658 



HANDBOOK OF PHVSIOLOGV 



CIRCULATION 



duced alone or in combination with aortic insuffi- 

 ciency, the anacrotic notch on the aortic curve was 

 separated from a synchronous vibration on the 

 ventricular curve by a pressure gradient. 



The changes of left ventricular contraction depend 

 on the degree of aortic narrowing. In mild degrees of 

 stenosis the ventricular pressure curves resemble 

 those produced by moderate augmentation of aortic 

 resistance; initial tension and the isometric pressure 

 gradient remain unaltered, but the pressure summit is 

 higher and displaced to a later moment of systole. 

 Isometric contraction is prolonged slightly, but the 

 total duration of systole is not affected. The extensive 

 experimental and clinical experience regarding the 

 pressure pulses in aortic stenosis can be appreciated 

 from the following papers: (22, 42, 68, 69, i 10, 153, 

 162, 164, 209, 213). 



As soon as the degree of stenosis becomes dynami- 

 cally significant the ventricular pressure curves are 

 more peaked. The pressure summit is reached earlier, 

 not later, in systole. When ventricular ejection is 

 seriously impeded, the ventricles approach an iso- 

 metric type of contraction in which the increased 

 residual volume and marked elevation of initial ten- 

 sion contribute to the production of high systolic 

 ventricular pressure. It is important to point out that 

 these experimental findings may differ considerably 

 from what is found in clinical aortic stenosis, where 

 the ventricular response is characterized by the grad- 

 ual narrowing of the orifice with marked myocardial 

 hypertrophy and by the relative degree of coronary 

 insufficiency due to unfavorable pressure circum- 

 stances in the aorta close to the coronary artery ostia. 



The aortic pressure curve, after the initial period of 

 rapid ventricular ejection, shows a diminished though 

 prolonged gradient of ascent, because of the impeded 

 blood flow through the stenosis. The central arterial 

 pressure curve vibrations correspond to the aortic 

 systolic thrill and murmur. All of these indicate the 

 obstruction to, and turbulence of, systolic blood flow 

 at the aortic orifice. The arterial systolic and pulse 

 pressure are typically decreased, and the diastolic 

 pressure normal or slightly elevated. When the pulse 

 pressure is narrow it may suggest severe aortic 

 stenosis. Unfortunately, as many authors have empha- 

 sized, it is often normal even when aortic stenosis is 

 severe. The radial pulse is usually of the flat, plateau 

 variety and delayed, "pulsus parvus et tardus." An 

 anacrotic wave is present in the peripheral arterial 

 pulse tracing. The anacrotic notch is the lower in 

 position, the greater the stenosis and the inpedance of 

 the systolic discharge. However, cases are reported 



with severe aortic stenosis, wliere the carotid pulse 

 was normal in every respect. 



The left atrial, pulmonary venous, and pulmonary 

 arterial wedge pressures may be typically altered in 

 aortic stenosis, presumably as a consequence of the 

 myocardial hypertrophy, impeding the inflow to the 

 left ventricle. Gorlin et al. (88, 89) have described an 

 increase of the amplitude of the a wave of the left 

 atrial pressure pulse. As a consequence, the pre- 

 systolic left ventricular tension is elevated. The atrial 

 pressure pulse may then be similar to what is found in 

 slight mitral stenosis in conformity with the findings 

 in the right side of the heart with the giant a wave in 

 pulmonary stenosis, simulating slight tricuspid nar- 

 rowing. The only way definitely to rule out valvular 

 changes in the atrioventricular valves, in the presence 

 of .severe semilunar valve stenosis with ventricular 

 hypertrophy influencing the atrial pressure trac- 

 ing, is through simultaneous pressure tracing from 

 the atrium and the ventricle, with determination of 

 the pressure gradients throughout the cardiac cy- 

 cle. 



Several studies have been published (81, 88, 89, 

 151, 174) regarding cardiac output, intracardiac and 

 vascular pressures in patients with aortic stenosis, 

 studied at rest. Cardiac output ranged from about 2 

 to 7.0 liters per min per m- BSA, with systolic ventric- 

 ular pressures up to almost 300 mm Hg, and the 

 pressure gradient over the aortic valve up to 180 mm 

 Hg. The calculated aortic valve area has varied from 

 0.3 to 1 .4 cm-. In cases with left ventricular fail- 

 ure the cardiac output was lower and the pulmonary 

 artery wedge or left atrial pressure markedly ele- 

 vated, as compared to those not in failure. 



In animal experiments the stroke and minute out- 

 put of the heart decrease as soon as the orifice is nar- 

 rowed by about 60 per cent. In contrast, the cardiac 

 output in human aortic stenosis is maintained within 

 normal limits until left ventricular failure super- 

 venes — then the cardiac output decreases markedly 

 together with an increase of the left atrial and pul- 

 monary vascular pressures usually giving rise to pul- 

 monary edema. Left ventricular hypertrophy, which 

 presumabh develops slowly, thus enables the heart to 

 keep up a normal stroke volume even in the face of 

 pronounced stenosis. This seems to constitute one of 

 the most important differences between aortic and 

 mitral stenosis — the atrial myocardium cannot com- 

 pensate for the narrowing of the orifice as effectively 

 as the \entricular myocardium. The maintenance of 

 an adequate blood flow even later in the course of 

 aortic \aKular disease, in contrast to mitral disease 



