Obstructive Pulmonary

Disturbance
&
Respiratory Failure
 Disturbance in Ventilatory
Function

•  Restrictive Lung Disorders

•  Obstructive Lung Disorders

Disturbance in Ventilatory
Function
 Obstructive Pulmonary
Disturbance

•  Reduced flow rates

– FEV1/FVC (less than 70%)
 Obstructive Pulmonary
Disturbance
•  Chronic obstructive pulmonary disease
(COPD)
–  Chronic bronchitis
–  Emphysema
•  Asthma
•  Bronchiectasis
•  Cystic fibrosis
 COPD
•  Disease state characterized by airflow
limitation that is NOT FULLY
REVERSIBLE. The airflow limitation is
usually progressive and associated with
an abnormal inflammatory response of
the lungs to noxious particles and
gases
»  Global Initiative for Obstructive Lung Disease
(GOLD)
 Chronic Bronchitis

•  chronic productive cough for 3 months

during each of 2 successive years in a
patient in whom others causes of
chronic cough have been excluded
Emphysema
•  Abnormal
permanent
enlargement of
the air spaces
distal to the
terminal
bronchioles
COPD
 Clinical Features
•  Cough
•  Sputum production
•  Hemoptysis
•  Dyspnea with exertion – dynamic
hyperinflation
•  Health status (quality of life)
•  Acute exacerbations
 Clinical Features
•  Coarse crackles occurring
early in inspiration
•  Wheezing
•  PROLONGED EXPIRATORY
TIME
–  Expiratory phase longer than
4 seconds
•  Barrel shaped chest, purse-
lipped breathing,
emaciation
•  Tripodding position
•  Pulmonary hypertension
Pink Puffer/ Blue Bloaters
Clinical Features
 Laboratory Findings
•  Chest Radiography
•  Computed Tomography
•  Pulmonary Function Tests
–  Spirometry, lung volumes, volume-
pressure relations, diffusing capacity,
arterial blood gases (ABG)
•  Erythrocytosis
•  Sputum Examinations
 Chest Radiography
•  Chronic bronchitis
–  Increased thickness of bronchial walls viewed on
end
–  Increased prominence of lung markings
•  Emphysema
–  Arterial deficiency (overinflation, oligemia and
bullae)
–  Increased markings ( “dirty chest” )
•  Overinflation
–  flattening of the diaphragm with a concavity of
superior surface of diaphragm
–  Increase in width of retrosternal space- less
sensitive
Chest Radiography
 Risk Factors

•  Exposure to toxic
fumes and gases
–  Cigarette smoking
-most important
risk factor
–  10-15% smokers
lead to COPD
 Risk Factors
•  Smoke from home cooking and heating
fuel
•  Occupational dust and chemicals
•  Gender: More common in men.
•  Increasing age
•  Others: Infection, nutrition and
deficiency of α1 antitrypsin
 Natural History of COPD
100
Never smoked or not
FEV1 (percent of value at age 25)

