66o 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



flowed back before the mitral valve opened. There 

 was thus really no competition for space in the left 

 ventricle between the regurgitated volume and the 

 inflow from the left atrium. The size of the leak was 

 the chief factor determining the decline of pressure 

 during isometric relaxation, and hence the degree of 

 regurgitation. Changes in heart rate, on the other 

 hand, did not seem to alter those factors. 



It was also demonstrated that increasing the pe- 

 ripheral resistance definitely increased the actual 

 volume of regurgitation. This followed the increase in 

 pressure gradient aorta to ventricular cavity during 

 diastole caused by the increased resistance. As long 

 as the myocardium was able to respond normally, this 

 increased the end-diastolic tension and thus the 

 systolic discharge. The final result was that the per- 

 centage of regurgitation remained unaltered. The 

 increased load imposed on the myocardium, when an 

 acute aortic leak was created, was reflected by in- 

 creased coronary blood flow and myocardial oxygen 

 consumption (195, 196). 



Moscovitz & Wilder (153) studied the pressure 

 pulses in tracings obtained by direct puncture of the 

 left atrium and ventricle, and of the aortic arch, 

 descending aorta and femoral artery in dogs, with 

 experimentally produced aortic lesions. Aortic insuffi- 

 ciency was created by partial evulsion of one aortic 

 cusp. They found that the characteristics of the aortic 

 pressure pulse in aortic insufficiency was a steep rise 

 to an early peak due to the high velocity of the ejected 

 blood, a steep fall in pressure with a lowered or 

 absent dicrotic incisure, and a widened pulse pressure. 

 At times a double-peaked or bisferious summit was 

 present. 



The isometric contraction phase of the ventricular 

 pulse was shortened because of the lowered aortic 

 diastolic pressure. During ejection the ventricular 

 pressure rose in a fashion parallel to that of the 

 aortic curve, with no detectable systolic gradient 

 between the two. The slope of left ventricular pressure 

 decline was unaff"ected unless the aortic leak was of 

 great magnitude. 



The anacrotic notch was a synchronous and super- 

 imposable event in the aortic and \entricular pulses 

 in the normal dog and in aortic insufficiency. 



As the normal central pulse was transformed into 

 the peripheral, the anacrotic shoulder rose to become 

 a primary peak. The systolic pressure increased, the 

 mean and diastolic pressures decreased, and the curve 

 was smoother as the pulse traveled towards the 

 periphery. This was found in normal and in aortic 

 \al\ular disease. 



Welch el al. (197) studied the effects of quantita- 

 tively varied experimental aortic regurgitation in a 

 specially constructed dog heart preparation. As 

 aortic regurgitant flow was increased, efTective 

 systemic flow decreased substantially. This was 

 always accompanied by a widening of pulse pressure 

 and a lower diastolic pressure. Calculated total 

 peripheral resistance rose as did the left \entricular 

 end-diastolic pressure, whereas mean left atrial pres- 

 sure exhibited only a slight elevation. The left 

 ventricular function curve (15, 175) was always 

 markedly depressed in the presence of aortic re- 

 gurgitation. These findings were in contrast to what 

 was found when mitral regurgitation was created 

 (29). It should be pointed out that in these studies the 

 heart rate was kept constant, thereby preventing the 

 modifying effect of changes in diastolic time. 



When mitral leaks were produced in the presence 

 of aortic regurgitation, the left ventricular end- 

 diastolic pressure fell, causing a further diminution 

 in both total and effective stroke volume beyond that 

 which had been produced by the aortic regurgitation 

 alone (fig. 5J. 



From these studies it was concluded that a compe- 

 tent mitral valve acts in two ways to protect the circu- 

 lation in the presence of aortic regurgitation. First, 

 it limits the ele\ation of left atrial and pulmonary 

 capillary pressures; second, it makes possible the 

 high left ventricular end-diastolic pressure, as a result 

 of which a more forceful ventricular contraction 

 occurs. 



The few clinical studies that have been made in 

 patients with aortic regurgitation tend to confirm these 

 findings. The common clinical observation that, once 

 left ventricular failure has occurred in patients with 

 aortic incompetence, the downhill course is rapid may 

 be explained as an effect of ventricular dilatation with 

 relative mitral incompetence. Thus, two debilitating 

 influences occur at the same time — myocardial failure 

 and mitral incompetence. 



Regan et al. (168) studied the influence of an in- 

 fusion of norepinephrine on eight patients with sub- 

 stantial aortic regurgitation (estimated to be about 

 61 per cent of aortic outflow). Norepinephrine 

 markedly increased total peripheral resistance and 

 pulmonary wedge pressure (from 8 to 29 mm Hg) 

 concomitant with a decrease in regurgitation — ■ 

 probably due to diminished diastolic pressure gradient 

 from the aorta to the left ventricle. In contrast to the 

 normals studied as controls, the heart rate did not 

 decrease and the pulmonary vascular resistance did 

 not increase. Whereas the small increment of left 



