A B S T R A C T Right ventricular performance was studied relative to right coronary artery flow in the chloralose-anesthetized, open chest dog. The right coronary artery was cannulated for measurement and control of flow and pressure. Under control conditions, right coronary artery occlusion caused no change in cardiac output, or right and left ventricular pressures, although right ventricular contractile force fell markedly. With right coronary artery flow intact, incremental pulmonary artery obstruction caused a corresponding decline in cardiac output and elevation of right ventricular end-diastolic pressure with eventual total right ventricular failure and systemic shock. With right coronary artery occlusion, identical degrees of pulmonary artery obstruction resulted in more pronounced changes in cardiac output and right ventricular end-diastolic pressure with right ventricular failure occurring at a much lower level of right ventricular stress.However, with right coronary artery flow intact, the right ventricular decompensation induced by pulmonary artery obstruction, could be reversed by raising right coronary artery perfusion to levels above normal, thus increasing right ventricular performance and restoring cardiac output.We conclude that right ventricular failure and resultant systemic hypotension due to severe pulmonary artery obstruction can be reversed simply by right coronary artery hyperperfusion, and that, although a normally contractile right ventricular free wall is not essential to maintain cardiac performance at rest, during right ventricular systolic stress, over-all cardiac performance becomes increasingly dependent on the right ventricle. The data further imply that increased myocardial impingement on right coronary artery flow dur-
The effects of alterations in the diastolic filling pressure of the right ventricle on left ventricular (LV) geometry and filling pressure were studied in six isolated, supported canine hearts. This experimental preparation permitted graded increments in right ventricular (RV) end-diastolic pressure while LV cardiac output, heart rate, and mean aortic pressure were held constant. Endocardial radiopaque markers were placed in the ventricular septum, the anterior wall, the posterior wall, and the free wall in a plane perpendicular to the aortoapical axis. LV end-diastolic dimensions were recorded by x-ray cinematography at 60 frames/sec. The effects of varied RV end-diastolic pressure (0-16 mm Hg) on LV end-diastolic pressure and dimensions were studied at several LV cardiac outputs (780-2880 ml/min) and at several initial LV end-diastolic pressures (1-18 mm Hg). Increments of 5 mm Hg in RV end-diastolic pressure increased LV end-diastolic pressure 2.3 mm Hg. The septum-to-free wall distance decreased by 4.5% from the control distance, but the anterior-to-posterior dimension increased by 4.4%.Thus, LV end-diastolic pressure and LV end-diastolic dimensions were significantly related to RV end-diastolic pressure; LV end-diastolic geometry was increasingly distorted at elevated RV end-diastolic pressure. These data suggest that the high RV filling pressures that characterize certain diseases can secondarily alter LV filling pressures and geometry.
A B STR A C T The effects on myocardial mechanics of acute, artificial aortic and mitral regurgitation were studied in the dog to determine the manner in which the changes in load induced by valvular regurgitation alter ventricular performance. With mitral and aortic regurgitant volumes of approximately the same magnitude as the forward stroke volume, immediate increases occurred in total stroke volume, left ventricular enddiastolic pressure, and peak ejection velocity, whereas contractility remained unchanged. Although calculated myocardial fiber tension rose, the rate of decline of tension during ejection was accelerated with regurgitation due to the more rapid decrease in ventricular size. Average tension therefore decreased relative to average pressure. As a consequence of the increased fiber length and this unloading, contractile element velocity, work, and power were increased. Despite unchanged contractility of the myocardium, the ejection fraction rose with both aortic and mitral regurgitation.When regurgitant beats were compared with control beats at a constant end-diastolic volume, ventricular stroke volume, work, power, and ejection fraction, as well as contractile element velocity, work, and power consistently increased. Thus, reduction of instantaneous impedance to ejection allowed the ventricle to empty further, reducing ventricular wall tension with a resultant Received for publication 5 June 1967 and in revised form 14 November 1967. increase in the velocity of shortening. External energy output was increased despite unchanged contractility and diastolic fiber length. It is concluded that the impedance to ejection and myocardial fiber tension during ejection govern the velocity and extent of contractile element shortening, and hence affect stroke volume, peak aortic flow rate, and ejection fraction. The alterations of ventricular function accompanying valvular regurgitation can be explained by an evaluation of the effects of these lesions on the instantaneous impedance to left ventricular ejection.
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