A small proportion of patients in chronic Type II (hypoxaemic, hypercapnic) respiratory failure will develop apnoea if their central hypoxic drive is removed by supplemental oxygen. However, this is seldom (if ever) abrupt and a period of deterioration and increasing drowsiness will alert medical and nursing staff to consider either (i) FIO2 reduction if overall condition allows, (ii) non-invasive or invasive mechanical ventilation if fatiguing or (iii) use of respiratory stimulants such as doxepram. The corollary is that close supervision and monitoring is necessary in all critically ill patients.

A normal pulse oximetry reading may obscure deteriorating gas exchange and progressive hypercapnia.

Oxygen toxicity is described in animal models. Normal volunteers will become symptomatic after several hours of breathing pure oxygen. Furthermore, washout of nitrogen may lead to microatelectasis. However, the relevance and relative importance of oxygen toxicity compared to other forms of ventilator trauma in critically ill patients is still far from clear. Efforts should nevertheless be made to minimise FIO2 whenever possible. Debate continues as to whether FIO2 or other ventilator settings (e.g. PEEP, VT, inspiratory pressures) should be reduced first. The authors' present view is to minimise the risks of ventilator trauma.

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