a. Clorhidropeptic hyper-secretion, through parietal cells with hyper-secretion, the persons

with sanguine group O I, high pepsinogen I serum, mediated hyper-secretion through
gastrin or vagal.
The gastrine, which is secreted by the G cells (from the antrum), stimulates the parietal
cells which secret HCl, in great amount.
b. Helicobacter pylori (H.p.) = increases the secretion of gastrin (increases the acidity)
c. Alteration of the factors of defence of the gastric mucosa which are:
- gastric mucus: destroyed by H.p.
- secretion of bicarbonates is low
- the sanguine flow is modified and it appears the local chronic ischemia
- urogastrin, which stimulates the increase of the epithelium, is low.

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The clinic signs:
- the abdominal pain as cramps, painful hunger or the epigastria burn.
 It appears at 30 - 90 min. postprandial in the gastric ulcer (G. U.) and at
2-4 h, and during the night in the duodenal ulcer (D. U.)
 It appears, with rhythmicity in the spring and in the autumn
 It is calmed to milk and alkaline medicaments.
 Localised in the epigastrium, in the G. U. and parombilical right in the
D.U.
- pirozis (through the irritation of the inferior oesophagus)
- nausea and vomiting
- eructation and acid regurgitations
- sialorrhea
- hiperorexia in U.D
- anorexia in U.G
- constipation (hipervagotonia)
- ulcerous dyspepsia (abdominal cramps, postprandial bloating)
Para clinic exams:
- the radiologic exam, puts in evidence:
 Niche (intense opacity, round because it retains the contrast substance).
 Convergence of the creases of the gastric mucosa towards the niche.
- digestive fibroscopy
- the exam of the gastric secretion, determining the cardiac debit of the basal acid
(DAB)
- cytological exam, from the sediment of the gastric juice for the H.p
- serologic exam (the identification Atc anti H.p. from the serum (class IgG) –
indirect sample
Differential diagnostic:
- the stress ulcer
- gastritis
- duodenitis
- gastric cancer
- Zollinger-Ellison syndrome
- acute pancreatitis
- acute esophagitis
- viral hepatitis (debut)
- biliary lithiasis
- myocardial infarct
- basal pleurisy

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 - pneumonia
Treatment:
Hygiene-dietetic regime:
- rest in bed
- sedatives
- reduced meals, repeated at fixed hours
- light aliments:
 lactates
 pasta
 soups, creams
 puree
 boiled meat
- exclusion of the condiments from the alimentation

Medicamentous treatment:
- administration of alkaline (neutralisers of the gastric acidity)
 compounds of Ca and Na (calcium carbonate, sodium bicarbonate)
 aluminium compounds (aluminium phosphate, aluminium hydroxide)
 magnesium compounds (magnesium oxide, magnesium carbonate)
- anticholinergic
 atropine 1f s.c. = 1 mg
 belladonna tincture
- blocker receptors H2 - histaminergics
 nizatidina (oxide) f = 50 mg/ml cp 150; 300 mg dose 2x150 mg/day
 cimetidine (tagamet) f = 50; 300 mg/ml; cp 200 and 300 mg dose
2x400 mg/day
 ranitidine (zantac) f = 50 mg/ml cp 150 and 300mg dose of 2x150
mg
- inhibitors of the carbonic anhydrase
 acetazolamide (ulcosilvanil) dose 25mg/kg/day
- gastrin inhibitors
 proglumid dose 400 mg i.v
- blockers of the proton pump
 omeprazole (losec) cp 20 mg Dose 20-40 mg
- protectors ale of the gastric mucosa
 bismuth salts (ulcerotrate)
- prostaglandins(misoprostol) dose 4x200 mg/day
- regulators of the digestive motility (metoclopramide)
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 - treatment of the infection with H.p.
 omeprazole 20 mg/day + amoxicillin 750 mg/day or helicocin +
ranitidine
Surgical treatment:
- partial gastrostomy and the gastro-duodenal termino-terminal anastomosis (Pean,
Bilroth)
- vagotonia (troncular or selective) with drainage and piloroplasty.
- antrectomia
- partial gastrostomy and the gastro-jejunal anastomosis termino-lateral (Reichel -
Palya)
5. Acute pancreatitis
It is a disease of the pancreas, which is characterised, through the acute edematous
inflammation or necrotico-haemorrhagic of the pancreas.
Aetiology:
- infection (viruses)
- alcohol
- biliary lithiasis
- metabolic factors
- medicaments (cortisone, sulphamides, furosemide, diuretics, oral contraceptives,
etc.).
Pathogen
Through the autodigestive theory, it is assumed that the protheolitic enzymes (phospholipase
A, tripsinogen, chemotripsinogen, pro-elastase) are activated in the pancreas, by a series of
factors such as: the viral infections, endotoxins, exotoxins, traumatisms and lead to the
digestion of the pancreatic tissue.
a. the acute pancreatitis nerotico-hemoragic
Clinic signs:
- abdominal pain in the bar:
 place in the epigastrium
 lancinant
 irradiates in the left hypochondria, at the base of the left hemithorax and the
left shoulder
- bilious vomiting, watery, in „coffee grounds”, or fresh blood.
- transit disorders or even dynamic ileus
- eructation
- meteorised abdomen, bloated
- collapse
- pallor, cold sweats, anxiety

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 - hypotension or even its collapse.
- fever
- filiform pulse, rapid
- timpanism
- ecchymosis in flanks (the left flank, Gary-Turner)
- associated pulmonary affections (pneumonia, atelectasis, pleurisy)
b. Acute oedematous pancreatitis:
- it has an image with clinic more reduced signs, sometimes masked
- epigastria pain, with the same localisation as the necrotic one, but of more
diminished intensity.
- dyspeptic syndrome
The para-clinic exam
- hyperamilasemia (5 times higher or even more)
- hyperamilasuria
- increase of the serum lipase
- hiperleucocitosis (10-20.000/mm3)
- hyper-glycaemia (moderate)
- low values of the calcium
- high values of cholesterol
- hepatic samples modified
- in advanced phases azote retention
- high hepatic transaminase
- electrolytic disorders
- decrease of SaO2
Imagistic:
- Rx abdominal simple = ileus reflex localised on the transvers colon and the first
thin ansa
- Rx with contrast substance, show the enhance of the pancreatic gland
- Rx thoracic = pleural reversion or parenchymatous opacities
- Echography: enhanced pancreatic lodge, intra and peri-pancreatic necrosis
- Computer tomography: enhanced pancreas in volume, with deleted contour
- Colangio-wirsungography endoscopic, when there are ampoular obstructions
- Scintigraphy radioisotopic with selenium, marked meteonin, show the glandular
necrosis
- Selective angiography of the celiac trunk shows vascular lacunas in the areas of
necrosis.
- EKG – dislevelment of the ST segment and inversion of the T wave.

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Differential diagnosis:
- gastro-duodenal ulcer
- intestinal occlusion
- acute cholecistitis
- aorta aneurism
- extra uterine pregnancy
- myocardia infarct
- pneumonia
- porphyria
Complications
- HDS
- Supra-infection
- Shock
- Intestinal occlusion
- Ascites
- Pulmonary complications
- Cardiac complications
- Renal complications
Treatment
1. Calming the pain with:
- antalgics
 Mialgin 100 mg at 6 h
 Fortral 50-100mg at 6 h
- anticholinergic
 Atropine 1 mg at 6 h, s.c or i.v.
 Scobutil 10 mg at 4 h
 Procaine in perfusion 20 - 40 ctg through lumbar infiltration or peridural.
2. Inhibition of the pancreatic secretion
- alimentary pause
- nasogastric aspiration probe
- gastric lavages, with alkaline solutions
- Mg oxide, calcium carbonate
- blockers of H2 (cimetidine 1 g/day)
3. anti-enzymatic therapy
 Gordox 500.000 uk/24 h
4. Inhibitors of the pancreatic secretion
Sandostatin 0,100-0,200 mg, de 3 times/day
5. Therapy with antibiotics
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 - Antibiotics with wide spectre
 cephalosporin associated with aminoglycosides
6. Prevention of the shock
- catheter in the central vein and the measuring of the PVC
- urinary probe, for monitoring the diuresis
- blood transfusion and macromolecular solutions
- rebalance H-E , according to the blood ionogram
- vasopressor drugs and tonicardiac for the sustenance of the heart and circulation
- fractionate and non-fractionate anticoagulants
- HHC-500-1000 mg
7. Parenteral alimentation
- Solutions of amino-acids and glucoses (30 calories kg/body)
8. The treatment of the complications (depending on the complication that appeared)
9. The surgical treatment in the necrotic-haemorrhagic pancreatitis for the clearance of the
necrosis

6. The biliary colic

It is represented by continuous pains or more rarely, caused by colic, localised in the right
hypochondria or in the epigastrium, with irradiation in the back and in the right shoulder, with
nausea, bilious vomiting, sometimes icterus and seldom fever.
Aetiology
- acute colecistitis
- lithiasic colecistitis
- colecist malformations
- vesicular hidrops
- mechanic icterus
- biliary icterus
The clinic signs and the disgnosis
- pain in the right hypochondria and in the epigastrium (the Murphy positive sign)
- dyspeptic syndrome (nausea, vomiting)
- headache
- psychomotorial agitation
- subfebrilities or fever
- lack of appetite
Para-clinic exams
- HLG
- Glycaemia
- Blood ionogram
- Moderated increase of the bilirubinemia and bilirubinuria
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 - Urine exam
- Urea, creatinin
- amilasemia, amilasuria
- enzymes CPK; ALAT
- pro-thrombin index
- thoracic and abdominal Rx
- abdominal ECO
- CT
- EKG
Differential diagnostic
- Right renal colic
- Acute appendicitis
- Extra-uterine pregnancy
- Right anexitis
- Intestinal colic
- Gastro-duodenal ulcer
Treatment
Antispastics:
- Piafen 1 - 2 f la 8 h
- Algocalmin 2 - 3 f/day
- Scobutil 1 - 2 f at 12 h
Anti-inflammatory
- Ketonal 1 – 2 f /24 ore
- Ketoprofen 1 – 2 f /24 ore
- Tador 1 f /24 ore
analgesics:
- Petidine (mialgin) 50-100 mg
- Fortral 1-2 f (50-100 mg),
In case of inflammation of the cholecyst, antibio-therapy with wide spectre.
Also in the aetiology of the acute abdomen we have:
- the renal colic
- extrauterine pregnancy
- salpingitis
- entero-mezenteric infarct
The renal colic
It is a painful lumbar symptom, with paroxistic pain, in the intra-renal cavities on top of the
obstacle.
Aetiology
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 - renal calculi
- tumours of the ureter
- blood clogs
- the caseum from the renal TBC
- traumatisms
Clinic symptomatology
The pain:
- intense paroxistic
- irradiates towards the genital external organs and the internal face of the hip
- appears suddenly
- the duration varies, from minutes → hours, and it is repeated
- lumbar unilateral localisation
- Giordano positive sign
General signs:
- pallor
- transpirations
- agitation
Vesical signs:
- dysuria, polakiuria
- vesicle tenesma
- haematuria (70 % of the cases sometimes piuria)
Digestive signs:
- abdominal meteorism
- dyspeptic syndrome
- muscular defence (it can be absent)
The para-clinic exam
The urine exam
- normal diuresis or oligoanuria
- urină tulbure, haematuria or opaque
- pH acid, in the uric lithiasis
- pH alkaline, in the phosphate lithiasis
- neutral pH, in the oxalic lithiasis
- urinary sediment (hematies, bacteriuria, cristaluria)

The exam of the blood

- normal urea and cretinin, in time slightly increased
- calcemia (modified)
- hemoleucogram (slight hyperleucocytosis)
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Imagistics
- the renal simple radiography, shows the radioopac calculi (90 %)
- urography (with odiston, ultravist) shows the calculi
- the echography shows, calculi bigger than 3 mm
- retrograde ureteropielography, shows the ureteral calculi
- C.T shows the diagnosis
- the magnetic resonance, shows the obstacle
Differential diagnosis
- urologic affections
 infarct renal
 renal hematoma
 prostatitis
- rachidian affections, lombago
- gastro-intestinal affections
 acute pancreatitis
 biliary colic
 splenic infarct
 gastro-duodenal ulcer
- gynaecologic affections
 the extrauterine pregnancy
 acute anexitis
 torsioned ovarian cyst
Treatment
a. The hydric restriction and then hydration 2 - 3 litres, after eliminating the obstacle
b. Antalgics and analgesics
- minor: - ketonal, algocalmin, novalgin i.v or i.m
- major: - mialgin, morphine, fortral
c. Non-steroidal anti-inflammatory
- ketoprofen 100 mg în 250 ml glucose 5 % de 3 times/day
- antispastics
 Scobutil
 Papaverine
Bockus – divides the affections which produce acute abdomen in 3 categories:
1. Abdominal pains, which need urgent surgery
- Acute appendicitis
- Intestinal occlusion
- Organ perforation

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 - Acute perforated cholecystitis
- Organ torsion
- Organ rupture
- Intestinal infarct
- Emboli of the aorta bifurcation
2. Abdominal diseases, which simulate the acute abdomen
- Acute pancreatitis
- Acute gastritis
- Painful ovulation
- Retroperitoneal bleeding
- Acute enteritis
- Acute hepatitis
- Gonococci peri-hepatitis
- Mesenteric lymphadenitis
- familial polyserositis
3. General diseases, which give acute false abdomen
a. cardio-vascular affections
- I.M.
- Pulmonary emboli, renal, splenic
- the stasis liver
- disequant aorta aneurism
- nodous polyarthritis
b. thoracic affections
- pneumonia
- pulmonary infarct
- spontaneous pneumothorax
- diaphragmatic pleurisy
- acute mediastinitis
- oesophageal rupture
- obstructed hiatal hernia
c. other affections
- diabetic gastric crisis
- diabetic acidosis
- porphyria
- Hennoch-Schonein purpura
- acute saturnism
- cortico-suprarenal insufficiency
- Zoster zone
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 - Adverse reactions to some drugs
The acute abdomen does not comprise:
- Septic abortion
- Parasitizes
- Subphrenic abscess
- Peritoneal carcinomatosis
- Obstructed hernias
The diagnosis of acute abdomen, is difficult to establish, due to the multitude of affections
that makes the differential diagnosis.

