SUMMARY OF PREMID TO FINAL

TOPICS
IN
CARDIOPULMONARY ANATOMY
AND PATHOPHYSIOLOGY

Submiited to:
Mr. Hector Victor Perez
(Instructor)

Submitted by:
Kiram, Laizanoor J.
Bsrt 2B
Mwf (10:00 -11:00 am)
PREMID TOPICS
AIRWAY RESISTANCE
 Is mainly defined as airflow obstruction in the airway in which the obstruction of
airflow may be caused by this:
1. Changes inside the airway because of the retained secretion
2. Changes in the wall of the airway because of abnormal structure in the bronchial
muscle
3. Changes outside the airway because of the tumor.
COPD
 Is the most common reason why airway resistance happens.
INTERNAL DIAMETER OF THE ENDOTRACHEAL TUBE
 Major contributor to increased airway resistance.
VENTILATOR CIRCUIT
 Significant amount of water in the ventilator circuit due to condensation.
AIRWAY OBSTRUCTION
 Most frequent causes of increased pressure change.
HYPOVENTILATION
 Result if the patient is unable to overcome the airway resistance by increasing the work
of breathing.
RESTRICTIVE LUNG DISEASE
 Shallower but it is faster
VENTILATORY FAILURE
 Failure of the lungs to eliminate carbon dioxide without supplemental oxygen. It leads to
hypoxemia.
THE NORMAL AIRWAY RESISTANCE
 0.5 to 2.5 cm H2O/L/sec in healthy adults.

MECHANICAL OBSTRUCTION
 Post intubation obstruction
 Foreign body aspiration
 Endotracheal tube
 Condensation in ventilator circuit

INFECTIOUS PROCESSES INCLUDES:

 Croup
 Epiglottitis
 Bronchiolitis
LUNG COMPLIANCE
 Defined as volume (lung expansion) per unit pressure change (work of breathing) there
are two types of compliance which are the:
 LOW COMPLIANCE
 Makes lung expansion difficult meaning that the volume changes in small per unit
pressure change.
 Lung expansion is difficult
 Lung are stiff or noncompliant
 Patient with low compliance reduce its functional residual capacity
 Patient often have a restrictive lung defect, low lung volume, low minute of
ventilation
 Patient have a problem with their inhalation-
 Refractory Hypoxemia may result in patient with low compliance.
 HIGH COMPLIANCE
 Induce incomplete exhalation and carbon dioxide elimination, meaning that the
volume change is larger per unit pressure change.
 Patient has a lack or absent of elasticity and recoil in lung
 Patient with Emphysema is example of high complaint.
 Patient with high compliance due to chronic air trapping, destruction in lung tissue,
and enlargement of terminal and respiratory bronchioles
 High compliant patient may have increase or high Functional Residual capacity and
total lung capacity.
 Patient have a problem in exhalation.
TWO DIVISION OF COMPLIANCE:
 STATIC COMPLIANCE
 Reflects the elastic properties of the elastic resistance lung and chest. It is measured
there is no airflow using PLATEU PRESSURE – PEEP
 PLATEU PRESSURE – needed to maintain inflation in the absence of airflow.
 DYNAMIC COMPLIANCE
 Reflects the airway resistance and the elastic properties of the lung and chest wall. It
is measured when air flow is present using PEAK AIRWAY PRESSURE- PEEP
 PEAK AIRWAY PRESSURE - use to deliver the tidal volume by overcoming the
nonelastic and elastic resistance.
DEADSPACE VENTILATION
 Wasted ventilation or a condition in which ventilation is in excess of perfusion.
 Air that being inhaled by the individual does not take any part for gas exchange due to
this three types of dead ventilation:
 ANATOMIC DEADSPACE
 -Volume occupying the conducting airways that does not take part in gas
exchange.
- This is the normal type of deadspace because it is normal that air remain in
our respiratory system.
 ALVEOLAR DEADSPACE
- Normal lung volume that has become unable to take part in gas exchange
because of reduction or lack of pulmonary perfusion.
- There is a present of ventilation in the alveoli but absent or low of perfusion in
the pulmonary circulation because of obstruction the pulmonary blood vessels.
 PHYSIOLOGIC DEADSPACE
- The sum of anatomic and alveolar deadspace volume under normal
conditions.
VENTILATORY FAILURE:
 Inability of our pulmonary system to remove the waste product or the CO2
 Hypercapnia may result in patient that has a increased in PaCO2

MIDTERM TOPICS
Chronic obstructive pulmonary disease
 is a disorder in which subsets of patients may have dominant features of chronic
bronchitis, and emphysema. The result is airflow obstruction that is not fully reversible
 Patients typically have symptoms of chronic bronchitis and emphysema.

