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Mechanical ventilation

Acute respiratory distress syndrome


Consensus conference definition:

  • acute onset
  • a condition known to be associated with the development of ARDS
  • bilateral infiltrates on frontal CXR
  • PAWP <18 if measured or absence of evidence of LA hypertension if not
  • PaO2/FiO2 <200 mmHg (26 kPa)

Definition of acute lung injury is the same except the severity of gas exchange impairment is less (PaO2 <300 mmHg)


  • Not well studied. Best estimate is about 3/100000/year with a mortality of about 60%
  • <20% of deaths are due to refractory respiratory failure


Develops very soon after the precipitating event. Usually within 12-72 hours and often within 6 hours


  • probably part of a systemic problem that is manifested in lung
  • all aetiologies eventually lead to clinically similar responses and injury of both epithelium and endothelium of lung. However it is conceptually useful to consider 2 separate main mechanisms of injury: a direct insult to the lung (primary ARDS) and the effects of systemic inflammatory response on the lung (secondary ARDS)
  • result of a complex interaction between:
    • pro- and anti-inflammatory mediators
    • resolution of inflammation as a result of apoptosis
    • activation of coagulation cascade
    • genetic pre-disposition
    • mechanical injury from mechanical ventilation
    • poor function of mechanisms responsible for clearing exuded fluid from lungs

Effects on cardiac function

  • increased pulmonary vascular resistance results in increased right ventricular load. Cardiac output is maintained by an increase in RV stroke work, pressure and volume until RV failure develops (rare)
  • RV failure results in decreased LV output because of decreased LV preload. Also ̃ back pressure on systemic venous and portal venous systems
  • LV function is depressed in septic shock

Multi-organ failure

  • common "complication" of ARDS
  • incidence of organ failure in ARDS:
    • renal 40-55%
    • hepatic 12%
    • CNS 7-30% (confusion, coma, agitation, fits)
    • GI failure 7-30% (haemorrhage, ileus, malabsorption, acalculous cholecystitis, pancreatitis)
    • haematological 0-26% (WBC < 1, platelets < 50, fibrinogen < 0.1 g/dl)
    • cardiovascular 10-23% (cardiac index < 2 l/min/m2 or MAP < 60 mmHg or reversible VF or asystole)
  • mortality closely related to number of organ systems involved. Varies from 15-30% for lung alone to > 80% for three or more organs.
  • not clear whether multiple organ failure is a consequence of ARDS or whether ARDS is simply one manifestation of a more widespread disease process that shows itself in the lung first because of the immediate requirements for gas exchange. Current evidence favours the latter hypothesis.

Extracorporeal membrane oxygenation (ECMO)

  • very expensive
  • not associated with improved survival

Drug treatment

No treatment has been shown conclusively to be of benefit in ARDS

Cyclo-oxygenase inhibitors

  • NSAIDs, especially ibuprofen improve shock and acute lung injury in models of sepsis
    - trend towards increased thoracic compliance and decreased airway pressures in patients with sepsis syndrome treated with ibuprofen but not statistically significant
  • Antagonism of thromboxane with ketoconazole not found to be useful in multi-centered randomized controlled trial


  • Not useful in the acute management of ARDS
  • May be of value in ARDS variants such as fat embolism
  • Have been suggested as potential treatment for later "fibroproliferative" phase. Very limited clinical data suggests that there may be a benefit.

Nitric oxide

- inhaled nitric oxide (40 ppm in air) reduces pulmonary hypertension and in concentrations of 15-20 ppm decreases shunting and improves gas exchange in ARDS by preferentially increasing blood flow to ventilated areas of the lung
- no systemic effects because nitric oxide scavenged rapidly by Hb
– 3 clinical trials have failed to show evidence of improved outcome in patients treated with NO


  • inhaled prostacyclin vasodilates as effectively as NO but does not confer as much oxygenation benefit


  • controlled trial of artificial surfactant failed to show an improvement in outcome. However this was probably due to the fact that the delivery system resulted in the surfactant being denatured

Cardiovascular management

  • treatment aimed at reducing pulmonary capillary hydrostatic pressure causes a reduction of pulmonary oedema formation in animal models of ARDS. There is also some evidence to suggest that protocols which lead to negative fluid balance improve outcome.
  • however patients with severe ARDS may have decreased ventricular compliance and preload reduction in these patients puts them at particular risk of falls in cardiac output and oxygen delivery
  • in severe ARDS PEEP may decrease RV output by increasing RV afterload. Maintenance of RV output is usually achieved through the use of inotropes and increasing preload. An alternative is to decrease RV afterload with PGE1 or prostacyclin but this approach is limited by systemic hypotension and increasing shunt fraction. Inhaled nitric oxide promising.


  • immediate prognosis related to number of organ systems involved:
    • lung only 15-30% mortality
    • 2 organs 45-55%
    • 3 or more > 80%

This figure rises to 100% if the multiple organ failure persists beyond 4 days

  • outcome also varies with the cause of ARDS. 90% of patients with ARDS secondary to fat embolus survive whereas nearly 100% of patients with ARDS following bone marrow transplantation die.

  • death is not usually due to respiratory failure.

Further reading

©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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