PHYSIOLOGY OF AORTA AND MAJOR ARTERIES 



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not been observed. We then attributed the velocity 

 change not to the heart rate but to a changing 

 hysteresis loop behavior of the wall. A long diastolic 

 interval could allow more time for recovery after a 

 stretch, and the diastolic size, and hence the distensi- 

 bility modulus, would be thereby reduced. It is less 

 clear now (96) that the difference in this size could 

 be sufficient to account for the difference in wave 

 velocity. Yet it remains possible that the correlation 

 with heart rate was still only coincidental, and that 

 when the pressure was abruptly lowered the slope of 

 the stretch curve could be shallower for the first few 

 beats than it would be after the pressure had re- 

 mained low for some time. 



Most especially, if we regard the pulse wave as an 

 independent phenomenon, the velocity of the wave 

 start would be affected least by a change in harmonic 

 frequency. The upper parts of the pressure pulse 

 could have their propagation speed affected to 

 greater degree by these frequencies or by the speed 

 of the pressure upstroke. A different velocity for the 

 parts of the wave was fully accepted by Bramwell 

 and Hill simply on the basis of their formula. They 

 went further (14) and held that the difference in 

 velocity could be such that the anacrotic rise of the 

 pulse would progressively steepen in transit until 

 finally the wave force would become unstable, and a 

 "breaker" (like that seen when an ocean wave enters 

 shallow water) would form. Evidence of such breaker 

 phenomena was seen when pulses were generated in 

 a bicycle tire. As will be described later, evidence is 

 not clear that the natural pulse does so progressively 

 steepen during propagation, and there is no evidence 

 at all for sudden pressure vibrations that would mark 

 a breaker. However, the calculated differences in 

 velocity between the start and the peak of a natural 

 wave are not large enough to create a breaker within 

 the length of the aorta. 



If there is a velocity differential between the parts 

 of the wave (and it would appear to be quite small 

 if present), 2 it could reflect the progressive increase 



2 There is an obvious discrepancy between the statement that 

 there is no clear evidence for a difference in propagation 

 velocity of the parts of a natural wave and our published 

 results (103) which showed clear differences in transit time for 

 the parts of an artificial wave. There are few inflections on the 

 natural pulse form which can be measured with the necessary 

 precision to establish a difference in propagation velocity. The 

 start of the wave and the incisural notch can be so timed, and 

 these two parts of the pulse contour appear to move with the 

 same velocity. Since we have no clear idea as to which tension- 

 length slope should be used to predict the velocity of the in- 

 cisura, or to which volume on the stretch-release curve this 

 slope should be referred, this identity of velocity with that of 



in the stiffness modulus as the reference volume in- 

 creases, without requiring a dependency upon the 

 harmonic frequencies. Landowne (72, 73) did show 

 that when small impact waves were formed at a 

 point on the human brachial artery, the speed of 

 their propagation was faster if they fell during the 

 systolic portion of the pressure pulse than during the 

 diastolic portion. The propagation velocity of these 

 small waves was much greater than that of the 

 natural wave. Van Citters (125) believes that the 

 velocity is of the order to be expected if they were 

 being transmitted by longitudinal strain through the 

 wall itself, rather than by fluid accelerations within 

 the artery. 



Landowne (71) has also shown that, with a rubber 

 tube or umbilical artery, either small impact waves or 

 rapidly repeated sinusoidal waves moved at a velocity 

 which bore a direct relation to the frequency. Our 

 experiments showing a dependency of wave velocity 

 upon the rate of stretch of rubber fit with this (46). 

 The umbilical artery has a uniquely large time- 

 dependent factor in its visco-elastic behavior (141), 

 so that it would not be at all unreasonable that the 

 velocity could also show a clear rate dependency. 

 These results should not be regarded as transferable 

 to the aorta, and perhaps not even to arteries such 

 as the femoral or carotid. We are left, then, with the 

 conclusion that the actual pulse wave velocity remains 

 to be explained in a quantitative way. A mathe- 

 matical analysis of the determinants of pulse wave 

 velocity is presented in the chapter by Hardung (49). 



We still have the fundamental question as to 

 whether there would be an appreciable time lag 

 between the pressure pulse and the fluid displace- 

 ment, or the movement of the pulse wave from 

 segment to segment through the tube. The idea of a 

 large lag was presented first in the papers of Peterson 

 (89, 90). He perfected a mechanism which could 

 produce a very rapid input of fluid into the ascending 

 aorta, and thereby generate pressure curves, of rather 

 strange form, which were propagated. The shape of 

 these curves was explained on the basis of a sum- 

 mation of three forces. First, a very small amount of 

 fluid would be driven into the aorta more rapidly 

 than the walls could stretch, so that, just as in a 

 rigid pipe, there would be a sudden rise in pressure. 



the wave foot may be coincidental, and not be evidence for or 

 against a dependency of wave velocity upon frequency. It 

 should also be stressed that while the wave parts of the artificial 

 wave moving through an excised aorta showed different 

 transit times, these times were not conditioned by the rate of 

 pressure rise or fall. 



