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Chronic obstructive lung disease


Chronic bronchitis: daily productive cough for at least 3 months of the year for 2 consecutive years

Emphysema: anatomical alteration of the lung characterised by an abnormal enlargement of the airspaces distal to the terminal and respiratory bronchioles associated with destructive changes of the alveolar walls and capillary membranes

NB Most patients with COPD have features of both disease processes.


- primary pathophysiological change in lung mechanics is airflow obstruction leading to expiratory flow limitation. Results from loss of elastic recoil pressure and airway narrowing.
- airway resistance is increased by mucosal oedema and hypertrophy, secretions, bronchospasm, airway tortuosity and turbulence and loss of lung parenchymal elastic tissues supporting small airways
- expiratory flow limitation cannot be overcome by increased expiratory effort because this tends to compress the airways - a tendency which is exaggerated in patients with COPD
- if a patient with COPD needs to breath harder the only way he can do so is to increase inspiratory flow and increase lung volume. In fact, during exercise the patient increases both end-expiratory volume and inspiratory flow: both are critically dependent on inspiratory muscle action. (Increase in lung volume makes respiratory muscles less efficient because of shortened fibre length and mechanical disadvantage).
- ie although the load is essentially expiratory the compensation is essentially inspiratory
- combined with high respiratory drive (which exists in patients with acute respiratory failure and COPD) and poor mechanical advantage may result in inspiratory muscle fatigue. (Fatigue = inability of muscles to continue to develop the amount of tension generated before fatigue, no matter what the degree of stimulation)
- thought that development of inspiratory muscle fatigue is of central pathophysiological importance in the development of acute respiratory failure in these patients
- intrinsic PEEP opposes inspiratory muscles
- other factors exacerbating decreased neuromuscular competence:

  • depressed drive eg sedative induced, hypothyroidism
  • muscle weakness eg secondary to hypokalaemia and hypophosphataemia (latter present in approx 20% of patients with acute respiratory failure and COPD; exacerbated by methylxanthines, beta agonists, corticosteroids and diuretics)
  • malnutrition

- additional causes of increased load:

  • increased resistive load eg bronchospasm, upper airway obstruction
  • increased lung elastic load: eg pulmonary oedema, pneumonia, atelectasis
  • increased chest wall elastic load: eg obesity, pleural effusion, pneumothorax, abdominal distension
  • increased minute ventilation loads: even if work of each breath remains constant an increase in respiratory rate increases the load. Minute ventilation requirements increased by excess CO2 production (eg excessive carbohydrate feeding, fever) and increased VD/VT (eg PE, hypovolaemia, shallower breathing)

- management of these patients should be directed towards decreasing load and increasing neuromuscular competence
- pulmonary capillary bed loss from alveolar destruction and hypoxic pulmonary vasoconstriction lead to pulmonary hypertension, secondary vascular changes and ultimately cor pulmonale. Increased hypoxia during acute respiratory failure increases PA pressure and may precipitate RVF
- combination of airway obstruction, parenchymal disease and pulmonary circulatory disturbance leads to extensive V/Q mismatching and increased hypoxaemia
- shunting also increases hypercarbia
- increased dead space
- dynamic hyperinflation of lung

Clinical features

  • usually have a history of cigarette smooking
  • cough
  • dypsnoea
  • wheeze
  • prolonged expiration
  • barrel-chest
  • cyanosis
  • signs of pulmonary hypertension and cor pulmonale



  • Image
  • hyperinflation (characteristically on PA CXR dome of diaphragm is below 10th interspace posteriorly).
  • increased bronchial and peribronchial markings (chronic bronchitis).
  • patchy areas of hyperlucency and fibrosis, flat hemidiaphragms, attenuated vascular markings (empysema)

Lung function tests

  • FEV1/FVC < 0.75
  • decreased PEFR and FEV1
  • increased residual volume (chronic bronchitis),
  • increase in residual volume and total lung capacity with decreased diffusing capacity for carbon monoxide (emphysema)

Acute respiratory failure


  • viral infection
  • bacterial infection: especially H. influenzae, Strep pneumoniae. Other organisms include Pseudomonas aeruginosa, Strep. viridans, Moraxella catarrhalis, Mycoplasma pneumoniae
  • congestive cardiac failure: chronic hypoxia results in pulmonary hypertension and subsequent right heart strain and hypertrophy. RV muscle fibres interdigitate with those of the LV and thus RV dysfunction in patients with COPD may be associated with LV dysfunction
  • pulmonary embolus
  • sputum retention
  • pneumothoraces and bullae
  • sedation



