Arterial oxygen desaturation after induction of anesthesia.

To the Editor:—Naguib et al. have presented a clinically relevant study of arterial saturation values after preoxygenation and different doses of suxamethonium, and discuss their results using the extensive reports relevant to this topic. Unfortunately, they perhaps did not search the published work back to times before the pulse oximeter was introduced. Before the pulse oximeter, the Hewlett Packard ear oximeter (Waltham, MA) was used to measure arterial oxygen saturation continuously. Although clumsy, it was accurate and gave reliable results. We used this device to be the first to report changes in oxygen saturation, measured continuously, at induction of anesthesia. We recorded arterial oxygen saturation in patients who were given thiopental and suxamethonium (although in greater doses than those used by Naguib et al.) and described the effects of preoxygenation. We showed convincingly that desaturation was more likely in obese patients and that even a small mask leak markedly impaired the efficacy of oxygenation. Naguib et al. suggested “shunting” as a reason for the hypoxemia they found, particularly in obese patients. This is not the most probable explanation. As they acknowledge, in anesthetized obese subjects, functional residual capacity is small, often close to residual volume, as shown in the study by Damia et al. In these circumstances, oxygen stores are small, and desaturation occurs more quickly as the small alveolar oxygen content decreases. This effect is shown clearly in the model predictions of Hardman et al. This model, which was more complete than the model studies considered by Naguib et al., showed much more rapid desaturation with a small functional residual capacity than with a greater pulmonary shunt.