J J M MEDICAL COLLEGE,

DAVANGERE.
DEPT OF ANESTHESIA

PHYSIOLOGY OF AUTONOMIC
NERVOUS SYSTEM
CHAIRPERSON
Dr RAMAPPA M.D
READER
DATE: 20-08-2010

PRESENTED BY
Dr PRITAM
Post Graduate
1

INTRODUCTION
Much of the action of the body in maintaining,
cardiovascular, gastrointestinal and thermal
homeostasis occurs through the autonomic
nervous system (ANS).
The ANS is our primary defense against
challenges, to maintain homeostasis. It
provides involuntary control and organization
of both maintenance and stress responses.
2

HISTORY
GALEN - spoke of sympathy
& consent of body & was
probably 1st to describe
Paravertebral nerve trunks.

THOMAS WILLIS
notion of
involuntary
movements
3

ROBERT WHYTT
recognized that adequate
stimulation is necessary for
visceral sensation & that all
sympathy must be referred
to brain

JACOB WINSLOW
COINED TERM SYMPATHETIC

XAVIER BICHAT divided nervous

system into 2 parts
La vie organique- Visceral nervous
system.
La vie animal- Somatic nervous system

CLAUDE BERNARD
i) Theory of chemical synapse
transmission.
ii) Described fundamental role
of ANS in maintaining
Homeostasis (la fixite du
milieu interior)

BROWN-SEQUARD
noted that sympathetic
stimulation constricts blood
vessels.

WALTER GASKELL
described white
communicanti rami &
recognized that the system
contained 2 antagonist set
of nerve fibers.
6

JOHN LANGLEY
i) Mapped 3 distinct divisions in
system.
ii) Coined term AUTONOMIC &
declared that
it was largely independent from
brain.

SHERRINGTON
initiated systemic study of
reflexes & described
Characteristics of reflex
function.
7

JJ ABEL
synthetized
Epinephrine

SIR HENRY DALE

isolated Choline.
8

DEFINITION
It is network of nerves & ganglia that
controls involuntary physiologic
parameters & maintains internal
homeostasis & stress responses.
It is primarily peripheral efferent system.
Autonomic - self governing
9

PURPOSE OF AUTONOMIC
NERVOUS SYSTEM
A major goal of anesthetic administration is
maintaining optimum homeostasis in the patient.
The intelligent administration of anesthetic
care to patients requires knowledge of ANS
pharmacology in order to achieve desirable
interactions of anesthetics with the involuntary
control system and to avoid responses or
interactions with deleterious effects.

10

FUNCTIONAL ANATOMY
Nervous System

Central Nervous
System

Peripheral
Nervous System

Somatic

Sympathetic

Parasympathetic

Autonomic

Enteric
Nervous
System

11

Difference between
Somatic

Autonomic

Organ supplied

Skeletal muscles

All other organs

Distal most synapse

Within CNS

Outside the CNS(i.e. ganglia)

Nerve fibers

Myelinated

Preganglionic - myelinated
Postganglionic- nonmyelinated

Peripheral plexus

Absent

Present

Efferent transmitter

ACH

ACH, Nor-adrenaline

Effect of nerve section

Paralysis and Atrophy

Activity maintained, no

formation

on organ supplied

Atrophy

12

13

CENTRAL AUTONOMIC ORGANIZATION

Cerebral cortex is the highest level of ANS integration.
The principal ANS organization is the Hypothalamus.
SNS functions are controlled by nuclei in the postero-lateral
hypothalamus.
PNS functions are governed by nuclei in the midline and some
anterior nuclei of the hypothalamus.
The anterior hypothalamus is involved in regulation of
Temperature.
The supra-optic hypothalamic nuclei regulates water
metabolism.

14

SYMPATHETIC NERVOUS SYSTEM

SNS originates from spinal cord in the thoracolumbar region.
Efferent SNS originates in the intermedio-lateral
gray column of T1-12 and L1-L3 segments of spinal
cord.

Nerve fibers, extend to three types of ganglia,

Paired sympathetic chains,
Unpaired distal plexus,
Terminal or collateral ganglia near the target organ.
15

 The 22 paired ganglia lie

along either side of the
vertebral column.
Sympathetic trunks
connect these ganglia to
each other and gray rami
communicans connect the
ganglia to the spinal
nerves.
SNS ganglion are almost
always located closer to
spinal cord than to organ
they innervate.