  • antibiotics for those with purulent sputum
    • antibiotics probably more useful in patients with severe disease (eg those who require admission to ICU0
    • choice of agent should be based on local resistance patterns
    • many recommend cephalosporins, azithromycin or clarithromycin , or fluoroquinolones
  • systemic corticosteroids
    • reduce need for mechanical ventilation or death
    • shorten length of hospital stay
    • optimal duration of treatment unknown
      • GOLD report recommended 10 day course
      • 8 week course not superior to 2 weeks
      • 10 day course superior to 3 days
  • b 2 agonists
  • ipratropium bromide
    • some but not all data suggests combination with beta agonists better than either alone
  • aminophylline: reports of benefits are conflicting
  • avoid sedatives unless ventilated
  • diuretics


  • no clear consensus regarding how much oxygen to give
  • the argument for restricting the amount of oxygen the patient receives is based on the assumption that chronically hypercarbic patients are dependent on hypoxic respiratory drive. There is no good evidence to support this
  • the argument for completely correcting the patient's hypoxia is based on the fact that hypoxia can kill and the premise that the rise in Pco2 often seen in these patients is not due to hypoventilation.


  • GOLD report concluded that physical methods may be beneficial in patients producing >25 ml/day of sputum or with lobar atelectasis
  • no evidence that postural drainage alters outcome

Artificial ventilation

  • largely subjective
  • the following are ominous:
    • respiratory rate > 36
    • use of all accessory muscles
    • thoracoabdominal paradox
    • even minor mental state changes
    • patient's subjective sense of exhaustion
  • ABG used only to confirm clinical assessment
Mode of ventilation
  • Non-invasive
    • decreases need for invasive ventilation and may be associated with improved outcome
    • CPAP alone can reduce work of breathing in COPD during weaning and during sleep
    • BiPAP weaning may be better than weaning on pressure support via an ETT
  • Invasive
    • aim is to support ventilation while reversible components improve, to allow respiratory muscles to rest and recover without wasting and to minimize dynamic hyperinflation
    • use low tidal volumes (8-10 ml/kg), low minute ventilation ( 115 m//kg) and long expiratory times in SIMV mode. High inspiratory flows allow short inspiratory time and therefore longer expiratory time for any given respiratory rate but use is controversial. Has been shown to reduce dynamic hyperinflation and alveolar pressure and improve gas exchange
    • if higher minute ventilation is required for excessive hypercapnic acidosis the degree of dynamic hyperinflation and its effects should be determined before increasing ventilation
    • if dynamic hyperinflation is significant discourage spontaneous ventilation with heavy sedation. However if it is not excessive spontaneous ventilation should be encouraged. Low level CPAP may reduce the work of breathing in spontaneous breathing modes by facilitating triggering (NB avoid PEEP in controlled ventilation)
  • flow-based algorithm for inspiratory to expiratory cycling in pressure support mode may not be suitable for some patients with COPD. Many older ventilators cycle from inspiration to expiration in pressure support mode when the inspiratory flow rate falls to 25% of the peak inspiratory flow rate. This tends to occur early in patients with COPD with the result the ventilator cycles while the patient is still trying to breath in. A cut-off of 5% which is used in some newer ventilators may circumvent this problem


  • 60-75% of patients with COPD and acute respiratory failure are successfully weaned however 1 year survival is only 32-50%. NB these studies are relatively old and the ventilators used relatively basic
  • prognostic factors with regard to weaning:
  • FEV1 when well
  • premorbid exercise tolerance
  • severity of dyspnoea (premorbid)
  • serum albumin
  • age, sex, co-existing illness, Po2, Pco2, ECG findings, cause of respiratory failure not related to weaning outcome
  • prognostic factors with regard to 1 year survival:
  • FEV1
  • premorbid exercise tolerance
  • ? serum albumin
  • ? cor pulmonale
  • ? severity of dyspnoea

NB once the patient has been weaned duration of ventilation not related to 1 year survival

Further reading

Hall CS et al. Acute exacerbations in chronic obstructive pulmonary disease. Drugs,2003; 63(14):1481-8

Pauwels RA et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO global initiative for chronic obstructive lung disease (GOLD) workshop summary. Am J Resp Crit Care Med, 2001; 163:1256-76

Charles Gomersall December 1999


Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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