The organ perforations

Are a part of the syndrome of acute abdomen provoking a chemic aggression over the
peritoneum and installing rapidly the acute peritonitis secondary to the perforation.
Etiopathogeny:
Through the most frequent perforations of organ we meet:
1. The appendicular perforation is produced by: the gangrenous and phlegmonous
appendicitis
2. The gastro-duodenal perforation is provoked by: the gastro duodenal ulcer
3. The perforation of the gallbladder is produced in the case of the vesicular hidrops, of the
acute cholecystitis or of the neoplasm of biliary ways
4. The perforation of the thin intestine is provoked by: the mesenteric infarct, intestinal
occlusions, sharp foreign bodies, the Chron disease, intestinal neoplasm
5. The perforation of the colon is provoked by: the necropsying rectocolitis, the colon
neoplasma, diverticulitis, foreign bodies
General signs: obnubilation, hippocratic facies, glimmering eyes, psihomotorial agitation,
tachycardia with arterial hypotension, tachypneea.
Diagnostic
- Anamnesis if it is possible for the patient who is conscious or from the relatives
concerning:
- The character of the pain: violent, colicative, intensity, duration, place, associations
with the dyspeptic (nausea, vomiting, diarrhoea, stopping the intestinal transit,
hiccup)
- The objective exam
 Inspection of the abdomen: if they participate to the breathing movements,
retractions, antalgic position
 palpation: wood abdomen, with generalised contracture, abolition of the
skin reflexes, skin hyperanaesthesia
 percussion: painful, mate, meteoric, pneumoperitoneum
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  auscultation: abdominal silentium, sometimes garguriments (intestinal
occlusion)
Para clinic exams:
- hyperglycaemia
- hyperleucocytosis with the deviation to left of the leucocitary formula, high urea
and creatinine

Imagistic:
- pneumoperitoneum (with the exception of the perforation of the biliary bladder)
- hydro-aeric images
- swallow nests

Treatment:
Only the urgent surgical intervention.
The mesenteric infarct
Definition
The obstruction of the arteries or of the mesenteric veins with consecutive intestinal necrosis.
Etiopatogeny
- Thrombosis
- Abdominal traumatisms
- Atrial fibrillation
- Peripheral arteriography
- Ischemic cardiopathy
Symptomatology
- Strong abdominal pain, violent or medium, with rough start and which is continued
- Pallor, sweat, obnubilation
- Tachycardia, arterial hypotension
- Psihomotorial agitation
- The palpation of the abdomen which does not give painful sensitivity
- Dyspeptic syndrome with nausea, vomiting, diarrhoea, melena dejections or fresh
blood
- Signs of paralytic ileus
Paraclinic exams
- The abdominal radiography on an empty stomach which shows the hydroaeric
levels
- the Doppler ecography of the mesenteric arteries
- EKG in more cases shows atrial fibrillation
- The mesenteric angiography – shows the affectation of the mesenteric arteries
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The clinic exam of the acute abdomen comprises:
- anamnesis
- objective exam
Anamnesis :
- when the pain appears
- the start
- the way of the start
- evolution
- localisation
- duration
- symptoms
Continuous pain:
- acute appendicitis
- acute pancreatitis
- peritonitis
Colicative pain:
- bilinear lithiasis
- renal colic
- mechanic ileus
Irradiations
- right shoulder = acute cholecystitis
- bar = acute pancreatitis
- irradiations in the genitals = renal colic
Associated symptoms:
- dyspeptic syndrome
- fever
- asthenia, adynamie
Alimentation – what the patient consumed
Medication – if some medicaments were consumed (contraceptive, anti-inflammatory, births,
abortions, menstrual cycle, etc)
Conditions of life and work (toxic environment, great efforts, etc.)
Objective exam
General signs:
- agitation,
- antalgic position
- eruptions
- cold teguments
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 - the state of nutrition
- oedema
- dehydration
- hyper-hydration
- peripheral collapse
The exam of the abdomen
The inspection in orthostatic position:
- participates to the respiratory moves
- vascular stars
- collateral circulation
- hernia in obese persons

Palpation:
- all the areas are palpated
- muscular defence
- pain in compression
Auscultation:
- abdominal silentium
- naises
- friction
Percussion:
- abdominal meteorism
- ascitis
Rectal touch:
- painful = acute appendicitis
= extra-uterine pregnancy
- blood = mesenteric infarct
= colon cancer
Gynaecologic consult
Paraclini exam
- HLG
- Urine summary
- Urea, creatinin
- Ts and Tc
- Glycaemia
- Blood group
- Blood and urine ionogram
- RA
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 - Hepatic samples
- electrophoresis
- Douglas puncture
- Paracentesis
- Rx abdominal
- mesenteric angiography and
- Echo-Doppler
- abdominal ECO
- abdominal CT
- magnetic resonance
- exploratory laparatomy
Hospitalised urgently:
- generalised peritonitis
- intestinal occlusion
- perforated or acute appendicitis
- internal bleeding
Treatment
- rest in bed
- post alimentary
- endovenous catheter
- colloidal solutions
- crystalloid solutions
- correction of the acidosis
- nasogastric probe
- probing the bladder
- wide spectre antibiotics
- anti-inflammatories
- antispastics, minor analgesics
- strong analgesics are not administered
- surgical intervention

II.12. THE POLYTRAUMATISMS. FIRST AID. THE TRANSPORTATION OF THE

TRAUMATISED PATIENTS.
Definition
The traumatism represents a dynamic transport of energy towards the live tissue, situates at an
inferior level, through a direct impact or through an interposed agent. After the impact, the
continuity of the morphologic structures and it is produced the alteration of the cellular
functions.
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If it is interfered rapidly and prompt in rescuing the patients who suffered poly-traumatisms
there are chances, but most of the times the intervention depends on the multiple difficult
factors which stop the healing of the patient.
These are:
- sudden start of the events
- the severity and variety of the lesions
- circumstances of the trauma
- the collective trauma
- the lack of sanitary materials, medicaments and devices at the place of the accident
- nonqualified volunteers who interfere, with a good intention at the place of the
accident but who do not have medical knowledge
- non-qualified medical personal who does not know the algorithm of the poly
traumatism
The therapeutic success in the case of the poly-traumatised patient depends on the methodical
intervention of experienced medical personnel, represented by the trauma team based on some
precise protocols. The general principle of these protocols is simple: it treats first the
traumatic lesion with immediate vital risk.
The trauma team must be multi-disciplinary, well trained, each member having a precise role
in the evaluation and treatment of the patient. (84)
For the poly traumatised patients we apply the principles of the Vital Support Advanced for
the Traumatised (Advanced Trauma Life Support = ATLS) support which appeared in the
USA, being known worldwide and applied in the majority of the countries around the world.
Deaths due to poly traumatisms comprise 3 peaks having a „trimodal” distribution.
1. The first peak of the deaths appears few minutes after the traumatism through:
- cerebral dilacerations or of the trunk +
- severe cardio-aortic lesions (ruptures)
There is no chance of salvation but through „prevention”.
2. The second peak of the deaths appears at minutes or hours from the production of the
traumatism through:
- extradural and subdural hematoma
- pneumo or hemothorax
- lesions of the viscera and intra-abdominal (spleen, liver)
- organic lesions with massive sanguine losses
3. The third peak of the deaths appears after few days or weeks after the traumatism
when it appears:
- sepsis
- multiple organic insufficiency (MSOF)
Approaching the traumatised patient is different from the one of the regular patient and it
comprises the following principles:
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 - the major vital threat must be cleared as a priority
- the interventions of resuscitation and rebalancing, anticipate the diagnosis
- the evaluation of the trauma does not need a special anamnesis in the first part
of the diagnosis
Due to these principles the number of the manoeuvres of resuscitation from the vital basal
support was enlarged, instead of A, B, C at A, B, C, D, E, the evaluation must be performed in
approximately 30 seconds as it follows (84):
A = control of the aerial way and of the cerebral spine
B = ventilation
C = circulation and control of the bleeding
D = evaluation of the neurologic state (neurology disability)
E = complete evaluation of the skin surface of the patient
Out of these evaluations it results that the death interferes faster when the respiratory ways are
not free and the lack of respiration dies faster than the loss of the blood volume, and the
expansion of the intracranial mass is a vital danger.
The doctor who is treating these cases must have the theoretic and practical knowledge about
the ATLS and to pass rapidly to:
- rapid and precise evaluation of the state of the trauma
- to fixate the priorities of the resuscitation and establishment of the patient
- to evaluate the complecity of the necessary treatment for the poly traumatised
patient, concretely and with the possibilities that exist.
Taking care of a poly-traumatised must comprise:
- the pre-hospital care
- cares for the medical recovery
The first measures to the primary initial evaluation
A. The aerial way and the ventilation
We will perform airway control (upper and lower). Check cervical spine injury, full
stomach, vital parameters.
Any workmanship release airways will be made only after stabilize the cervical spine. If
that is traumatized will move to immobilize manually by keeping the head in a neutral
position by placing sandbags on both sides of the head and join with plaster passed over
the patient head. The most useful means of fixing the cervical spine is rigid cervical collar.
Upper airway will clean: secretions, blood, vomiting, fragments of teeth or teeth.
The ventilation – will monitor the effectiveness of ventilation. If ventilation is efficient,
give oxygen, and if necessary can move on respiratory resuscitation measures. The
ventilation efficiency evaluation is done by tracking SpO2 pulse oximetry life, and note
the colour of the skin (cyanosis). (84)

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 If that is not effective pulmonary ventilation will move to endotracheal intubation or
nasotracheal I.O.T. can be done from the onset of injury in case they cannot release the
upper airways.
Where facial trauma I.O.T. or INT will not be done quickly move to tracheostomy.
B. Circulation
It then moves quickly to assess hemodynamics by identifying pulsations in large arteries:
carotid, femoral and checking blood pressure. Follow insurance venous line by two
appropriately sized vein. If this path is not possible will address the large veins: the
subclavian vein, femoral or ultimately discovering surgical ante-cubital vein or saphenous
vein and the introduction of endovenous catheter.
It then passes the type crystalloid fluids management, colloids and blood after blood group
determination. If the patient is in severe bleeding shock and there is no time to determine
blood group is administered emergency 0I blood group, Rh negative and resorting quickly
to haemostasis surgery.
It has vasopressor support to maintain the temporary indication of perfusion pressure of
vital organs (brain, heart, lung, kidney).
The secondary evaluation of the traumatised patient
It makes were finalzat after the first stage of care measures (ABC).
In this phase will then fully examine all vital organs and anatomical regions of the body and
neurological examination.
Next will perform laboratory tests, imaging and general nursing measures.
1. Anamneses: if the patient is conscious we will pass to the anamnesis, the
circumstances in which the accident appeared.
The trauma may be caused by accidents of circulation, decrease through precipitation,
through white weapons (knifes etc.).
2. The clinic exam comprises:
- Complete examination of the cephalic extremity (bone parts and soft parts)
- Examination of the maxillo-facial area, where it interferes with the superior
respiratory ways
- Examination of the throat and vertebral spine
- Complete examination of the thorax
- Complete examination of the abdomen
- Examination of the perineum, genitals and rectum
- Examination of the extremities
- Examination of the nervous stimulant
3. The paraclinic exam
- blood group
- hematologic and coagulation samples

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 - biochemical samples
Imagistic
- cranium radiography
- lateral radiography of the cervical spine
- thoracic radiography
- basin radiography
- extremities radiography
- ECO
- C.T
- RMN
- urography
- angiography
- sonography
- EKG
- EEG
4. The monitoring comprises :
- TA
- PVC
- AVC
- PCP (pulmonary artery)

Treatment of the special lesions

1. Cranial lesions
- For the patients with spontaneous respiration it is administered O2, is followed the
neurologic functions and it is monitored the vital parameters
- For the comatous patients I.O.T. (attention to the vomiting from the full stomach)
- For the patients with cerebral contusions with intracranial hematoma the hematoma
is evacuated
- For the patients with penetrant cerebral lesions it practice the debridation of the
devitalised tissues, the clearances of the hematoma and the small bone remains
- For the patients with fractures of the cranial box is practiced the debridation,
cranioplasty

The medical treatment comprises:

- Maintenance of the pressure of cerebral perfusion (PPC)
- Diminution of the intracranial pressure (PIC)
- Prevention of the cerebral oedema (medicamentous, with the increase of the PaO2
and decrease of the PaCO2

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 2. The traumatism of the vertebral spine and of the spine marrow
- Respects the general principles of the cranial traumatism with the mention for
maintaining the pressure of pressure of the marrow (Pa medial – Pextrinsic) and the
reduction of the medullar compression through surgical treatment for the
decompression and stabilisation of the vertebral spine
- The circulatory and ventilator dysfunctions will be corrected
- The prevention of the spinal shock which is the consequence of the functional
interruption of the sympathetic innervation under the lesion of the marrow
producing vasodilatation and arterial hypotension.
When the lesion is localised on top of the place of origin of the cardio-accelerator nerves (T1-
T4) difficult signs appear:
- bradycardia
- bradyarrhythmia
- atrio-ventricular block
- cardiac harass
All these symptoms occur due to vagal tone which is not contrary to the sympathetic tone.
C3 and C4 injuries requiring I.O.T. and mechanical ventilatory support.
Spinal shock is accompanied by hypothermia is the consequence of heat loss through
peripheral vasoplegie.
As the medicinal therapy of acute injury to the spinal cord is the administration of
methylprednisolone at a dose of 30 mg as a loading dose and continued on 5 mg / KGB / h in
perfusion for 24 hours.
3. The facial traumatism
Expresses itself: abundant nasal or buccal bleeding, damage to the dental arch, foreign bodies
in the mouth and throat that can obstruct the upper airways.
Sublingual in hematoma trauma jaw, dental arch affected and to limit her movements,
resorting to nasotracheal intubation (INT).
4. The neck traumatism
Accompanying neighborhood lesions from lesions of the cervical column, subcutaneous
emphysema, esophageal rupture, damage large vessels, etc.
Open neck injuries can be: cartilage fracture, transecţiunea larynx-tracheal rupture of vessels,
etc.
Penetrating trauma injuries produce large vessels with massive haemorrhage
Treatment of these injuries relate to freedom airway and stopping bleeding.
5. The thoracic traumatism
Interests an important portion of the body and it can comprise:
- Larynx
- Trachea
- Heart
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 - Great vessels
- The thoracic duct
- The lung
- Ribs, clavicle, shoulder blades, etc.
Through the severe thoracic traumatism is produces the respiratory insufficiency with
hypoxemia when it is indicated the mechanic ventilation.
The analgesia for this type of traumatism is indicated through epidural thoracic catheter, that
facilitates chest movements.
6. The abdominal traumatism
Interests the viscera and peritoneum. Investigations are eviscerated by imaging methods
(native abdomen, CT, laparotomy, etc.). Abdominal wounds requiring require a thorough
investigation or surgical exploration. Lesions may present as abdominal wall lesions
intraperitoneal injury, retroperitoneal injury. (84)
7. The genito-urinary traumatism
Requires traumatized bladder catheterization probe Foley and kidney injuries with prolonged
hypotension requiring surgery. Urethra injury produces acute urinary retention.
8. The basin traumatism
The severe lesions of the basin produce open fractures with massive bleedings both internal
and external.
9. Bone traumatism
The fractures of the bones with dislocation produce lesions of the proximity of the vessels and
nerves.
The transportation of the traumatised patients
Is performed after the well-established rules, otherwise the transport incorrectly can cause
injuries even fatal effects.
For the poly-traumatises the transport includes:
- The primary transport
- The secondary transport
The primary transport is made from the place of the production until the hospital and it must
fulfil the following conditions:
- To prevent the worsening of the traumatic shock
- To keep the haemostasis
- To maintain the vital constants
The primary transport is made with:
- stretcher, on small distances to the transport vehicle and from it to the hospital.

Positioning the patient on a stretcher is done by 2-3 people (stretcher).

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The stretcher bearers sits on the same side of the injured person is put down on his knees,
hugging the injured, and the cephalic extremity supports his head.
The stretcher will be brought to the stretcher bearers that will put the patient on a stretcher
with care. If there is a trauma spine or poly-trauma, the three stretcher-bearers will take the
traumatised between legs and they will raise him on the stretcher, sited sideways or they will
push the stretcher under the ill → Dutch bridge.

Stretcher

Position the patient on a stretcher is supine, head slightly raised. In hiportensiune caused by
multiple trauma (peripheral circulatory failure), descends below the head and legs up to the
vital organ perfusion.
If comatose patients, the sick will be transported in lateral decubitus or semiventral. Patients
with head injuries transported in a sitting position. Patients with abdominal trauma transported
supine with the knee flexed, supporting legs in the popliteal region with rolls pillows.
Patients with facial injuries transported in prone face and high forehead supported under.
Patients are sedated shake before determining their position on the stretcher and immobilized.
The stretcher is carrying two or four people, changing between them who will walk without
shaking or rocking uniform stretcher. Turning to transport is changing steps, and before the
patient will be directed forward and in reverse slope so as to be located above the head.
During transport of the patient will be overseen by a nurse or stretchers from behind. In the
absence of the primary fair ground transportation and other means can improvise.
- seats
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 - blankets, rugs fixed on wood pillars
- door wings
- planks
the transportation of the patient with motorised means is made:
- with ambulances
- with airplanes
- with helicopters
- sanitary ships
In the ambulance the patient will be seated on the middle of the stretcher for the sanitary
personnel to have access.
The means of transportation will have:
- devices for artificial respiration
- oxygen
- EKG
- defibrillators
- emergency case
- drugs
The secondary transportation – refers to the transport of the patient from a hospital to another,
junctions or at home.

The transportation inside the hospital

This transport is prepared taking all necessary safety precautions to prevent complications.
Before the transportation we will check bandages, haemostasis, immobilization devices,
medical documents and patient pain will be relieved.
The transport in the junctions
Is made by the stretcher bearers with an attendant and permanently monitored.
Obligatory we will transport the following categories of patients:
- with severe cardio-respiratory insufficiency
- in shock
- exhausted, feverish, adynamic
- suspect of myocardial infarct
- with disorders of balance and nervous disorders
- with major lesions of the inferior limbs
Transhipment of bed polytrauma patient on a stretcher is made by placing the stretcher over
the bed, hanging it from one secure grip.
Travel by trolley.

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The trolleys have height operating tables.

Transport with wheelchair.

In fact wheelchair is made of metal tubing trolley with wheels fitted with pneumatic rooms.
By this means of transport after transporting the patient has been stabilized in terms of vital
functions and trauma has been resolved.

The rolling bed:

It is an ideal form of transport polytrauma patient, both in hospital and in-hospital. The bed is
fitted with wheels rolling on four legs. With this transport the patient no longer being
transhipped from one place to another (trolley, masses of surgery, radiology tables, etc.).
The child transportation
The transportations of the new-borns and babies
It is made only with a caretaker the same as in adults.
- with respiratory and cardiac affections
- with convulsions
- meningitis
- septicaemia
- severe infections
- congenital cardiopathies
- with surgical affections which need surgical intervention
All of these are transported in the incubator with their mothers at the sections of intensive
care.
The ambulance or any other means of transport (airplane, helicopter, ship, etc.), must have:
- oxygen source
- cardiac monitor
- complete case for emergencies (laryngoscope, intubation probes, aspirator)
- syringes
- pumps
- perfusion
- tucks
- aspirator of secretions Nelaton probe (no. 12-14)
- portable mechanic ventilator
- casolette with sterile compresses
- clean sheets

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 - drugs for emergencies
(breathing analeptics, tonicardiacs, adrenaline, analgesics, etc.)