16

Sympathetic response is not confined

to segments from which stimulus
originates. This allows for a more
dramatic
response,
with
diffuse
discharge of the SNS
After entering the Paravertebral
ganglia of lateral sympathetic chain, the
Pre-ganglionic fibres follows 1 of the 3
courses.
1.Synapses with post ganglionic fibres in
ganglia at the level of exit.
2.Course upwards or downwards in the
trunk of SNS chain to synapse in
ganglion at other level.
3.Track for variable distance through the
sympathetic chain and exist without
synapsing to terminate in an outlying,
unpaired, SNS collateral ganglion.
17

Paired sympathetic chain ganglia

Superior
Middle and
Cervico-Thoracic ganglion (stellate ganglion formed by
fusion of inferior cervical and thoracic ganglia).
The sympathetic distribution to the head and neck
enable and mediate
vasomotor,
pupillodilator,
secretory and
pilomotor functions.

SNS post ganglionic neurons outnumber the pre

ganglionic no. in an average ratio of 20:1 to 30:1.

18

Unpaired pre-vertebral ganglia

Reside in the abdomen and pelvis anterior to the vertebral
column.
Celiac ganglion innervated by T5-T12 innervates the
liver, spleen, kidney, pancreas and small bowel and
proximal colon (many preganglionic fibers from T5 to T12
may pass through the paired paravertebral ganglia to form
the splanchnic nerves).
Superior mesenteric ganglion innervates the distal
colon.
Inferior mesenteric ganglion innervates the rectum,
bladder and genitals.
19

Terminal/Collateral ganglia
Small, few in no. & near
their target organs.
E.g Adrenal medulla

20

PARASYMPATHETIC NERVOUS
SYSTEM

Arises from Cranial n. III, VII, IX, X as well

as from Sacral segments S2-4.
Ganglia occur proximal to or within the
innervated organ. This location of ganglia
makes the PNS more targeted and less robust
than SNS.
Pre ganglion fibres originate in 3 areas of the
CNS.
Mid brain,
Medulla oblongata and
Sacral part of spinal cord

21

 Fibres arising in the

Edinger-Westphal
nucleus of the
Occulomotor nerve
course in the midbrain to synapse in
the ciliary ganglion.
This pathway
innervate the
smooth muscle of
iris and the ciliary
muscle.

22

 In Medulla, the facial

nerve gives off
parasympathetic fibres
to the chorda tympani
and greater superficial
petrosal nerve
These subsequently
synapse in the ganglia
of the submaxillary or
sublingual glands and
the pterygopalatine
ganglion respectively
23

 Glossopharyngeal
nerve synapses in
the Otic ganglion.
These post
ganglionic fibres
innervate the
parotid, salivary
and lacrimal glands.

24

 The Vagus n. transmits fully

of the traffic of the PNS.
It supplies heart,
tracheobronchial tree, liver,
spleen, kidney and all GIT
except distal colon.
Most vagal fibres synapse at
small ganglia on and about
thoracic and abdominal viscera
PNS may synapse with a 1:1
ratio of nerve to effector cells,
the vagal innervations of the
Auerbach plexus may connect 1
nerve fibre to 8,000 cells.

25

 The Sacral segments emerges from S2S4.

Innervates organs of the pelvis and
lower abdomen
Preganglionic cell bodies

Located in visceral motor region of spinal

gray matter

Form splanchnic nerves

26

27

Difference between
Sympathetic
Origin

Dorso-lumbar (T1 to L2)

Parasympathetic
Craniosacral (III, VII, IX, X,
S2-S4)

Distribution

Wide

Limited to head, neck and trunk

Ganglia

Away from organs

On / close to the organ

Post-ganglionic fibre

Long

Short

Pre-post ganglionic fibre

1:20 to 1:100

1:1 to 1:2 except in enteric

ratio
Transmitter

plexus
Nor-adrenaline (major)

ACH

Acetylcholine (minor)
Stability of transmitter

NA stable, differ for wider activity

Ach rapidly destroyed locally

Imp. Function

Tackling

Assimilation of food,

stress

and emergency

conservation of energy

28

29

ENTERIC NERVOUS SYSTEM

ENS is the system of neurons and their supporting
cells are found in the walls of GIT, including neurons
within the pancreas and gall bladder.
It is derived from the neuroblasts of the neural crest
that migrate to GIT along the Vagus nerve.
ENS having extraordinary degree of local autonomy.
Digestion and peristalsis, occurs after spinal cord
transaction or during spinal anaesthesia, although
sphincter function may be impaired.

30

It contains
Myenteric /Auerbach plexus
Submucous /Meissner plexus.
Acetylcholine is principle excitatory trigger of nonspecific portion of ENS. It causes muscle contraction.
Role of cholinergic neurons are Excitation of
external muscles, activation of motor neurons
augmenting secretion of water & electrolytes &
stimulation of gastric cells.
Nicotinic antagonist causes abolition of enteric
reflexes while cholinergic overload or over-reversal of
muscle relaxant causes hyper-reactive enteric reflexes.
31

FUNCTIONS OF ANS
Sympathetic
Fight or flight
E division
Exercise, excitement,
emergency, and embarrassment
Parasympathetic
Rest and digest
D division
Digestion, defecation, and
diuresis
32

Antagonist
ic Control
Most internal organs are
innervated by both
branches of the ANS which
exhibit antagonistic control

A great example is heart

rate. An increase in
sympathetic stimulation
causes HR to increase
whereas an increase in
parasympathetic
stimulation 33
causes HR to
decrease

 Exception to the dual innervation rule:

Sweat glands and blood vessel smooth muscle are only innervated
by symp and rely strictly on up-down control.

