Effects of Acute Valvular Regurgitation on the Oxygen Consumption of the Canine Heart

Abstract

The effects on myocardial oxygen consumption and mechanics of acute, simulated aortic and mitral regurgitation were studied in open-chest, anesthetized dogs to determine how changes in the mechanical performance of the ventricle alter oxygen consumption. When regurgitation was induced acutely with effective stroke volume (total stroke volume less regurgitant volume) and heart rate held constant, left ventricular end-diastolic volume, total stroke volume, the ejection fraction, left ventricular wall tension, and the extent of shortening of the contractile element and the circumferential fibers all increased. With volumes of regurgitation approaching effective systemic blood flow, oxygen consumption increased only moderately, despite the increases in tension and shortening. When valvular regurgitation was induced while peak ventricular wall tension was held relatively constant, stroke volume doubled and the extent of both contractile element and circumferential fiber shortening increased. Confeactile element work in generating tension was unchanged; that which led to fiber shortening increased substantially. Myocardial oxygen consumption did not increase significantly. Thus, marked increases in the efficiency of the contractile elements and myocardial fibers occurred. The low energy cost per unit of work expended in shortening as opposed to that used for tension development therefore allows the excess stroke volume of valvular regurgitation to be maintained at only a small added oxygen cost to the ventricle.ADDITIONAL KEY WORDS aortic insufficiency mitral insufficiency cardiac energetics contractile element work myocardial tension• Although the effects of valvular regurgitation on cardiovascular dynamics have been studied intensively for many years (1, 2), relatively little information is available concerning the effects of these lesions on myocardial energy requirements. Although acutely induced aortic and mitral regurgitation have been shown to increase myocardial oxygen consumption (MVO 2 ) (3-5), the mechanism by which these increases are mediated has not been defined. It has recently become possible to define From the Cardiology Branch, with greater precision the relative importance of the various determinants of M\ 7 O2. These include the tension developed by the myocardium (6-9), the contractility of the myocardium as reflected in the velocity of shortening of the unloaded fibers (V maj ) (9-12) and myocardial shortening against a load (7, 13-15). Also the effects of acutely induced, simulated, aortic and mitral valvular regurgitation on myocardial mechanics have been examined (16) and such an approach now permits an analysis of the effects of these lesions on MV0 2 . MethodsA bilateral thoracotomy was performed in 11 dogs (avg wt, 20.7 kg) anesthetized with sodium

Coronary Hemodynamics and Regional Myocardial Metabolism in Experimental Aortic Insufficiency

“…A current hypothesis is that flow is normally less in the subendocardium during systole due to this pressure gradient, but greater in the subendocardium during diastole due to autoregulation of flow by coronary resistance vessels (21) The previous studies raised an important question concerning the adequacy of subendocardial flow in aortic insufficiency, and one of the main purposes of the present investigation was to obtain information bearing on this question. It was felt that information on regional tissue flow would not permit a reliable assessment of the nutritional adequacy of such flow because oxygen consumption of the ventricle is reported to be increased in aortic insufficiency (14). Accordingly, metabolic data were sought that would reflect the balance between oxygen supply and demand in the inner and outer regions of the left ventricle in animals with aortic insufficiency.…”

Left Ventricular Response to Mitral Regurgitation

“…Almost a century ago, Evans and Matsuoka 23 found that increased flow work added little to the energy requirements of the heart. Later, Urschel and associates 24 demonstrated that myocardial oxygen consumption increased only minimally during experimental MR, despite a doubling of the total stroke volume. Thus, the LV response to acute MR includes an increase in preload, a decrease in afterload, an increased EF, and an increased total stroke volume.…”

Indications for surgery for aortic regurgitation

“…The Laplace law (wall stress = [pressure × radius]/2 × wall thickness) provides a useful framework for the understanding of hemodynamic changes in AR [4]. The acute volume overload forces the normal-sized LV to reach the limits of it preload reserve while imposing excessive afterload [5], resulting in marked increase in LV wall stress with resultant decrease in myocardial oxygen consumption [5,6]. This leads to acute afterload mismatch, causing acute depression in LV, ejection fraction (LVEF) [5].…”