The algorithm of the poly-traumatised

1. The mobilisation of the rescue team which goes to the place of the accident (the anti-
shock team)
2. Retrieving the person from the accident by experienced persons and who have
knowledge about the poly-traumatisms
- help
- 3 or 4 persons who transport the stretcher
- immobilising the spine and the limbs
- the position of the traumatised person in the ambulance
3. Assuring the permeability of the superior breathing ways (clearance of the foreign
bodies, blood, dental prosthesis)
4. Oxygenotherapy
- On the probe
- With the respiratory device
5. Monitoring the cardiac function inclusively external cardiac massage
6. Monitoring the bleedings: provisory haemostasis auto-hemo-transfusion
7. Provisory immobilisation of the traumatised segments
8. Steps for preventing the shock, calming the major and minor pains with analgesics
(opiates)

II.13. THE COMA

Definition
Coma is a pathologic state, characterised through a delineation of diverse degrees of
unconsciousness, of sensitivity and voluntary motility.
In the coma is kept in a relative way the functions of the vegetative life meaning: respiration,
circulation, nutritive exchanges and secretions.
Coma is started through the depression of the function of the vegetative subcortical centres
(bulbar, di-encephalic).
There are two types of coma:
1. The metabolic coma – is a global disorder of the cerebral metabolic processes through
two mechanisms:
 The interruption of the alimentation with energetic under-layer (ischemia,
hypoxia, hypoglycaemia)
 The alteration of the neuro-physiologic answer of the neuronal membrane (the
cases of drug intoxications, alcohol, endogenous toxins, etc.)
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 2. The anatomic coma with the mechanical destruction of the important areas from the
cerebral trunk and cortex.
The alteration of the conscience presents several degrees:
 alteration of the attention
 mental confusion with affection of the reasoning
 temporal-spatial disorientation
 somnolence
In come the cerebral superior functions are abolished so that the perception, integration and
interrelation with the environment are compromised.
When hospitalising the patient:
 he does not open his eyes spontaneously or at verbal stimuli
 does not talk
 does not answer to the verbal stimuli
Ethiopathogeny
The coma is installed through a process of primitive disorder of the state of vigilance with the
alteration of the ascendant reticular system (SRAA) localised at the level of the
mesencephalon (cerebral peduncles) lowering in adiacent rostal regions (diencephal) and
caudal (protuberance).
SRAA is situated in the central part and anterior to the Sylvius apeduct contact with the
occulomotor ways, being alimented by sensitive afferences, the spinocellular and sensorial
ways.
SRAA is projected diffuse towards the cortex through the thalamus or direct and it has a
chemical complementary medication: dopaminergic and noradrenergic.
In the come is implemented the process of loss of conscience in which SRAA is blocked.
Differential diagnosis:
- akynetic mutism: connected to bithalamic or bifrrontal lesions (awake patient, conscious,
without any motorial or verbal initiative)
-<<the locked-in syndrome>>: connected to a pretuberantial lesion (infarct most of all)
(awake patient, conscious, but totally paralysed, with the exception of the moves of verticality
and of opening the eyes; superior intact functions and normal EEG).
- the psychogenous areactivity, simulation, histerie or melancoly: psychiatric origin (awaken
and conscious patient).(95)

The clinic exam comprises:

a. Anamneses: - made from the persons who accompany the patient:
- how did the coma start, wether it was preceded by: weakness, headache,
convulsions, vomiting, diplopia.
- if he consumed alcohol in great amount.
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 - if the patient has any chronic visceral suffering
- the way the coma installed (insidious, suddenly)
- past of HTA
- past hepatic, renal, respiratory, cardiac
- chronic treatment
- psychiatric past (suicidal tentative)
- intoxication

b. The objective exam

The exam of the teguments
Teguments:
 dehydrated, with low turgor (diabetic coma, hyperosmolar)
 sweat (hypoglicemic coma)
 hot, febrile (infectious coma)
 cyanotic (hypercapnic coma, CO2 intoxication)
 icteric (hepatic coma)
 pale-terous (uremic coma)
 with haemorrhagic spots, ecchymosed (hepatic coma)
 the fever suggests a systemic infection, cerebral lesion with the alteration of the center
of the thermoregulation
The respiratory apparatus
Respiration:
- Cheyne – Stokes (lesions in the cerebral trunk),: alternation hyperpnoea and apnoea
with progressive transition
- Biot
- Kussmal (metabolic acidosis from the hepatic and uremic coma), alternation
inspiration, pause expiration, pause.
The general aspect of the thorax: emphysematous, in careen, dystrophic
The cardio – vascular apparatus
- myocardia infarct
- atrial fibrillation, extrasystole
- arterial hypertension (hypertensive encephalopathy, cerebral bleeding)
- arterial hypertension: ethanol intoxication, with barbiturates, myocardia infarct
The digestive apparatus
- abolished deglutition, hepatosplenomegaly, collateral circulation, icterus, flapping
tremor = hepatic coma
The neurologic exam

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 It is estimated conscious state Glasgow Through Scale (neurological balance sheet) care
is based on assessment of verbal response, motor and open the Eye. Quality is assessed
maximum response of the UN Between 15 POINTS, WHAT indicating un aware sick
normal neurological POINTS AND un 3 minimum, care means brain dead. THIS
SCORE version coma prognosis indicates the immediate period after the assault.

The Glasgow scale, for appreciating the coma

The score
The time for answering (number and
points)
I. The best motor answer
Executes the command 6
Localises the painful stimulant 5
Retraction answer 4
Abnormal flexion 3
Abnormal extension 2
The lack of answer 1
II.The best verbal answer
Oriented 5
Confuse conversation 4
Inadequate words, dysarthria 3
Non intelligible sounds 2
The lack of answer 1
III. Opening the eyes
Spontaneous 4
At verbal stimulation 3
At painful stimulation 2
Absent 1
TOTAL score = I+II+III

The coma aetiology

A. Coma of cerebral origin
1. traumatisms:
 commotion
 contusion
 hematoma
 fracture of the cranial base
2. physical factors:

303
  insolation
 blights
 burns
 electrocutions
3. inflammations:
 meningitis
 meningoencephalitis
 encephalitis
4. expansive intra-cranial processes:
 tumours
 abscesses
 cyst
 tubercular
5. cerebral diffuse oedema
 eclipse
 acute nephropathy
 encephalopathy hypertensive
6. vascular lesions
 emboli
 thrombosis
 parenchymatous bleeding
 meningioma bleeding
B. Coma of extra-cerebral origin
1. hidro-electrolytic and acidobasic disorders
 cellular hyper-hydration, extracellular, global
 respiratory acidosis
2. restarted cardiac harass
 partial drowning
 asphyxia
3. endocrinopathy
 thyreotoxicosis
 myxoedema
 Addison disease
4. acute exogenous intoxications
 alcohol
 carbon monoxide
 mushrooms
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  drugs
5. acute endogenic toxicosis
 uremic
 diabetic
 hepatic insufficiency
 portal, renal encephalopathy
The neurologic exam presents a peculiar importance through it being able to establish the
degree of the come, meaning:
a. the state of consciousness: loss of consciousness, the sick presents a state of profound
sleep, pathologic reacting only to strong stimuli such as moans or movements
b. the state of perceptivity: appreciated through the intensity of the necessary stimuli for
obtaining the motor answer and they are:
 painful (stinging, pinching, pressure)
 sensorial (acoustic)
c. the vegetative functions:
 cardio-vascular
- normal
- changes of the arterial tension (hipo or hypertension)
- rhythm troubles
- infections
 respiratory
- normal
- dynamics disorders
 digestive
- vomiting + hiccup = uremic coma
- vomiting = intracranial hypertension
- deglutition: alteration time I oral, in the superficial coma and the alteration time II
pharynx – oesophagus in severe coma
d. state of reactivity is characterised the spontaneous or provoked moves
 cervical reddor (meningitis, bleeding, cerebral tumours)
 maintaining some flasc positions: the lifted limbs fall on the part of the paralysis
 the paralysed cheek is deviated to the healthy part
 the Babinski part
- unilateral in hemiparesis
- bilateral in encephalitis, cerebral oedema, hypertensive encephalopathy
 rigidity through de-cerebration
 abolishing of the abdominal cutaneous reflex from the paralysed part

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  ROT (osteo-tendinous reflexes)
- Abolished in the severe comas
- living: coma degree I and II
e. the ocular globes
- look towards the cerebral lesion: conjugate deviation of the occulat globes towards
the left or right hemisphere
- they float in the peduncle lesion
- lowered in the pontine area
- fixated median in intra-ventricular bleeding
- pupils
- Midriatic
o unilateral: intracranial hematoma, peduncular lesions
o bilateral: atropine intoxication
- Miotics
 Intoxications with pesticides, opioids
 Bleedings: ventricular, cerebral trunk
The exam of the eye bottom (F.O.) in sub-arachnoidian bleeding, intracranial hypertension,
hypertensive encephalopathy.
The para-clinic exam
- Biochemical exams: the blood ionogram, urea, creatinin, glycaemia, plasmatic
osmolality, R.A, hepatic tests, oximetry.
- toxicological analysis from the blood and urine
- radiographies
- computer tomography (CT)
- magnetic resonance (MRI)
- EEG investigation
- The lumbar puncture and the exam of the LCR
Pathology
a. Disorders of the osmotic pressure (O.P.)
- hipo-osmolality < P.O < 260
< Na < 110 mEq/l cerebral oedema
- hiper-osmolality P.O > 330 mosm/l
o Hypernatremia
o Hyperglycaemia
o Hypercloremia
o High urea uremic coma, ethylic, hyperosmolar
b. Disorders of the glucid balance

306
 - hypoglycaemia (Gl < 50mg %)
- in insulin dependent diabetes
- hepatic coma
- ethilic coma
c. Disorders of the protein metabolism
- high prothrombin time
- high NH3 = uremic coma, coma through dehydration
d. disorders of the lipidic metabolism
- high lipids and cholesterol = diabetic coma, mixematous, ethylic.
e. Disorders of the acido-basic balance
- pH < 7,3 under 10mEq/l
- metabolic acidosis = uremic coma, diabetic, alcohol intoxications, paraldehyde
The coma diagnosis on apparatuses
The respiratory apparatus
We will follow permanently:
- amplitude
- frequency
- type of the respiration
- intercostal tirage
- secretions
- aspirate of gastric content (post vomiting)
- thoracic radiography
- gasometry
- cyanosis
The cardio-vascular apparatus
We will follow:
- arterial tension
- pulse (P)
- cardiac frequency (Fc)
- the EKG trajectory
- central venous pressure (CVP)
The renal device
We will follow:
- urea
- creatinin
- diuresis
- blood ionogram
- urinary ionogram
307
The nervous system
We will follow:
- the state of vigilance
- the degree of the coma
- the osteotendinous reflexes
- opening the eyes
- motor optimal answer
- verbal optimal answer
- pupils
Thermoregulation
We will follow:
- the cutaneous temperature axillar and rectal
Treatment
In order to establish a correct treatment, we will keep an algorithm of action:
1. Establishing the positive diagnosis or at least the diagnosis suspicion
2. The complete anamnesis from the attendants (if there are)
- aetiology of the coma
- the correct examination of all the apparatuses and systems
3. The Noble safety position
- latero-ventral position with the posterior tren twisted ventral, the thorax disposed
on a part and one hand under the head
- - Clear upper respiratory passages and removing secretions from the mouth and
nose
- - Fitting pipe Guedel
- - In tuxedos column, release upper airway by lifting the jaw, head back extension
with pipe fitting Guedel
- 4. Transport the patient to the hospital
- When the diagnosis is certain (known history) and there are possibilities of
treatment at home, indicate the treatment provided to be better monitored
- When the diagnosis is uncertain, with unclear etiology and vital functions are
impaired, the patient will be transported to the hospital in the position described,
taking care that the extreme cephalic to be at a lower level than the rest of the body,
monitoring them permanent O2 and rebalancing hydroelectrolytic.
- Ambulance transport will take place in good condition, the patient is covered with
blankets and the vehicle speed will be adequate without turbulences.
The hospital the patient will be admitted to the intensive care unit, where he will
take reanimator physician and neurologist.
- 5. Monitoring the vital signs

308
 - T.A.
- Pulse
- PVC
- respiration
- diuresis
4. Oxygeno-therapy
- O2 will be administered on the nasal probe, 4 l / min
5. The complete
6. The clinic exam
- we will examine completely all the devices
- we will start the complete exam of the NCS, of the cranial nerves
- we will establish the Glasgow score
7. The treatment will be started at the house of the patient with the correct positioning of the
patient, by assuring the vital functions
Setting the venous line and of the perfusion with physiologic serum 9 ‰

8. At the hospital: treatment will be immediate objective of preventing a worsening of

suffering brain.
Will it heal faster:
- hypoglycemia
- hyperglycaemia
- hypoxia
- Hypotension
- hyperthermia
- Substance known antidote to poisoning
- Installation of the 4 wells
• endotracheal probe
• flexula
• gastric probe
• bladder probe
- Harvesting biological medical tests
- Various imaging (radiography, ECO, CT, MRI)
- LCR exam

Diabetic ketoacidosis coma

Corrections glucose
- Low Doses of insulin (low-Doses) 10-12 I.U. crystalline insulin i.v. bolus,
followed by administration of 4-15 I.U. 9 ‰ NaCl solution, to check blood sugar
every hour
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 The rehydration:
- Hypotonic solution Na + HCO 3 1/3 9 ‰ 14 ‰ distilled H2O + 1/3 at 1 - 2 l quickly
- 5% glucose buffered insulin after blood sugar levels fall below 300 mg.
- Total solutions within 24 hours = 5 - 10 l youth and
3-5 l elders

Electrolyte imbalance
- Correction of hypokalemia after blood ionogram potassium phosphate, potassium chloride
preferably (15 to 20 mEq / L)
Corrections cetoacidosesi
- In severe acidosis sodium bicarbonate
(500 ml isotonic sodium bicarbonate the pH <7.1)
Hypoglycaemic coma
- It is administered glucoses 33 % or hypertonic glucoses 10 - 20 %, 100 ml i.v.
- In severe hypoglycaemia hypertonic glucoses + corticotherapy
Diabetic hyperosmolar coma
- correction of hyperglycaemia
- rehydrate
- rebalancing hydroelectrolytic
- antibiotics
- prevention of thrombosis
- etiological treatment
Coma in exogenous poisoning
- Antidote (if any)
- Gastric lavage (if any)
- Supportive care
- Support metabolic function
• combat hypoglycaemia
• fighting acidosis
- Removing toxic
• diuresis
• alkalizing solutions
• dialysis
- To support renal function
• loop diuretics
• infusion solutions 4-5 l / 24 hours
• bladder to monitor urine output probe
- Supportive care
- Prevention of respiratory infections
310
• antibiotic with broad spectrum (cephalosporin)
- Vitamins of group B and C
- Patient sedation (diazepam, hydroxyzine, DORMICUM)
- Food facility: parenteral and naso-gastric probe
Anoxic coma (anoxic encephalopathy)
- ventilation artificial
- sustaining the cardiac functions
 correcting the rhythm disorders
 pacemaker
 cardiac surgery
The hypercapnia coma
- Assisted intermittent positive pressure ventilation
- Combating respiratory infections (antibiotics, thinned secretions)
- Heart failure (digital diuretics)
Mixedematous coma
- Substitution treatment with thyroid hormones (thyroxine T4 0.25 - 0.5 mg iv)
- Respiration (Hyperbaric Medicine)
- Correction of hypothermia
- Corticosteroids (HSHC; 100-300 mg / day)
- Correction shock (haematic fluid and electrolyte rebalancing)
- Antibioterpie broad spectrum
Thyrotoxicosis coma
- Administration of antithyroid substance (sodium iodide 1- 2 g / day its slow infusion iv)
- Α + β blockers (propranolol 120-240 mg / day)
- Antiarrhythmics (Lidocaine 1%)
- Oxygen (nasal tube)
- Sedatives (phenobarbital, 0.4 g / 24 hours)
- Antipyretics (Perfalgan)
- Corticosteroids (hydrocortisone hemisuccinate 500-2000 mg / 24 hours)
- Rebalancing hydroelectrolytic (H-E)
- Antibiotic with broad spectrum (Fortum, Medocef)
Hepatic coma
- Solution of glucose 5, 10, 20% i.v 2 to 3 l
- Diet (1500 - 2000 calories)
- Suction probe (note esophageal varices)
- Treatment of hypokalemia and hyponatremia
- Vitamins (B group and C)
- HSHC (500 - 1000 mg i.v.)
- Combating bleeding (Phytomenadione 1-3 f / day calcium, Venosta, Adrenostazin)