a. CHRONIC BRONCHITIS
 is defined clinically as the presence of a chronic productive cough for 3 months during
each of 2 consecutive years.
 Also known as “BLUE BLOATERS” is a term derived from cyanosis the bluish
color of the lips and skin.
 Patients may be obese
 Frequent cough and expectoration are typical
 Use of accessory muscles of respiration is common
 Coarse rhonchi and wheezing may be heard on auscultation
 Patients may have signs of right heart failure (cor pulmonale), such as edema and
cyanosis

b. EMPHYSEMA
 is defined pathologically as an abnormal, permanent enlargement of the air spaces distal
to the terminal bronchioles, accompanied by destruction of their walls and without
obvious fibrosis.
  Also known as “PINK PUFFER” because of the red complexion or flush
complexion and a rapid respiratory rate.
 Patients may be very thin with a barrel chest
 Patients typically have little or no cough or expectoration
 Breathing may be assisted by pursed lips and use of accessory respiratory muscles;
patients may adopt the tripod sitting position
 The chest may be hyper resonant, and wheezing may be heard

TWO MAJOR TYPES OF EMPHYSEMA:

1. PANACINAR EMPHYSEMA (panlobular emphysema)

 involves the entire alveolus distal to the terminal bronchiole. The panacinar type is
typically most severe type of emphysema and generally develops in patients with
homozygous alpha1-antitrypsin (AAT) deficiency.

2. CENTRIACINAR EMPHYSEMA (centrilobular emphysema)

 is characterized by focal destruction limited to the respiratory bronchioles and the central
portions of the acini. This form of emphysema is associated with cigarette smoking and is
typically most common type of emphysema

DIAGNOSIS
1. BODE
- index is a tool used by health care professionals to predict the mortality rate from COPD.
2. CHEST RADIOGRAPH
- useful in eliminating other cardiopulmonary disorders.
3. COMPUTED TOMOGRAPHY
- is more sensitive than standard chest radiography and is highly specific for diagnosing
emphysema.
4. LUNG VOLUME AND DIFFUSING CAPACITY
- it helps assessing the severity of COPD especially if the patient shows air trapping or
obstruction.
5. OXIMETRY AND ABG PULSE OXIMETRY,
- combined with clinical observation, provides instant feedback on a patient's status while
ABG are helpful in determining the patient oxygen and acid-based status.
6. ALPHA 1 - ANTITRYPSIN DEFICIENCY
- screening used to help view the lack of alpha1 antitrypsin in patient a consideration
screening to COPD patient.
7. EXERCISE TESTING
- is helpful in the differential diagnosis

TREATMENT AND MANAGEMENT

  Smoking cessation, it is used to encourage smokers especially the patient to stop or quit
smoking.
 Bronchodilators is used to prevent occurring the symptoms of COPD
 Inhaled corticosteroids may help stratify the likelihood of efficacy of treatment.
 Rehabilitation a program that reduced the risk of COPD

ASTHMA
More than 2000 years ago Asthma first recognized by “HIPPOCRATES”.
Two (2) Types of Asthma
1. EXTRINSIC ASTHMA
 (Allergic or Atopic Asthma)
 It is linked with exposure to specific allergen (Antigen) like dust, mites, molds, yeast,
pollens, fungi, etc.
2. INTRINSIC ASTHMA
 (Nonallergic or Nonatopic Asthma)
 It is not directly linked with specific Antigen or Extrinsic inciting factor.

Clinical Guidelines are developed and disseminated by:

(1) NAEPP – The National Asthma Education and Prevention Program
 Year 1991 NAEPP published the first Evidence-based Asthma Guidelines.
 Under coordination with National Heart, Lung, and Blood Institute (NHLBI) of National
Institutes of Health (NIH)
 Four (4) Components of Care
1. Assessment and monitoring of Asthma
2. Patient education
3. Control of factors contributing to Asthma severity
4. Pharmacologic Treatment
 The NAEPP Stepwise Asthma Management Chart (Used for optimal treatment of specific
age groups- 0 to 4 years, 5 to 11 years, and 12 years and older)
 NAEPP Guidelines
1. Six steps of asthma management based upon degree of asthma control
2. Four levels of asthma intermittent and 3 levels of persistent- mild, moderate,
severe.
3. Adjustment to management based upon degree of asthma control
4. Use of actions plans for children and adult are recommended.