susceptible to smoke
75
Smoked regularly and
susceptible to its effects

50
Stopped at 45
Disability
25
Stopped at 65

Death

0
25 50 75
 Disease Trajectory

Symptoms

Exacerbations

Exacerbations
Deterioration
Exacerbations

End of Life
 Pathogenesis

Noxious particles
& gases
Host factors

Antioxidants Lung inflammation

Antiproteinases

Oxidative stress Proteinases

COPD pathology Repair mechanisms

 Pathophysiology
Normal COPD
 Spirometry
•  Diagnosis
•  Assessing
severity
•  Assessing
prognosis
•  Monitoring
progression
 Treatment
•  Avoidance of risk factors
–  Smoking cessation
–  Reduction of indoor pollution
–  Reduction of occupational exposure
•  Influenza vaccination
 Treatment
•  Bronchodilators
–  Short-acting β2-agonist
–  Long-acting β2-agonist
–  Anticholinergics
–  Methylxanthines
 Treatment
•  Inhaled Corticosteroids
–  Improvement in airflow
–  Reduced the frequency and severity of
exacerbations
–  Reduce the rate of health status decline
–  Reduced hospitalization and mortality
 Treatment
•  Oxygen Therapy
–  Extends life in hypoxemic patients
–  Reduction of hematocrit
neuropsychological improvement
–  Improvement in pulmonary hemodynamics
–  Diminish dyspnea and work of breathing
•  reduction of airway resistance
∀ ↓ minute ventilation needs
 Treatment
•  Pulmonary Rehabilitation
–  Improved independence and quality of life
–  Decreased hospital days
–  Improved exercise capacity
 Acute Exacerbation
•  New respiratory event or complication
superimposed upon established COPD
•  Common causes
–  Infection, pollution
•  Prevention
–  Inhaled glucocorticoids
–  Anticholinergic tiotropium and ipratropium
–  Long-acting beta agonist
–  Influenza vaccine
Asthma
 Definition
•  Chronic, inflammatory disorder of the
airways
•  Mast cells, eosinophils, T lymphocytes,
macrophages, neutrophils and epithelial cells
play a role
•  In susceptible individuals, inflammation
causes recurrent episodes of wheezing,
breathlessness, chest tightness and cough
especially at night or early morning
 Definition
•  Associated with widespread but
variable airflow obstruction
•  reversible with treatment or
spontaneously
•  Inflammation - causes
hyperresponsiveness to variable
stimuli
 Risk factors
•  Strongest risk factor: family history of atopic
disease ( 3x-4x)
•  Serum IgE
•  Low or high birth weight, high intake of salt
•  Prematurity
•  Maternal smoking during pregnancy
•  Parental smoking
•  obesity
 Risk factors
•  Fish oil: protective
•  Breast feeding: increase risk of allergies
and asthma
•  Outdoor air pollution : not a major risk
factor
•  Indoor house allergen
–  dust mite
–  cat dander
–  cockroach
 Pathophysiology
•  Disturbances clearly
seen during attacks
•  Narrrowing of the
airways: maximal in
small bronchi 2-5
mm in diameter
•  Consequences:
increase work of
breathing
 Pathophysiology

