Circulation, Vol 74, 1114-1123, Copyright © 1986 by American Heart Association
RM Lang, KM Borow, A Neumann and D Janzen
Systemic vascular resistance (SVR) is a frequently used clinical index of
left ventricular afterload. However, SVR may not adequately assess left
ventricular afterload (i.e., ventricular internal fiber load during
systole) since it reflects only peripheral vasomotor tone. In contrast,
left ventricular end-systolic wall stress (sigma es) reflects the combined
effects of peripheral loading conditions and left ventricular chamber
pressure, dimension, and wall thickness. To determine the relationship
between SVR and sigma es, left ventricular afterload and contractility were
pharmacologically altered in eight dogs instrumented with central aortic
microtip and Swan-Ganz thermodilution catheters. Left ventricular wall
thicknesses and dimensions were measured from two-dimensionally targeted M
mode echocardiograms. Aortic, right atrial, and left ventricular end-
systolic pressures as well as cardiac output were recorded. SVR and sigma
es were determined under control conditions as well as during infusions of
nitroprusside, methoxamine, dobutamine, and norepinephrine. Control data
acquired before each drug infusion were similar. When compared with
baseline values, SVR underestimated the magnitude of change in left
ventricular sigma es by 22% when afterload alone was decreased
(nitroprusside), 54% when afterload alone was increased (methoxamine), and
50% when afterload was decreased and contractility was augmented
(dobutamine). Most importantly, when afterload was minimally decreased in
association with augmented contractility (norepinephrine), SVR increased by
21% while sigma es fell by 9%. Thus, discordant changes in left ventricular
afterload (i.e., sigma es) and SVR can occur during pharmacologic
interventions. SVR is an unreliable index of left ventricular afterload,
reflecting only peripheral arteriolar tone rather than left ventricular
systolic wall force. This emphasizes the fact that a true measure of left
ventricular afterload must consider the interaction of factors internal and
external to the myocardium.
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