Coupon Accepted Successfully!


Chronic obstructive pulmonary disease (COPD) 

Definitions COPD is a common progressive disorder of airway obstruction (FEV1 <80% predicted; FEV1 /FVC <0.7) with little or no reversibility Q.


Basic physiology:


During an obstruction in airways, there is decrease in expiratory flow which become were pronounced when expiration is more forceful.


The major site of increased resistance in most individuals with COPD is in airways 2 mm diameter. (Ref. Hari. 18th ed.,  Pg- 2154)


Chronic bronchitis

  1. It is defined clinically Q as cough, sputum production on most days for 3 consecutive months of, 2 successive years Q.
  2. FEV1 reduced, MMEFR reduced, Increase RV, Normal diffusion capacity.

REID INDEX – Ratio of the thickness of submucosal glands to that of the bronchial wall.


Normal 0.44 ± 0.09 in chronic bronchitis 0.52 ± 0.08


Extra Edge:

Reid index is increased in chronic bronchitis.




Definition: It is defined histologically Q as enlarged air spaces distal to terminal bronchioles, with destruction of the alveolar walls.


Pathology– Permanent and destructive enlargement of airspaces distal to the terminal bronchioles with out obvious fibrosis and with loss of normal architecture. 3 types

  1. Centriacinar – Central or proximal part of respiratory unit – acinus upper lobe involvement. Commonly seen in male smokers (MCQ).
  2. Panacinar – Uniform destruction of acinus. Lower zone involvement. It is associated with α1 – AT deficiency (MCQ).
  3. Paraseptal – Involvement of distal acinus. It is found near the pleura and often causes pneumothorax. 

Compensatory emphysema – Normal lung tissue undergoes hyperinflation as a compensatory mechanism in response to the damage occurring in part of the same lung or opposite lung.

Alveolar septa are preserved. In emphysema VC, DLCO, TLC, FEV1, FVC. (LQ 2012)


Important Points:

  1. Pink puffers (Emphysema) and blue bloaters (Chronic bronchitis) (Two Ends of a spectrum)
    1. Pink puffers have increase alveolar ventilation, a near normal PaO2 and a normal or low PaCO2.
    2. They are breathless but are not cyanosed.
    3. They may progress to type 1 respiratory failure.
  2. For chronic bronchitis.
    1. They are cyanosed Q,
    2. Blue bloaters have reduced alveolar ventilation, with a low PaO2 and a high PaCO2. (Type II respiratory failure)
    3. Their respiratory centres are relatively insensitive to CO2.
    4. They rely on hypoxic drive to maintain respiratory effort so supplemental oxygen should be given with care so always give low flow oxygen. 

Important Points: Both Chronic bronchitis and emphysema patient may go on to develop cor pulmonale Q.


There are two types of emphysema that cause clinically significant airflow obstruction:


Panacinar emphysema

Centriacinar emphysema

Acini are uniformly involved from level of respiratory bronchiole to terminal blind alveoli

Central or proximal parts of acini formed by respiratory bronchioles are affected whereas distal alveoli are spared

Lesions are more common in lower zone and bases

Lesions are more severe and common in upper lobes

Occurs in association with α1 antitrypsin deficiency

Occurs predominantly in smokers

Is the commonest pattern.



  1. Airflow limitation 
  2. Hyperinflation
  3. Cachexia – It causes weight loss a classical feature of emphysema due to Increase TNF α
  4. Muscle dysfunction – Proximal limb girdle ms. are usually affected due to.
    Protein loss, malnutrition, glucocorticoid use.

Clinical features Symptoms: Cough, sputum, dyspnea, and wheeze.

Chronic bronchitis patients are usually obese Q whereas weight loss Q is the feature of emphysema.


Signs :

  1. Tachypnea; use of accessory muscles of respiration; hyperinflation
  2. Decrease crico sternal distance (<3cm)

Important clinical signs of emphysema:

  1. Barrel shape chest          
  2. Reduced area of cardiac dullness           
  3. Liver dullness shifted more down ward.
  1. Reduced chest expansion
  2. Resonant or hyperresonant percussion note
  3. Wheeze; cyanosis; cor pulmonale.
  4. Paradoxically inward movement of chest wall during inspiration (Hoover Sign) the result of alteration of the vector of diaphragmatic contraction on the rib cage as a result of chronic hyperinflation.
  5. Patients with severe airflow obstruction may also exhibit use of accessory muscles of respiration, sitting in the characteristic "tripod" position to facilitate the actions of the sternocleidomastoid, scalene, and intercostal muscles.
Important Points about emphysema
  1. Breathlessness (Dyspnea) is a characteristic presenting symptom
  2. Obstructive pattern is seen on PFT
  3. Diffusion of carbon monoxide is reduced (↓DLCO)
  4. Long term bronchodilator therapy does not improve lung function


  1. Acute exacerbations         
  2. Polycythemia Q (In ch bronchitis) 
  3. Respiratory failure
  4. Cor pulmonale Q                      
  5. Pneumothorax (ruptured bullae Q) (In emphysema)      
  6. Pulmonary artery hypertension Q (In ch bronchitis)


Pulmonary Hypertension in COPD has been attributed to multiple factors including:

  1. Hypoxia
  2. Pulmonary vasoconstriction (secondary to hypoxia)
  3. Acidemia​
  4. Hypercapnia

Mechanical effect of high lung volume of emphysema on pulmonary vessels

  1.  Loss of small vessels in vascular bed
  2.  Regions of emphysematous lung destruction 

Important Points: Lung function: obstructive + air trapping (FEV1 <80% of predicted, FEV1 / FVC ratio <0.7%.


