834 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



to physiological change, and only if a constant so 

 derived for one individual could be applied to 

 another. All these assumptions have seemed so 

 precarious that the German formulas have not 

 received favor in this country. 



Yet the hope remains that some means can be 

 devised by which the stroke volume can be predicted 

 from the values of the pressure pulse. This would 

 allow a quantitation of beat-to-beat changes, and 

 also of the acute change in ejection volume that occur 

 as the cardiovascular status is rapidly changed. We 

 have no direct method applicable to closed-chest 

 animals that can measure these stroke volume changes. 

 Until we do, an indirect approach can serve a limited 

 but useful purpose. 



Another attempt at making this sort of indirect 

 calculation was made by Bazett and co-workers (10). 

 They divided the arterial reservoir into four parts: 

 /) the aortic arch and its large branches; 2) the 

 whole of the descending aorta through the iliacs; 

 3) the subclavian-brachial systems; and 4) the 

 femoral-leg system. They recognized that the pulse 

 pressure would be different in these regions, and 

 therefore concentrated instead on the pressure change 

 taking place during diastole, when the previously 

 stored blood was being discharged through the re- 

 sistance vessels. They assumed that, by the time of 

 the incisura, the whole arterial reservoir would be 

 draining as a single unit, and that the pressure 

 change could therefore be that from the level of the 

 incisura of a central pulse to the end-diastolic value. 

 Unfortunately, their central pressure pulses were 

 rather inadequately recorded. Next, using calcula- 

 tions based on the size of the larger vessels of each 

 arterial region as taken from autopsy data, and 

 using assumptions and empirical adjustment of the 

 derived diastolic volume values, they arrived at 

 figures for the total diastolic volume for each region. 

 The change in volume from this level was then 

 equated as a function of the pulse wave velocity 

 through the region, or 



,v. v V, v 4 , 



V 



V 3 



where AC is the total stored volume, the I"s are the 

 calculated diastolic volumes of the four parts of the 

 reservoir, and the v\ the respective wave velocities 

 (which could be measured only rather crudely). 

 With more modern technology, the basic data could 

 be much more accurately recorded. The formula 

 would still be rather cumbersome, and the necessarv 



measurements many. Two of the major weaknesses 

 still present are that V cannot be directly obtained, 

 any more than the A of Frank's equation can be, 

 and that the v values of necessity must be taken from 

 a single large artery in each of the regions. This 

 assumes that this artery can fairly represent the whole 

 system, and also that this velocity gives a true indica- 

 tion of vessel distensibilitv. 



We presented another approach to the problem, 

 worked out on the dog rather than on the human. 

 For reasons which have been covered previously, 

 we regarded the wave velocity as a most dubious 

 measure of vessel distensibilitv. Instead, we sub- 

 stituted volume-pressure relations taken from data 

 obtained by stretching isolated rings, and by inject- 

 ing saline into occluded arteries of dead animals. 

 We necessarily assumed that the values obtained 

 would be practically the same for different animals. 

 To make some correction for differences in body size, 

 all values were expressed per square meter of body 

 surface area. We also assumed that the transmission 

 time through the various arterial beds would be the 

 same for all animals, at the same diastolic pressure 

 level. After making the studies described above, in 

 which we calculated the presumed cardiac ejection 

 curve on the basis of a summation of volume uptake 

 values of the arterial regions taken serially as they 

 were invaded by the pulse wave, as described above, 

 we settled on the premise that such a summed total 

 uptake, with a calculated systolic drainage added, 

 should equal the stroke volume at the time of valve 

 closure. Hence we could work with a single central 

 pressure pulse, laying back the transmission time to 

 each of the four major divisions of the arterial bed, 

 from the incisura. The pulse pressure to be quan- 

 titated for each bed would then simply be the pres- 

 sure shown at this interval before valve closure. In 

 other words, the point at which this time interval 

 intercepts the pressure pulse curve indicates the 

 pressure developed in the bed in question at the end 

 of systole. This assumes that there was no change in 

 pulse contour during propagation. More rightly, it 

 assumes that any contour change present during 

 propagation would be constructed by a redistribution 

 of the volume of blood ejected into the ascending 

 aorta to create the given central pressure pulse. At- 

 tempted modifications based on actual pulse contours 

 taken at various points in the aorta did not alter the 

 value of the calculated stroke volume to significant 

 degree. 



Without introducing any empirical correction 

 factor, the agreement between the predicted and 