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- Antibiotics (neomycin 6-8 g gastric tube)
- Blakemore balloon - Sengstaten hemorrhages
- Treatment of renal failure (IR) - hemodialysis
- Liver transplantation
Uremic coma

- Restriction lime (1-2 g / day)

- Fluid restriction (less than 1 l / z)
- Loop diuretics
- Ultrafiltration, dialysis
- Correction of hyperkalemia (exogenous restriction, ion exchange resins, glucose, calcium
gluconate)
- Correction of metabolic acidosesi (restriction of protein intake)
• sodium bicarbonate 14 ‰
• dialysis
- Correction of hypocalcemia (calcium gluconate)
- Restriction rate of protein (0.5 g kgb / day)
- Parenteral nutrition
- Correction of anemia (blood transfusions, erythropoietin)
- Antibiotics (note nephrotoxic antibiotics: kanamycin, streptomycin, gentamicin, etc.)
- Treatment of convulsive syndrome (barbiturates, phenytoin)
- Prevention of upper gastrointestinal bleeding (H2 blockers)
- Kidney transplantation in chronic renal failure

II.14. ACUTE RENAL INSUFFICIENCY

Definition – sudden and significant decrease in glomerular filtration responsible for increased
creatinine. IRA is often accompanied by oliguria (diuresis lower at 500 ml / 24H), but diuresis
may be preserved. Urinary retention (bladder globe) should be identified and eliminated
systematically. (95)
Classification:
Depending on the cause:
- Prerenal (functional)
- Renal (organic)
- Post-renal (obstructive)
- Global
Aetiopathogenetic
- functional
- organic
Depending on the cause,
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The renal insufficiency, pre-renal acute (the most frequent cause of IRA)
It is characterised by:
 Hypovolemia: (extracellular dehydration)
- Internal and external bleedings
- Hydroelectrolytic losses:
o skin (sweating, burns)
o digestive (vomiting, diarrhea, gastrointestinal fistula)
o renal (excess of diuretics)
o iatrogenic (paracenteze)
- Seizure (hidroelectrolytes, sector III)
o ascites, peritonitis, intestinal obstruction
- Cardio-circulatory failure
o pump failure (myocardial infarction, cardiac tamponade)
- Severe peripheral circulatory
o Septicaemia
o Acidosis
o states of shock

I.R.A ischemia Pre-renal cause:

renal cause - prolonged shock
- arterial hipo-tension
- smoking
Renal cause
Acute
tubular - adm.of anti- hipertensives
necrosis - adm.of non-steroidal anti-inflammatory
(N.T.A.)
Mechanisms
Directly produced nephrotoxicity:
- antibiotics (aminoglycosides, amphotericin)
- osmotic substances (dextran, manitole)
- antineoplastic m e d i c a m e n t s
(interferon, cyclosporine)
- contrast substances (ultravist pobilan)
Aggression of the urinary endogenous pigments:
- pathologic haemoglobin
- infection with gram negative/anaerobic germs
- endotoxic shock
- transfusion incompatibility

313
Acute interstitial nephritis
- Immunoallergic (penicillin, cephalosporins, dextrans)
- Infection (pyelonephritis acute diffuse)
- Dysmetabolic (postterapie chemotherapy)
Glomerular nephritis
- Glomerulonephritis – post infectious / viral
- Rapidly progressive glomerulonephritis
- Idiopathic glomerulonephritis, type I, II and III
Angiopathies - thrombotic microangiopatia
- Scleroderma
- Malignant nephroangiosclerosis
- Disorders of the great vessels (aortic dissection, renal artery obstruction)
Post-renal IRA
- By obstructions: tubule-caliceal
- Ureters (stones, tumours)
- Lower urinary tract obstruction (prostate adenoma, strictures, tearing)
- Echography systematically to all IRA cases, to eliminate an obstacle: pielocaliceal
expansion. (95)
Global IRA
- Through pre-renal and post-renal affection

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 The ethiopathogenetic
classification

Circulatory disorders
through hypovolemia
Low renal blood flow
- bleeding,
- anaphylactic shock,
- depletion hydroelectrolytic,
- hepato-renal syndrome,
- anesthesia
- cardiac insufficiency

Renal hipo-perfusion

Renal ischemia

Decrease of the glomerular

filtrate

Oliguria 400 > ml/day

Decreases the ability to concentrate urine: creatinine ↑

urea↑
After the appearance of the proximal convoluted ischemia is the most sensitive to ischemia.
After 1-2 hours of ischemia histopathological changes occur in the proximal convoluted
tubule cells to tubular epithelial cell necrosis, where they occur and altered permeability.
After a short time, cellular necrosis and curvy portion extends from the distal convoluted
tubule. This creates casts (hyaline cylinders and dummies leukocyte) that occluding the
ascending branch of the loop of Henle (nephron) distally. Decreases the glomerular filtration
which with the arteriolar vasoconstriction close the vicious circles and so the oliguria,
nitrogen retention, hyperkalemia appears.
The positive diagnosis of the IRA
 Not specified symptoms
- asthenia
- vomiting
- HTA, dyspnoea, EPA
- cardiac arrhythmia
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  Urinary symptoms
- massive proteinuria
- hematuria
- pyuria
- back pains
- modified diuresis <400ml / day
• Signs of nitrogen retention
- Increased plasma urea> 17 m mol / l
- Increased plasma creatinine> 150 m mol / l
- Creatin clearance <50ml / day
Etiologic diagnostic (clinic, laboratory, para-clinic)
- IRA functional
- Decreases diuresis
- Oliguria <400 ml / 24 hours
- Hipercatabolism protein
- Nitrogen retention
(Urea <200 ml%)
- Urinary density> 1020
- Osmolarity> 500 mOsm / l
- Urinary urea> 10 g / l
- Urinary sodium <20 meg / l
- Prolonged severe hypotension (oligoanurie)
- Dehydration extracellular
- With hypotonic extracellular fluid overload intracellular osmotic
Imagistic: echography, tomography
Other investigations: EKG, cystoscopy
Dg IRA organic has 4 stages:
St I Debut < 24 h urine pH acid, urinary sediment with hematies and leucocytes
St II Oligoanuric - diuresis < 400 ml/24 h
Humoral syndrome
- Blood urea> 100 mg%
- Increased creatinine of 0.5 - 1 mg% / day
- Increased serum uric ac
- Alteration of electrolyte and acid-base balance with fluid retention (fluid overload> 400ml /
day)
- Hiposodemie 130 meg / day by dilution + losses (vomiting, diarrhea, aspiration)
- K ranges (normal, hyper, hypo)
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- hypocalcemia
- hypermagnesiumia
Clinical image
- Oligoanurie D p = 50 - 150 ml / day
- Urinary urea <10 g / l
- Digestive signs (anorexia, nausea, vomiting, gastrointestinal bleeding)
- Cardiovascular signs: acute heart failure, cardiac arrhythmias
- Neuropsychiatric signs: drowsiness, confusion, agitation, cramps
- Haematological signs: anemia, hemolysis, bleeding
- Urinary infections: cystitis, pyelonephritis, sepsis
St III Retake of the diuresis
- diuresis > 400 ml/day -> 4000 ml/24 h
- urea and creatinin remain high
St IV Healing
- is normalised the values of the urea and cretinin
Dg IRA organic from glomerular nephropathies
- acute nephrotic syndrome
- high ASLO titrage
- low serum complement
- autoantibodies
- immune circulate complexes
- hiponatremy
- biopsy renal establishes the diagnostic
- ecography / renal urography
Dg IRA organic from the interstitial nephropathies
- fever
- chills
- back pain
- polakidisurie
- proteinuria
- pyuria
- hematuria ± eosinophilia
- urography = kidney volume increased + underlying or intrinsic obstacles
- renal puncture = infiltrated lymphoplasmacytic
Dg IRA organic from the angiopathies
- clinic modifications, para-clinic depending on the aetiology
- hypertensive encephalopathy
- modifications of the eye bottom
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Dg differential
Is made depending on the evolution of the diuresis
- anuria
 rare in NTA, 70 % oliguria
 frequent in the cortical necrosis and the glomerular nephropathy
- urinary sediment
 IRA functional = poor in granule cylinders
 NTA = rich in granule and epithelial cylinders
 Glomerulopathies – rich in hematic cylinders
Para-clinic investigations
- simple renal
- urography
- ECO
- angiography
- computerized tomography
- cystoscopy
- bioptic renal puncture
Complications
- uremic coma
- high IRA
- IRA acute -> complications

Complications:
- infectious (pneumonia, urinary infections, septicaemia)
- cardio-pulmonary (EPA, arrhythmia, crisis, angora)
- haemorrhagic (HDS, purpura, suffusions)
- iatrogenic (escars, phlebitis, septicaemia, infections)
Treatment:
1. IRA functional
- correction:
 hypovolemic
 electrolytic misbalances
- administration of perfusion intravenous solutions
- plasmexpanders: dextran, plasmagel, macrodex
- blood
- positive inotropic agents
 Isoproterenol

318
  Dopamine / dobutamin
 Hydrocortisone hemisuccinate
 Diuretics: Furosemide: 40 mg in 250 ml gucose 5 %
Long persistence of the functional renal insufficiency may take to the acute tubular
necrosis (NTA) (95)
2. The NTA treatment
- Avoiding hyperhydration (fluid restriction)
- Reducing hiperazotemiei
- Maintaining balance blood
- Evitararea hyperkalemia and correction acidosesi
- Strict fluid balance
The amount of liquid administered is calculated: L (ml) = 400 ml + diuresis (ml) + other
losses
The liquids are administered
- Orally
- Endovenous (ENP)
Caloric intake + Protides:
• 1,500 calories / day
• carbohydrate 100 g / 24 h
• ENP: glucose 10%, 20% + insulin (1 I.U. 5 g glucose)
• the repeated dialysis, increase caloric intake to 2,500 calories / day.
• Balanced Building maintenance ionic depending on serum and urinary ionogram
• hiposodemia = NaCl 9 ‰ infusion therapy
• hyperkalemia = treatment with ion understood, changes resins
(Polystyrene sulfonate Na)
• will reduce K-rich diet (bananas, tomatoes, apples)
• severe hyperkalemia: treatment with 10% Ca gluconate, 10 - 20ml iv
• acidosis progressive treatment (sodium bicarbonate ground mole) of sodium bicarbonate
8.4% = deficit bases mEq / L x 0.35 x G
The treatment of the complications:
- HTA
- EPA
- arrhythmia
- hemodialise
The NTA treatment (phase for retaking the diuresis)
It is to avoid
- dehydration
- depletion of Na, K
- supra-infections
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 - mixed rebalance (oral + endovenous)
- liquids are administered NaCl, K under control TA and of the blood ionogram
PEV, and oral balanced alimentation with the reintroduction of the proteins (eggs,
cheese, milk)
3. The IRA organic treatment (depending on the aetiology)
- infections: antibiotics, cephalosporin
- Immunological mechanisms: prednisone 1 mg / kg / 24 hours (2-4 weeks)
- Glomerulopathies antibiotics, corticosteroids, immunosuppressants
- Hemolytic syndromes platelet plasma
- Nefroangioscleroza malignant captopril, ENAP.
- IRA post renal treatment: surgery
- NTA and treatment of glomerulonephritis:
• peritoneal dialysis
• hemodialysis
4. The IRA post-renal treatment
- The surgical treatment is based on the etiology
Measures of general nursing
Drug administration will be done at the doctor's instructions.
- The only therapeutic indication, he does nurse, oxygen therapy.
- Any complication after administration of drugs or complications that occur during
hospitalization, nursing, will announce immediately.
Sanitary education
- the nurse will train the patient how to self-administer the medication that will be living and
working arrangements further.

Labor protection
- the nurse will be obliged to comply with safety, meaning to protect themselves with gloves,
masks, special equipment in order to avoid illnesses.
II.15. THE HIDRO-ELECTROLYTIC MISBALANCE

Rebalancing is maintaining electrolyte volume and composition of normal body when intake
is insufficient or losses are too high. Water and electrolyte metabolism is a vital function of
the body along for cardiovascular, respiratory and renal. To maintain this function in balance
requires constant correction and balanced by intake of water and electrolytes. The patient will
be permanently watched clinical, biological and hydrological balance.
The total water from the organism
- 55 % masculine sex
- 47 % feminine sex
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The human body contains 45-80% of water, depending on the age, sex, degree of obesity.
Elder and obese contain a lower percentage of water with the risk of dehydration or fluid
overload grown.
The water body is arranged in three sectors:
1. intracellular Sector (BC) = 30-40% of G
2. the extracellular (E.C) = 20% G
3. trans-cellular sector (water in the digestive tract, bile, CSF, lymph system (15 mlkg / Body)
The extra-cellular sector
- interstitial sector (I.T) 15 %
- intravascular sector (I.V.) 5 %
Among these sectors there is an ongoing exchange.
Fluid and electrolyte balance is regulated by hormonal hormones: aldosterone and
antidiuretic.
A. Aldosterone is a mineralocorticoid hormone synthesized in the adrenal cortex glomerular.
He works in the distal renal tubular cells and retaining rezorbând Na so correct hypovolemia.
Under stress there are three types of adjustments by aldosterone.
1. Adjusting short: when hypovolemia and hyponatremia rapidly stimulates aldosterone
secretion and release.
2. Adjusting average: renal hypoperfusion and hyponatremia release renin, which acts on
angiotensinogen. Angiotensinogen is converted into angiotensin I, which is converted into
angiotensin II by stimulating vasoconstriction and aldosterone release.
3. Adjust headlamps: ACTH stimulates the secretion and release of aldosterone.
B. antidiuretic hormone (ADH) is synthesized nuclei supraoptici neuro-pituitary-thalamic.
ADH regulation is done by stimulation by a number of factors: hypovolemia, osmolarity,
pain, stress, drugs.
The antidiuretic ADH - permeates the distal convoluted tubule and collecting tube and makes
the water flow in the gap → concentrated urine and urine volume decreases removed.
Thirst is produced by exciting the thirst center in the hypothalamus by cellular dehydration.
NaCl intake increases water requirements. Adjusting the amount of water and electrolytes is
done with the kidney.
Diuresis = 500-1500ml / 24h.
Urine output is produced, depending on the dietary Na. Diuresis may be less by lack of Na or
be a saline diuresis (excessive Na).
balance Water
Need for a proper fluid resuscitation, this being achieved by a ratio between INPUT and
OUTPUT.
Inputs
- integrated water ≈ 1000 ml
- alimentary water ≈ 1200 ml
321
 - water from oxidations ≈ 300 ml
 Total inputs 2500 ml
Outputs
- diuresis ≈ 1500 ml
- insensible perspiration ≈ 850 ml (12-15ml/kgbody/24 h)
- dejections ≈150 ml
 Total 2500 ml

Insensible perspiration resulting from:

- Skin perspiration (500ml / 24 hours)
- Exhalation (350ml / 24 hours)
Insensible losses that grow: Pulmonary hyperventilation, increased temperature in the
operating room, fever (for each degree above 37 ° C water is lost 500ml)
- Internal organs direct exposure to air
- Sweating (2 g NaCl / L of sweat).
Dehydration is the loss of body water volume, which is produced by:
- Loss of Na
- Low water intake
- Loss of water
The clinical picture of dehydration:
- Thirst (deficit of 1,5 liters of water)
- oliguria
- Increased urinary density
- Hypernatremia (over 150 Meg Na)
- Weight loss
- Decreased skin elasticity and turgor
- Dry mouth and lips
- Rough language
- Difficulty swallowing
- Low voice hoarse
- Hypotonia eyeballs
- Hypotension pulse threadlike
- Muscle cramps and abdominal
- Mental confusion
- hallucinations
- Psychomotor agitation.
When the water drops below 20% of the body weight of death appears.
- Plasma protein ↑
- Blood urea ↑
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- Cl Na in urine ↑
Treatment
- Hydration with isotonic solution: a 9% S.F
- 5% glucose
- Oral hydration with isotonic solution + flat water
HYPERHYDRATION
Represents the water retention, without Na = water intoxication.

