PHYSIOLOGY OF AORTA AND MAJOR ARTERIES 



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fig. 7. Carotid pressure pulse (.4) and ascending aorta flow 

 (C). [From E. Wetterer (131).] B = change in volume uptake 

 curves for arterial bed regions. Broken line of C = the summed 

 uptake values taken from B. D = change in volume uptake as 

 calculated from a hysteresis loop, as taken from fig. 3. The 

 summed uptake values are given in C as the dotted line. 



ment simply accompanies the movement of the pulse. 

 This displacement is toward the periphery in systole, 

 but some may be toward the heart for a period in 

 diastole. It should not be difficult to understand that 

 the molecules involved in such displacements in the 

 lower aorta, for example, are not the same ones as 

 left the ventricle during the corresponding ejection. 

 The stroke volume is of the order of a fourth of 

 the aortic volume. In contrast, a stream flow is 

 established in the stiffer resistance vessels, which 

 approach more nearly the characteristics of a rigid 

 tube. Another way of saying this is that flow through 

 the aorta starts and stops, rather than being con- 

 tinuous. 



At present, the aortic flow curves available offer no 

 clear indication of the amount oi time lag between 

 pressure and fluid displacement. Spencer (119) 

 makes the statement that in the upper aorta pressure 

 and flow start together, but he offers no supporting 

 figure. If this is true, any phase lag will be based 

 simplv on a relatively slower increase of flow than 

 of pressure. On the other hand, the left ventricle 

 usually develops a pressure above the aortic level 

 before ejection apparently begins, which excess is 

 then gradually lost (98). Thus there appears to be a 

 true time lag of about 5 msec, similar to that en- 



visioned by Peterson. But a study of pressure pulses 

 taken from adjacent parts of the aorta offers no clear 

 evidence that a similar excess and time lag exist 

 there. Thus, after the initial delay between ventricle 

 and ascending aorta, the pressure pulse seems to be 

 propagated at a steady rate through the aorta (98, 



99)- 



At present, a major obstacle in the interpretation 

 of the presented flow curves is a lack of a reference 

 standard against which they can be compared. 

 Quantitatively, the curve from the ascending aorta 

 should integrate to the stroke volume less the coronary 

 flow. But our knowledge of the time contour of 

 cardiac ejection rests only on cardiometer curves, 

 which come from open-chest animals and bear 

 distortions that make one question the value of a too 

 detailed study of their time-flow dimensions. Flows 

 taken from other aortic regions can be related to the 

 stroke volume only if one assumes a distribution of 

 volume between the parts of the arterial bed. 



Construction of a Hypothetical Ejection Curve 



It might be of interest to construct a hypothetical 

 ejection curve, derived from the contour of the 

 central pressure pulse (104). This requires that all 

 animals be assigned the same wave transmission time 

 and the same arterial distensibility, the latter taken 

 from an average of stretch curves of isolated rings. 

 Certainly no claim can be made for the accuracy of 

 such curves. All we do know is that the total stroke 

 volume derived in this way usually agrees reasonably 

 well with that given by a direct measurement (94). 

 In this construction the arterial funnel, as shown in 

 figure 5, is divided into segments, the lengths of which 

 are approximately 10 msec of transmission time. The 

 total volume uptake of the arterial region is then 

 divided by the number of segments included, with the 

 various segmental uptake curves starting in sequence 

 every 10 msec. This derivation assumes that: a) the 

 aortic pressure pulse, as taken from the ascending 

 aorta, has no distortion because of a contained 

 acceleration transient; b) the wall stretch shows no 

 hysteresis lag; c) the control pulse is propagated as an 

 entity, without damping and without augmentation; 

 and d) there is no time lag between pressure change 

 and the corresponding fluid displacement. 



Suppose we take first the pressure pulse presented 

 by Wetterer (131) corresponding to his ascending 

 aorta flow pulse shown in figure 7. This pulse is ob- 

 viously from an open-chest animal, the length of 

 systole probably indicates that the animal was cold, 



