It is routine practice during general anaesthesia (GA) to administer more than the 21% oxygen in which we mostly spend our lives. It is essential to understand the physiology underlying this practice if we are to keep patients safe by avoiding both hypoxaemia and hyperoxia during GA. 1 Four pathophysiological changes occur, which explain the answer to the question posed in the title of this article.(i) Abnormal respiratory muscle activity Induction of GA is followed within seconds by profound relaxation of all skeletal muscles, to a much greater extent than seen with physiological sleep. The effects on airway muscles are well known to all anaesthetists, and artificial airways are used routinely to bypass this part of the respiratory tract. The spinal muscles relax, increasing thoracic spinal curvature; relaxation of intercostal muscles leads to a reduction in the cross-sectional area of the ribcage; and the diaphragm is displaced in a cephalad direction, particularly in dependent regions because of the weight of the abdominal contents. Together, these three changes to the chest cavity shape cause an immediate reduction in functional residual capacity (FRC) of 15e20% compared to the value when awake and supine. In effect, the patient takes a prolonged expiration as they lose consciousness and when breathing recommences, this is from a lower lung volume. The reduction in FRC is similar in patients breathing spontaneously and those whose lungs are ventilated artificially, and is much greater in obese patients. 2
(ii) Formation of atelectasisIn older patients, the reduced FRC may be less than the closing capacity and so airway collapse will occur throughout the lung. Even if FRC remains above the closing capacity, the changes in chest wall and diaphragm shape commonly result in direct compression of lung tissue in the caudal and dependent regions behind the diaphragm. This leads to atelectasis in 75e90% of patients, which is easily detected by CT. There is some evidence that use of oxygen 100% at various stages of GA may exacerbate the formation of atelectasis. Blood flow through atelectasis constitutes an intrapulmonary pathological shunt and will adversely affect arterial oxygenation. The amount of shunt through these areas varies between individuals and is likely to be influenced by the efficacy of their hypoxic pulmonary vasoconstriction reflex. 3 This becomes particularly important during one-lung ventilation. Increasing F I O 2 will have no effect on this situation as the extra oxygen does not reach these closed lung regions. Atelectasis can be reduced at induction by avoiding oxygen 100%: in one study the use of 80 or 60% oxygen before induction reduced the atelectasis area on CT scans by 76 and 96%, respectively, compared with oxygen 100%. 4 Alternatively, use of moderate amounts of CPAP (6 cm H 2 O) before induction of anaesthesia prevents atelectasis formation. 5 During maintenance of anaesthesia the use of PEEP helps to limit the amount of atelectasis that forms, but once formed, a recruitment manoeuvre wi...