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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



and venous return curves up to those depicted by the 

 dashes and dots. Therefore, within 2 min, the venous 

 return and cardiac output will have returned to ap- 

 proximately two-thirds normal, and the right atrial 

 pressure will have risen another 2 mm Hg up to +6 

 mm Hg. But, even this is an abnormally low cardiac 

 output which is still insufficient to supply all the tissues 

 of the body with adequate amounts of blood. Further- 

 more, there is intense sympathetic vasoconstriction 

 throughout the circulatory system during this period 

 of time as well as sometimes a decreased arterial pres- 

 sure; the intense sympathetic vasoconstriction (134) 

 and the decreased arterial pressure (135) both de- 

 crease renal output. Furthermore, the semishock 

 state that exists at this stage causes the adrenal glands 

 to secrete large quantities of aldosterone. This, in 

 turn, promotes rapid reabsorption of sodium from 

 the renal tubules, associated also with rapid reabsorp- 

 tion of water (48). The net effect on the kidneys, 

 therefore, is to reduce renal output greatly or, at 

 times, even to stop renal output completely. Over a 

 period of the next few days, fluid is progressively re- 

 tained in the circulatory system, thus shifting the 

 venous return curve in figure 1 8 further and further 

 to the right (99, 105). The solid venous return curve 

 depicts approximately that which will obtain after a 

 week or so of fluid retention. 



Simultaneously with the changes that take place 

 in the venous return curve, the heart will also be 

 changing. If the infarction is an uncomplicated one 

 and recovery from the infarction begins immediately, 

 then the cardiac output curve of figure 18 will pro- 

 gressively rise. The solid cardiac output curve depicts 

 approximately that which one would expect after a 

 week of recovery. As illustrated by the point at which 

 the solid cardiac output curve equates with the solid 

 venous return curve, we find that the cardiac output 

 and venous return will have now returned almost 

 completely to normal but that the right atrial pressure 

 again will have risen another 2 mm Hg. This is charac- 

 teristic of the chronic stage of congestive heart failure, 

 that is, the cardiac output may be normal or slightly 

 below normal, but the venous pressures are essentially 

 always greatly elevated. 



Another effect that occurs as the cardiac output 

 approaches normal is that the degree of sympathetic 

 activity throughout the body also gradually becomes 

 reduced toward normal. Furthermore, the body is 

 no longer in a shocklike state so that the output of 

 aldosterone also becomes reduced. As a consequence, 

 renal output once again returns toward normal, thus 

 preventing further retention of fluid. Therefore, the 

 circulatorv svstem has now reached a new steady 



state, with the cardiac output and venous return 

 essentially normal, renal output once again essen- 

 tially normal, but the right atrial pressure consider- 

 ably elevated. 



It should be noted again that the analysis illus- 

 trated in figure 1 8 is that for myocardial damage 

 affecting both ventricles approximately equally. The 

 course of events depicted by the dotted line is typical 

 of that normally observed following acute generalized 

 myocardial infarction (13, 71, 73, 75, 106-108, 121, 

 162, 163, 166). We shall see that the more complicated 

 graphical analysis presented later in the chapter is 

 much more satisfactory than the simple graphical 

 analysis when one side of the heart fails to a greater 

 extent than the other side. 



ANALYSIS OF DECOMPENSATION AND COMPENSATION IN 



congestive heart failure. Figure ig illustrates an 

 analysis of decompensation in severe cardiac failure. 

 This shows by the two dashed curves the analysis for 

 the normal circulatory system in a normal 10-kg dog. 

 Then, at the bottom of the graph, it shows the typical 

 cardiac output curve for a severely damaged heart 

 after all sympathetic reflexes and all recovery that 

 are possible have taken place (38). If we assume that 

 the cardiac output curve suddenly falls from the 

 normal down to this depressed curve, then we find 

 that the cardiac output immediately falls to point A y 

 about two-fifths normal, with a right atrial pressure 

 of approximately +4 mm Hg. This cardiac output 

 is far too little to cause normal renal function, and, 

 for the same reasons discussed above, renal output 

 becomes severely depressed. As a result, fluids are 

 retained in the body, and the mean systemic pressure 

 progressively rises, shifting the venous return curves 

 to the right and progressively elevating their plateaus. 

 Thus, during the ensuing days, with the progressive 

 retention of fluid, the equilibrium points in figure 19 

 proceed to B, C, D, E, F, and G. It is especially in- 

 teresting that cardiac output curves of severely dam- 

 aged hearts do not rise to a plateau but, instead, rise 

 to a peak and then begin to descend (117). Therefore, 

 after the process of decompensation has proceeded 

 past the peak at point E, further retention of fluid 

 causes a reduction in cardiac output rather than an 

 increase. 



The significant factor in decompensation is that 

 even at its greatest peak, the cardiac output curve 

 never reaches the necessary cardiac output level re- 

 quired to re-establish normal renal function. Con- 

 sequently, fluids continue to be retained indefinitely 

 until death of the animal. 



