Is PA-PWRmax truly a preload-independent index of myocardial contractility in anesthetized humans?
This study tested the hypothesis that the preload-adjusted maximal power index (PA-PWRmax) is a load-independent index of human myocardial contractility. Based on the ventricular pressure-volume relationship and derived from stroke work, the index is the product of instantaneous ventricular pressure and volume changes, divided by a correction term of end-diastolic volume (EDV2) or end-diastolic area (EDA3/2) to adjust for preload effects. Echocardiographic measures of instantaneous ventricular area change may be used to obtain PA-PWRmax noninvasively. We prospectively evaluated 28 human subjects undergoing cardiac evacuation before cardiopulmonary bypass procedures. Continuous peripheral arterial pressure, pulmonary arterial pressure, and echocardiographic views of the left ventricle in the transgastric short-axis view were recorded. Simultaneously gated instantaneous fractional shortening (FS) and PA-PWRmax indices were calculated, with FS = (EDA - ESA)/EDA and PA-PWRmax = [MAP (EDA - ESA)]/ EDA3/2, where ESA = end-systolic area and MAP = instantaneous mean arterial pressure. FS decreased uniformly with cardiac evacuation and decreasing pulmonary artery diastolic pressure (t = -5.4; 95% confidence interval, -10 to -0.046; p < 0.001), as did PA-PWRmax (t = -5.8; 95% confidence interval, -2.25 to -1.08; p < 0.001). FS and PA-PWRmax showed a strong downward correlation (r = 0.81). Unlike previous studies of autonomically denervated animals, our study did not find PA-PWRmax to be preload independent, perhaps because of the instantaneous homeostatic mechanisms of the human autonomic nervous system linking contractility to loading conditions.
Lester
Steven J
SJ
Adult Echo Laboratory, University of California, San Francisco, San Francisco, Calif, USA.
Shin
Henry
H
Lambert
A Stephane
AS
Miller
Joseph P
JP
Cahalan
Michael K
MK
Seeberger
Manfred D
MD
Foster
Elyse
E
Schiller
Nelson B
NB
D000768:Anesthesia, General; D002302:Cardiac Output / Q000502:physiology*; D006439:Hemodynamics; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D011446:Prospective Studies; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology*