Chronic obstructive pulmonary diseases are diffused lung diseases affecting the respiratory system for long term causing partial or complete obstruction in airflow even after forceful breathing that is not fully reversible.

 These are mainly classified as-

  1. Chronic bronchitis
  2. Emphysema

Common pathology-

  1. Chronic inflammation
  2. Number of mucus gland increases
  3. Goblet cells hyperplasia
  4. Decreased ciliary movement
  5. Lung parenchyma destruction
  6. Inhibit  function of alveolar macrophages

Chronic bronchitis(blue bloaters)-

It is clinically defined as excess tracheobronchial mucus production sufficient enough to cause persistent cough with expectoration on most days for at least 3 months of a year for more than 2 or more years consequently.

Blue bloaters- called so because of their bluish appearance of skin and lips due to lack of oxygen in spite of taking deeper and longer breaths.


  1. Simple chronic bronchitis-

In this type of chronic bronchitis mucoid sputum is produced.

  1. Chronic mucopurulent bronchitis-

In this type mucopurulent sputum is seen in absence of bronchitis or localised suppurative disease.

  1. Chronic obstructive bronchitis-

Dominant airway obstruction and marked by severe dyspnea and wheezing (similar to asthma)

  1. Chronic asthmetic bronchitis-

Long term continuous sputum production  with late onset of disease.


  1. Smoking- This is the major cause of copd.
Fig-Pathogenesis of COPD due to smoking
  1. Atmospheric pollution
  2. Occupational hazard
  3. Infection
  4. Familial and genetic factors
  5. Passive smoking

Clinical features-

  1. Insidious onset
  2. No family history
  3. History of smoking
  4. Cough with expectoration (start as attack of winter cough or smoking usually)
  5. Gradually increases
  6. More in winter and high atmospheric pressure
  7. Orthostatic cough and more in morning
  8. Sputum-
  • Infectious- yellow and mucopurulent sputum
  • Non-infectious- white and mucoid
  1. Dyspnea
  2. Wheeze
  3. Inspiration: expiration is 1:4 instead of 1:2


  • Respiratory failure
  • Cor pulmonale
  • Heart failure

Differential diagnosis-

  • Cystic fibrosis
  • Asthma
  • Tuberculosis
  • Bronchiolitis


  • Pulmonary function test
  • Graded exercise test
  • Chest X-ray


  • Smoking management
  • Drug therapy
  1. Antibiotics
  2. Corticosteroids
  3. Mucolytic agent- acetylcysteine
  • Oxygen therapy
  • Diuretics

Physiotherapy management-


  • Lifestyle modification
  • To clear airways
  • To improve breathing
  • To correct posture

1.Lifestyle modification-

  • Smoking cessation is the first and most important step in case of smoking induced copd.
  • Use of masks and other protective aids in polluted air especially in occupation induced copd like in workers of coal mines.
  • Keeping habitat clean and infection free as they are prone to acquire infection due to reduced immunity.
  • Taking a rich nutritive diet to improve healing.

2. To clear airways-

Due to overproduction of mucus, obstruction to airways creates difficulty in breathing.

1.Chest physiotherapy- 

  • Use of nebulizer or humidifier for humidification of thick secretions.
  • Suctioning by suction pump (if patient can’t remove actively)
  • Manual therapy techniques by trained physiotherapist- Percussion



  • Forced expiratory techniques-

Huffing ( to move secretions from peripheral to central airways)

Coughing ( to through secretions from larger airways to out from mouth)

  • Active breathing techniques-

Active cycle of breathing techniques (ACBT)

Autogenic drainage (AD)

Single, Double or triple cough along with deep breathing.

3. To improve breathing-

  • Deep breathing exercises
  • Thoracic expansion exercises
  • Pursed lip breathing (to relieve dyspnea)
  • Spirometry

4.To correct posture-

  • Biofeedback by correcting posture in front of mirror
  • Shoulder retraction and shoulder shrugging exercises
  • Shoulder blade squeeze
  • Cobra stretch
  • Diaphragmatic breathing to correct faulty breathing pattern

Emphysema (pink puffers)-

Emphysema is abnormal permanent dilation and destruction of airway distal to terminal bronchioles with destruction in their wall.

Fig-Relevant anatomical structures

Pink puffers – as there is destruction of walls of distal tend to breath fast to avoid collapse and so they have pink skin and are of lean mass due to overexertion.


  1. Anatomical type-
  2. Central
    • Central acinar emphysema (CAE)
    •  Centrilobular emphysema (CLE)
    • In this type only respiratory bronchioles are abnormally dilated having high ventilation:perfusion (V:Q) ratio whereas the peripheral part has decreased ventilation so low V:Q ratio.
    • Mainly caused due to smoking.
    • This is the most common type.

2. Paraseptal emphysema

  • Only distal portion that is alveolar ducts and alveoli are dilated
  • Also called as distal or peripheral emphysema
  • Least commonly from of emphysema
  • They generally do not cause obstruction in Airways
  • There may be blood formation which causes pneumothorax.

3. Total or pan acinar emphysema

  • All structures are dilated
  • These are caused due to Alpha 1 antitrypsin deficiency cigarette smoking or intravenous injection of oral ritalin
  • Seen in lower lungs mainly.