Exception to the antagonism rule:

Symp and parasymp work cooperatively to achieve male sexual
function. Parasymp is responsible for erection while symp is
responsible to ejaculation. Theres similar ANS cooperation in
the female sexual response.
34

AUTONOMIC INNERVATION
Heart:
The heart is well supplied by SNS
and PNS. These nerves affect
cardiac pumping is 3 ways -

By changing the rate (Chronotropism)

By changing the strength of contraction
(Inotropism)
Modulating coronary blood flow.

The PNS cardiac vagal fibres

approaches the stellate ganglion and
then join the efferent cardiac SNS
fibres.
35

 The PNS fibres are

distributed mainly to SA
and AV node and to a
lesser extent to the atria.
The main effect of Vagal
cardiac stimulation to the
heart is chronotrophic.
Vagal stimulation
decreases the rate of SA
node discharge and
decreases the excitability
of the AV junction fibers.
36

 SNS has the same supraventricular

distribution as the PNS but with
strongest representation, to the
ventricles. SNS efferents to the
myocardium funnel through the paired
stellate ganglion.
Right stellate stimulation decreases
systolic duration and increases the
heart rate.
Left stellate ganglion stimulation
increases mean arterial pressure & left
ventricular contractility without causing
a substantial change in the heart rate.
The dominant effect of ANS on
myocardial contractility is mediated
primarily through SNS.

37

Peripheral circulation :
SNS nerves are imp regulators of the peripheral
circulation stimulation produces both vasodilatation &
vasoconstriction with vasoconstriction effect being
predominant.
Blood vessels in the skin, kidney, spleen and mesentery
have a extensive SNS distribution where as those in the
heart, brain and muscle have less SNS innervation.
Basal vasomotor tone is maintained by impulses from the
lateral portion of the vasomotor center in the medulla
oblongata that continuously transmits impulses through
SNS maintaining partial arteriolar and venular constriction.

38

Lungs :
Lungs are innervated
by both SNS and PNS.
Postganglionic SNS
fibres from upper
thoracic ganglia
(stellate) pass to the
lungs to innervate the
smooth muscles of the
bronchi and pulmonary
blood vessels.
PNS innervation of
these structures is
from the vagus nerve.

39

 Both SNS and the vagus

nerve provide active
bronchomotor control.
SNS stimulation
produces
bronchodilatation and
pulmonary
vasoconstriction.
Vagal stimulation
produces
bronchoconstriction &
may increase secretion
of bronchial glands.

40

ANS Neurotransmitters
Predominant SNS neurotransmitter-nor
epinephrine.
Predominant PNS neurotransmitterAch.

41

Synthesis & Metabolism of ACH

42

Catecholamines
A catecholamine is any compound having a catechol nucleus (a
benzene ring with 2 adjacent OH group) and an amine
containing side.
Endogenous catecholamines in humans are dopamine, NE and
EPI.
Dopamine is a neurotransmitter in CNS and primarily involved
in co-ordinating motor activity in the brain. It is a precursor
of NE. NE is synthesized and stored in the nerve endings of
postganglionic SNS neurons.
Catecholamines are often referred to as adrenergic drugs
because their effector action is mediated through receptors
specific for the SNS.
43

44

Regulation :
Increased SNS activity as in chronic stress stimulates
the synthesis of tyrosine hydroxylase & dopamine
hydroxylase.
Glucocorticoid from the adrenal cortex pass through
the adrenal medulla and stimulate increase in
phenylethanolamine N methyl transferase that
methylates NE to EPI.
The release of NE is dependent upon depolarization of
the nerve and an increase calcium ion permeability. NE
inhibits its own release by stimulating presynaptic
prejunctional alpha 2 receptors.

45

Inactivation :
Catcholamine are removed from the synaptic cleft by 3
mechanism.
These are

(a) reuptake into the presynaptic terminals,

(b) extraneuronal uptake, and
(c) diffusion.

