156 



HANDBOOK OF PHYSIOLOGY -^ CIRCULATION I 



FIG. 4. Relation between efficiency and 

 isotonic load for frog sartorius muscle. [From 

 Hill (138).] P is actual load, Pt, is isometric 

 tension. 



FIG. 5. Work performed in after loaded 

 contractions a? a function of load. The dots 

 show the work when the loads were applied at 

 the length which corresponded to a tension of 

 55 g, and the circles that developed at the 

 length corresponding to a tension of 1 20 g. 

 [After Rosenblueth el al. (249).] 



40 



20 



0.3 



0.9 



200 400 600 700 



a diminution in the functional capacity of the organ 

 e\cn thougli the contractility of the component cells 

 may be normal. An attempt will be made in later sec- 

 tions to consider direct effects on the contractility of 

 heart tissue itself, and to separate them from altera- 

 tions in shape or innervation that affect the per- 

 formance of the heart as a pump. 



An interesting example in which the type of analysis 

 outlined above may be helpful is provided by experi- 

 ments on cardiac oxygen consumption first re- 

 ported by Evans & Matsuoka (73) and confirmed 

 many times subsequently (6, 99, 104, 166, 167, 174, 

 262). The stroke work of the heart is given approxi- 

 mately by the product of stroke volume and arterial 

 pressure. An increase in stroke work caused by an in- 

 crease in stioke \olume is associated with a very small 

 increment in oxygen consumption; but increased 

 stroke work caused by raising arterial pressure is 

 accompanied by a considerable rise in oxygen con- 

 sumption. In other words, work output/energy input 

 or mechanical efficiency is lower when work is aug- 

 mented by raising blood pressure than by raising 

 stroke volume. This phenomenon could be accounted 

 for at least in part if the heart were working in the 

 region of the peak of its load-efficiency curve (fig. 4), 

 since an increase in load by elevation of arterial pres- 

 sure would cause a drop in efficiency. Another factor 

 may also play a role, if it can be established that Po 

 (equation i ) does not change greatly. Reference to 

 figure 2 will show that if the heart muscle working at 

 point A on its force-velocity curve against a load d 

 (on the force axis) and velocity c is presented with an 

 increased load / (on the force axis), it would then be 

 working at point B on that curve at a considerably 

 decreased velocity {e). However, measurements show 

 that when the load is increased by increasing aortic 

 pressure, the velocity of shortening is not decreased 

 (212); and it is apparent that the heart muscle must 

 be working on a cur\ c which passes through point D, 

 thus reflecting a change in contractility and or veloc- 

 ity of the muscle. 



.■\lthough a length-tf*nsion curve such as that shown 



OR U A B 



-VOLUME 



FIG. 6. Changes in dynamic pressure-volume curves of dog 

 heart in response to an increase in inflow pressure. (See text for 

 description.) 



in figure i can be obtained experimentally with a 

 cardiac muscle strip, the corresponding pressure- 

 volume curve for an intact heart is impossible to ob- 

 tain, and this section will be concluded with a 

 discussion of the difficulties encountered. Consider an 

 isolated perfused heart in which volumes and pressures 

 can be measured. Referring to figure 6.4, the cardiac 

 cycle begins at the black dot corresponding to volume 

 A and end diastolic pressure m, a point on the resting 

 pressure-volume curve. The aortic diastolic pressure 

 is at a level p. When the heart contracts, pressure 

 rises isometrically to p (point D in the figure) and then 

 shortening occurs to point C which is on the contracted 

 pressure-volume curve.* Isometric relaxation then 

 occurs and finally the heart returns to the original 

 point as shown by the direction of the arrows. In this 

 example the end-diastolic volume is OA, the stroke 

 volume is DC, and the stroke work is the area en- 

 closed by the arrows. Construction of the resting and 

 contracted pressure-volume curves, t'l'and RS, could 

 theoretically be accomplished as follows. For the 

 resting curve, increase the input pressure stepwise and 

 measure the corresponding (end-diastolic) volumes. 

 For the contracted curve, increase the output pres- 

 sure stepwise and again measure the (systolic) volume 

 at each pressure le\el. However, a series of elegantly 

 performed experiments by Rosenblueth and co- 



* There is some doubt as to whether the ventricle reaches 

 equilibrium with the oiUput pressure during systole {248). That 

 is, shortening may stop before point C is reached. See also sec- 

 tion I. 



