ADVERSE-EFFECTS OF HYPOXEMIA ON DIASTOLIC FILLING IN HUMANS

Citation
Ri. Cargill et al., ADVERSE-EFFECTS OF HYPOXEMIA ON DIASTOLIC FILLING IN HUMANS, Clinical science, 89(2), 1995, pp. 165-169
Citations number
28
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
01435221
Volume
89
Issue
2
Year of publication
1995
Pages
165 - 169
Database
ISI
SICI code
0143-5221(1995)89:2<165:AOHODF>2.0.ZU;2-I
Abstract
1. Abnormalities of myocardial relaxation may occur as a consequence o f myocyte hypoxia. We have therefore examined the effects of hypoxaemi a on right and left ventricular diastolic function in 10 healthy male subjects. 2. After resting to reach baseline haemodynamics, subjects w ere rendered hypoxaemic by breathing a variable nitrogen/oxygen mixtur e. Oxygen saturation (Sao(2)) was maintained at 85-90% for 20 min and then at 75-80% for a further 20 min. Haemodynamic and diastolic fillin g parameters were measured noninvasively at baseline and at the end of each period of hypoxaemia. 3. Diastolic filling of both ventricles wa s significantly impaired by hypoxaemia. In comparison with baseline, l eft ventricular isovolumic relaxation time and transmitral E-wave dece leration time corrected for heart rate were significantly prolonged at SaO(2) 75-80%: mean difference in corrected relaxation time, 9.8ms (9 5% confidence interval 1-19); mean difference in corrected deceleratio n time, 34 ms (95% confidence interval 11-56). Similarly, right ventri cular isovolumic relaxation time and transtricuspid E-wave deceleratio n time were significantly prolonged at Sao(2) values of 75-80% compare d with baseline: mean difference in relaxation time, 20.3 ms (95% conf idence interval 3-38); mean difference in deceleration time, 33 ms (95 % confidence interval 11-55). 4. During hypoxaemia there were dose-rel ated increases in heart rate, cardiac output and mean pulmonary artery pressure, but no effects on mean arterial pressure. 5. Hypoxaemia sig nificantly impairs relaxation of left and right ventricles in normal h umans, These changes may reflect impairment of intracellular calcium t ransport secondary to the effects of myocyte hypoxia.