Termination of NE at the effector site is almost entirely by

reuptake of NE into the terminals of presynaptic neurons
(uptake 1) and this is stored in the vesicle for reuse.
A small amount is deaminated in the cytoplasm of the neuron
by MAO to form dihydroxyl mandelic acid.
46

 Uptake 1 is an active energy requiring temperature

dependent process that can be inhibited.
Extraneuronal uptake (uptake 2) is a minor pathway
for inactivation of NE and NE that is taken up by the
extraneuronal tissue is metabolized by MAO and
COMT to form VMA.
The importance of uptake 1 & uptake 2 is diminished
when sympathomimetics are given exogenously,
uptake 3 is the predominant pathway for
catecholamines given exogenously and is clinically
important. The uptake 3 is slow metabolism.
47

RECEPTORS

48

Cholinergic receptors

Cholinergic
receptors
Nicotinic
NM

NN

Muscarinic
M1

M2

M3

M4

M5

49

Nicotinic receptors
Pentamers of 5 types of
glycoprotein subunits:
(a1-a10), (b2-b5), , & .
Each subunit has 4
hydrophobic helical
membrane-spanning
domains labeled M1-M4.
The M2 regions, which
contain rings of negatively
charged a.a & leucine
residues, form the pore
walls & provide hydrophilic
environment for ions.
50

51

Muscarinic receptors
These are 7 transmembrane domain, Gprotein coupled receptors.
M1, M3,& M5

52

Muscarinic receptors
M2 & M4

53

54

55

56

Adrenergic Receptors
Adrenerg
ic
receptor
s

receptor
s

receptor
s

57

1 Adrenergic receptor
G protein-coupled receptor (GPCR) associated with the
Gq heterotrimeric G-protein .
It consists of 3 highly homologous subtypes, including
1A, 1B, and 1Dadrenergic

58

2 Adrenergic receptor

G protein-coupled receptor (GPCR) associated

with the Gi heterotrimeric G-protein .
It consists of 3 highly homologous subtypes,
including 2A, 2B, and 2C adrenergic

59

 Adrenergic receptor
It is a G-protein coupled receptor associated
with the Gs heterotrimeric G-protein.
They are further divided into 1,2 & 3.

60

61

62

 RECEPTORS IN
CARDIOVASCULAR SYSTEM
Coronary arteries :
Sympathetic nerves cause coronary
vasoconstriction which is mediated by
postsynaptic 2 receptors.
Larger epicardial arteries posses mainly
1 receptors (1 agonists have got little
influence on coronary resistance).

63

Myocardium :
Myocardial postsynaptic 1 receptors mediate perhaps as
much as 30-50% of the basal ionotrophic tone of the
normal heart.
The increase in density of myocardial 1 adrenoreceptors
shows a relative increase in failure and myocardial
ischaemia, thus enhancing of myocardial 1 receptor
numbers and sensitivity
Intracellular mobilization of cytosolic calcium by the
activated 1 myocardial receptor during ischemia appears
to contribute to arrhythmias. The 1 receptor also
increases the sensitivity of contractile elements to calcium.
64

-PERIPHERAL VESSELS
Activation of presynaptic 2 vascular receptor inhibit
NE release, produces vasodilatation.
Whereas postsynaptic 1 and 2 vascular receptors
subserve vasoconstriction.
Postsynaptic 1 and 2 receptors co-exist in both the
arterial and venous sides of the circulation with
relative distribution of 2 receptors being greater on
the venous side.
Nor epinephrine is the most potent venoconstrictor of
all the catecholamine
65

-RECEPTORS IN CNS
There is a close association between and
for BP and HR control.
Cerebral and Spinal cord presynpatic 2
receptors also involved in inhibition of
presynpatic NE release.
Central neuraxial injection of 2 agonists such
as clonidine act at these sites to produce
analgesia, sedation and CVS depression
66

-RECEPTORS IN THE KIDNEY

The greatest density of adrenergic receptors
innervation is present in the thick ascending loop of
Henle followed by DCT and proximal tubule. Both 1
and 2 are found but 2 is dominating, a1 receptor
predominantes in the renal vasculature and elicits
vasoconstriction which modulates renal blood flow.
Tubular 1 receptors enhance sodium and water
reabsorption leading to anti-natriuresis where as
tubular 2 receptors promotes sodium and water
excretion.
67

-receptors in CVS
1 and 2 receptors are present in myocardium & are functionally
coupled to adenyl cyclase.
Post synaptic 1 receptors are distributed predominantly to myocardium
in SA node and ventricular conduction system.
2 receptors have the same distribution but are presynaptic. Activation
of 2 presynaptic receptors accelerates the release of NE into the
synaptic cleft.
The effect of NE on ionotropism in the normal heart is mediated
entirely through the postsynaptic 1 receptors whereas the ionotropic
effects of EPI are mediated through both the 1 and 2 receptors.
2 receptors may also mediate the chronotrophic response to EPI
because selective 1 antagonists are less effective in suppressing
68
induced tachycardias than the non selective 1 antagonist propranolol.