(2) GINA – Global Initiative for Asthma

 Year 1993 GINA was established, in collaboration between the US (NHLBI, NIH and
WHO)
 GINA’s Specific Goals
 1. Increase the awareness of asthma and its public health consequences
2. Promote identification of reasons for the increased prevalence of asthma.
3. Promote study of the association between asthma and the environment.
4. Reduce asthma morbidity and mortality
5. Improve management of asthma
6. Improve availability and accessibility of effective asthma therapy.
Anatomic Alterations of the Lungs
1. Reversible bronchial smooth muscle constriction
2. Airway inflammation
3. Increased airway responsive to assortment of stimuli
Eosinophils – It infiltrates airway mucosa along with other inflammatory cells
Charcot- Leyden Crystals – Formed from breakdown of eosinophils in patient with Allergic
Asthma.
Goblet Cells –Proliferate;
Bronchial Mucous Glands –Enlarge over the time, smooth muscle layers’ hypertrophy and
increase 3 times their normal thickness.
Cilia –Are often damaged
Remodeling –Process of mucosa basement membrane becoming thicker than normal.
Smooth Muscle Constriction Causes:
 Bronchial Mucosa Edema
 Excessive Bronchial Secretions
 Air Trapping
 Alveolar Hyperinflation
Major Pathologic or Structural Changes during asthmatic episode:
 Smooth muscle constriction of bronchial airways (Bronchospasm)
 Excessive production of thick, whitish bronchial secretions
 Mucous plugging
 Hyperinflation of Alveoli (Air Trapping)
 In severe cases, atelectasis caused by mucous plugging
 Bronchial wall inflammation leading to fibrosis
RISK FACTORS IN ASTHMA (Divided into two factors)
 HOST FACTORS
 GENETICS
1. Production of allergen specific IgE antibodies
2. Airway hyper responsiveness
3. Inflammatory mediators
4. T-helpers Cells (Th1 and Th2) – lymphocytes that recognize foreign pathogens or normal
tissue.
 Th1 – Cell Mediated Immunity; deals with infections by viruses and bacteria.
 Th2 –Humoral Mediated Immunity; deals with bacteria, toxins and allergens.
 OBESITY –Asthma is more commonly seen in obese people BMI >30kg
  SEX and GENDER –Before 14 years old asthma is 2 times more prevalent in young boys
(5-7 years old) while girls experience onset of asthma at puberty; more common in adult
women than men.
ENVIRONMENTAL FACTORS
 ALLERGENS (Outdoor and Indoor Pollution)
 Outdoor Pollution –Asthma exacerbation in areas with increased air pollution.
 Indoor Pollution –Smoke, fumes and biomass fuels.
 INFECTIONS – (Viral Upper or Lower Airway Infection) Respiratory Syncytial Virus
(RSV), Parainfluenza Virus, or Rhinovirus Infection.
 OCCUPATIONAL SENSITIZERS –Causes about 1 in 10 cases of asthma among
working age.
 Occupational Asthma –Caused by exposure to an agent in work environment,
predominantly seen in adults.
 TOBACCO SMOKE –Associated with greater risk of developing asthma-like clinical
manifestations at childhood when exposed prenatally or after birth. Infants with smoking
parents is four time more likely to develop asthma.
 DIET – Cow’s milk or Soy protein formulas for infants have higher incidence of
wheezing.
 OTHER RISK FACTORS
 DRUGS -20% patients are sensitive to Aspirin and NSAIDs (Nonsteroidal Inflammatory
Drugs). Beta-blockers and intraocular drugs for glaucoma are associated with asthma
exacerbations.
 FOOD ADDITIVES AND PRESERVATIVES –Sulfites; commonly found in processed
potatoes, shrimps, dried fruits, beers, causes severe asthma exacerbations.
 EXERCISE-INDUCED BRONCHOCONSTRICTION (EIB) –Vigorous exercise causes
asthma and a common trigger of asthma in children. Running in cold air causes
bronchospasms.
 GASTROESOPHAGEAL REFLUX DISEASE (GERD) –Regurgitation, significantly
contributes to bronchoconstriction where patient may complain of burning, belching, and
bitter or acid taste.
 SLEEP (NOCTURNAL ASTHMA) –Difficulty of breathing at night with asthma
patients.
 EMOTIONAL STRESS –Meditated with histamine release from mast cells that
contributes to asthma exacerbations.
 PERIMENTRUAL ASTHMA (CATAMENIAL ASTHMA) –Symptoms of asthma
worsen in women during menstrual and premenstrual periods.
 ALLERGIC BRONCHOPULMUNARY ASPERGILLOSIS(ABPA) –Exaggerated
response of immune system to aspergillus fungus, which causes airway inflammation and
bronchospasms.
DIAGNOSIS OF ASTHMA
 In children: Based on symptoms and findings.
 In adult: Based on medical history and physical examinations.
DIAGNOSIS AND MONOTORING TESTS FOR ASTHMA
 FEV1, FEV1 /FVC Ratio, & PEFR –Test that measures severity, reversibility, and
variability of airflow limitation (AL).
 FEV – Increased >12% (>200ml) after administration of bronchodilator suggest
reversible AL consistent with asthma.
 FEV1 /FVC Ratio –Normal value is >0.75-0.80. Any lesser value indicates AL.
 PEFR –60L/min (20% prebronchodilator after inhalation of bronchodilator) or Diural
variation of more than 20% suggest asthma.

DIFFERENTIAL DIAGNOSIS:
 Children 5 y/o and Younger: Challenging group because respiratory symptoms like
wheezing and coughing are common in children w/o asthma (esp. 3 y/o).
o Alternative diagnosis for wheezing: Infections, Congenital Problems, Mechanical
Problems.
o Diagnoses: Trial treatment of bronchodilator and inhaled glucosteroids.
 Older Children and Adults: Careful history and physical examination with demo
reversible and variable airflow obstruction will confirm diagnosis of asthma.
o Alternative diagnoses: Upper airway of inhaled bodies, Vocal Cord dysfunction,
CHF (Pulmonary edema).
 Elderly: Cardiac Asthma wheezing, breathlessness, and cough caused by left ventricular
heart failure.

