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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



the systolic peak tends to come late. ( )n the other 

 hand, this maintenance of a high, late systolic pressure 

 may also reflect a change in the acceptance by the 

 aorta of ejected blood. For example, if the aortic 

 pressure is acutely raised, the first result is a reduced 

 stroke volume and a tendency toward shortening of 

 the ejection period. This is presumably because the 

 energy cost of ejection has been raised. As the heart 

 size increases, the stroke volume shows some tendency 

 to increase, and the duration of ejection becomes 

 longer. The systolic peak comes later in systole. 

 This pattern is clearest in animals with chronic hy- 

 pertension. Part of this change may be due to a 

 change in cardiodynamics (although not documented 

 as such). A more likely explanation is that as the 

 pressure rises, the front of the wave moves more 

 rapidly through the whole receiving arterial reservoir, 

 so that by midsystole the whole reservoir may be so 

 nearly filled that the vessels act more as rigid conduits 

 than as extensible tubes. As discussed previously, this 

 tends to maintain the pressure at higher levels in 

 the ascending aorta. 



Conversely, when the aortic pressure is acutely 

 lowered, the first few beats show a prolongation ot 

 systolic duration, with the systolic peak remaining 

 in midsystole. After the first few beats, as the heart 

 size becomes smaller, the stroke volume is reduced, 

 and the peak tends to occur earlier (45, 94). At low 

 pressures, the wave front moves so slowly through the 

 reservoir that volume is still being readily accepted 

 by the lower aorta, and hence by the ascending aorta, 

 toward the end of systole. 



The location of the systolic peak and the contour of 

 the main part of the systolic portion of the pulse 

 contour depend upon the varying characteristics of 

 both the arterial reservoir and the cardiac ejection 

 curve. This can also be taken to mean that the form 

 of the ejection curve is molded by the rate of aortic 

 acceptance of blood. Hence when the pressure is 

 elevated, and the wave moves more rapidly through 

 the vessels, the whole reservoir is filled in less time. 

 Toward the end of systole, then, cardiac ejection 

 need only compensate for the drainage loss, and the 

 pressure can be held relatively high until ventricular 

 relaxation begins (106). Conversely, when the aortic 

 pressure is lowered and the pulse moves more slowly, 

 the ejection of the same amount of blood will produce 

 a greater rise in pressure in the upper aorta. If the 

 pressure peak is still being propagated into the more 

 distal vessels toward the end of systole, we would 

 expect a fall in pressure in the ascending aorta, for 

 the small amount of cardiac ejection could not 



compensate for the fluid displacement required to 

 construct the pulse wave. 



The incisural vibration is formed in the ascending 

 aorta and is propagated at an orderly rate not greatly 

 different from that of the wave foot (98, 99). In 

 many cases, and particularly when the systolic peak 

 is reached late in the ejection period, it develops as 

 soon as the ventricular pressure falls below the aortic 

 level. In other cases, an appreciable pressure differ- 

 ence between ventricle and ascending aorta is de- 

 veloped before the notch appears. This is particularly 

 true in pulses which have a high anacrotic shoulder 

 and a collapsing pulse late in systole (98). Valve 

 closure is also delayed when the aortic pressure is 

 low. At times it may not appear until the isometric 

 relaxation phase of the ventricle is almost complete 

 (106). 



It may be more than coincidence that the delay 

 of the incisura is seen in those cases where the wave 

 front is still moving through the reservoir. Valve 

 closure must require a certain amount of flow reversal 

 in the ascending aorta. It seems reasonable that this 

 reversal could be accomplished more readily when 

 outflow from the upper aorta is minimal (as with 

 high pressure). 



In most normotensive pulses the incisura has been 

 damped out by the time the pulse enters the ab- 

 dominal aorta. With elevated pressure, it may be 

 seen as far as the femoral artery. With a lowered 

 pressure level, it may be lost in the thoracic aorta. 

 This difference is presumably attributable to the 

 various visco-elastic properties of the wall at the 

 different pressure levels. Whether the incisura is still 

 present or not, the pulse of the lower aorta and the 

 leg arteries shows a deep early diastolic trough. This 

 is accentuated in fever, hyperthyroidism, and aortic 

 regurgitation. Three different factors contribute to 

 the presence and size of this trough. First, it is in- 

 fluenced by the late systolic fall in pressure of the 

 central pulse. Second, the trough contains the remnant 

 of the incisural vibration. Third, the trough appears 

 to be set by the same mechanism that gives rise to 

 the augmentation of the systolic peak, especially 

 when this augmentation appears attributable to the 

 achievement of resonance in the aortic system (2, 7, 



99)- 



The fundamental form of the diastolic part of the 



pulse is probably the same for all pulses, no matter 



where recorded, except for the size of the periodic 



oscillations which are superimposed. Where such 



oscillations are minor, the slope appears exponential 



(140), but the relation of the rate of pressure fall to 



