8 3 o 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



speeding of the upper portions of the pulse as the 

 modulus of extensibility is increased. This would 

 probably cause an augmentation of the pulse pressure. 

 This effect seemingly would be operative only if wall 

 hysteresis were of minimal importance. However, I 

 am not convinced that there is any difference in 

 transit time of the wave foot and of the incisura, for 

 example. 



c) The same sort of peaking could indicate an 

 attenuation of mismatched harmonic frequencies. 

 If the electrical analogy is apt, there would be no 

 augmentation of the pulse pressure in this case, how- 

 ever, but simply less attenuation of the matched 

 frequencies. In a hydraulic system, of course, it 

 might be that attenuation of one part of the pulse 

 might yield fluid and energy for another frequency, 

 which conceivably could produce pulse pressure 

 augmentation. Such a redistribution of energy has 

 not been shown to be true. 



d) There could be a reflection of the whole or a 

 part of the incident wave, whether the vascular 

 bed did or did not achieve resonance as it has been 

 described. The maximum possible increase in pulse 

 pressure by reflection would be to twice the original 

 value, which would be realized only if the whole 

 pulse pressure showed complete reflection, and the 

 pulse recording was very near the reflection "end" 

 of the system. Usually the pulse pressure in a femoral 

 artery is less than twice that of the central pulse. 

 However, Alexander has shown femoral pulse pres- 

 sures in the dog which are greater than twice the 

 value. 



e) As an extension of d), or perhaps as a result of 

 another property of the bed entirely, when the aorta 

 does show resonance, augmentation of the pulse 

 pressure is appreciably greater than when a standing 

 wave is not seen. 



/) In some cases where the cycle length is short, 

 the diastolic pressure swell (presumably the reflected 

 wave) may begin late in the diastolic period. If a 

 new systolic upstroke coincides with the upswing of 

 this swell, very high pulse pressure values can be 

 obtained. This mechanism of augmentation by "su- 

 perposition" was illustrated by pulses recorded from 

 the system of man ( 1 08 ) . 



Aside from changes in pulse pressure and the form 

 of the systolic peak, there are other aspects of pulse 

 contour transformation which have no clear explana- 

 tion. The pulse formed in the ascending aorta shows, 

 after a variable but short period in which the pressure 

 rise from the diastolic level is slow, a rather abrupt 

 assumption of a steep and constant slope of pressure 



rise. This anacrotic rise is maintained unchanged for 

 at least 30 msec. It is then usually lost rather abruptlv, 

 often with a temporary interruption of pressure 

 rise. This halt is called the shoulder of the pulse. 

 The steeper the preceding slope, the more con- 

 spicuous is this shoulder. The rate of anacrotic pres- 

 sure rise is clearly related to the amount of sympathetic 

 stimulation of the left ventricle, which serves to speed 

 the whole contractile process. Thus, with such stimu- 

 lation, maximal outflow is reached earlier in systole, 

 the shoulder tends to be at a relatively high pressure 

 level, and the systolic peak of the pulse occurs earlier. 

 A shortening of the length of the ejection period 

 can be used as the basis of an assay method for 

 sympathomimetic stimulation (100). With extreme 

 cardiac stimulation, particularly when the stroke 

 volume is reduced because of inadequate venous 

 return, the shoulder may be so abrupt as to throw 

 the whole aorta into vibrations. Under such circum- 

 stances, the height of the shoulder may be greater 

 than that of any other part of the pulse, which 

 makes the shoulder height represent the systolic 

 pressure. In such cases, the pulse pressure may have 

 higher values than would be anticipated from the 

 stroke volume (94), in the peripheral vessels as well 

 as in the ascending aorta. 



The slope of pressure rise preceding the shoulder 

 was found by Hamilton & Dow (42) to be propagated 

 unchanged through the aorta. Alexander (4) showed 

 some loss of steepness in the abdominal aorta, while 

 I (99) found it to remain constant in the thoracic 

 aorta and then to steepen in the abdominal aorta. 

 The slope change is never marked, however, so that 

 all three studies are compatible with the general 

 conclusion that this first part of the pressure wave 

 seems to move as an unchanged unit. All three also 

 agree that the steep upstroke continues for a longer 

 time interval the further from the heart the recording 

 is made. This might lead one to the conclusion that 

 this early part of the wave cannot be thought of as 

 being propagated by repetitive accelerations of tiny 

 segment volumes. It was pointed out earlier that the 

 length of what is called a "small segment" of the 

 aorta is undefined. The segment may have an ap- 

 preciable length, and the volume contained, which 

 is accelerated as a unit, have an appreciable mass. 

 Thus it may be that the propagation of the first 

 part of the pulse wave would involve fluid accelera- 

 tions which would have many of the physical prop- 

 erties of a volume surge with inertia. If so, one 

 would expect the "surge" to produce a progressiveh 

 greater pressure rise in the lower regions of the aortic 