4. Irregular or mixed emphysema

  • There is no fixed pattern as the acinus is irregularly involved.
  • This is a combination of the above 3 types.
  • Generally seen around scar tissues.
  • Common types seen in autopsy.

b. Other types-

  1. Congenital/congenital lobar emphysema

Partial obstruction of the bronchus as there is only one lobe of the lung is distended.

  1. Unilateral/Swyer and James emphysema

Bronchial obstruction or bronchitis causes emphysema of one whole lung that interferes in development of lungs in childhood.

  1. Senile emphysema

There is decreased metabolic rate in elders so there is less healing and elastic recoil property of the airway is affected resulting in airspace dilation.

  1. Compensatory emphysema

When one part of the lung is out of function, the other part has to work more to compensate for its function resulting in damage to the Airways causing compensatory emphysema.

  1. Generalized bilateral hypertrophic emphysema

Both lungs are involved and survival is difficult in active breathing so require ventilatory support.


  • Smoking
  • Pollution
  • Occupational ha hazards
  • Infection
  • Alpha-1 antitrypsin deficiency
Fig- Etiopathology of Emphysema


Clinical features-

  • Progressive dyspnea which is initially only present on exertion but as disease progress occurs at rest too.
  • Drowsiness
  • Headache
  • Cough with expectoration is present if there is infection or chronic bronchitis along with emphysema
  • Barrel chest deformity-

Anterior posterior diameter becomes equal to transverse diameter and chest is fixed in full inspiration, further elevation is only by accessory muscles.

Download movement of trachea during systole called “tracheal tug” is present.

  • Abnormal respiratory pattern-

Fish like inspiration followed by forceful expiration to prevent early closure of alveoli.

  • They used to attain specific COPD posture having thoracokyphosis and rounded shoulders.
Typical COPD posture
  • Due to such posture there is increase in thoracic pressure so the jugular vein is felt in expiration.
  • Vocal fremitus is absent.
  • Tachypnoea
  • Nocturnal hypoxia


  • Papilloedema
  • Cor pulmonale
  • Respiratory failure


  • GOLD criteria( Global initiative in obstructive lung disease)
  • History of smoking
  • History of asthma
  • Family history of copd


  • Pulmonary function test
  • Chest X-ray
  • Blood investigation
  • High resolution ct scan
  • Sputum examination
  • ECG


  • Lifestyle modification
  • Physiotherapy management-
  1. Lifestyle modification
  2. Maintain tracheobronchial hygiene
  3. Improve breathing pattern
  4. To correct posture
  1. Lifestyle modification-

Due to abnormal posture and incorrect breathing pattern they tend to have breathlessness with activity, restricting them from leading a normal life. This can be resolved by lifestyle modification such as-

Stair climbing- Inhale while taking the first step then exhale during the second step and can maintain exhalation till third step in later stages. This will reduce the load of breathing making it easy to climb up.

  1. Maintain tracheobronchial hygiene-

Active physiotherapy-

  • Active cycle of breathing technique(ACBT)
  • Autogenic drainage(AD)
  • Forced expiratory technique

Active assisted physiotherapy-

These are of 2 types

  1. Manually assisted
  2. Mechanically assisted
  3. Manual assistance-
  • Neurophysiological facilitation of respiration
  1. Mechanical assistance-
  • Positive end expiratory mask
  • Flutter

Passive physiotherapy-

  • Postural drainage
Fig- Postural Drainage
  • Manual hyperinflation
  • Airway suction
  • Percussion, vibration, shaking and compression
  • Nebulizers, humidifier and bronchodilator
  1. Improve breathing pattern-
  • To improve breathing pattern firstly the use of accessory muscles should be ceased by upper limb exercises along with respiratory training. This forces the diaphragm to work and reduce use of accessory muscles.
  • Proper positioning- position the patient in such a way that abdominal contents exert upward force on diaphragm giving it stimuli for activation, high side lying is most useful in respiratory training.
  • Respiratory muscle training- Incentive spirometry, Glossopharyngeal breathing, respiratory muscle training devices like Intermittent positive pressure breathing (IPPB) and periodic continuous positive airway pressure (PCPAP).
  • Thoracic expansion exercises.
  1. To correct posture
  • Joint restrictions- Passive mobilisation of cervical and thoracic apophyseal , costochondral and costotransverse joints by the physiotherapist or self mobilisation exercises.
  • Posture correction by visual, auditory and sensory feedback
  • Lengthening, shortening and strengthening of appropriate muscles.
  • Motor re-education- holding and maintaining various postures along with postural perturbation and electrical stimulation for neural tissue provocation. 


  • Jennifer A. Pryor and Barbara A. Webber ( Physiotherapy for respiratory and cardiac problems)
  • Praveen Kumar and Michael Clark ( Clinical medicine)
  • Nicki R. Colledge, Brian R. Walker and Stuart H. Ralston ( Davidson’s principles and practice of medicine )
  •  J. Larry jamson, Anthony S. Fauci, Dennis L. Casper, Stephen L. Hauser, Dan L. Longo and Joseph Loscalzo (Harrison’s manual of medicine)
  • Lee Goldman and Andrew I. Schafer ( Goldman – Cecil medicine)
  • Harsh Mohan ( Textbook of pathology)