Causes:

- Normal water intake, but decreased clearance

- Excessive ingestion and lack of urine output (vol. LEC ↑)
We are seeing a cellular fluid overload and decreases serum Na, up to 123 meg / l.
Clinical:
- delirium
- hallucinations
- seizures
- Intracranial hypertension
- cramps
- Brain hemorrhage
- Left ventricular failure
- hyponatremia
- coma
Treatment:
- Water restrictions
- Hypertonic solutions:
o 10% glucose,
o mannitol 10%, 20%
- Treatment of the renal apparatus
THE DISORDERS OF THE ELECTROLYTIC METABOLISM
Electrolytes
Sector
- Intracellular K, Mg, phosphates, proteins = cation
- Extracellular Na, Cl, Na = bicarbonate anion
Water distribution in the body is determined by the concentration of electrolytes. 95% of the
osmotic pressure is given by Na, governing the three sectors.
Deficit Na (Na +) and Cl is calculated depending on the outcome ionogram blood and urine.
Formula
Na deficit = (mEq Na+ normal – Na+ actual) x G x 0, 6.
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Normal values 140- Na = 142 mEq / l
Necasurul daily Na is: 1-4 mmol / kg / 24h approximately 100 mEq / 24 hours (6 -7 g Cl).
1 g NaCl = 16 mEq and 16 mEqCl.
There are times when serum glucose and lipid parotids is increased and false hyponatremia
occurs. In this case use the formula:
glicemia(mmol / l )  5
Corrected Na = actual Na +
3

Disorders of the electrolytic metabolism

Hyponatremia: Na falls below 135 mEg / l
Aetiology

- vomiting
- diarrhea
- Digestive fistulas
- sweating
- Accumulation of fluid intraperitoneal
- In surgery, by insufficient intake
- bleeding
- trauma
- Burns
Biological
- Urea, creatinine increased
- Ionogram blood (Na↓ under 135 meg / l)
- Ht and Hb ↑ (haemoconcentration)
1/4 -1/3 LEC loss of circulatory failure with TA ↓, and D↓

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 Na RETENTION

1.Na ↑ + water retention 2. Na retention = hipernatremia

equivalent (renal insufficiency,
hyperaldosteronism)

Osmotic pressure = Osmotic pressure of

normal the CRL ↑

Oedema (G ↑)
(Cardiac insufficiency)

Treatment

- I.v intake Na Na Cl .: 9% a the formula:

Na deficit (mmol) = 0.6 x T x 140 (sodium levels)
- Treatment case

Hypernatremia - occurs when water losses are higher than those of Na, Na increases in this
situation.
Clinical:
- Impaired consciousness
- Seizures
The diagnosis is made on clinical examination, especially on ionogram blood, showing
elevated Na.
Aetiology
Loss of water (sweating, fever)
- Renal losses: polyuria osmotic after a hyperglycaemic coma
- Administration of mannitol
- Losses digestive (vomiting, diarrhea, fistulas)
Treatment
- Is slow in 2-3 days
Administer:
- 5% glucose

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- dextran
HIPOKALIEMIA
- The normal values of the K + = 3.5 to 4.5 mEq / L.
- The daily requirement of K + is 0.7 to 3 mmol / kg / 24h or 2-4 g / 24 hours.
- 1 g KCl = 12 + 12 + MeQk mEqCl
- Parenteral molar KCl solution is administered in the 7.4% 1 ml = 1mEq
- contraindications
- Oliguria (diuresis less than 500 ml / 24 hours)
- The day of surgery when intracellular K + goes into the extracellular space and its
concentration is increased blood after ionogram
- Management solution rapidly mole

Hypokalemia K <3.5 mmol / l

98% of K, is found in the cell.
K deficiency is dangerous to a patient or digitized cardiac antiarrhythmic therapy.
K deficit, it highlights the blood ionogram.

The EKG signs:

- the U wave ample
- prolonged ST segment
- extended QU interval
Aetiology
-
- Impairment loss
- Treatment with corticoids
- Primary aldosteronism
- Vomiting, diarrhea
- Treatment
- K per os administration of 3-5 g / day
- 7.4% KCl solution 6-8 g / day
- ECG monitoring Aldactone

HIPERKALIEMIA is a serious emergency, which occurs if there is cropped and

quickly, may cause death K> 5.5 mmol / l
Ionogram blood, diagnose and track EKG
- ST segment in S italic
- Widening of the QRS
- A-V block
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Aetiology

- Medicament (diuretics, salt medicinal intoxication Digitalis)

- Chronic renal failure or acute terminal
- Acute adrenal insufficiency
- symptoms
- Ventricular tachycardia (in the worst forms of advanced)
- Ventricular fibrillation
- Treatment
- Na bicarbonate 8.4% 50 -100 ml in 5 -10 min.
- 10% glucose + 10 u.insulin
- Polisteren sulfate (Kayexalate)
- hemodialysis
- Treating alkalosis

To correct hyperkalemia we administer 500 ml glucose 10% i.v. + 20-30 U.I insulin within 30
minutes.

Hypocalcemia

Calcium

Normal 2.2mmol / l
Required 0.1- 0. 4 mmol / l
1 ml of 10% gluconic Ca = 0. 48 mEq

As <2. 2 mmol / l = hypocalcemia

Clinical:
- tetany (favored by alkaloids)
- seizures
- laryngospasm
- EKG QT = widened
- striated and smooth muscle contraction
- anxious facies
- palpitations
- sweating
Treatment:

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The calcium administration as clorure or calcium gluconate 10% i.v. very slowly until the
dessapearance of the muscular contracture.
Dose 1-2 vials
Diazepam 5 mg = 1f. i.m.
HIPERCALCEMIA
As a> 2.7 mmol / l for a normal proteinuria
More than 3 mmol / l = dangerous
Aetiology
- neoplasms
- hyperparathyroidism
Clinical symptoms
- Digestive signs: constipation, nausea, vomiting, abdominal pain, anorexia,
- Cardiovascular signs: cardiac arrhythmias, QT shortened,
- Neurological signs: impaired alertness, behavior, muscle weakness, coma
- Signs Urinary: polyuria with thirst, dehydration global renal failure
Treatment
- Fast admission in Intensive Care
- Limit intake of Ca
- Rebalancing hydroelectrolytic
- Administration of phosphorus per os (3g / day)
- Forced diuresis with furosemide
- Hemodialysis
HIPOMAGNESEMIA
Magnesium

The decrease of blood calcium alăuri produce muscular contractions.

And similar symptoms accompanied with hypocalcemia.
The daily requirement from 0.1 to 0.4 mmol / 24 hours, 10 to 20 mEq / 24 hours
1 f MgSO4, 4.1 mEq
HIPOPHOSFATEMIA
Phosphates
Decrease phosphates in producing prolonged parenteral nutrition polyneuritis.
Zinica needs 25-40 mmol / 24h
Do not administer more than 0.02 mmol / kgb / h
It is administered in the form of ampoules 20mmol K or Na phosphate.
THE CALORIC INTAKE

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 - it is closely linked to nitrate intake and fluid.
- caloric intake / day in adults is 30-40 kcal / kgb / 24h (Elwyn)
- 50% of the calories are made of sugars (glucose, fructose, sorbitol)
- 30% of the calories are made of protides
- (amino acid solutions: Infesol, Aminomel)
- 20% of calories from fat is made (Lipofundin, Intralipid)
The nitrogen requirements
N = 0.15 to 0.30 g / kg / 24 h
The minimum required is 5.2 g / 24 hours.
Protide needs 1-2g / kg / 24 hours.
The energy needs of a patient is calculated as follows:
Calorie needs / 24 hours = MB x 1.25 x factor stress

MB = basal metabolism which is given by Harris - Benedict is:

- For women: 665 096 9563 G + J + 1.850 - 4.676 V
- Men: 66.473 + 13.752 G + J 5003 - 6755 V
G = weight
I = the height (in cm)
V = age in years

Stress factor
For sleep stable state
- 1,05 – 1,10 –postoperative state
- 1,10 – 1,45 – denutrition, neoplasm
- 1,25 for peritonitis
- 1,30 – 1,35 – severe poly-traumatism, sepsis
The parenteral nutrition

1 kcal = amount of energy required to raise the temperature of one kilogram of H2O from
14.5 ° C to 15.5 ° C.
1 kcal = 4.1868 KJ
1 g glucide (G) = 4. 1 kcal
1 g protein (P) = 4. 2 kcal
1 g fat (L) = 9. 3 kcal
1 g alcohol = 7. 1 kcal
The work of internal heat is converted into heat and energy needs of the rest measures
resulting from the oxidation of G, P, L (O2 consumption and CO2 production).

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Parenteral nutrition is indicated in critically ill nutrition. Parenteral nutrition is achieved pine
i.v. preparations carbohydrates different concentrated preparations of amino acids, lipids
emulsified.
But this type of diet is supplemented with enteral nutrition. Parenteral nutrition alone induce
intestinal mucosal atrophy, it is immunosuppressive decreases IgA, emphasizes the response
to injury with uncontrolled hyperglycemia, increased release of pro-inflammatory cytokines
and stress hormones.

Enteral nutrition is achieved by administration per bone, oral or nasogastric probe, stoma
(gastro-jejuno stoma) of various foods in particular preparations containing nutrients, minerals
and vitamins. This type of diet is carried out with pumps, automatic syringes or perfuseers.
ACIDO-BASIC IMBALANCE
pH = concentration of the ions of d H-, from the liquids of the organism.
pH = 7,35-7,40, slightly alkaline, because it protects, the acid aggressions, from the cellular
metabolism.
Increase of the concentration of ions H + -> ↓ pH -> acidosis.
Decrease of the concentration of ions H + -> ↑ pH -> alkalosis.
A-B balance = to maintain constant pH.
This balance is achieved by two compensatory mechanisms:
1) mediated mechanisms (buffer) = plasma buffers, neutralizing any rapid change in the
concentration of H + ions by means of their salts with weak acids or bases.
Role highest, 75%, with balance-B, it has buffer bicarbonate / carbonic acid.

2) mechanisms final (definitive), the removal of excess H + or OH, with the involvement
of the lungs or kidneys.

Acidosis = acid accumulation.

The acid is neutralized by sodium bicarbonate -> H2CO3 removes lung after dissociate CO2
and H2O.
When the base fluid invading the body -> alkalosis intervenes carbonic acid, which rapidly
neutralize (under physiological conditions) by converting the NaHCO2. Here comes the
kidney that removes excess bicarbonate.
Normal bicarbonate 27 mEq / l acid, carbonic 1.35 mEq / l, and their ratio is 27 / 1.35 or 20/1.
The balance A-B = the function renal/ventilation
METABOLIC ACIDOSIS
It appears when:
- the amount of bicarbonate decreases
- pH 7,38 or
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 - pH normal if the acidosis is completed through compensatory hyperventilation
- hyperkalaemia

Clinic: compensatory hyperventilation, through polypnoea

Aetiology
Nodosed Anions „ ANIONIC HOLE” is calculated depending on the formula:
(Na+K) – (HCO3) + Cl- = 17 mmol/l,
The anionic hole, where the metabolic acidosis is over 20 mmol / l
- Diabetic acidosis (lunch prolonged ingestion of alcohol)
- Lactic acidosis (severe shock, severe hypoxia, hepatic coma, diabetes, acute pancreatitis)
- Aspirin poisoning, antifreeze
- Loss of bases diarrhoea, digestive fistula
Treatment
It is administered sodium molar bicarbonate of 8, 4 % or 14 ‰
1 ml = 1 mmol Na+ and 1 mmol HCO3
The amount of bicarbonate administered, is calculated on the formula:
Bicarbonate deficit = 0, 4 x G x (20 – the level of plasmatic bicarbonate)
1 g of Na bicarbonate contains: 12 mmol bicarbonate 12 mmol sodium
THAM 36 g in 500 ml Sorbitol
METABOLIC ALKALOSIS
It is produced when the bicarbonate > 27 mmol/l
pH > 7,42
Pa O2 (a moderated increase), which tries to maintain the normal pH.
Hypo K + hypo Cl

Clinic
- hypoventilation
- neuromuscular manifestation
Aetiology
 acid loss in:
- vomiting
- digestive aspirations
- diuretics
- corticoids
 hyperaldosteronism
 hypercalcemia
 alkaline excess
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Treatment
 elimination of the cause
 re-establishing the deficit of
K and Cl
 the correction of the dehydration
 more rarely acidifying

RESPIRATORY ACIDOSIS
PaCO2 > 42 mmHg
pH < 7,38
Slow increase of the bicarbonates, has no time to interfere.
Clinic
Image of respiratory insufficiency
Aetiology
Alveolar hypoventilation, of central or peripheral origin (muscles, wall, pleura)
Treatment
 etiologic treatment
 mechanic ventilation
 THAM or bicarbonate

RESPIRATORY ALKALOSIS
Hypocapnee
- PaCO2 > 38 mmHg
- pH > 7,42
Diminution of the bicarbonates, has as an objective the maintenance of the pH towards normal
values.
Clinic
Neuromuscular manifestations
Aetiology
- secondary to lung hypoventilation
- brainstem lesions
- salicylic acid poisoning
- assisted ventilation
- associated with a metabolic acidoses
Treatment
- treatment of the underlying disease that caused alkalosis
- rebalancing H-E (electrolyte)
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II.16. THE BURNS
Definition
Burns is a set of functional changes and lesions, caused by an agent acting termovulnerant.
Destroy skin deep thermal injuries, which is a barrier protecting the body from the
environment.
The skin has a vital role in thermoregulation in hydro-ionic homeostasis and in defending the
outer body infections.
A strong thermal agent on the skin produces the vulnerable:
- Massive displacement of water more fluid spaces
- High heat losses
- Loss of protein
- Susceptibility to bacterial infection
- Agencies that produce burns:
- Liquids (chemicals: acids, alkalis)
- Solid (incandescent)
- Gaseous (vapours, aerosols overheat)

The gravity of the burns depends on:

- Heating degree of causative agent
- The concentration of chemical substances
- The duration of action of the thermovulnerant agent
- Health or sickness of a person
- The environment of the person concerned
- Duration of the action of the thermovulnerant agent
After the appearance of lesions and profoundness
There are 4 degrees of burns:
The I degree - is an inflammatory process on the surface is characterized by a painful local
hyperaemia of the skin accompanied by edema. Healing burns this takes a few days, after
which the skin returns to its normal appearance and only interested in the superficial layer of
the epidermis.
The 2nd degree - in addition to erythema, blistering skin which is transformed into blisters
filled with serous exudate or serosanghinolent. Occur within minutes or hours after the onset
of infection and potentially increased. It includes all layers of the epidermis to the basal germ.
Appear to shatter pain and infected. Her healing takes 1-2 weeks if cared for properly and heal
without cmplicaţii.
The 3rd degree - epidermis and dermis and partially destroyed completely. Form and content
bloody blisters that have potential for infection pronounced. Healing is scarring sequelae.

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The 4 th degree - full thickness skin care and charring of tissue necrosis occurs. That infected
bedsores are formed easily. Healing is done only after becoming necrotic tissue within weeks
or months. Scar tissue is formed with a tendency to withdraw limiting movements.
Burns Grade II, III and IV affects the entire body giving serious disorders, according to their
breadth and depth.
- Kidney disorders with oliguria and anuria
- Circulatory disorders of blood plasma extravasation and haemoconcentration
- Disorders of the central nervous system with agitation, restlessness then apathy
The burn unit is a three-dimensional, which is characterized by surface and depth
Findings of body surface burned area
The extent of burn was calculated in percentage units, compared to body surface
area which is from 16 to 20,000 cm2. To calculate the area burned using "RULE's
NEW" (Wallace) applies only to adults.

- Head and Neck: 9%

- The front or rear of the body 18%
- Limb 9%
- 18% lower limb
- Perineum 1%

The cartography of the burns

Internet source
334
It also estimated body surface area burned with "palm" the patient is considered 1% of the
body surface. These rules appreciate his body only estimates, and for the exact calculation of
body surface burned there Maps (Tostnikov, Burkov) and tables that allow a mapping that
looks and surface variation by age (Lund and Browder). These tables can appreciate exactly
and area burned child that is slightly different from the adult.

