Left ventricular systolic performance during acute hypoxemia.

Abstract

STUDY OBJECTIVE: Although some of the cardiovascular responses to hypoxemia are well described, effects on myocardial contractility have not been defined. Such effects are readily assessed by noninvasive techniques and we have therefore evaluated Doppler-phonocardiographic parameters of systolic left ventricular contractility in normal humans rendered hypoxemic. DESIGN: Eight healthy male volunteers were studied. Parameters were measured after resting to achieve baseline haemodynamics, after 20 min moderate hypoxemia (SaO2 85 to 90%), and after a further 20 min of severe hypoxemia (SaO2 75 to 80%). Hypoxemia was induced by breathing a variable N2/O2 mixture. MEASUREMENTS: Pulsed-wave Doppler analysis of ascending aortic blood flow was combined with phonocardiography to measure indices of systolic left ventricular function at baseline and at the end of each period of hypoxemia. RESULTS: There was a significant, dose-related increase in cardiac output in response to hypoxemia, from 5.5 +/- 0.26 L/min at baseline to 6.1 +/- 0.08 L/min during moderate hypoxemia and to 7.0 +/- 0.23 L/min during severe hypoxemia. Likewise, heart rate increased significantly in dose-related fashion although stroke volume was not affected by either level of hypoxemia. Hypoxemia had no significant effects on systolic or diastolic blood pressures, but caused a significant reduction in systemic vascular resistance. Aortic peak and mean acceleration and acceleration time were not affected by moderate or severe hypoxemia. Although the systolic time intervals measured shortened significantly during severe hypoxemia, these were no longer significant when appropriate corrections were made for heart rate. CONCLUSIONS: Although cardiac output increases during hypoxemia, this is due to increases in heart rate but not to any effect on stroke volume. Parameters of left ventricular systolic function and myocardial inotropic state were also not affected by severe hypoxemia. Systolic left ventricular function and myocardial contractility are thus well preserved in normal humans during hypoxemia.