Table: GOLD Criteria for COPD Severity Reference(Ref. Hari. 18th ed., Table 260.1 Pg- 2156)


GOLD Stage





At Risk

Chronic cough, sputum production




With or without chronic cough or sputum production

FEV1/FVC <0.7 and FEV1 80% predicted



With or without chronic cough or sputum production

FEV1/FVC <0.7 and, 

FEV1 50 to 80% predicted



With or without chronic cough or sputum production

FEV1/FVC <0.7 and, 

FEV1 30 to 50% predicted


Very Severe

With or without chronic cough or sputum production

FEV1/FVC <0.7 and FEV1 <30% predicted Or FEV1 <50% predicted with respiratory failure or signs of right heart failure


Important Points:



  1. Mild Antimuscarinic eg ipratropium or beta 2-agonist inhalation.
  2. Moderate Regular ipratropium or long-acting inhaled beta 2-agonist (salmeterol) + inhaled steroid (fluticasone)
  3. Severe Combination therapy with regular short-acting beta 2-agonist and anticholinergic.

The only three interventions that influence the natural history of COPD patients

  1. Smoking cessation
  2. Oxygen therapy in chronically hypoxemic patients
  3. Lung volume reduction surgery (in selected patients with severe emphysema)

Indications for surgery in EMPHYSEMA

  1. Recurrent pneumothorax
  2. Isolated bullous disease
  3. Lung volume reduction surgery (selected patients).

BODE Index is used for COPD Survival Prediction


BODE stands for Body mass index, airflow Obstruction, Dyspnea and Exercise capacity.


Recent Advances – New Drugs

  1. Bupropion is a non-nicotine agent that is indicated as an aid to smoking cessation.
  2. Varenicline is a nicotinic receptors agonist and is used for treating nicotine addiction. 

Obstructive sleep apnea syndrome


This disorder is characterized by intermittent closure/collapse of the pharyngeal airway which causes apneic episodes during sleep. These are terminated by partial arousal.


Sleep Apnea:

  1. By convention sleep apnea is defined by breath cessation for at least 10 seconds.
  2. Most patients with sleep apneas have cessation for 20-30 seconds. The duration of breath cessation may be as long as 2-3 minutes.
  3. Sleep apneas can be central or obstructive 


  1. Central sleep Apnea
    Sleep apnea occurs due to transient cessation of neural drive to all respiratory muscles
  2. Obstructive sleep Apnea
    Sleep Apnea occurs due to transient occlusion of the oropharyngeal airway despite continued respiratory drive.

Clinical features: The typical patient is a obese Q, middle-aged man (or a post. menopausal woman) who presents because of snoring or daytime somnolence Q.


Poor sleep quality

  1. Morning headache.
  2. Decreased libido
  3. Cognitive performance 

Important Points: - Complications of OSA

  1. Pulmonary hypertension;               
  2. Type II respiratory failure.  


  1. Polysomnography (which monitors
    1. Oxygen saturation,
    2. Airflow at the nose and mouth,
    3. ECG,
    4. EMG
    5. Chest and abdominal wall movement during sleep) is diagnostic.


  1. Weight reduction
  2. Avoidance of tobacco and alcohol
  3. CPAP via a nasal mask during sleep is effective
  4. Surgical procedures to relieve pharyngeal obstruction tonsillectomy, uvulopalatopharyngoplasty Q, or tracheostomy.

Primary Pulmonary Hypoventilation


Characterized by:

  1. Impaired chemoreception resulting in decreased ventilatory drive.
  2. Chronic hypercapnia and hypoxemia in the absence of identifiable neuromuscular disease or mechanical ventilatory impairment. 


  1. Mostly in males aged 20-50 years.
  2. Early: lethargy, fatigue, daytime somnolence, disturbed sleep and morning headache.
  3. Late: Cyanosis polycythemia, pulmonary hypertension, congestive heart failure.  

Important Points: Dyspnea is uncommon despite severe arterial blood gas derangements




The key diagnostic feature is respiratory acidosis in the absence of respiratory muscle weaknesses or impaired ventilatory mechanics.


  1. Bronchodilators such as beta-agonists, anticholinergic agents, and methylxanthines are helpful in treating patients with obstructive lung disease and severe bronchospasm.
  2. Treatment also is aimed at assisting ventilation

Test Your Skills Now!
Take a Quiz now
Reviewer Name