Lund and Browder’s table

Age
0–1 1–4 5–9 10 – 15 16 Adulţi
Segments
Head 19 17 13 14 9 7
Neck 2 2 2 2 2 2
Ant.face of
the trunk 13 13 13 13 13 13

Post.face of
13 13 13 13 13 13
the trunk
Buttocks 5 5 5 5 5 5
Genitals 1 1 1 1 1 1
Arm 8 8 8 8 8 8
Forearm 6 6 6 6 6 6
Hands 5 5 5 5 5 5
Hips 11 13 16 17 18 9
Calf 10 10 11 12 13 14
Legs 7 7 7 7 7 7

The profoundness of the burn

It is estimated by knowing the etiology, inspection and palpation of wound assessment tool
and sensitive nerve endings. It is expressed in "degrees by burning" and there are several
rating scales. After Dupuytren are 6 degrees of sunburn and after school there are four degrees
Romanian burning, which have been described.
Prognostic Index
After burn assessment is important to know the vital prognosis is determined according to
certain parameters. The Romanian school prognostic index calculated by multiplying the
percentage of area burned by the depth of the burn.
Example:
For burning 50%, of which 22% grade III lesions, and 28% grade IV lesions.
IP = 22 x 3 + 28 x 4 = 66 + 112 = 178
335
If you do not take into account the age and associated diseases posed by the patient, IP shall
be construed:
- 0 - 40 – good prognostic
- 50 - 80 – the complications appear at 50% of the cases
- 80-100 – complications are majoritarian
- 100-140 – all the cases evolve with complications
- 140-180 – deaths in 50% of the cases
- Over 200 – deaths in all the cases
Children and old age can not be established correctly extreme prognostic index. Zawaki in
1979 after a study shows that the best prognostic index should include three parameters:
- Airway oedema
- Surface of fourth degree burns
- History of bronchopulmonary
The burn severity depends on them being serious when includes: face, eyes, ears, hands, feet,
perineum or those associated with inhalation burns or electrical shock.
Care and treatment measures:
According to early care and non-emergency treatment, depends on the speed and quality of
patient’s life.
1. Stealing inpatient act as causative agents
2. Managing a major analgesic: pethidine, fentanyl, morphine
3. Wrapping the patient in a clean sheet
4. Emergency transport the patient to hospital
At the hospital:
- Remove clothing under mild sedative or anesthesia
- Healthy hair growth regions wash with soap and water
- Burned areas with sterile saline wash, remove devitalized epithelium and clothing burned
debris in the wound
- Fitting an intravenous line (peripheral or central) and electrolyte rebalancing treatment with
shock combat (soil. Glucoză5% soil. Ringer, izogrup izoRh blood bicarbonate and mannitol
20% sodiu14 ‰)
- Mounting a probe bladder to monitor urine output
- If the upper airways suffered burns or patient is in shock, the first step to entering the
hospital is clear upper respiratory passages
- After cleaning the wound we cover the wound with a sterile dressing soaked in a solution of
boric acid 2% and chloramine 2%

- Wet bandage over a compression bandage is applied with cotton wool for moisture
absorption and prevent oedema

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- Tetanus prophylaxis, serum tetanus or tetanus toxoid
- Collection of biological samples and blood group
- Inpatient hospitalization in a ward heated by 4-5 ° C higher than in wards other conditions.
Bed linen sterile. If burning is minimal patient will remain naked and sits on top of an awning
to support a sheet or blanket, sterile
- Mobilization of the patient to prevent bedsores permanently
- Permanent pain therapy
- Toilet patient and personal hygiene will be strictly observed (short fingernails)
- Calculating daily water balance
- Observation of complications occurring and their treatment
- The alimentation: rich in liquids, vitamins and mineral salts
The local treatment: the burned wound dressing is rarely made only when soaked, to protect
newly formed tissue through the healing process. For extensive burns the patient is sinking
into a well disinfected bath tub, after patient was placed on a sterile bed sheet, sinks into water
and is left for 20-30 minutes. In the water from the bathtub is placed a solution of potassium
permanganate, which helps to peel the bandages easier. Then we remove the patient from the
water with the sheet and we dry the skin with sterile sheets, from where we are carrying the
patient in the bandages or bed room. The burned wound will be cleaned by the doctor and the
nurse, the patients will be dressed in sterile clothing and they will stay in sterile conditions
under i.v. narcosis with midazolam, we clean the wound of necrosis and we perform the
bandage.
Complications
 sepsis
 syndrome of abdominal compartment
 syndrome of compartment at the level of the extremities
 pneumonia
 venous profound thrombosis
 the stress ulcer
 hypothermia (97)
The drug treatment
- Correction fluid losses during the first 24-48 hours after injury when there are
massive fluid loss through evaporation and water retention in the extracellular
spaces (Area III). It makes an aggressive compensation of losses is mandatory to
prevent hypotension, hypo-perfusion and shock. Liquids have retained their
composition similar to plasma.
Liquids used in rebalancing:
- lactate Ringer
- glucose serum 9‰
337
 - colloid (Dextran 40, Reomacrodex, izogroup blood izo Rh etc.)
To balance the correct patient is burned using standard protocols which calculates the volume
of fluid required using body weight (KGB) and body surface area burned (in%).
1. The Brooke formula:
Sol. crystalloid 1, 5 ml/kg % burned surface/24 h
+
colloid 0, 5 ml/kg % burned surface/24 h
+
glucose 5 % 2000 ml /24 h
2. The Parkland formula:
Ringer lactate 4ml/kg%/24 h

After the calculated fluid deficit, half the amount will be given within 8 hours of
production burn, and half of the remaining liquids can be given in the next 16 hours. Hidro-
electrolytic and colloidal aggressive rebalancing will be administered until stable
hemodynamics. Throughout rebalancing fluid volume will monitor vital parameters and
biological.
In order to reabsorb the fluid from the space III, it takes 36-72 hours, it will establish
the functional integrity of the membrane capillaries. Clinically this can be observed by
increasing urine output and a decrease in edema. From the day 3 to day 5 of the producrea
burn hypermetabolic state is installed which is characterized by hemodynamic modification in
the sense that increase cardiac output and peripheral resistance decreases. In this phase of O2
consumption and increase energy. It is vulnerable period of development of sepsis with Gram-
negative microbes
If burning all over the chest, chest wall compliance decreases, hypoxia and
hypercapnia occurs. In this case efctuată IOT must not extend quickly to hypoxia. And CNS
suffers extensive burns and great depth from burns gr. II, when encephalopathy occurs
commensurate with the seriousness of the burn. In patients with heartburn and digestive tract
is affected by intestinal gastric stasis and paralysis. Therefore, there is mounted a tube-
feeding. Bleeding gastric mucosal erosions may cause smaller or larger depending on the
severity of the burn. So the liver parenchyma is changed, this is expressed through increased
transaminase (SGOT and SGPT). Catabolic hormones (catecholamines, corticosteroids)
increase and this is highlighted in the blood.

Hematologic system suffers extensive burns, it distinguished by hemolytic anemia and

thrombocytopenia. Disseminated intravascular coagulation (DIC) caused by sepsis can occur
at any time unless keeps perfect sterility. If the sepsis caused by the infection was burned
surface of the healing process decreases as the chance of skin transplantation. The most
338
common microbial contaminants found in burns are staphylococcus, streptococcus,
Streptococcus hemolytic, gram negative (Klebsiela, Proteus, and Pseudomonas). Local
treatment is indicated as antimicrobial agents:
- the silver nitrate in solution 0, 5 %
- the silver sulphadiasin 1 %
- the cream of mophenida 10 %
If a patient is agitated burned will move on to sedation with diazepam, hydroxyzine,
DORMICUM, diuretics and cardiac conditions complicated by heart failure (digoxin,
mannitol 10 to 20%).
Broad-spectrum antibiotics when there is a confirmed systemic infection or prophylactically
prior to surgery. Prevention starts early articular sequelae by therapeutic gymnastics, joints
and muscles after the fever has ceased, and overall has improved.
The surgery treatment
 the precocious excision and the skin grafts: decrease the risk of installation of the
sepsis, it attenuates the SIRS (97)

II.17. THE BLOOD TRANSFUSION

Definition
The introduction blood transfusion of blood or blood components in the circulatory system.
The first blood transfusion was performed in 1818 by Blumdel.
In 1920 Landsteiner discovers blood groups and dr. Wiener discovered the Rh factor in 1941.
The early twentieth century, is revealed immunological mechanism result of antigen-antibody
reactions, which underlies accidents transfusion.
He divided people into four blood groups. Each individual has a system of antibodies that are
found in the plasma (Atc), which are called agglutinins, and the erythrocyte are agglutinogens
(Atg).
Landsteiner, divides the sanguine system into 4 groups:
GR O I – no agglutinogen, has agglutinin αβ.
GR A II – has agglutinogen A and agglutinin β
GR B III – has agglutinogen B and agglutinin α
GR AB IV – has agglutinogen A and B
The distribution of human serum agglutinins is the placement rules MUTUAL REVERSE,
meaning that it cannot coexist with Agglutinogen agglutinin the same way.
Rh factor discovery in 1941, shows that 84% of people have agglutinogen or + Rh factor,
erythrocyte regardless of OAB group, and 16% are Rh negative and it does not possess Rh
factor.

339
Under physiological conditions there agutinina antiRh, but is formed if transfused blood Rh
positive person Rh negative and as if a mother Rh negative and the baby is Rh positive occurs
isoimmunization, reactions antigen-antibody jaundice, hemolytic or eritroblastoză.
By determining blood groups is established compatibility between recipient and donor blood
(lack of reaction antigen-antibody).
You cannot manage to contain agglutinogens blood erythrocyte plasma agglutinins same way
recipient.

Blood transfusion blood administered izogroup, izoRh donor-recipient.

Exception to 750 ml blood groups O I do universal donor, the intake of agglutinins is
diminishes and do not produce side effects.

Group IV AB is the universal recipient, does not possess agglutinins may receive limited
blood from all groups
There are more methods of determining the blood groups:

1. The Beth – Vincent method – searches the agglutinogenes A and B. In this determination
it is used high hemotest serum and research blood.

α, β β α

OI A II B III AB IV

The relation RECEIVER - DONOR

Practical elements for reanimation, anaesthesia and intensive care, dr. Aurel Mogoşeanu, 1987, Timişoara

340
2. The Simonine method – searches the agglutinin α and β + known hematies OAB + research
plasma.

OI A II B III
serum serum serum

OI AII BIII AB IV

Practical elements for reanimation, anaesthesia and intensive care, dr. Aurel Mogoşeanu, 1987, Timişoara

THE DETEMINATION OF THE

Testimony + Research Testimony

blood Rh+ blood +
● ± blood Rh-

Direct compatibilities
3. Jeambreau, at cold: blood donor + plasma receiver
4. Jeambreau, at hot: the blood in the thermostat at 37ºC, for 30-40 minutes
5. Oelecker (the biological sample): it is transfused 20 ml from the transfused blood which
was heated at 37ºC, then the transfusion is stopped and we observe if the patient presents
adverse reactions: urticarial reaction, trembles, temperature, lumbar pains, anaphylactic
shock.
The indications of the transfusion
- Restoration of circulating blood volume

341
 - Combating disorders of hemostasis or platelet deficiency of coagulation factors
- Increasing transport capacity O2

Numerous studies have demonstrated that both adaptive responses, increasing CO2 and
O2 extraction occur in the early stages of anemia izovolemice. These responses enable
the maintenance of a balance of O2 tissue to a 10-12% Ht. Below this critical O2 offer
no longer cover the needs of tissue oxygen and tissue hypoxia occurs.

Factors associated with decreased tolerance to anemia

Any factor that alters one of the two mechanisms for response (or cardiac output or
oxygen extraction) will reduce the patient's tolerance to anaemia.
Factors associated with decreased CO:
-hypovolemia
-heart failure
- negative inotropic agents
-valve and coronary diseases
Factors associated with decreased O2 extract:
-sepsis
-SDRA (Acute respiratory distress syndrome)
-SIRS (Systemic inflammatory response syndrome)
-syndrome ischemia reperfusion
-drugs vasodilators
Factors associated with altered gas exchange:
-SDRA
-chronic obstructive pulmonary disease
Factors associated with increased consumption of O2
-fever
-pain
-sepsis
-hyperventilation (87)
Blood components
1. The integral blood
- Ensures correct circulating blood volume
- Improves the transport capacity of O2
- Ensure coagulation factors

The donor collects in plastic bags mixed with a stabilizer ACD (citric acid, citrate, sodium
citrate and glucose in distilled water) in an amount of 500 ml.
Keep up to 21 days (preserving blood collected in special solutions is the temp. Of 4-6ºC).
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Fresh blood (collected in the first 24hrs) provides intake of platelets, clotting factors V and
VIII.
Before administering blood transfusion is testing for HIV and viral hepatitis markers.
By preserving whole blood, platelets reduce their viability after 24h, factors V and VIII
degrades after 24 hours, coagulation factors II, VII, IX, XI remain stable and granulocytes
reduce their viability after 2-3 days.
If prolonged blood storage more risk microaggregate platelet, white blood cells and fibrin
thrombi.
2. Erythrocyte mass is a product that is obtained by centrifuging the whole blood erythrocyte
sedimentation and resuscitation in the nutrient solution and 0.9% saline.
Keeping this blood derivative can be up to 35-56 days.
It is indicated in anaemia volume unchanged and fluid therapy haemorrhagic shock. Shelf
8-10 days.
3. Fresh frozen plasma (P.P.C) at - 60ºC. It is a blood derivate which is obtained by frosting
at 18ºC, after the figurate elements were extracted.
In coagulation disorders is indicated deficiency of factors V and VIII and for the correction of
antithrombin III. There is a nutrient solution. Her administration has the risk of transmission
of viral diseases (HIV, hepatitis). Retention period is 6 months.
4. The cryoprecipitate is a plasma concentrate containing Factor VIII, I, XIII, and
fibrinogen. Its operation is done after thawing at 37 ºC. It is used for the recovery of factor
VIII in haemophilia A, Willebrand disease, CID. The average adult dose is 8-10 units of
cryoprecipitate. Be kept for a year at 37ºC.
5. Plasma without cryoprecipitate is fresh plasma, frozen, with factor VII, I, XIII and
fibrinogen and is indicated as plasma expandir.
6. The placentae concentrates (thrombocyte concentrate: CT)
TC is obtained from fresh blood by platelets through repeated centrifugation and separation in
50ml unsprung plasma and stored at 22ºC. TC unit contains a minimum of 5.5 x 10 to the
power 10 platelets. TC administrered in the first 24-48 hours of preparation and kept at room
temperature for up to 5 days.
7. The leucocyte mass – derivate which is obtained in a special device specially programmed
for centrifuge and the absorption of the leukocyte layer between the plasma and erythrocytes.
The administration is made in leukopenia.
8. Polyvalent immunoglobulin (specific)
D specific immunoglobulins IgG is administered within 48 hours of the birth of a child Rh (+)
of mother Rh (-), or in cases with Rh immunization alpha.
Viral hepatitis prophylaxis is administered immunoglobulin IgG antiHBs.
9. The granulocyte concentrates need ABO compatibility. It is administered for sick people
with granulocitopenia under 500/mm³. It is used less in adults and more frequent for the new
born with medullar granulocitopenia.
343
10. The human albumin 5% or 25%
Is a compound which is prepared from the blood contained in the human placenta.
5% human albumin solution containing 88% albumin and is given as plasma expander for
restoring volume expansion and oncotic pressure.
When administered to a volume of 1000 ml 5% human albumin, plasma volume expands with
500ml. Do not use in nutritional purpose and cirrhotic patients.
25% albumin solution is indicated for the effect of depletion in patients with cerebral edema
or edema reduction hypoproteic. In her administration is no risk of viral transmission because
it is prepared at temperatures of 60ºC, for several hours.
Ways of blood administration
1. Massive transfusion:
comprising administering an amount greater than the volume of blood circulating blood in
situations of massive blood loss (haemorrhage large multiple accidental trauma,
cardiovascular surgery, liver surgery, etc.); 1.5 ml / kg / min.
In this type of transfusion due installs acid sodium citrate used as a preservative, which
induces decrease ionized calcium and magnesium, causing arrhythmias.
2. Autologous transfusion
It consists of harvesting a unit of blood per week for 4-5 weeks before surgery (CPDA is
recoletază on special solutions 1 and 2), the last sampling is 72 hours prior to surgery.
Blood taken during surgery the patient is returned.
The condition for this type of transfusion is that the patient benefiting from this method have
minimal transfusion 11gHb and Ht be minimum 34%.
3. Preoperative auto-transfusion
Is taking blood from the surgical wound using a special device and its reimbursement Cell
Saven surgery. Auto-transfusion with preoperative hemodilution is as follows: after induction
of anesthesia is recoletează 750-1000ml blood from the patient and compensated plasma
expander, then the blood taken after the patient is returned during hemorrhagic operator.
Hematocrit patient transfusion in this way must be kept to a minimum 25%.
The accidents and incidents of the blood transfusion
Once they arise are classified into acute (immediate) and delayed. The acute transfusion
occurs during or within 2-3 hours. Late reactions occur days, weeks or months after
transfusion. In the case of infection with human T-cell leukaemia virus, appear in late years.
1. Acute haemolytic accidents – are produced by distinguishing the erythrocytes of the
donor by the antibodies of the receiver: natural or acquired.