-Peripheral vessels
Post synaptic vascular receptors are virtually
all of the 2 subtype.
The 2 receptors are located in the smooth
muscle of the blood vessels of the skin, muscle,
mesentery and bronchi.
Stimulation of post synaptic 2 receptors
produces vasodilatation and bronchial
relaxation.
69

-receptors in the kidney

Kidney contains both 1 and 2 receptors 1 being
predominant.
Renin release from JG apparatus is enhanced by
stimulation.
1 receptor evokes renin release from the kidneys.
Renal 2 receptors also appear to regulate renal
blood flow at vascular level.
70

DOPAMINERGIC
RECEPTORS
Dopaminer
gic
Receptors

DA1

Postsynapti
c

DA2

Presynapti
c

Postsynapti
c

71

Peripheral vessels
Greatest numbers of DA1-postsynaptic receptors are found
on vascular smooth muscle cells of the kidney and
mesentery.
The vascular receptors are like the 2 receptors linked to
adenyl-cyclase and mediate smooth muscle relaxation.
Activation of these receptors produces vasodilatation
increasing blood flow to the organs. Concurrent activation
of vascular presynaptic DA2 receptors also inhibits NE
release at the presynaptic 2 receptors.
Higher doses of dopamine can mediate vasoconstriction via
the postsynaptic 1 and 2 receptors.
72

73

Central nervous system

Dopamine receptors have been identified in the
hypothalamus where they are involved in
prolactin release.
They are also found in basal ganglia where they
coordinate motor function.
Central action of dopamine is to stimulate the
CTZ of medulla producing nausea and vomiting.
74

GIT, Kidney & Mesentery

Dopamine receptors are found in the smooth muscle
of esophagus, stomach, small intestine enhance
secretion, production & decrease intestinal motility.
DA1 receptors are located on renal tubules which
inhibits sodium reabsorption with subsequent
natriuresis and diuresis. It reduces afterload via
dilatation of the renal and mesenteric arterial beds.
The natriuresis may be the result of combined renal
vasodilatation, improved cardiac output and tubular
action of DA1 receptors.
JG cells also contain DA2 receptors which increases
renin release when activated. This action modulates
the diuresis produced by DA1 activation of tubules.75

FUNCTIONAL RESPONSE
MEDIATED BY ANS

76

Effector
organ

Adrenergic
response

Receptor

Cholinergic
response

Receptor

Rate of
Contraction

Increase

Decrease

M2

Force of
Contraction

Increase

Decrease

M2

Bronchodila
tation

Bronchocon
striction

M3

HEART

LUNG
Bronchiolar
smooth
muscle

77

Effector
organ

Adrenergic
response

Arteries
(most)

Vasoconstriction 1

Veins

Vasoconstriction 1

Skeletal
muscle

Vasodilatation

Endothelium

Receptor

Cholinergic
response

Receptor

Release
EDRF

M3

78

Effector
organ

Adrenergi Receptor
c
response

Cholinergi Receptor
c
response

GENITO-URINARY & SMOOTH MUSCLE.

Baldder
wall

Relaxation

Contraction

M3

Ureter

Contraction

Relaxation

M3

Sphincter

Contraction

Relaxation

M3

Uterus
(pregnant)

Relaxation
Contraction

2
1

Variable

M3

Penis/Vas
deferens

Ejaculation

Erection

M3
79

Effector
organ

Adrenergic
response

Receptor

Cholinergic
response

Receptor

Increase
secretion

Increased
secretion

M3

Relaxation
Contraction

22
1

Contraction
Relaxation

M3
M3

Increase
secretion

M3

Gastro-Intestinal tract

Glands

Smooth
muscle
Walls
Sphincters
Secretions

80

Effector organ

Adrenergic
response

Receptor

Cholinergic
response

Receptor

------

------

Increased
secretion

M3

SKIN
Hair follicles
Smooth muscles

Contraction
Piloerection

Thermoregulation

------

---------

Apocrine (stress)

Increased
secretion

SWEAT GLANDS

81

Effector
organ

Adrenergic
response

Receptor

Cholinergic
response

Receptor

EYE
Iris
Radial muscle
Circular
muscle

Contraction
----------

1
-----

-----------Contraction

M3

Ciliary muscle

Relaxation

Contraction

M3

Ciliary
epithelium

secretion of
Aqueous
Humour

---------

82

AUTONOMIC REFLEXES
DURING ANAESTHESIA
AND SURGERY

83

OCULO-CARDIAC REFLEX (TRIGEMINOVAGAL REFLEX)

Bernard Aschner & Guiseppe first described this reflex in 1908.
Stimulus

Traction on Extra ocular muscle.

Pressure on eyeball.

Afferent

Increase in intraocular pressure.

