Anesth Analg 2002;94:1421-1426
© 2002 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Propofol Alters Left Atrial Function Evaluated with Pressure-Volume Relations In Vivo
Franz Kehl, MD,
Tobias T. Kress,
Boris Mraovic, MD,
Douglas A. Hettrick, PhD,
Judy R. Kersten, MD,
David C. Warltier, MD PhD, and
Paul S. Pagel, MD PhD
Departments of Anesthesiology, Medicine (Division of Cardiovascular Diseases), and Pharmacology and Toxicology, Medical College of Wisconsin and the Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin; and Arrhythmia Management Research, Medtronic, Inc, Minneapolis, Minnesota.
Address all correspondence and reprint requests to Paul S. Pagel, MD, PhD, Medical College of Wisconsin, MEB-M4280, 8701 Watertown Plank Rd, Milwaukee, Wisconsin 53226. Address e-mail to pspagel{at}mcw.edu
The effects of IV anesthetics on left atrial (LA) function in vivo are unknown. We tested the hypothesis that propofol alters LA mechanics evaluated with pressure-volume relations in barbiturate-anesthetized dogs (n = 9) instrumented for measurement of aortic, LA, and left ventricular (LV) pressures (micromanometers) and LA volume (epicardial orthogonal sonomicrometers). LA myocardial contractility (Ees) and dynamic chamber stiffness were assessed with end-systolic and end-reservoir pressure-volume relations, respectively. Relaxation was determined from the slope of LA pressure decline after contraction corrected for peak LA pressure. LA stroke work and reservoir function were assessed by A and V loop area, respectively, from the steady-state pressure-volume diagram. LA-LV coupling was determined by the ratio of Ees to LV elastance. Dogs received propofol (5, 10, 20, or 40 mg · kg-1 · h-1) in a random manner, and LA function was determined after a 15-min equilibration at each dose. Propofol decreased heart rate, mean arterial blood pressure, and the maximal rate of increase of LV pressure. Propofol caused dose-related reductions in Ees, dynamic chamber stiffness, and Ees/LV elastance. An increase in V loop area and declines in LA stroke work, emptying fraction, and the active LA contribution to LV filling also occurred. Relaxation was unchanged. The results indicate that propofol depresses LA myocardial contractility, reduces dynamic chamber stiffness, maintains reservoir function, and impairs LA-LV coupling but does not alter LA relaxation in vivo.
IMPLICATIONS: Propofol depresses contractile function of left atrial (LA) myocardium, impairs mechanical matching between the LA and the left ventricular (LV), and reduces the active LA contribution to LV filling in vivo. Compensatory decreases in chamber stiffness contribute to relative maintenance of LA reservoir function during the administration of propofol.
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