Physiology of apnoea and the benefits of preoxygenation

Abstract

This article will concentrate on factors that accelerate or delay the onset of severe hypoxaemia during apnoea (Fig. 1). In the anaesthetized patient, the oxygen consumption (VO2) remains fairly constant at 250 ml min. This is delivered to the tissues by haemoglobin whose oxygen is then replenished, on return to the pulmonary circulation, by the diminishing store of oxygen within the lungs. The alveolar partial pressure of oxygen (PAO2) decreases steadily, not only because the oxygen is being removed from the lungs but also because this oxygen removal generates a substantial negative intrathoracic pressure if the airway is obstructed. Although the arterial partial pressure of oxygen (PaO2) decreases in direct relation to the PAO2, the arterial haemoglobin oxygen saturation (SaO2) remains .90% as long as the haemoglobin can be re-oxygenated in the lungs. The SaO2 only starts to decrease when the store of oxygen in the lungs is depleted and the PaO2 is of the order of 6–7 kPa. Its subsequent decline is of a constant and rapid nature, about 30% every minute. At the start of this rapid decline, the SaO2 is still 90–95%. This inflection point we will define as ‘critical hypoxia’. It is for this reason that oximetry is not a good tool for predicting impending severe hypoxaemia. However, because oximetry detects the decrease in SaO2 before any clinical signs are apparent, it has proved invaluable in detecting critical situations and has helped improve clinical practice to avoid these situations. Various factors significantly influence the time period from the onset of apnoea to critical hypoxia.