FUNCTIONAL ANATOMY OF CARDIAC PUMPING 



77 1 



in fig. 15). The fact that the ventricular and aortic 

 pressures continue to rise even after the flow rate 

 starts to drop is not surprising, since during the period 

 of reduced ejection, blood continues to accumulate 

 in the aortic arch. Because aortic pressure at any one 

 instant is determined both by the distention of the 

 arterial walls with blood coming from the ventricle 

 and by the runoff into the periphery, the pressure 

 continues to rise as long as more blood enters the 

 aortic arch than runs off toward the periphery. There 

 is no fixed and easily definable time relation between 

 the summits of the flow and pressure curves, because 

 the factors determining the position of each of the 

 summits are numerous and variable (149). 



Some aspects of the time relation between the flow 

 and pressure curves A and B are illustrated in figure 

 15. During exercise the rapid ejection occupies a 

 relatively shorter portion of the total ventricular 

 ejection. In this example the whole ventricular 

 ejection lasts 374 msec at rest and only 234 msec 

 during exercise. However, the delay between the 

 summits of the flow and pressure curves is 109 msec, 

 in both cases, or 29 per cent of the whole ventricular 

 ejection at rest, and 46 per cent during exercise. In 

 other words, during exercise the aortic pressure 

 continues to rise relatively longer after the aortic flow 

 rate has started to drop, indicating that there is 

 relatively more blood accommodated in the central 

 arteries (arterial compression chamber) during 

 systole. This also means that, when ventricular 

 ejection ceases, there is a higher aortic pressure and 

 consequently a larger amount of peripheral runoff 

 during early diastole. Such conditions help to main- 

 tain greater tissue perfusion in the active organism. 



The configuration of the aortic flow curve is not 

 the same in the organism at rest and during exercise 

 or sympathetic stimulation. At rest, the descending 

 limb of the flow curve first declines gently, then 

 progressively faster, forming thereby a shallow hump 

 (see fig. 15.4). During exercise the ascending limb is 

 steeper and the descending limb declines precipi- 

 tously (fig. 15B). This pattern indicates: /) an increase 

 in the myocardial contractile force, which continues 

 to exert its strong effect after the end of the iso- 

 volumetric contraction phase and achieves a more 

 rapid flow acceleration; 2) a longer duration of flow 

 at near maximal velocity (Olmstead, personal 

 communication); and 3) a faster return to the begin- 

 ning of myocardial relaxation. Despite shortening of 

 the ejection phase, the stroke volume, which can be 

 calculated from the area under the curve, is approxi- 

 mately the same during moderate exercise as it is at 



rest. However, during strenuous exercise (running of 

 dog at 16 miles per hour over rough terrain) the 

 stroke volume appears to be increased by approxi- 

 mately 25 to 40 per cent (Olmstead, personal com- 

 munication). Whether or not there is always an 

 increase in stroke volume during exercise is still a 

 matter of debate among various investigators [see also 

 Rushmer (139)]. 



Toward the end of the reduced ejection phase the 

 intraventricular and aortic pressures drop quickly. 

 The ejection stops and forward flow in the ascending 

 aorta ceases shortly after closure of the semilunar 

 valves as seen by the crossing of the flow curve through 

 the horizontal zero flow line in figure 15. Flow in the 

 root of the aorta near the valves momentarily reverses 

 its direction, because of a translocation of blood into 

 the sinuses of Valsalva and the coronary vessels, 

 which helps to close the aortic valves. Although there 

 is a brief backflow near the valves, in the more 

 distal part of the aorta the flow continues forward for 

 a while, since the energy momentarily stored in the 

 distended aortic arch propels the blood to the area of 

 lower pressure, i.e., the peripheral vessels (compres- 

 sion chamber effect). The precise moment of valve 

 closure cannot be easily correlated with the pressure 

 and flow curves. It can be stated from the flow curve 

 that the valves must have closed at least by the time 

 when the downward deflection is suddenly stopped 

 (fig. 1 5) and after which blood again is propelled 

 forward in the ascending aorta. How much blood is 

 regurgitated into the ventricles and how much flows 

 into the coronary arteries while the valves are in the 

 process of closing, has not yet been determined. 



4-5: Isovolumetric relaxation. It is also difficult to 

 establish the exact moment when the myocardial 

 fibers start to relax after maximal shortening. Wiggers 

 (156) took the steepening of the decline in the ventric- 

 ular pressure curve prior to the deepest point of the 

 aortic incisura as the beginning of the relaxation 

 process and referred to the brief interval from the 

 beginning of muscular relaxation to semilunar valve 

 closure as the protodiastolic phase. Since little is 

 gained by singling out this interval, which cannot 

 be accurately measured, the phases of protodiastole 

 and isovolumetric relaxation will be treated here as a 

 single process as Wiggers ( 1 59) also suggested in his 

 recent discussion on this subject. 



It appears reasonable to assume that, just as the 

 contraction began asynchronously, some myocardial 

 fibers will begin to relax earlier than others. However, 

 no direct measurements are available to document 

 this hypothesis. At the end of isovolumetric relaxation, 