Acute intravascular haemolysis is caused by ABO incompatibility system whose agglutinins

have haemolytic action in the presence of complement. This produces haemolysis of red
blood cells with haemoglobin and hemoglobinuria donor.
344
Clinic signs:

- Malaise
- chills
- fever
- Pain in the transfusion
- dyspnea
- nausea
- vomiting
- Hypotension
- Chest pain and wings
- shock
- Diffuse bleeding
- oliguria
- hemoglobinuria
- kidney failure
- Jaundice late
Biological samples
- hemoglobin
- Hemoglobinuria (> 5 mg%)
- Serum haptoglobin <50mg%
- Increased serum bilirubin1. Măsuri şi tratament
- Discontinuation of the infusion
- Changing transfuse infusion which is administered 0.9% saline
- Collection of blood for blood group
- Verification of compatibility tests
- Direct Coombs
- - Foley catheter for urine analysis and monitoring them
- (Urinary flow rate is maintained at 75 -100ml / hr)
- Duret 20% mannitol, furosemide
- Alkaline urine (40-70mEq sodium bicarbonate)
- CID and shock treatment
- Renal vasodilator
2. hemolytic transfusion reactions occur 3-21 days late after transfusion through a
secondary response.
Clinic: reticulocytosis autoimmune hemolytic anemia, elevated indirect bilirubin
test positive Combs, haemoglobinuria with oliguria.
3. post-transfusion purpura - is characterized by severe thrombocytopenia, which
occurs due to antiplatelet antibody development
345
 4. Allergic reactions: are fairly common and starts with hives or anaphylaxis.
Tranfuzării antibodies arise because donors hypersensitive or antigens of the
recipient hypersensitive and occur in the administration of whole blood, plasma,
red cells, cryoprecipitate.
5. febrile reactions - shiver: occur due to the presence alloantibodies anti
antileucocitari and rare HLA antigens to the surface of the cell donor.
6. bacterial infection - is due to non-compliance with aseptic and antiseptic rules
both in harvesting and conservation of blood and its derivatives. Contamination of
the most common Gram negative occurs which develops at 4 ° C. It is manifested
clinically by: abdomiale colic, nausea, vomiting, fever, chills, dyspnea,
hypotension, and shock. Urgent interruptions transfusion, antibiotics, blood seeding
culture medium, shock treatment.
7. immunosuppressive effect - tansfuzia nonspecific immunosuppressive effect on
the recipient.
8. Transmission of disease through blood:sifilisul (concentratul trombocitar)
- Malaria (donors who have visited countries where the disease)
- Viral hepatitis: the most common complication of hepatitis B (10%)
- Infection with Epstein-Barr virus: herpes virus infection
- Infection with cytomegalovirus (CMV) is a herpes virus which is 10% of the
donors
- Infection with AIDS virus has a frequency of 1 / 1,250,000. Screening tests are
reliable in 96% of cases as the period of positivity donors who have AIDS is 3
months.
9. Coagulation disorders
- Thrombocytopenia: produce diffuse bleeding wounds, punctures
- Hypothermia - if administered unheated blood that causes the body temperature drops
below 30-32 ° C, causing severe heart rhythm disorders, increase potassium levels,
increase blood viscosity.
- Increasing the affinity of Hb for O2 by lowering HBO2 2-3 DPG and curve moving to
the left so diminishes offer O2
- Complications of lung edema pulmonr by injury, A.R.D.S given platelet
microaggregates and leukocytes that are formed in the preserved blood.
10. Incompatible transfusion group - appears at the beginning transfusion appears malaise
with impaired general condition, chills, hives, hypotension, bleeding, renal failure until
haematuria, jaundice.
General anaesthesia may mask the symptoms of transfusion reactions such as the haemolytic
and non-haemolytic. Signs of haemolytic reactions include hypotension, tachycardia,
hemoglobinuria and micro vascular bleeding, but they can be mistakenly attributed to other
causes of the patient anesthetized. (87)
346
 Emergency steps:
- Interruption transfusion and replacing it with crystalloid solution (kit changes and infused)
- Corticosteroids (HSHC)
- Antihistamines (Claritin) and anti-mastocitar (Ketotifen)
- Diuretics (furosemide, diuresis minimum 1 ml / kg / h, 20% mannitol)
- Alkaline urine (8.4% sodium bicarbonate)
- exanghinotransfusion
- Plasmapheresis intakes 500ml
- Shock treatment
- haemodialysis
After each blood vial withheld incompatible blood or blood derivatives to be sent to the
Centre harvest compatibility tests that will be restored as well as serologic (Coombs - Anti -
IgA). If incompatible transfusion biological samples will be collected quickly (bilirubin,
platelet count, pro-thrombin time, fibrinogen, compatibility tests, blood cultures).
Emergency transfusion
There are more special and emergency situations when it is not possible to conduct
compatibility tests. In this situation izogroup izoRh administer blood test direct compatibility
with incomplete (red cells when placed in contact with the donor recipient serum at room
temperature, and after centrifugation read macroscopic agglutination.

II.18. ACUTE EXOGENOUS INTOXICATIONS

Definition:
Entering the body of toxic substances, the diferte ways:
- digestive
- respiratory
- dermal
- parenteral
Toxicity can occur:
- accidentally 10-15%
- voluntary suicide purposes 80-90%
- with criminal intent
60% are drug poisoning, followed by alcohol intoxication, fungicides. Insect venom, snakes
may be due to severe poisoning.
Etiopathogeny
1. Respiratory by:
- - Respiratory mucosa irritation of the airways, with altered alveolar-capillary
membrane permeability, paralysis of respiratory muscles, depression of the
respiratory center, blocking the respiratory enzymes acute respiratory failure →

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 2. Cardiovascular
- - Atrioventricular blocks
- - Abnormal heart rhythm (bradycardia)
- - Decreased myocardial contractile force
- - Decreased blood volume
- - heart attack
3. Neurological Disorders
- Altering awareness
- Altering the function of sensory-sensory
- Changing vegetative function
- Headache, insomnia, anxiety, nervousness, somnolence
- Delirium, aphasia, paresthesia, convulsions
- coma
4. Visual impairment
- visual disturbances
- mydriasis
- miosis
5. Digestive disorders
- Toxins acting on the liver and digestive organs Schedule
- Action on the digestive tract inflammation →
- Gastrointestinal bleeding
- Dyspepsia (nausea, vomiting)
- diarrhea
- Haematemesis, melaena
- Hepatocellular damage by blocking biliary jaundice →
6. Changes kidney
- Nephrotic lesions (sulfonamides, lead, gold, etc.)
- Parenchymal lesions (mannitol, phenylbutazone, kanamycin)
- Urinary retention (as sulfuric acid and hydrochloric acid)
7. Changes in Blood
- Toxic action on hemoglobin
- Coagulation disorders
8. Hydroelectrolytic modifications (H-E) and acido-basic (A-B)

- vomiting, diarrhea, hyper or glandular hyposecretion

- global dehydration
- hypo or hyperkalemia
- hypocalcemia

348
- hyponatremia
- Acidosis or alkalosis
=> shock, coma, collapse, paralytic ileus, paralysis, convulsions, IRA, abnormal heart rhythm,
respiratory failure.
Diagnostic
It includes: clinical examination + history + exam paraclinically
Anamnesis: the patient consciously or carers:
- What was ingested, time, quantity, duration of exposure, the route enters the body, the toxin
name, time elapsed since ingestion, ingestion or exposure reason.
General clinical examination - performed quickly
Exam of the teguments and mucosa
- Clammy skin = poisoning with organophosphorus compounds, mushrooms,
aspirin, nicotine, methyl alcohol
- Facies congestive = alcohol poisoning
- Jaundice skin = poisoning with mushrooms (Amanita Phaloides), paracetamol,
carbon tetrachloride, chloroform
- Cyanotic skin with blisters = carbon monoxide poisoning
- Cyanotic skin intensely = nitrite poisoning
Exam of the consciousness state
- Coma with agitation = intoxication with alcohol, salicylates, organophosphorus
compounds, antihistamines
- Coma with seizures = antidepressant poisoning derivatives
- Coma with mydriasis, tachycardia = + atropine poisoning
- Coma with hypotonia = poisoning barbiturates, tranquillizers, chlorpromazine
- Coma with hypotonia + depressed = intoxication with opiates
Exam of respirator apparatus – action of the toxic manifests over the aerial ways, over the
alveolar-capillary membrane over the breathing centres and breathing musculature
- Bronchial hypersecretion = chlorine poisoning, substance organophosphorus
pesticides
- Bronchospasm = intoxication with halogen (iodine, chlorine, bromine)
- Acute pulmonary edema (EPA) = poisoning ammonia, halogens, pesticides,
nitrous vapors, hydrogen sulphide (HS)
- Paralysis of the respiratory center = intoxication with opiates, barbiturates,
alcohol, pesticides
- Paralysis of respiratory muscles = poisoning with pesticides, cleaning substances
organophosphorus
Exam of the cardio-vascular apparatus

349
 - Ventricular tachycardia with digitalis intoxication, antiarrhythmics,
sympathomimetic
- QT prolongation = intoxication, antiarrhythmic, antidepressant, heavy metals,
lithium
- Bradycardia and atrioventricular blocks = amantadine poisoning, digital, beta
blockers, calcium blockers, pesticides, carbonates
Exam of the digestive apparatus
- Will examine the oral cavity, esophagus, stomach and duodenum, to highlight
various injuries, ask occur after ingestion of toxic
- To examine the liver, liver repeated testing is done, especially in poisoning with
mushrooms (Amanita Phalloides), paracetamol
Exam of the urinary apparatus
- The diuresis will be monitored and also the aspect of the urine, plus the para-clinic
analysis (urography, eco, urea, creatinin, uric acid, density etc.)
Exam of laboratory
- Tests for the control of the organ function
- Glycaemia
- Toxicological exam from the blood, urine and gastric content
Treatment
Objectives:
1. supportive treatment
2. preventing absorption of toxic
3. eliminate toxic
4. administration of the antidote
1. Treatment of sustaining the vital functions
It will be appreciated affecting vital functions (airway, ventilation, circulation, excretion)
consciousness, deep coma.
Patients with acute poisoning exogenous will be internal in the intensive care unit (TI) where
therapeutic conduct will be determined depending on the severity of poisoning and the
condition in which the admission.
For admission to TI there are some special criteria:
- Lack of response to verbal stimuli
- Change of respiratory function requiring endotracheal intubation (I.O.T)
- Seizure
- Hypoventilation manifested by PaCO2> 45 mmHg
- SBP <80 mmHg
- Cardiac arrhythmia
- Atrioventricular block gr. II and III
- QRS> 0.12 seconds
350
The first measures have as an objective the sustenance of the vital functions through:
- Placing the patient supine
- Remove dentures, food from the mouth and liquid vomit
- Probe naso-gastric
- Intubation O.T (if applicable)
- Oxygen by mask or nasal tube at a rate of 8-10l / min
- Fitting an intravenous line
2. Prevention of the absorption of the toxic:
- Will mount a naso-gastric probe or probe Faucher, to empty stomach or induce
vomiting
- Will be given as quickly as antidote or neutralizing absorbent to minimize
absorption and intestinal gastric
- Will evacuate as quickly, intestinal contents through purgative drugs and enemas
For provoking the vomiting we administer:
- Simple water, in great amount, 300 - 400 ml, then it is exerted with a spatula,
oropharinphes
- Animal or plant charcoal is administered 4-6 tablespoons in 1000 ml water. Gastric
lavage is effective within 4 hours after ingesting the toxin. Gastric lavage is done
after the patient was intubated endotracheal then Faucher probe is inserted into the
stomach, the patient is placed in Trendelenburg and left lateral decubitus position.
The probe is inserted activated charcoal 2.1 g / kg in 500 ml of water and then
extracted with backsiphonage (total 10.6 l of water).
Activated carbon is produced by burning various organic materials (wood, stone fruit).
Carbonaceous residue is activated by steaming and strong acids. This process produced a fine
powder of porous granules with a surface area of 1000 m² / g. Toxic coal snaps into granules
and inactivated.
In 1 g of activated charcoal is between 100 -1000 mg absorb toxic. The method of
administration of activated charcoal is the first therapeutic measure applied Intoxication:
paracetamol, salicylates, meprobamate, digoxin, theophylline, antidepressants.
Removing toxic, the skin is done by removing toxic and washing clothes soaked with water
10 to 15 minutes.
Gastric lavage is not indicated:
- In the intoxication with petrol derivatives, which creates foam with the water
- In the ingestion of corrosive substances (risk of oesophageal or gastric perforation)
3. The elimination of the toxic:
- Induce diuresis by forcing hemodialysis
- Reduce tubular reabsorption of toxins, osmotic solution is made and diuretics

351
 - Osmotic diuresis will be made alkaline with 10 to 20% glucose, 10% mannitol,
20% sodium bicarbonate and furosemide 4.2 14 ‰ f (40 - 80 mg).
Hemodialysis removes subtanţele low molecular weight proteins that are labile bonds, volume
of distribution and clearance decreased spontaneously.
Not dialyse benzodiazepines and barbiturates dialyse only of phenobarbital, but not
completely.
Indicate haemodialysis and salicylate poisoning, ethylene glycol, methanol and lithium.
Hemoperfusion using exchange resins and activated carbon. It Amanita phalloides indicated
Intoxication.
Haemofiltration technique: heparinate blood is passed through a column of absorbing toxins
that secure.
Exanguino transfusion is indicated poisoning that produce severe haemolysis or jaundice
marked.
Forced diuresis is contraindicated in heart failure, renal failure, hypertension.
The treatment of the convulsions
- The patient was immobilized in bed
- Management of the anticonvulsant (diazepam 10-20 mg) iv endotracheal
intubation after
- Combat hypoglycaemia, hypocalcaemia, acidosis, pulmonary oedema, cerebral
oedema.
The treatment of the respiratory disorders
- - Removing the intoxicated from the environment
- - Managing specific antidote
- - 400-500 ml bleed, oxygen, aminophylline, endotracheal intubation and cortisone
in acute pulmonary edema
- - Broad-spectrum antibiotics to fight with lung infection
The treatment of the cardio-vascular disorders
- In toxic shock, takes stock losses and administered crystalloid fluid (NaCl 0, 9%, 5-
10% glucose), macromolecular substances (dextran, marisang) blood needed
- Vasoactive therapy in shock and paralysis of vasomotor centers, norepinephrine in
the 4-8mg Doses of 500-1000 ml saline or dextrose 5%
- Small Doses dopamine in the 5-10 mcg / kg / min in case of hypotension
The coma treatment
- Is made in order to maintain the vital functions and to prevent complications
- We will assure the caloric intake of minim 20 - 25 cal/kgbody/day
The treatment of the major emergencies
If an intoxicated patient showing coma with altered vital signs (BP, AV, breathing,
etc.) the endotracheal intubation resorts quickly and the mechanical ventilation (no

352
 indication of non-invasive ventilation). Endotracheal intubation cannot define a
threshold score Glasgow.
In case the patient is in shock rebalancing will initiate expansion hydroelectrolytic for
volume- and administration of vasopressors, and hypotension if administered dopamine
is maintained if they revealed a cardiac contractile dysfunction.
4. The treatment with specific antidote
There is no antidote for all toxic substances.
If there is, the general steps will be applied for the treatment of poisoning.
Administration of antidote supportive treatment does not exclude vital functions. Antidote
exists only for a few toxic.
The organophosphorus compounds poisoning and cyanide antidote is the administration of the
first therapeutic gesture.
Subsequently supportive treatment of vital functions and symptomatic treatment of
complications (arrhythmias, convulsions, pulmonary edema, etc.), rebalancing
hydroelectrolytic and nutrition are basic steps in solving cases with acute exogenous
poisoning.
Antidotes foe some toxic substances which are more usual:

Nr.
Toxic substance Antidote Treatment
ct
Organo-phosphoric 1-2 mgi.v. it is repeated at 10
1. compounds (muscarinic Atropine minutes
effects) I.O.T.+ mechanic ventilations
Metanole Sol. 5% i.v. in glucoses 100-
2. Ethylic Alcohol
(blindness, coms, acidosis) 150ml, 2-3 ml/min
Opium and the affined 5-10mg,i.vla interval de
Nalorphyne
compounds 10-15 min
(psychomotorial agitation, it 0,01mg/gkbody
3. Naloxone
appears somnolence, i.v or s.c
depression, bradypnea,
Respiratory paralysis, coma) Levalorphan 0,5/1mgi.vsaus.c