GENERAL MANAGEMENT OF ASTHMA

 Primary goals of Asthma Management:
- Attain and maintain control of the clinical manifestations associated with asthma.
- Maintain normal activity levels, including exercise.
- Maintain pulmonary function as close to normal as possible.
- Prevent asthma exacerbations.
- Avoid adverse effects from asthma medications.
- Prevent asthma mortality.
INTERRELATED COMPONENTS TO MANAGE ASTHMA:
 Component 1- Develop Patient/Doctor Relationship.
 Component 2- Identify and Reduce Exposure to Risk Factors (aka triggers)
 Component 3- Assess, Treat, and Monitor Asthma.
1. Assessing asthma control
2. Treating achieve control
3. Monitoring and maintaining control
 Component 4- Manage Asthma Exacerbations (aka Asthma Attack/Episode)
 Component 5- Special consideration.
  PREGNANCY –At pregnancy, asthma severity changes. Acute exacerbations should be
treated aggressively to avoid fetal hypoxia.
 OBESITY –Asthma is difficult to control in obese patients; weight loss improves
condition.
 SURGERY –Airway hyperresponsiveness, airflow limit, and mucus hypersecretion
predisposes patients with asthma to intra and postoperative respiratory complications.
 RHINITIS, SINUSITIS, AND NASAL POLYPS –Upper airway disease can adversely
influence airway function
 OCCUPATIONAL ASTHMA –Avoidance of relevant exposure is important
 RESPIRATORY INFECTION –Provoke wheezing and increased symptoms
 GASTROESOPHAGEAL REFLUX –More common in asthmatic patients and with
obstructive sleep apnea
 ASPIRIN-INDUCED ASTHMA(AIA) –28% adults with asthma suffers from
exacerbations due to aspirin and other NSAIDs
 ANAPHYLAXIS –Serious allergic reaction to previously encountered antigen that is life
threatening and can both mimic and complicate severe asthma with airway swelling.
RESPIRATORY CARE TREATMENT PROTOCOLS
 AEROLIZED MEDICATION PROTOCOL
 PMDI –Pressurized Metered Dose Inhaler
 DPI –Dry Powder Inhaler
 SVN –Small Volume Nebulizer
 GREEN ZONE –Stable patient
 YELLOW ZONE –Caution
 RED ZONE –Patient is in danger
 OXYGEN THERAPY PROTOCOL –May be required to treat hypoxemia, decrease work
of breathing, and decrease myocardial work.
BRONCHOPULMUNARY HYGIENE PROTOCOL
 Enhanced mobilization of bronchial secretions caused by excessive mucous production.
MECHANICAL VENTILATION PROTOCOL
 STATUS ASTHMATICUS –Severe asthmatic episode that does not respond to
pharmacologic therapy associated with acute ventilatory failure that require continuous
mechanical ventilation (CPAP/BPAP) to maintain adequate ventilatory status.
KEY POINTS: SIGNS OF POORLY CONTROLLED ASTHMA
1. Frequent nocturnal awakening
2. Frequent use of rescue inhaler
3. Frequent symptoms
4. High peak flow variability

