HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



things. /) The loops given by an isolated ring may be 

 much wider than those found in the living aorta. 

 Evidence was cited above that this might be true. 

 2) The velocity may be dictated not by the wall 

 extensibility, but rather by the force of elastic recoil. 

 Calculation from a stretch-release curve would indeed 

 give smaller values. The question is what amount of 

 stretch should be used to produce pertinent stretch- 

 release curves, j) The distensibility slope of the aorta 

 during life may be entirely different from that indi- 

 cated by the isolated rings. The data of Peterson 

 (91), for example, seem to have it greatly different. 

 4) Factors which act to slow the pulse wave should 

 be introduced into the formula. To the extent that 

 the aorta acts as a rigid tube, fluid resistance toward 

 flow can act in this manner, as will a phase lag be- 

 tween the pressure pulse and the corresponding fluid 

 displacement. Many workers now accept the presence 

 of an appreciable lag. As will be seen, acceptance of 

 such a lag cannot be readily reconciled with the 

 failure to find a correlation between wave velocity and 

 the rate of pressure rise, as mentioned above. 



Phase Lag and the Harmonics of the Arterial System 



Since phase lag is formulated in terms of the 

 frequency of harmonic components, the first step is 

 to perform a Fourier analysis of the pressure wave. 

 For this, a sinusoidal fundamental wave must be 

 selected. Since such a fundamental is not readily 

 apparent in the contour of the natural pulse wave, it 

 is selected on the basis of a time duration (123, 124). 

 Usually the length of the pulse cycle is used. As 

 emphasized by McDonald in the introduction to his 

 book (84), such a mathematical analysis can start 

 from one of two premises. First, we can assume that 

 each pulse is an isolated or transient phenomenon, 

 with the aortic volume being almost static when a 

 new cardiac ejection and sudden flow acceleration 

 are begun. Second, we can say that the heart rate is 

 virtually stable, so that the ventricle is repeatedly 

 pulsing the arteries at a set frequency. The latter 

 premise makes the cycle length a true measure of the 

 wave fundamental, makes the harmonics relatively- 

 reproducible from beat to beat, and makes all the 

 mathematical compilations very much easier. A 

 change in heart rate will vary the contained har- 

 monics and alter the phase lag between pressure and 

 fluid displacement. It will, then, alter the wave 

 velocity. 



But the fact that an analysis on the basis of a 

 uniform heart rate is easier to make does not mean 

 that the premise is correct. Much evidence can be 



quoted for the stand that each pulse is indeed an 

 independent event. Strict regularity of the pulse rate 

 is infrequent, usually being found only in rather 

 prolonged experiments in animals under deep anes- 

 thesia. In the unanesthetized dog or human, variation 

 from cycle to cycle is clear. In this variation the 

 diastolic period is affected predominantly or ex- 

 clusively. The pulse contour during systole, and its 

 duration, is affected but little. Further, when the 

 heart rate changes outside the limits of such beat-to- 

 beat variations, systolic durations and contour are 

 altered far less than is the cycle length (100). If the 

 fundamental is reset each time this cycle length 

 changes, a different harmonic picture will be re- 

 quired to construct the same systolic pressure contour. 

 If the fundamental is taken as the average cycle 

 length for a number of pulses, then we must proceed 

 cautiously in interpreting the influence of the 

 harmonic pattern on the contour of any single pulse 

 of the group. 



The whole approach seems more hazardous, too, 

 when it is recalled that the length of systole almost 

 never equals half the cycle length. This makes the 

 heart quite unlike most pumps. Perhaps it would be 

 more logical to use twice the length of the systolic 

 period as the fundamental wave. This might be done 

 for a central pulse, but certainly not for a peripheral 

 one, where the incisura has been lost through damp- 

 ing. 



Believing in the principle of a stable heart rate, 

 McDonald (84) would have the velocity of the wave 

 foot increasing with the heart rate. He offers no 

 experimental support for the claim. We have looked 

 often for evidence of such a dependency on heart 

 rate and, with the single exception presented below, 

 have not found it. However, McDonald has calculated 

 that in a vessel the size of the aorta neither the viscous 

 resistance factors nor the pulse frequency would 

 affect the velocity to significant degree. In a smaller 

 vessel, such as the femoral artery, he calculates that 

 the viscosity would slow the velocity by about 10 

 per cent, and an increased heart rate might restore 

 it to the value expected from the Bramwell and Hill 

 formula. Much larger changes than these would be 

 needed to correct the formula if the data given by 

 the crosses in figure 6 are correct. 



We did offer evidence (46) that a slower foot 

 velocity was seen in the early part of the response 

 of an animal to an injection of acetylcholine, when 

 the heart rate was slow, than was seen later when, 

 at the same diastolic pressure levels, the heart rate 

 increased. A similar effect at higher pressures has 