Normal airway

Airway during Post-mortem airways

acute attack
 Pathophysiology
•  Airway narrowingà affects gas
exchange
•  Severity of obstruction not uniform à
uneven blood flow à v/q mismatch
•  Arterial oxygen tension in acute severe
asthma: 60 and 69 mm Hg
 Pulmonary function testing
•  FEV1- most widely used and best
standardized test for airflow obstruction
•  Hallmark of asthma: 12% improvement
AND >200 ml improvement of FEV1 after
bronchodilator
•  FEF 25-75 – selective of obstruction of small
airways, a normal value makes asthma
unlikely
 History
•  Cardinal symptoms
–  Wheezing
–  chest tightness
–  shortness of breath
•  Precipitants
–  Exercise
–  exposure to allergens
–  viral respiratory infections
•  Day to day variability of symptoms
•  Cough
–  nonproductive,
nocturnal, chronic,
sometimes
persisting for years
•  Worsened
–  exercise, inhalation
of cold air, allergen
exposure, upper
respiratory infections
 Clinical Features
•  Sputum production: dominant symptom
•  Frequently misdiagnosed “ recurrent
acute bronchitis”
•  Clue: youth, family history of atopy,
symptoms of breathlessness and
wheezing
•  Marked predominance of eosinophilia in
sputum
 Physical Examination
•  Polyphonic expiratory wheezing (absence
does not indicate airflow obstruction )
•  Overinflation of thoracic cage
 Laboratory Studies
•  Peak flow and FEV1
•  Asthma recommended spirometry:
at the time diagnosis is made
change in the severity of symtoms
within 2 years in all cases
 Laboratory Studies
•  Measurement of bronchial responsiveness
highly sensitive
non specific
•  Elevated IgE levels
positive skin prick Supportive evidence of asthma
blood eosinophilia
 Goals of Asthma Management
•  Prevent chronic and troublesome symptoms
•  Maintain “normal” pulmonary function test
•  Maintain normal activity levels
•  Prevent recurrent exacerbations of asthma
•  Provide optimal pharmacotherapy with
minimal or no adverse effects
•  Meet patient and family expectations
 Short Term Relievers
•  Reverse
bronchoconstriction
•  Beta adrenergic agonist
–  albuterol, salbutamol
•  Relaxes airway smooth
muscle
•  Best delivered by
inhalation
 Bronchodilators
•  Beta-agonist
–  Salmeterol and formoterol- long acting
( >12 hours )
–  onset of action is slow
–  best use in combination w/ inhaled
corticosteroid
•  Anti-cholinergic
–  ipratropium bromide
–  Tiotropium – long acting
•  Methylxanthines (theophylline)
 Long Term Controllers
•  Improve overall asthma control
•  Do not relax airway smooth muscle but
reduce bronchial reactivity
•  Modulate ongoing inflammatory reactions
•  Inhaled corticosteroids
–  Oral or intravenous routes à acute attacks
–  Inhaler – for long term use
•  leukotriene receptor antagonist
•  putative inhibitors of mast cell degranulation
(cromolyn sodium)
 Long Term Controllers
•  Leukotriene receptor antagonist
–  Zafirlukast and montelukast
–  Orally
–  Effective in aspirin induce asthma
•  Theophylline
§  Inexpensive
§  Anti inflammatory effect
§  Induces histone deacetylase activity
§  Down regulating expression of inflammatory
genes
 Aims of Treatment of Acute Asthma
Exacerbations
ü  Relieve airway obstruction as quickly as
possible
ü  Relieve hypoxemia
ü  Restore lung function to normal as soon
as possible
ü  Plan avoidance of future relapses
ü  Provide a written action plan in case of
further exacerbations
 Acute Severe Asthma
•  Most common precipitant: respiratory viral
pathogen
•  Clues to life threatening attack:
–  Altered sensorium
–  Upright posture
–  Diaphoresis
–  Telegraphic speech
–  Cyanosis
–  Fatigue
–  pulsus paradoxus
–  intercostal retractions
–  PF < 25% of predicted <1.0 L
 Bronchiectasis
•  Pathologic irreversible dilatation of the
bronchi caused by destruction of the
bronchial wall, usually resulting in
suppurative infection in an obstructed
bronchus
•  Etiology
–  Most common cause – bacterial infection
–  Predisposing conditions
 Bronchiectasis
•  Clinical Features
–  Chronic cough production of purulent sputum
–  Recurrent chest colds or pneumonia
–  Hemoptysis
–  Pleuritic pain
•  Physical Examination
–  Rales over the area of involvement on
repeated examinations
 Bronchiectasis
•  Diagnostics
–  Chest radiography
–  High-resolution CT scan
•  Treatment
–  Antibiotics
–  Postural drainage
–  Immunization against influenza and pneumonia
–  Surgical resection
–  Bronchodilation
–  Oxygen therapy
Respiratory Failure
 Respiratory Failure
•  One of the most
common reasons
patient are admitted
to the ICU
•  In some ICU setting,
75% of patients
require mechanical
ventilation during their
stay
 Respiratory Failure
•  Can be categorized mechanically based
on pathophysiologic derangements in
respiratory function
–  Type I (Acute Hypoxemic)
–  Type II (Ventilatory Failure)
–  Type III (perioperative)
–  Type IV (hypoperfusion)
 Type I (Acute Hypoxemic)
•  Occurs when alveolar flooding and
subsequent intrapulmonary shunt
physiology occur
•  May be a consequence of pulmonary
edema, pneumonia or alveolar
hemorrhage
•  paO2 <
 Type II (Ventilatory Failure)
•  Occurs as a result of alveolar
hypoventilation and inability to effectively
eliminate carbon dioxide
•  Mechanisms
–  Impaired central nervous system drive to
breathe
–  Impaired strength with failure of
neuromuscular function
–  Increased loads on respiratory system
 Type III (Perioperative
Respiratory Failure)
•  Occurs as a result of lung atelectasis
•  Atelectasis occurs so commonly in the
peri-operative period
•  After GA, decrease in functional residual
capacity leads to collapse of dependent
lung units
 Type IV (Hypoperfusion)
•  Hypoperfusion of respiratory muscles in patients
in shock
•  Patients in shock suffers from respiratory
distress due to pulmonary edema, lactic acidosis
and anemia
•  In this setting, up to 40% of cardiac output may
be distributed to the respiratory muscle
•  Intubation and mechanical ventilation can allow
redistribution of the CO to vital organs while the
shock is treated
 Thank You
Thank You

“Whatever you do, work at it

with all your heart, as
working for the Lord, not for
men.”
- Colossians 3:23