PREFINAL TOPICS
RESPIRATORY FAILURE
This describe as:
• Exchange of oxygen of pulmonary capillary with alveoli
• Carbon Dioxide elimination
• Combination of both.
CLINICAL SCENARIOS
 The connection of this two the anatomic alterations of the lungs, the pathophysiology
mechanism, and the clinical manifestation.
THERE ARE SIX MAJOR ANATOMIC ALTERATIONS OF THE LUNGS THAT CAN
RESULT IN RESPIRATORY FAILURE:
1. Atelectasis – occur from mucus plugging, upper abdominal surgery, pneumothorax, or flail
chest.
2. Alveolar consolidation – caused of pneumonia
3. Increased alveolar capillary membrane thickness – ARDS, pneumoconiosis, or pulmonary
Edema
4. Bronchospasm – example like asthma
5. Excessive bronchial secretions – example like chronic bronchitis
6. Distal airway and alveolar weakening – example like emphysema.
RESPIRATORY FAILURE IS COMMONLY CLASSIFIED AS EITHER:
 Hypoxemic (Type I) respiratory failure
 Hypercapnic (Type II) respiratory failure
The HYPOXEMIC (TYPE I) RESPIRATORY FAILURE – is used when the primary problem is
not enough of oxygenation exchange with alveoli and the pulmonary capillary and it decreases
the PaO2.
The HYPERCAPNIC (TYPE II) RESPIRATORY FAILURE – is used when the primary
problem is the alveolar hypoventilation which means that it increased the PaCO2 and without the
supplemental of oxygen, a decreased of PaO2. And is it commonly called ventilator failure.
THE MAJOR PATHOPHYSIOLOGY CAUSES OF HYPOXEMIC RESPIRATORY FAILURE
ARE:
1. Alveolar hypoventilation – is it abnormal condition of respiratory system that develops
when the volume and distribution of alveolar ventilation is not enough for the body’s
metabolic needs. And also it increased the PaCO2 level, and without supplemental
oxygen, a decreased PaCO2.
 COMMON CAUSE OF HYPOVENTILATION:
• Central nervous system depressants
• Head trauma
• COPD
• Obesity
• Sleep apnea
• Neuromuscular disorders
RESULTS OF HYPOVENTILATION:
• Hypoxia
• Hypercapnic
• Respiratory acidosis
• Pulmonary hypertension with cor pulmonale.
2. Pulmonary shunting – portion of the cardiac output that moves from the right side to the
left side of the heart without being exposed to alveolar oxygen (PAO2).
TWO CATEGORIES:
• ABSOLUTE SHUNT (TRUE SHUNT)
-Are commonly classified under two major categories: ANATOMIC SHUNT AND
CAPILLARY SHUNT.
-ANATOMIC SHUNT occur when blood flows from the right side of the heart to the
left side without coming contact with an alveolus for gas exchange.
-Normal shunt is 3% of cardiac output.
-COMMON CAUSES OF ANATOMIC SHUNT: Congenital heart disease,
Intrapulmonary fistula, Vascular lung tumors.
-CAPILLARY SHUNT caused by alveolar collapse or atelectasis, alveolar fluid
accumulation, or alveolar consolidation or pneumonia.
• RELATIVE SHUNT (SHUNT- LIKE EFFECT)
- Are caused by an airway obstruction, an alveolar capillary diffusion defect, or a
combination of this two.
- AIRWAY OBSTRUCTION leads to poor ventilation of the distal airway. As the
result, the pulmonary capillary blood flow is greater than the alveolar ventilation in
short, a decreased V/Q ratio exists.
 - ALVEOLAR CAPILLARY DIFFUSION DEFECTS occur when an abnormality in
the structure of the alveolar-capillary membranes slows the movement of oxygen with
the alveoli and the pulmonary capillary blood.
3. Ventilatory- Perfusion (V/Q) Ratio Mismatch
• Alveolar ventilation – about 4 L/min.
• Pulmonary Capillary blood flow – is about 5 L/min.
• Anatomic dead space- volume of gas in the conducting airways: nose, mouth
pharynx, larynx and lower portions of the airways down but not including the
respiratory bronchioles.
• Alveolar dead space- this is when the alveolus is ventilated but not perfused with
blood, the volume of air in the alveolus is dead space, that is, the air within the
alveolus is not physiologically effective in terms of gas exchange.
• Physiologic dead space – is the sum of the anatomic dead space and alveolar dead
space.
• Pulmonary embolism – the lungs receive less blood flow in relation to ventilation.
•Asthma, Emphysema, Pulmonary Edema, or Pneumonia – the lungs receive less
ventilation in relation to blood flow. When this condition develops, the V/Q ratio
decreases.
• Decreased V/Q ratio – leads to a relative shunt, or shunt like effect, which in turn
leads to venous admixture and a decrease PaO2.
• Dead-Space/ Tidal Volume Ratio – provides a good reference to the patients
wasted ventilation.
DECREASED PARTIAL PRESSURE OF INSPIRED OXYGEN (DECREASED PiO2)
 Hypoxemia – can also develop from decrease inspired oxygen.
 Alveolar-arterial oxygen tension difference – can be used to identify the primary cause of
the hypoxemic respiratory failure- alveolar hypoventilation, pulmonary shunting, or V/Q
mismatch.
CONDITIONS SUCH AS OBESITY OR DRUG OVERDOSE LEAD TO:
 Alveolar hypoventilation
 Hypoxemic respiratory failure
HYPERCAPNIC RESPIRATORY FAILURE (TYPE II) (VENTILATORY FAILURE)
 Primary problem is alveolar hypoventilation
 Patient with this kind of respiratory failure demonstrate an increased PaCO2 and without
supplemental oxygen, a decreased PaO2.
MAJOR PATHOPHYSIOLOGIC MECHANISM THAT RESULT IN HYPERCAPNIC
RESPIRATORY FAILURE:
1.) Alveolar Hypoventilation
2.) Increased Dead-Space Disease
3.) V/Q ratio mismatch

TYPES OF VENTILATORY FAILURE:

