• K G Hickling.
• Department of Intensive Care, Christchurch Hospital, New Zealand.
• Clin Intensive Care. 1992 Jan 1;3(2):67-78.

AbstractMany animal studies have demonstrated that mechanical ventilation with high peak inspiratory pressures (PIP) can result in a form of acute lung injury closely resembling ARDS, ie characterised by hyaline membranes, granulocyte infiltration, increased pulmonary and systemic vascular permeability, and eventually proliferation of fibroblasts and type II pneumocytes. These studies have led to a concern that, in some patients, orthodox ventilatory management in severe ARDS may result in additional lung injury and, possibly, remote organ dysfunction. Mortality may be increased as a consequence. In an attempt to avoid such ventilator-induced lung injury in severe ARDS, several modifications of ventilatory management have been evaluated. We have previously reported the technique of low volume pressure limited ventilation with permissive hypercapnia, using tidal volumes of 5-7 ml/kg and allowing the PaCO 2 to rise substantially (maximum PaCO 2 17.2 kPa [129 mmHg]), mean maximum 8.3 kPa [62 mmHg]). In an uncontrolled study the mortality was significantly lower than that predicted by Apache II (16% vs 39.6%, p less than 0.01). Acute hypercapnia can cause many physiological disturbances but most of these appear to be due to the resulting intracellular acidosis and should not occur in hypercapnia of gradual onset, allowing the intracellular pH to be normalised. The time scales for compensation of intracellular and extracellular acidosis are markedly different. However, even severe acute hypercapnia appears to be remarkably well tolerated. Several clinical studies suggest that the avoidance of high PIP may reduce mortality in ARDS, but a randomised trial will be required to establish whether pressure limitation and permissive hypercapnia do improve outcome.

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