LEFT-VENTRICULAR SYSTOLIC PERFORMANCE DURING ACUTE HYPOXEMIA

Citation
Ri. Cargill et al., LEFT-VENTRICULAR SYSTOLIC PERFORMANCE DURING ACUTE HYPOXEMIA, Chest, 108(4), 1995, pp. 899-902
Citations number
21
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
108
Issue
4
Year of publication
1995
Pages
899 - 902
Database
ISI
SICI code
0012-3692(1995)108:4<899:LSPDAH>2.0.ZU;2-S
Abstract
Study objective: Although some of the cardiovascular responses to hypo xemia are wed described, effects on myocardial contractility have not been defined. Such effects are readily assessed by noninvasive techniq ues and we have therefore evaluated Doppler-phonocardiographic paramet ers of systolic left ventricular contractility in normal humans render ed hypoxemic. Design: Eight healthy male volunteers were studied, Para meters were measured after resting to achieve baseline haemodynamics, after 20 min moderate hypoxemia (SaO(2) 85 to 90%), and after a furthe r 20 min of severe hypoxemia (SaO(2) 75 to 80%). Hypoxemia was induced by breathing a variable N-2/O-2 mixture. Measurements: Pulsed-wave Do ppler analysis of ascending aortic blood flow was combined with phonoc ardiography to measure indices of systolic left ventricular function a t 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 d uring moderate hypoxemia and to 7.0+/-0.23 L/min during severe hypoxem ia, Likewise, heart rate increased significantly in dose-related fashi on although stroke volume was not affected by either level of hypoxemi a. Hypoxemia had no significant effects on systolic or diastolic blood pressures, but caused a significant reduction in systemic vascular re sistance, Aortic peak and mean acceleration and acceleration time were not affected by moderate or severe hypoxemia. Although the systolic t ime intervals measured shortened significantly during severe hypoxemia , these were no longer significant when appropriate corrections were m ade for heart rate. Conclusions: Although cardiac output increases dur ing hypoxemia, this is due to increases in heart rate but not to any e ffect on stroke volume. Parameters of left ventricular systolic functi on and myocardial inotropic state were also not affected by severe hyp oxemia, Systolic left ventricular function and myocardial contractilit y are thus well preserved in normal humans during hypoxemia.