 Hypercapnic respiratory failure is commonly referred to as ventilator failure.
1) ACUTE VENTILATORY FAILURE (High PaCO2 and low pH)
2) CHRONIC VENTILATORY FAILURE (high PaCO2 and normal pH)
ACUTE VENTILATORY FAILURE- (acute respiratory acidosis) is a condition in which the
lungs are unable to meet the metabolic demands of the body in terms of CO2 removal)
CHRONIC VENTILATORY FAILURE – (compensated respiratory acidosis) is defined as a
great-than-normal PaCO2 level with a normal pH status.
ACUTE ALVEOLAR HYPERVENTILATION SUPERIMPOSED on CHRONIC
VENTILATORY FAILURE
 The patient with chronic ventilator failure can also acquire an acute shunt-producing
disease (e.g., pneumonia or pulmonary edema)
ACUTE VENTILATORY FAILURE (HYPOVENTILATION) SUPERIMPOSED ON
CHRONIC VENTILATORY FAILURE
 When the patient with chronic ventilator failure does not have the mechanical reserve to
meet the hypoxemic challenge of a respiratory reserve to meet the hypoxemic challenge
of a respiratory disorder, the patient begins to breathe less.
STANDARD CRITERIA FOR MECHANICAL VENTILATION
1) APNEA
2) ACUTE VENTILATORY FAILURE
3) IMPENDING VENTILATOR FAILURE
4) SEVERE REFRACTORY HYPOXEMIA
PROPHYLACTIC VENTILATORY SUPPORT – Is often provided to patients in whom the risk
of pulmonary complications, or hypercapnic respiratory failure, or hypoxemic respiratory failure
is high.
HYPERCAPNIC RESPIRATORY FAILURE – is treated with ventilator support techniques to
manage the patient’s PCO2 levels and acid-base status.

MECHANICAL VENTILATION PROTOCOLS:

(TDP) – Therapist driven protocol programs with a mechanical ventilation protocol rather than
with one of the relatively simple protocols.
Protocol 10-1 – provides an example of a Ventilator Initiation and Management Protocol.
Protocol 10-2 – provides an example of a Ventilator Weaning Protocol
TUBERCULOSIS
 Infectious chronic bacterial infection that primarily affects our lungs, though it may
involve any part of our body.
CLASSIFIED AS EITHER:
 PRIMARY TUBERCULOSIS – (also called as primary infection stage) Mycobacterium
tuberculosis- a rod-shaped bacterium with a waxy capsule. The TB begins when the
inhaled of bacilli implant in the alveoli. The bacilli multiply over 3 to 4 week period, the
initial response of the lungs is an inflammatory reaction that is similar to acute
pneumonia.
TUBERCLE OR GRANULOMA - The lung tissue that surrounds the infected area slowly
produces a protective cell wall.
GHON NODULES – When detected on a chest radiograph, these initial lung lesions.
GHON COMPLEX – The combination of tubercles and the involvement of the lymph nodes in
the hilar region.
DORMANT TB (also called LATENT TB) – are not infectious and cannot spread the TB bacilli
to others.
POST PRIMARY TUBERCULOSIS – (also called reactivation TB, reinfection TB, or
secondary TB) it describe the reactivation of TB months or even years after the initial infection
has been controlled.
MOST NEW TB CASES ARE ASSOCIATED WITH THE FOLLOWING RISK FACTORS:
- Malnourished individuals
- People in institutional housing (nursing homes, prisons, homeless shelters)
- People living in overcrowded conditions
- Immunosuppressed patients (Organ transplant patients, cancer patients)
- Human immunodeficiency virus (HIV) – infected patients (TB is a leading cause of death in
HIV patients)
DISSEMINATED TUBERCULOSIS – (also called extra pulmonary TB, military TB, and
tuberculosis- disseminated) refers to infection from TB bacilli that escape from a tubercle and
travel to other sited throughout the body by means of the bloodstreams or lymphatics system.
Most common location is the apex of the lungs.
ENDOBRONCHIAL TB – it may develops via direct extension to the bronchi rom an adjacent
tubercle cavity or the spread of the TB bacilli via infected sputum.
COMPLICATIONS OF TB:
- Hemoptysis
- Pneumothorax
- Bronchiectasis, extensive pulmonary destruction
- Malignancy
- Chronic pulmonary aspergillosis.
THE MAJOR PATHOLOGIC OR STRUCTURAL CHANGES OF THE LUNGS
ASSOCIATED WITH TB ARE THE FOLLOW:
- Alveolar consolidation
- Alveolar- capillary membrane destruction
- Caseous tubercles or granulomas
- Cavity formation
- Fibrosis and secondary calcification of the lung parenchyma
- Distortion and dilation of the bronchi
- Increased bronchial secretions
TUBERCULOSIS – one of the oldest known to man and remains one of the most widespread
diseases in the world.
DIAGNOSTIC METHODS FOR TB:
• Mantoux tuberculin skin test – which consist of an intradermal injection of a small amount a
purified protein derivative (PPD) of the tuberculin bacillus.
• Acid- fast bacilli (AFB) – it is because M. tuberculosis organism has an unusual, waxy coating
on the cell surface, which makes the cells impervious to staining an ACID- FAST BACTERIA
(AFB) test or also called sputum smear.
ZIEHL-NEELSEN STAIN- reveals bright red acid- fast bacilli against a blue background
FLUORESCENT ACID-FAST STAIN- reveals luminescent yellow-green bacilli against a dark
brown back ground.
• Sputum Culture – the nontuberculous strains of Mycobacterium can shown up on an AFB
smear, a sputum culture is often necessary to differentiate M. tuberculosis from other acid-fast
organism.
• QuantiFERON- TB Gold (QFT- G) test – is a whole- blood test used for diagnosing M.
tuberculosis infection, including the latent TB infection.
PHARMACOLOGIC AGENTS USED TO TREAT TUBERCULOSIS -Used to treat the M.
tuberculosis consist of two to four drugs for 6-9 months
SIX-MONTH TREATMENT PROTOCOL – The first 2 months (called the induction phase) the
patient take daily dose of isoniazid (INH), rifampin, pyrazinamide, and either ethambutol or
streptomycin.
NINE-MONTH TREATMENT PROTOCOL – The first 1-2 months the patient takes a daily
dose of isoniazid and rifampin, followed by twice-weekly isoniazid and rifampin until the full 9
month period has been completed.
RESPIRATORY ISOLATION PROTOCOL – patients hospitalized with active tuberculosis are
kept in respiratory isolation until three sputum AFB smears are negative, taken over three
consecutive days.