Long & short ciliary nerves (branch of Trigeminal nerve)

Center

Main Sensory nucleus of Trigeminal n.

Efferent

Vagus n.

Effects

Sinus

bradycardia,

Cardiac

fibrillation & Asystole.

Dysrhythmias,

Ventricular
84

CAROTID SINUS REFLEX

Stimulus BP & HR
Afferent

Glossopharyngeal n.

Center

Receptors present in Carotid

vessels & Aortic arch.

Efferent

Vagus n.

Effect

BP & HR
85

NASOCARDIAC REFLEX
Stimulus

Irritation of nasal cavity (by nasal

specules, nasal retractor or ET tube)
when anaesthesia is inadequate.

Afferent

Maxillary

&

Ethmoidal

division

of

Trigeminal n.
Center

Brainstem nuclei.

Efferent

Vagus n.

Effect

BP & HR.
86

PHARYNGEAL REFLEX
Stimulus

An airway introduced in anaesthesia that

is too light, irritation by mucus

Afferent

Glossopharyngeal

Efferent

Vagus

Effect

Swallowing followed by Laryngospasm

87

LARYNGEAL REFLEX (THE KRATSCHMER REFLEX)

Stimulus

Noxious, mechanical or chemical stimulation of laryngeal

mucosa.

Afferent

Superior laryngeal nerve (br.of Vagus)

Center

Receptors of Hypopharynx, Supraglottic & Glottic region.

Efferent

Recurrent laryngeal nerve (br. of Vagus)

Effect

Closure of Vocal cords.

Transient check or arrest of respiration.

Sensitivity of this reflex is reduced by age, CNS depressant drugs &

Anaesthetics.

88

TRACHEAL REFLEX : (VAGO-VAGAL REFLEX)

First described by Brace & Reid.

Stimulus

ET intubation, cuff inflation, suctioning, foreign

body in trachea.

Afferent

Vagus

Center

Dorsal nucleus of Vagus

Efferent

Vagus

Effect

Laryngospasm, Bronchospasm, bucking.

Cardiac arrhythmias, hypotension.

89

ABDOMINAL REFLEX
Stimulus

During operations within the abdominal

cavity autonomic nerves get stimulated by
traction pressure on the viscera.

Afferent

Splanchnic nerves

Efferent

Vagus

Effect

Respiration-apnea followed by tachypnea with

or without laryngospasm.
CVS- Bradycardia, hypotension

Peritoneal, mesenteric reflex, & celiac plexus reflex have same effects.
90

AUTONOMIC
DYSFUNCTION

91

TESTS OF AUTONOMIC SYSTEM

FUNCTION

These tests measure how the various systems in the body,

controlled by autonomic nerves, respond to stimulation. The
data collected during testing will indicate functioning of ANS.
These tests help to identify patients with autonomic
neuropathy and is predictive of mortality and morbidity.
Early autonomic dysfunction is defined as a single abnormal
or two borderline-abnormal results on the tests involving
changes in heart rate.
Definite involvement comes when two of the tests of changes
in heart rate are abnormal. Severe dysfunction is defined as
abnormalities in the blood pressure assessments.
Tests are done to monitor BP, blood flow, heart rate, skin
temperature and sweating.
92

Indications for ANS testing

Syncope
Central autonomic degeneration ex. Parkinsons
Pure autonomic failure
Postural tachycardia syndrome
Autonomic and small fiber peripheral
neuropathies ex.- diabetic neuropathy
Sympathetically mediated pain
Evaluating response to therapy
Differentiating benign symptoms from autonomic
disorders

93

Parasympathetic function tests

HR response with valsalva manoeuver
Valsalva manoeuver: valsalva ratio is an index of HR
response to BP changes that occur during valsalva
manoeuver resulting from mechanical and
cardiovascular effects.
Measure baseline HR and BP 3 minutes before this test
Patient takes a deep inhalation, a complete exhalation,
inhales again and then blows into a mouthpiece for 15
seconds
Expiratory pressure is maintained at 40 mm Hg. This
pressure can be measured by having the patient to
exhale through a mouth piece attached to a transducer
94

 BP and HR are measured throughout the manoeuver for

60 seconds after temination of the manoeuver
An average of 2 trials are taken for analysis
Caution while performing the test in elderly with
pulmonary disease who may not be able to perform the
test satisfactorily
As intraocular pressure is known to rise, the test must
not be performed in those with recent retinal surgery
VR values are aggregated. There is a decrease with age.
95

 VR=Max HR/Min HR. a normal VR indicates an

intact baroreceptor mediated increase and
decrease in HR. a decreased VR reflects
baroreceptor and cardiovagal dysfunction.
Normal value is a ratio of >1.21
Stimulus

Expiration of 40mm Hg for 15sec.

