PHYSIOLOGY OF AORTA AND MAJOR ARTERIES 



827 



pressure rise seen with a natural pulse, and they 

 were truly independent phenomena. 



McDonald (84) believes that because the natural 

 pulse is but one of a continuous train of waves with 

 virtually identical wave lengths, each ejection could 

 serve to reinforce the component frequency which 

 happens to match the transmission time through the 

 resonating part of the reservoir. This premise would 

 permit development of resonance with the first transit 

 of each wave. But, by extension, this premise would 

 also require that the pulse pressure augmentation 

 be a function of the heart rate. Again, all we can say 

 is that neither the pressure augmentation nor the 

 period of the diastolic oscillations has been shown to 

 have any relation to heart rate per se when the 

 diastolic pressure remains the same. The reciprocal 

 oscillations between aortic arch and abdominal aorta 

 pulses in the dog appear to be the rule and not the 

 exception. They appear with the first beat after a 

 prolonged cardiac arrest, as with vagal stimulation; 

 they are not clearly accentuated at any given heart 

 rate; it is most difficult to so alter the cardiovascular 

 status through nerve stimulations or injected drugs as 

 to make them disappear. 



The prompt achievement of resonance by the 

 aorta would seem to require, then, that the whole 

 vessel could act as a unit, and "mold" any ejection 

 wave into a pattern consistent with its own resonant 

 properties. Alexander (7) has used the analogy of 

 an orchestral chime, which, when struck, vibrates 

 at a frequency set by its own geometry, unaffected 

 by the characteristics of the impacting force. Use of 

 this analogy is not easily reconciled with the theorem 

 that wave propagation is from tiny tube segment to 

 adjacent segment. Instead the pressure rise in the 

 upper end of the aorta would have to be aisle, by 

 some mechanism, to throw the whole aorta into vibra- 

 tions. Yet there is no evidence that this pressure rise 

 "signals ahead" of the propagated pulse wave. There 

 is no pressure change in the lower aorta at the time 

 the central pulse is first being ejected. 



One question which must be decided is whether it 

 is the propagated pressure wave itself which sets the 

 aorta into resonance. No alternative suggestion has 

 yet been advanced, unless one can read into a paper 

 describing the genesis of the ballistocardiographic 

 waves the notion that whole body thrusts might in- 

 duce this resonance pattern within the vessels (43). 

 The propagated wave in an aorta has much in com- 

 mon with an artificial wave being propagated 

 through a stoppered rubber tube, although the latter 

 does not readilv create immediate resonance. The 



aorta should be even less conducive to the attainment 

 of resonance than the rubber tube. There certainly 

 is no single reflection point, for exit vessels are 

 distributed along the whole length of the system. One 

 would expect, then, innumerable returning waves 

 bearing no necessary time relation to each other. 

 Further, the exit vessels are not blind end tubes, bur 

 continue on to become the resistance vessels of the 

 arterial tree. This has led some to the conclusion 

 that the aortic reservoir should be considered as more 

 comparable to an open-end tube, the resonant wave 

 of which would then be twice as long as that of a 

 closed-end tube (60, 134). On the other hand, Hamil- 

 ton (38) has maintained that the sudden increase in 

 the resistance to flow in these vessels will serve to 

 produce the positive reflection. While such reflections 

 could take place wherever the flow pattern is changed, 

 as at a vessel bifurcation, or even in the curvature of 

 the aortic arch, these reflections within the tube 

 would be small when compared to those arising from 

 the small resistance vessels. He has documented this 

 belief by experiments done on a rubber tube model 

 fitted with many small rigid tubes of high-flow re- 

 sistance, but with a greater aggregate cross-sectional 

 area, placed in series with the rubber tube (41). 



Alexander (1, 4, 8) recorded pulses from the arch, 

 the abdominal aorta, and the femoral artery of dogs 

 under a variety of physiological conditions. Usually 

 the two peripheral pulses showed simultaneous 

 peaks, although at times they did not. If the central 

 pulse was subtracted from the peripheral one, to 

 give the contour of the reflected wave, two different 

 waves in the subtraction curve could be seen. The 

 first of these was taken to represent the propagated 

 peak of the incident wave, •"distorted" by damping 

 and the other factors which may give rise to contour 

 change during propagation. The second, a swell of 

 more sinusoidal form, was the first of the resonant 

 oscillations. When the two waves coincided, the 

 femoral pulse pressure was at its greatest. In some 

 central pulses, a late systolic trough could be seen 

 that appeared simultaneously with the distal resonant 

 swell. When the length of the ventricular ejection 

 period was slowed through induced hypothermia 

 (7), this trough came far enough ahead of the incisura 

 to be clearly recognizable. 



The resonant swell obtained by such a subtraction 

 did not have the same wave length as the central 

 pressure pulse. In fact, there is no real evidence that 

 the whole of the incident pulse is reflected. When 

 subtraction curves of the same tvpe were obtained 

 for human subclavian pulses (108), a reflected wave 



