446 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



Pressure -mm Hg 

 ISO 1— 



100 — I 



Jl 



_J I I i_ 



■< / second >- 



'5 cm 



FIG. 1 6. Simultaneously recoidcd aortic and radial-artery 

 pressure pulses in a 12 -year-old boy who had severe valvular 

 aortic stenosis. Note similarity of two contours, decreased 

 systolic pressure, anacrotism of radial pulse (lower tracing), 

 and absence of central postdicrotic wave of aortic contour 

 (compared with figure 15). 



maximum is greatly prolonged in both pressure pulses, 

 and the radial systolic pressure is less than the aortic 

 systolic pressure. 



The demonstrations by Katz et al. (145) that an 

 anacrotic incisura exists in the central pressure pulse, 

 and by Feil & Katz (loi) that the phenomenon occurs 

 in patients with aortic stenosis, suggested that the 

 turbulence started at the moment of the anacrotic 

 incisura is transmitted as a wave to the periphery. 

 Dow (81), who followed the changes in pressure 

 pulses in the aorta at various distances from the aortic 

 valve, concluded that so much resistance is developed 

 during early systole that the central pulse assumes an 

 anacrotic and tardus characteristic. Since the violence 

 of ejection is reduced, characteristics of the central 

 pulse are propagated more clearly to the periphery. 



The mechanisms responsible for the transformation 

 of pressure pulse contours during transmission to the 

 peripheral arterial system and the explanation of the 

 amplification of the systolic pressure remain obscure. 

 These appear to be related phenomena in the aortic- 

 radial and aortic-femoral systems and are difficult to 

 explain fully by a "standing-wave" hypothesis (198). 

 It is probable that these phenomena are related to the 

 resonant and damping characteristics of the arterial 

 system (158, 257). 



The central aortic pressure pulse in patients with 

 subvalvular aortic stenosis may appear normal, 

 whereas the peripheral arterial pulse contour may be 

 abnormal. In figure 17, pressure pulses obtained 

 during catheterization of the left side of the heart in 

 a patient with valvular stenosis are compared with 

 similar contours from a patient with subvalvular 



stenosis. Evidence of severe obstruction to left ventric- 

 ular outflow is present in both patients. The radial- 

 artery pulses are equally abnormal in contour. The 

 aortic contour in the patient with subvalvular aortic 

 stenosis resembles a normal contour to a surprising 

 degree. The postdicrotic wave on the aortic contour, 

 which suggests a normally functioning aortic valve in 

 the patient with subvalvular aortic stenosis, is absent 

 in the patient with valvular stenosis. These diagnoses 

 were confirmed surgically, and both lesions were 

 successfull)- corrected. Brachfeld & Gorlin (37) 

 found that the pulse contours in subaortic stenosis 

 were variable. They reasoned that a tight mem- 

 branous subvalvular stenosis would be hemodynami- 

 cally similar to the valvular aortic stenosis, but in 

 those cases of subvalvular stenosis in which the 

 muscular element is of the greatest significance a 

 somewhat different physiologic obstruction to flow is 

 obtained. With sudden opening of the aortic valve, 

 the violent systolic discharge subsequent to a period 

 of isometric contraction allows a normal percussion 

 wave to escape. Witli continued isotonic contraction, 

 the hypertrophied septal portion of the outflow tract 

 may permit the occurrence of a delayed "tidal" wave 

 form. This secondary peak often coincides in time 

 with the delay seen in pure valvular stenosis. 



In experimental animals the pulmonary and right 

 ventricular effects of aortic stenosis depend on the 

 degree of stenosis and the compensatory reaction of the 

 left ventricle (261). If both are favorable, the com- 

 paratively slight increase in blood volume is accommo- 

 dated by expansion of the left atrium and the venous 

 tributaries from the lungs. In such instances, pressures 

 in the pulmonary artery and the dynamics ot the 

 right ventricle are not altered. If, however, the 

 stenosis is severe, or if left ventricular compensation 

 does not quite meet the demands, the pressure 

 increases backward throughout the circuit and 

 elevates pulmonary arterial pressure through aug- 

 mented resistance. This may eventually lead to right 

 heart failure. 



Gorlin and associates (120) found that the "critical" 

 area of the orifice in aortic stenosis was 0.5 cm'-. 

 They also found that although the left ventricular 

 stroke work was increased at rest, the pulmonary- 

 artery wedge pressure was near normal in 80 per cent 

 of the cases they studied. On exercise, however, the 

 pulmonary-artery wedge pressure increased in nearly 

 all cases, but total and effective ventricular stroke 

 work, output and systolic pressure failed to increase 

 and sometimes decreased. This suggests that the 

 obstruction to outflow was such that aortic outflow 