Amyl Nitrite for

sustaining the vital Inhalation 1 vial at 5 minutes
functions

4. Cianhidric Acid Sol 3%i.v.slow 20ml, repeated at

Sodium Thiosulfate
la 30 min until 100 ml

Sodium nitrite
Solution 3 % i.v. 10 ml

5. Bromures NaCl0,9% Physiologic serum 9 ‰, 1000ml,

353
 (insobriety, headache, mental
confusion, vomiting, coma.
Mercure and mercurial
6. derivate (stomatitis, vomiting,
oligoanuria, collapse)
Plumb
(nausea, vomiting, abdominal
7.
pain, violent, bradycardia,
agitation, HTA)
Arsen (pesticide),
(painful vomiting, abdominal
pains, diarrhoea, arterial
8.
hypotension, fever,
scarlatiform eruptions)
Paracetamol
(nausea, vomiting, sweat,
9.
icterus, encephalopathy
hepatic)
Isoniazid
10 (nausea, vomiting, dizziness,
convulsions, acidosis, coma)
Carbon Oxide
(insobriety state, decrease of
11 the muscular force, arterial
hypotension, rhythm disorders,
cyanosis, tachipnea)
Barbiturates
(muscular hipotonia,
12
bradypneea, areflexion,
hypothermia, coma)
Meprobramat
(insobriety state, muscular
13
hipotonia, abolishment of the
osteotendinous reflexes, coma)
Sodium hydroxide (oedema,
buco pharyngeal burns,
14
sialorrhea, dysphagia,
sangvinolent vomiting)
Gas
15 (ocular irritation, delirium,
conculsions, coma, collapse)
Mushrooms
(abdominal pains, anorexia,
vomiting, diarrhoea,
16
bradycardia, hypersecretion
traheobronchial, bradycardia,
sight disorders)
at 4 h
Total 4000ml/24ore
Edetamin 2g/day i.v. at intervals of 12 h,
EDTA,Ca for 5 – 7 days
EDTA The same dose as at the mercury
3 mg/kg body, in sol 10%i.m.
Dimercaptopropanol profound la 4-6 h, for 5-6 days
BAL +1 glass of milk
-gastric wash -dexa spray
-urine alkalinisation
140 mg/kg body, then 70 mg/kg
N- acetilcistein
body in 200 ml gluc.5%, la 4
- gastric wash
ore, for 3 days
Perfusion i.v. in doses equivalent
Vitamin B6
with integrated isoniazid
When COHb >25 % is
administeredO2 hyperbaric 3
atm, for 30 minutes
X -sustaining the vital functions –
taking the patient out of the toxic
environment
O2 100% + re-balance H-E
It is applied the general schema
for trteatment of the
intoxications
- osmotic diuresis
- H-E rebalance
No antidote Tratamentul la fel ca şi la
barbiturice
Locale wash (not gastric)
- symptomatic treatment
X
- general treatment of the
intoxications
- O2
No antidote
-intubation OT
- mechanic ventilation
G Penicillin
300.000-1.ooo.ooo UI/kg
Body/day
X - ascorbic acid i.v
-thyamine
-sustaining the vital functions
-dialyse
354

Cocaine
(euphoria, excitation, nausea,
vomiting, psychosis,
17
convulsions, HTA,
tachycardia, respiratory
insufficiency)
Marijuana
(euphoria, relaxation,
18 temporary disintegration,
tangential speaking,
concentration disorders)
Tricyclic antidepresives
(imipramine, amitriptyline,
19
doxazepine): midriasis, dry
mouth, retenţie de urină
Benzodiazepine
(somnolence, calm coma,
20
depress of the respiration and
circulation)
Salicylates
(polypnoeea, metabolic
21 acidosis and alkalosis
respiratory, abdominal cramps,
vărsături, hemoragie digestivă)
Botulism
(toxin botulin) – nausea,
22 vomiting, diarrhoea, abdominal
distension, dysarthria,
dysphagia
Clorurate Insecticidees
23
(DDT, lindan)
II. 19. FIRST AID IN CASE OF DROWNING AND INSOLATION
THE DROWNING
The International Liaison Commitee On Resusciation (ILCOR) - defines drowning as a
"process that results in respiratory dysfunction primary, secondary immersion / submersion in
-plasmapheresis
-exanghino-transfusion
-medication with protective role
of the hepatic cell
0, 5 -5 micrograms/kg/body/min
0, 05-0, 1mg/kg/body i.v.
Diazepam 0, 1-0, 2mg/kg/body
X
i.v.
Sodium Nitroprusiate
Propranolol
X As for the cocaine
-gastric wash with activated
charcoal
-forced diuresis
- extra-renal clearance
X
-hyperventilation
- sodium bicarbonate
Physiostigmin, neostigmine 2
mg i.v. slowly
Flumazenil It is applied the classical schema
0, 5-1mgi.v. for treatment of the intoxications
-gastric wash
-activated charcoal
X -forced diuresis with the
alkalinisation of the urine
-haemodialysis
-permeabilisation of the
Botulin Antitoxin– breathing way
Trivalent preparate - ventilator support
(ABE) 12 - gastric lavage
-high enemas
Gastric lavage with charcoal and
purgation
No antidote - calcium gluconate 10 ml i.v. at
6h
-phenobarbital 1 f i.m.
355
a liquid medium. This definition implies that the Aryan upper tract of the victim there is an
air/liquid hindering ventilation. The victim may survive or die after this process, but
independent of the outcome, the victim was involved in an incident by drowning ". (86)
Immersion means that the victim is covered by water or any other fluid. For drowning to
occur it is necessary that at least the face and airway to be submerged.
Submersion implies that the entire body, including the airway is below the water surface or a
liquid.
ILCOR recommended that you accept the following terms earlier, not to be used: dry and wet
drowning, active and passive drowning, silent drowning, secondary drowning and near-
drowning versus drowned.
Style reported Utstein style should be used for cases of drowning in order to improve the
consistency of information in studies. (86)
The drowning is the aspiration of fluid into the lungs.
Hidrocution - is cardio-respiratory arrest, without inhalation of water through laryngospasm
and post hidrocution agonizing breaths, water can enter the lungs.
Aetiology
A. The aspiration of sweet water produces
- Hemo-dilutions: in 3-4 min pass 500 ml of water through the alveolar-
capillary membrane
- haemolysis
- hyperkalaemia
- fibrillation ventricular
B. The aspiration of salty water (sea water), is hypertonic, favors the pass of an
amount of liquid from the plasma in the lungs, and the alveoli are filled rapidly
with liquid.
Results: - EPA
- Increase of the electrolitemia

Diagnostic and symptomatology

- hipercapneea plus apnoea and/or hypoventilation
- hypoxemia
- metabolic acidosis
- cardio-vascular disorders
Treatment and care: - it is applied the protocol of CRRC
- is made at the place of the drowning
(the sequence is respected).
1. quickly to remove the victim from the water,
2. mouth to mouth (and water is practiced, getting the victim to the surface)

356
3. vigorous compressions 30-60 sec, on the slope at the base of the lung or abdomen, the
victim being held in lateral decubitus (plus breathing)
4. cardio-respiratory I.O.T.,
5. venous fast
6. combat E.P.A. (Glycosides, diuretics, HSHC)
7. fight hypertension (hypotonic solutions, dextrose 5% NaCl 9 ‰)
8. combat cerebral edema (mannitol 20%),
9. combating acidosesi mixed (14 ‰ sodium bicarbonate),
10. diuretics (furosemide, 10% mannitol, 20%);
11. oxygen,
12. monitoring vital signs (BP, AV, respiration, temperature, diuresis)
13. monitoring of pulmonary capillary pressure
(Probe Swan-Gantz)
14. general symptomatic treatment.
THE INSOLATION
Heatstroke, the totality of cerebral disorders, with generalized response produced by
sunlight.
It has two forms:
1) heat syncope - anaemia caused by cerebral cortex inhibited.
2) attack of sunstroke - cerebral oedema, intracranial hypertension by direct damage to the
meninges.
Diagnostic and symptoms
• intense headache
• photophobia
• hypertension followed by hypotension
• absence of perspiration
• coma
Immediate steps of care taking:
- Place the patient back in the shade or in a cool room.
- Sprinkle sick or apply compresses with cold water (moderate) or water with alcohol.
- Wraps cold, cold compresses on the skull applications.
- Ice bags in armpits and groin region.
The patient is transported at the hospital where it is continued the treatment started at the
place of the fact and it follows:
- Oxygen-therapy
- Rebalancing venous with hydroelectrolytic
- (Glucose 10%, 20%, 9 ‰ NaCl)
- Correction acidosis

357
 - (Sodium bicarbonate + 14 ‰ THAM)
- Monitoring vital signs
- (T0, TA, P, R, PVC, diuresis, SaO2)
- Sedatives (diazepam, hydroxyzine)
- Balance disorders fluid-coagulant therapy (fractionated heparin: Clexane,
inohep, Fraxiparine)
- Rahicenteză extraction 15-20 mL cerebrospinal fluid
- Administration of hypotensive (magnesium sulphate)
- Administration of vasopressors (nicetamid)

Abbreviations

L.A.A. – local anaesthetic analgesic substance

ACD – citric acid
G.A. – general anaesthesia
V.A. – ventricular allure
A.D.S. – adult respiratory distress syndrome
ARDS – acute respiratory distress syndrome
ASAT (TGO) – oxalo-acetic glutamic transaminase
ALAT (TGP) – pyruvic glutamic transaminase
A-B – acido-basic
CO2 – carbon dioxide
CMV – cytomegalic virus
D.H.B.P. – dehydrobenzoperidol
D.T.C. – detubocurar
E.K.S. – electrocardioscopy
E.K.G. – electrocardiogram
E.E.G. – electroencephalogram
H.S.H.C – hydrocortisone hemisuccinate
EPA – acute pulmonary oedema
Ht – haematocrit
HIV – human immunodeficiency virus
SH – sulphured hydrogen
H-E – hydro-electrolytic
i. m. – intramuscular
i.v. – intravenous

358
P.I. – pulmonary insufficiency
I.O.T. – oro-tracheal intubation
i.t. – intrathecal
IRA – acute renal insufficiency
Kgb – kilogram body
K – potassium
C.R.L. – cephalorachidian liquid
Na – natrium
N2O – azote protoxide
O2 – oxygen
PaO2 – partial pressure of the oxygen in the arterial blood
P.C.P. – the pressure in the pulmonary capillary
Pa CO2 – partial pressure of the carbon dioxide
P.C.W.P. – capillary pulmonary pressure
V.C.P. – venous central pressure
CRR – cardio respiratory resuscitation
SaO2 – oxygen saturation
s.c. – subcutaneous
C.N.S. – central nervous system
SIRS – systemic inflammatory response syndrome
SDRA – acute respiratory distress syndrome
AIDS – Acquired Immunodeficiency Syndrome
T.A. – arterial tension
Tb. – tablets
C.V. – current volume

359
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SUMMARY

INTRODUCTION 3
THE PAIN
Chapter I – ANAESTHESIA 16
I.1. DEZIDERATES 16
I.2. DEFINITION AND OBJECTIVES 18

I.3. THE DEVICES IN ANAESTHESIA 20

I.4. THE SUBSTANCES USED IN ANAESTHESIA 21
1.4. A. ANAESTHETICS USED IN THE PARENTERAL 21
ADMINISTRATION
a. BARBITURATES 22
b. BENZODIAZEPINES 24
c. PHENOLS 25
d. IMIDASOLE DERIVATIVES 26
e. PHENICYLINS 26
f. OTHER ANESTHETIC SUBSTANCES 27
g. OPIOIDES 27
h. ATARACTICS 31
i. MAJOR NEUROLEPTICS 32
j. ANTIHISTAMINICS AND ANTIMASTOCYTAR 33
k. ANTICHOLINERGICS 33
l. RELAXANT NEURO-MUSCULAR SUBSTANCES 34
m. ANTAGONIST SUBSTANCES 38
1.4.B. THE INHALANT ANECTHETICS 39
I.5. TYPES OF ANAESTHESIA 46
I.5.1. THE GENERAL ANAESTHESIA 46
I.5.1.a. THE TRACHEAL INTUBATION 57
I.5.1.b. THE COMPLICATIONS OF THE TRACHEAL INTUBATION 63
I.5.1.c. THE DIFFICULT INTUBATION 66
I.5.1.d. THE PRE-ANAESTHESIA 67
I.5.1.e. THE ANAESTHETIC RISK 70
I.5.1.f. CHOICE OF THE ANAESTHESIA 71
I.5.1.g. THE INDUCTION 74
I.5.1.h. THE MAINTENANCE 76

367
I.5.1.i. THE AWEKENING 79
I.5.1.j. THE COMPLICATIONS OF THE GENERAL ANAESTHESIA 81
I. 6. TECHNIQUES OF GENERAL ANAESTHESIA 90
I.6.1. THE GENERAL PIVOT HALOTHANE ANAESTHESIA 90
I.6.2. THE HIPNOANALGESIS 93
I.6.3. THE ACUPUNCTURAL HYPNOANALGESIS 94
I.6.4. THE NEUROLEPTANALGESIS TYPE II (NLA TYPE II) 94
I.6.5. THE RELAXING SURGERY 95
I.6.6. THE ATARANALGESIS 96
I.6.7. THE i.v. ANAESTHESIA POTENTIATED WITH SPONTANEOUS 98
BREATHING
I.6.8. THE GENERAL ANAESTHESIA IN THE C-SECTION 100
I.6.9. THE ANAESTHSIA FOR CHILDREN 101
I.6.10. THE ANAESTHESIA IN PATIENTS WITH HIGH RISK 105
I.7. THE REGIONAL ANAESTHESIA 111
I.8. TECHNIQUES OF LOCOREGIONAL ANAESTHESIA 115
I.8.1. THE LEADING ANAESTHESIA 116
I.8.1.A. THE SPINAL ANAESTHESIA SUB-ARACHNOIDIAN 116
(RACHIANAESTHESIA) IN UNIQUE DOSE
I.8.1.B. THE SUBARACHNOIDIAN CONTINUOUS ANAESTESIA 126
I.8.1.C. THE PERIDURAL ANAESTHESIA (EPIDURAL) IN UNIQUE 128
DOSE
I.8.1.D. THE CONTINUOUS PERIDURAL ANAESTHESIA 132
I.8.1.E. THE CAUDAL ANAESTHESIA IN UNIQUE DOSE 136
I.8.1.F. THE CAUDAL CONTINUOUS ANAESTHESIA 138
I.8.1.G. THE COMBINED ANAESTHESIA: THE RACHIANAESTHESIA 140
AND THE PERIDURAL WITH A SINGLE SPINAL NEEDLE
I.9. THE ANAESTHESIA IN THE SURGICAL EMERGENCIES 142
I.10. THE ANAESTHESIA AND THE ANALGESIA IN OBSTETRICS 147
I.11. THE POSTANAESTHESIC PERIOD 150
I.12. THE INTRAVENOUS THERAPY IN ANAESTHESIA AND 153
INTENSIVE CARE
I.13. THE ENTERAL ALIMENTATION OF THE CRITIC PATIENT 157
I.14. THE PHARMACOLOGY OF THE VEGETATIVE NERVOUS 162
SYSTEM (VNS) IN ANAESTHESIA
Chapter II - EMERGENCIES IN INTENSIVE CARE 174
II.1.GENERAL OBLIGATORY DATA FOR THE PRACTICE OF THE 174

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EMERGENCY MEDICINE
II.2. THE MONITORING OF THE PATIENT IN THE MEDICO- 182
SURGICAL EMERGENCIES
II.3. THE CARDIO-RESPIRATORY-CEREBRAL RESUSCITATION 189
(R.C.R.C)
II. 4. DIAGNOSTIC CRITERIA FOR THE DONOR IN CEREBRAL 214
DEATH
II.5. CARDIAC EMERGENCIES 219
II.5.a. THE ACUTE MYOCARDIAL INFARCT (A. M. I.) 219
II. 5. b. THE ARTERIAL HYPERTENSION (HTA) 228
II.5.c. CARDIAC INSUFFICIENCE 229
II.6. THE ACUTE RESPIRATORY INSUFFICIENCY (ARI) 233
II.7. THE BRONCHIAL ASTHMA 245
II.8. THE SHOCK 250
II.9 MODS – MULTIPLE ORGAN DYSFUNCTION SYNDROME 267
II.10 THE SYSTEMIC INFLAMATORY RESPONSE SYNDROME (SIRS) 268
II.11. THE ACUTE ABDOMEN 269
II.12. THE POLYTRAUMATISMS. FIRST AID. THE TRANSPORTATION 290
OF THE TRAUMATISED PATIENTS.
II.13. THE COMA 300
II.14. ACUTE RENAL INSUFFICIENCY 312
II.15. THE HIDRO-ELECTROLYTIC MISBALANCE 320
II.16. THE BURNS 333
II.17. THE BLOOD TRANSFUSION 339
II.18. ACUTE EXOGENOUS INTOXICATIONS 347
II. 19. FIRST AID IN CASE OF DROWNING AND INSOLATION 355
Abbreviations 358
Bibliography 360

369