CANCER OF THE LUNGS

CANCER is a overall term that apply to abnormal new tissue growth that described the
development of unrestrained multiplication of cells. This abnormal growth of new tissues is
known as NEOPLASM or TUMOR it may be benign or malignant.
a. Benign tumors are noncancerous growth in the body, they don’t spread in the body and do not
invade tissues.
b. Malignant tumors the cells are abnormal and can grow uncontrollably, they are cancerous cells
which invade in other organs.
BRONCHOGENIC CARCINOMA is a malignant neoplasm or tumors of the lung arising from
the epithelium of the bronchus or bronchiole.
TYPES OF CANCERS
1. NON-SMALL CELL LUNG CARCINOMA (NSCLC) is divided into adenocarcinoma,
squamous cell carcinoma (SCC), and large cell carcinoma representing 35-40% of all
lung cancer.
 a. Adenocarcinoma this tumor is composed of malignant glandular epithelium which
located in mucous gland of the tracheobronchial tree.
 Adenocarcinoma tend to be smaller than other bronchogenic carcinomas and located in
the periphery of the lung a distinctive type of adenocarcinoma is Bronchial alveolar cell
carcinoma.
 NOTE: most common type in women and nonsmokers
b. Large cell carcinoma this tumor is composed of large, undifferentiated malignant cells
accounts for 10-15% of lung cancers.
c. Squamous cell carcinoma cancer begins in the in the squamous cell they line the inside of
the airway in the lungs is found in the central parts of the lung account for 25-30% of all
lung cancer.
 NOTE: most common type in men and closely related to smoking.
2. SMALL CELL LUNG CARCINOMA (SCLC) the tumor is composed of small cells is
strongly related to smoking. It is a very progressive tumor, generally having metastasized
at the time of diagnosis.
SIGNS AND SYMPTOMS
1. Cough
2. Chest pain
3. Shortness of breath
4. Coughing up blood
5. Wheezing
6. Hoarseness
7. Recurring infections such as bronchitis and pneumonia
8. Weight loss and loss of appetite
9. fatigue

STAGING
1. NON-SMALL CELL LUNG CARCINOMA (NSCLC)
A chest CT scan is the standard for staging lung cancer. The TNM (Tumor Node Metastasis)
staging system from the American Joint Committee for Cancer Staging and End Reporting is
used for all lung carcinomas except small-cell lung cancer. The TMN takes into account the
following key pieces of information:
 T describes the sized of the primary tumors
 N describes the spread of cancer to regional lymph nodes
 M indicates whether the cancer has metastasized.
 2. SMALL CELL LUNG CARCINOMA (SCLC)
a. Limited stage this means that the cancer is only on one side of the chest and can be treated
with a single radiation field. This generally includes cancers that are only in one lung and that
might also have reached the lymph nodes on the same sided of the chest.
b. Extensive stage this describes cancers that have spread widely throughout the lung to the other
lung, to lymph nodes on the other side of the chest to other parts of the body.

GENERAL MANAGEMENT OF LUNG CANCER

SURGERY
a. Pneumonectomy the entire lung is removed in this surgery
b. Lobectomy an entire section (lobe) of a lung is removed in this surgery
c. Segmentectomy or wedge resection a part of a lobe is removed in this surgery
d. Sleeve resection removal of tumors in the large airways
RADIATION THERAPY used a high-intensity rays (such as x-rays) to kill cancer cells.
a. External beam radiation therapy
b. Stereotactic radiosurgery (SRS)
c. Brachytherapy (internal radiation therapy)
CHEMOTHERAPY is the general term for any treatment involving the use of chemical agents or
drugs that are selectively destructive to malignant cancer cells.