Afferent

Baroreceptors, Glossopharyngeal & Vagus nerves.

Central

Nucleus Tractus Solitarus

Efferent

Vagus & sympathetic nervous system.

Response

Heart rate response to blood pressure changes

Increase/Decrease in BP (phases I-IV)

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HR variability with respiration (respiratory sinus arrhythmia)

Respiratory sinus arrhythmia is recorded with patient

supine & breathing at fixed rate of 6 breaths/min with
slow inhalation & exhalation. This provides close to
maximum HR variability.
6-8 cycles are recorded with one or two trials being
performed.
Timed breathing potentiates normal sinus arrhythmia that
occurs during the normal respiratory cycles
Reduced HR variability with respiration is seen in aging,
autonomic peripheral neuropathies and central autonomic
degenerations.
Other factors which can influence this test are poor
respiratory efforts, hypercapnia, salicylates poisoning,
obesity
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 E/I Ratio: sum of longest RR intervals divided

by sum of shortest RR intervals. Normal value
is a mean difference of >15 BPM.
Stimulus

Deep breathing (6cycles/min)

Afferent

Pulmonary receptors, Cardiac mechanoreceptors, Vagus &

Glossopharyngeal nerves, Respiratory centre.

Center

Nucleus tractus solitaries

Efferent

Vagus

Response

Heart rate increases during Inspiration.

Heart rate decreases during Expiration.
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The 30:15 ratio (HR response to standing)

With patient in supine position baseline HR is
measured
Patient is asked to quickly stand up
HR variability is measured for at least 1 min of active
standing
A normal ratio is greater than 1 & reflects intact
vagally mediated HR changes.
An abnormal ratio indicates parasympathetic
cardiovagal dysfunction
Misinterpretations of this test can occur in
hypovolemia, medical deconditioning, and
hypothyroidism.
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After standing

HR

Exercise,

reflex/withdrawl

of

parasympathetic

tone.
Approx 15sec later

HR

Compensatory response to decreased venous return,

cardiac output & BP.

At approx 30 sec

Relative bradycardia

Stimulus

Decreased central blood volume.

Afferent

Baroreceptors, Ergoreceptors, Vagus & Glossopharyngeal nerves.

Center

Nucleus tractus solitaries, Rostral ventrolateral medulla.

Efferent

Vagus

Response

HR increases at approx 15 sec.

HR decreases at approx 30 sec.

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Sympathetic function tests

Blood pressure response to sustained hand grip

Sustained hand grip causes reflex increase in
heart rate & cardiac output without changing
systemic vascular resistance.
Diastolic BP thus normally increases.
BP is measured every min for 5 min.
The initial diastolic BP is substracted from the
diastolic BP just before release.
The normal value is difference of >16mm Hg.
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Blood pressure response to standing

The patient moves from resting supine
to standing position.
The standing Systolic BP is substracted
from the supine Systolic BP.
The normal value is difference of
<10mm Hg.

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Head Up Tilt Table Test

This test determines BP & HR response to an
orthostatic challenge as a measure of sympathetic
function.
Used to access orthostatic intolerance caused by
sympathetic nervous system dysfunction & to
detect any predisposition to vasovagal syncope.
Patient lies supine on a tilt table & a belt is placed
around the waist to secure them in case of syncope.
BP & ECG are monitored throughout the tests &
recorded.
Baseline BP is recorded for atleast 3 min.
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 Patient is slowly tilted upright to an angle of

60-80.
Patient is asked to report any symptoms.
Patient is returned to horizontal supine
position.
HR & BP are monitored in supine position until
it returns to baseline.
IV Isoproterenol, a pharmacological measure
to potentiate orthostatic challenge to the tilt
table test, is frequently used.
A normal tilt table test is one in which there
are no symptoms & a modest fall in BP.
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Stimulus

Decreased central blood volume.

Afferent

Baroreceptors, Vagus & Glossopharyngeal nerves

Center

Nucleus

Tractus

Solitarus,

Rostral

ventrolateral

medulla,

Hypothalamus.
Efferent

Sympathetic vasomotor

Response

Pattern, degree & rate of BP changes.

HR increase/decrease.
3 patterns:
a)Vasodepression resulting in hypotension without bradycardia.
b)Marked bradycardia (<40/min) with or without fall in BP.
c)Both bradycardia & Hypotension.

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 Other tests used are-

Sympathetic Cholinergic Sweat Function

Quantitative Sudomotor Axon Reflex Test.
Silastic Imprint Test.
Thermoregulatory Sweat Test.
Microneurography.

