STENOSIS AND INSUFFICIENCY 



659 



is also demonstrated by the behavior of the peripheral 

 and renal blood flow (106, 107). 



Sancetta & Kleinerman (174) studied the cardiac 

 output at rest and in exercise in nine patients with 

 aortic stenosis, seven of them in chronic left ventricu- 

 lar failure, indicated by increased pulmonary \ascu- 

 lar pressures. The cardiac index w as i .98 and 4.04 

 liters per min per ni- BSA in those not in failure, and 

 ranged from 1.58 to 2.35 liters per min per m- in 

 those in failure (wedge pressure 12 to 20 mm Hg) at 

 rest. On slight exercise (increase in oxygen consump- 

 tion 45 to I 10%) the cardiac output increased from 

 o to 43 per cent, less in those in failure. The brachial 

 arterial pressia-e ranged from 87/48 to 135/57 (one 

 patient had arterial hypertension 187/115) and 

 showed insignificant changes on exercise. Others have 

 reported similar findings (81, 88, 89). 



Pulsus alternans — varying systolic pressure from 

 beat to beat — has been taken as an indication of myo- 

 cardial failure. 



Cooper ('/ al. (39) studied 50 patients with aortic 

 stenosis (28 acquired, 22 congenital) by means of left 

 heart catheterization. Persistent left \entricular 

 pulsus alternans was observed in 15 patients with 

 acquired stenosis. Those patients more frequently had 

 congestive heart failure, angina pectoris, and cardio- 

 megaly, and their left ventricular systolic pressures 

 and left \entricular-aortic pressure gradients were 

 significantly higher. The hemodynamic parameter 

 (the blood flow was not determined) that afforded 

 the best separation of those patients with acquired 

 aortic stenosis and persistent pulsus alternans from 

 those without alternans, was the product of the left 

 ventricular systolic pressure and the heart rate. This 

 product closely correlated with the tension-time index, 

 which has been suggested to reffect myocardial 

 oxygen requirement. The authors suggest that a 

 disparity between the oxygen requirement of the 

 heart and the oxygen available to it can so alter 

 myocardial contractility as to result in alternation in 

 the strength of the ventricular contraction. 



Ferrer et al. (72), who studied the hemodynamics of 

 2 1 patients with pulsus alternans in the pulmonary 

 and/or systemic circulation, observed alternation in 

 only 4 patients with mitral valvular disease and i with 

 aortic. The authors found no consistent relationship 

 between the appearance or disappearance of pulsus 

 alternans and several other factors in these patients, 

 and particularly not with variations in stroke volume 

 and vascular pressures. There was no alternating 

 end-diastolic pressure, which one would expect if the 

 Starling law applies in these conditions. 



Aortic Incompetence 



The immediate effect of an acute aortic leak is a 

 reduction in the net stroke volume, a decrease of the 

 aortic pulse pressure, and an increase in the diastolic 

 ventricular volume. The myocardium usually re- 

 sponds at ooce to the greater initial length and ten- 

 sion with a more vigorous contraction. The total 

 stroke volume thus immediately increases consider- 

 ably. Of the blood ejected into the aorta, part reaches 

 the descending aorta, whereas part is regurgitated 

 back into the ventricle because of the larger pressure 

 gradient existing between the ventricular cavity and 

 the root of the aorta. This pressure gradient during 

 diastole is governed by the size of the leak and the 

 peripheral resistance, which thus also determines the 

 amount regurgitated. In the past it was believed that 

 most of the regurgitation occurred after the mitral 

 \alve opened and the ventricular cavity was filled 

 from the left atrium. As a consequence, it was con- 

 sidered that the competition between the forward and 

 backward flowing blood prevented any marked 

 regurgitation. In addition to the size of the leak, the 

 regurgitated amount is governed by the diastolic 

 time — the longer this is, the more time for equilibra- 

 tion of pressure between aorta and the ventricular 

 cavity. 



These considerations were put to an experimental 

 test by Wiggers & Maltby (203), w ho produced acute 

 aortic regurgitation in dogs. They found a typical 

 change of the lett ventricular pressure curve with an 

 increased end-diastolic tension, greater steepness, 

 larger amplitude, and higher systolic pressure during 

 the earlier systolic part of the curve, and a steep 

 decline late in systole, i.e., a true "systolic collapse." 

 This was thought to be due mostly to the lower 

 arterial resistance against which ejection began when 

 aortic incompetence was created. The increased total 

 systolic discharge, occurring as a result of the in- 

 creased initial tension, also played a part and was 

 responsible for the increase in the height of systolic 

 pressure. With these changes in pressures, most of the 

 systolic discharge occurred earlier in systole than it 

 did before the leak was created, causing the rapid 

 systolic collapse. 



Wiggers and Maltby also found that the greater 

 part of the decrease of pressure sometimes occurred 

 during isometric relaxation. In all but maximum size 

 leaks, this early diastolic decline of aortic pressure 

 occurred in two stages clearly separated by a halt and 

 change of pressure gradient. A considerable portion 

 of the backflow, increasing with the size of the leak. 



