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Effects of halothane, sevoflurane and propofol on left ventricular diastolic function in humans during spontaneous
M Filipovic1, J Wang, I Michaux
1Department of Anaesthesia and Medical Intensive Care Unit, University of Basel/Kantonsspital, CH-4031 Basel, Switzerland. miodrag.filipovic@public-health.oxford.ac.uk
Background:
There is limited knowledge of the effects of anaesthetics on left ventricular (LV) diastolic function in humans. Our aim was to evaluate these effects in humans free from cardiovascular disease.
Methods:
Sixty patients (aged 18-47 yr) who had no history or signs of cardiovascular disease were randomized to receive general anaesthesia with halothane, sevoflurane or propofol. Echocardiography was performed at baseline and during spontaneous respiration at 1 minimum alveolar concentration (MAC) of the inhalational agents or propofol 4 microg ml(-1) (step 1), and repeated during positive-pressure ventilation with 1 and 1.5 MAC of the inhalational agents or with propofol 4 and 6 microg ml(-1) (steps 2a and 2b). Analysis of echocardiographic measurements focused on heart rate corrected isovolumic relaxation time (IVRT(c)) and early diastolic peak velocity of the lateral mitral annulus (E(a)).
Results:
IVRT(c) decreased from baseline to step 1 in the halothane group (82 [95% CI, 76-88] ms and 74 [95% CI, 68-80] ms respectively; P=0.02), remained stable in the sevoflurane group (78 [95% CI, 72-83] ms and 73 [95% CI, 67-81] ms; n.s.) and increased in the propofol group (80 [95% CI, 74-86] ms and 92 [95% CI, 84-102] ms; P=0.02). E(a) decreased in the propofol group only (18.8 [95% CI, 16.5-19.9] cm s(-1) and 16.0 [95% CI, 14.9-17.9] cm s(-1); P=0.003). From step 2a to step 2b, IVRT(c) increased further in the propofol group (109 [95% CI, 99-121] ms and 119 [95% CI, 99-135] ms; P=0.04) but remained stable in the other two groups. E(a) did not change from step 2a to step 2b.
Conclusions:
Halothane and sevoflurane did not impair LV relaxation, whereas propofol caused a mild impairment. However, the impairment by propofol was of a magnitude that is unlikely to cause clinical diastolic dysfunction.