106

DISEASES ASSOCIATED
WITH PROGRESSIVE
NEUROLOGICAL
IMPAIRMENT OF
AUTONOMIC NERVOUS
SYSTEM

107

 They can be primary, familial or due to

secondary systemic disease or idiopathic.
Primary :
1. Idiopathic Orthostatic Hypotension
2. Shy-Drager type of Orthostatic
Hypotension
Familial :
1. Riley-Day Syndrome (Autonomic
neuropathy in infants and children)
2. Lesch-Nyhan Syndrome
3. Gill Familial dysautonomia
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Secondary to systemic diseases:

Aging
Diabetes Mellitus
Chronic Alcoholism
Chronic Renal Failure
Hypertension
Rheumatoid Arthritis
Carcinomatosis
Chaga's disease
Tetanus
Spinal cord injury Transection
Acute
Chronic

Neurological diseases
Tabes Dorsalis
Syringomyelia
Amyloidosis

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Ageing
Approximately 20% of people over 65 years of age have
postural hypotension.
Half of these patients are symptomatic i.e they
experience dizziness, faintness or loss of consciousness.
It is well known that the reflex regulation of heart rate
which is mediated primarily by parasympathetic
mechanisms declines progressively with age.
There will be a selective or earlier impairment of
parasympathetic function with aging with a minimal or a
more gradual involvement of the sympathetic nervous
system
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Diabetes Mellitus
Diabetic autonomic neuropathy is a well known clinical entity.
It may result from neuronal degeneration or metabolically
related neuronal dysfunction.
The afferent central or efferent reflex pathways each can
be involved.
It has been suggested that the Vagal neuropathy occurs
earlier in the course of DM than the sympathetic neuropathy.
The most sensitive test of cardiac parasympathetic
impairment is that of determining RSA during forceful
breathing. Intolerance to upright posture is often evident.
The presence of symptomatic postural hypotension is
associated with a poor prognosis. These patients are prone to
sudden cardiac death.
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For those scheduled for surgery there are several

implications that are important to anaesthesiologist.
Esophageal dysfunction and gastric hypotonia
increase the risk of regurgitation and aspiration.
Bradycardia, hypotension and cardiopulmonary
arrest have been reported.
Abnormal blood pressure falls with induction and
highest requirement for intraoperative pressor
agents to maintain stable haemodynamics.
ANS dysfunction may also interfere with control of
ventilation, making diabetics more susceptible to
respiratory depressant effects of drugs.
Painless myocardial infarction and unexplained
cardio respiratory arrest have been reported.
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Autonomic changes in Spinal Cord

Transection
It can cause various degrees of autonomic
dysfunction depending on site, extent & timing of the
lesion.
Many autonomic reflexes are inhibited by Supraspinal
feedback that is lost after spinal cord transaction.
In Paraplegic patient, small stimuli can cause
exaggerated sympathetic discharges.
The only intact efferent component of baroreflex
pathways in Quadriplegic patients is Vagus.
There are fundamental differences between acute &
chronic spinal cord transaction.
113

 First, a transient state of decreased

excitability occurs, known as Spinal Shock. It
may last for days to weeks.

In these patients, the periphery is generally atonic &

peripheral blood vessels are dilated.
In case of recent High Thoracic lesion, basal supine
blood pressure is usually low & accompanied by plasma
catecholamine levels that are approx 35% of normal.
In case of recent Low spinal injuries, compensatory
tachycardia is exhibited from intact part of ANS.
In cases of chronic High spinal lesion, patient may
fail to respond to hypovolemia with increased heart
rate & may exhibit bradycardia. Renin-angiotensinaldosterone system compensates for maintenance of
blood pressure in these patients.
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 The phenomenon of Autonomic

dysreflexia can occur with stimulation
below the lesion.
Bladder & bowel distension can elicit
Mass Reflex.

Dramatic rise in blood pressure.

Marked reduction in flow to periphery.
Flushing & sweating in areas above the lesion.
In addition there may be contraction of
bladder & bowel, skeletal muscle spasm &
penile erection.
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PREVENTION AND TREATMENT OF

ADVERSE AUTONOMIC REFLEXES
Atropine commonly used for both prevention and treatment.
Topical anaesthesia can eliminate the reflex.
Intravenous lidocaine is more effective than topical
anaesthesia.
Cessation of applied stimulus immediately.
Vasopressors injected if there is persistent hypotensive
response.
Depth of anaesthesia should be increased. Most of the
intrathoracic and intraabdominal reflexes are observed
during surgery when anaesthesia is to light or relaxation is
inadequate.
116

REFERENCES
1.
2.
3.
4.
5.
6.

Miller`s Anaesthesia- 7th ed.

Barash Clinical Anesthesia- 6th ed.
Stoelting`s Principles of Anesthesiology-3 rd ed.
Collin`s Anesthesiology
Ganong`s Review of Medical Physiology-23rd ed.
K.D Tripathi`s Essentials of Medical
Pharmacology 5th ed.
7. ISACON 2009.

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