CanadasummwRY The effects of progressive isocapnic hypoxia on the systolic time intervals were studied in 10 healthy human subjects. We induced hypoxia by a rebreathing method and monitored the arterial oxygen saturation continuously and non-invasively by means of an ear oximeter. Arterial oxygen saturation (Sao2) was allowed to fall to a level of 75 per cent and was then held constant for five minutes. As SaO2 fell, heart rate increased linearly, with a mean increase of 0-83 beats/min per one per cent fall in SaO2. The pre-ejection phase index decreased from a mean of 127x2 ms at full oxygen saturation to 120x1 ms at steady-state hypoxia levels, while the ratio of the pre-ejection phase to left ventricular ejection time decreased from a mean of 0 330 to 0-301. The left ventricular ejection time index increased from 417-4 ms to 429-3 ms, while no statistically significant difference was found in the length of electromechanical systole.The use of systolic time intervals (STI) is a wellestablished method for assessing cardiovascular function non-invasively (Weissler and Garrard, 1971a, b;Lewis et al., 1977;Weissler, 1977). As hypoxia is common in clinical practice, its effect on systolic time intervals (STI) has received considerable attention, but the reported findings are conflicting, as the duration of hypoxia was variable, and in most studies the Pco2 was allowed to vary, making it difficult to assess the effect of hypoxia alone. We recently reported the effect of acute, progressive hypoxia on heart rate in healthy subjects using a technique that enabled us to study physiological responses independent of changes in Pco2 (Slutsky and Rebuck, 1978). We found that heart rate was best fitted to an inverse linear relation to arterial oxygen saturation and a power function to Po2. The purpose of the present study was to extend these findings, determining whether the tachycardia induced by isocapnic hypoxia was associated with changes in electromechanical systole.
SubjectsTen subjects (5 men, 5 women), aged 24 to 40, who were staff members of Toronto General 'Present address: Pulmonary Division,