FINAL TOPICS
PNEUMONIA
 Refers to the outcome development of inflammatory that affects mainly the gas exchange
area of the lung. Which caused by bacteria, viruses, fungi, protozoa, parasites,
tuberculosis, anaerobic organisms, aspiration, etc. The patient with this condition
experience chills, sweating, chest pain, dry cough and febrile.
There are major pathologic alterations accompanied with pneumonia, these are:
Inflammation of the alveoli, Alveolar consolidation, Atelectasis, Etiology and Epidemiology.
• Bronchopneumonia- refers to a patchy pattern surrounded by the lung parenchyma in which the
infection is limited to the segmental bronchi. This is commonly involving the right and left lungs
and usually found in the lobes of the lower lung.
• Lobar pneumonia- refers to the end result of a worst scenario or long-term bronchopneumonia
in which the infection has spread from one lung segment to another until the entire lung lobe is
involved.
• Interstitial pneumonia- refers to a diffuse and often bilateral inflammation mainly associated by
the alveolar septa and interstitial space.
• Double pneumonia by layperson-is when the right and left lungs are involved.

Clinical Settings, and Pathogens, Associated with Pneumonia:

• Community-Acquired Pneumonia- is a type of pneumonia which has been acquired from a
normal social contact.
• Community-Acquired Atypical Pneumonia- refers to a patient commonly administered a
variety of both pulmonary and extra pulmonary findings. Here, the organism spurts identification
by standard bacteriologic tests, and there is only one moderate amount of sputum.
• Hospital-Acquired Pneumonia- is an infection which develops in the hospital environment.
 Staphylococci- refers to a common cause of hospital-acquired pneumonia and becoming
increasingly antibiotic resistant.
• Ventilator-acquired pneumonia- may develop more than 48 to 72 hours after endotracheal
intubation.
• Aspiration Pneumonia- refers to a pulmonary result of the entry of material from the stomach
or upper respiratory tract into the lower airways.
• Chronic pneumonias- associated with granulomas include tuberculosis and fungal diseases of
the lung.
Risk Factors for Pneumonia
 Age over 65 years
 Aspiration of oropharyngeal secretions
 Viral respiratory infections
 Chronic illness and debilitation
 Chronic respiratory disease
 Cancer (especially lung cancer)
 Prolonged bed rest
Common causes are:
 Streptococcus pneumonia- which refers for more than 80% of all the bacterial
pneumonias.
 Streptococci- are mostly transferred by aerosol from a cough or sneeze of an infected
individual.
There are two major groups of Staphylococcus:
(1) Staphylococcus aureus- responsible for most “staph” infections in humans
(2) Staphylococcus albus and Staphylococcus epidermidis- are part of the normal skin flora.
 Staphylococcal pneumonia- follows commonly a predisposing virus infection and is seen
most often in children and low immune system adults.
 K. pneumonia- is commonly hospital-acquired disease which has the organism that have
long been accompanied with lobar pneumonia, specifically in men older than 40 years
and those who drink alcohol beverages for a long time.
 Klebsiella- is a type of gram-negative bacillus which is a normal inhabitant of the human
gastrointestinal tract. The organism could be directly transferred by aerosol or indirectly
by contact with freshly contaminated particles.
 Mycoplasma pneumonia- has a common symptoms of cough that tends to come in violent
attacks, generating only a small amount of white mucus. This often experience among
children and early adults.
 Viral pneumonia- is where the patient may become short of breathed, cough, and
producing a small amount of white sputum.
 Parainfluenza viruses- are transmitted by aerosol droplets and by direct person-to-person
contact.
 Adenoviruses- are transmitted by aerosol. Pneumonia caused by adenoviruses generally
occurs during the fall, winter, and spring.
SLEEP RELATED BREATHING DISORDERS- SLEEP APNEA
 This refers to a type of serious disorder which breathing repeatedly stop and starts. The
patients with this condition usually experienced shallow breathing, followed by elevating
efforts to inhale. The onset diagnosis of sleep apnea with a comprehensive sleep
evaluation, that includes a history from the patient, specifically noting the presence of
snoring, sleep fragmentation, periods of apnea during sleep, non-refreshing sleep, and
persistent daytime sleepiness.
The four types are:
1) Obstructive sleep apnea (OSA) syndrome- is categorized by repeated episodes of
complete or initial obstructions in the upper airway during sleep.
Signs and Symptoms Associated with Obstructive Sleep Apnea are:
 Loud snoring
 Observed episodes of breathing cessation during sleep
 Abrupt awakenings accompanied by shortness of breath
 Difficulty staying asleep
 Moodiness or irritability
 Lack of concentration
 Memory impairment
  Awakening with a dry mouth or sore throat
 Morning headache
 Excessive daytime sleepiness
 Depression
 Nocturnal enuresis
 Sexual impotence.

2) Central Sleep Apnea Syndrome- happens because the brain is in abnormal condition
which inappropriately sends signals to the muscles that helps control breathing.
classified as:
 Primary Central Sleep Apnea- which is an unknown cause
 Secondary Central Sleep Apnea

3) Mixed Sleep Apnea- is a combination of symptoms of obstructive and central sleep

apnea.
4) Sleep Related Hypoventilation- refers to the abnormal slow breathing during sleep.
Stages of sleep:
 Eyes open-wake (stage W)
 Eyes closed-wake (drowsy)
 Non-REM sleep (stage N1-light sleep)
 Stage N2
 Stage N3 (Deep Sleep)
 REM sleep