VENOUS RETURN 



III5 



EFFECT OF OPENING THE CHEST ON VENOUS RETURN, 

 CARDIAC OUTPUT, AND RIGHT ATRIAL PRESSURE. Figure 



i 7 illustrates the changes that occur in the circulation 

 when the chest is opened. The dashed curves repre- 

 sent the normal circulatory conditions and then the 

 long dashed curve represents the immediate effects 

 on the cardiac output curve caused by opening the 

 chest. The new equilibrium point, point A, shows 

 that the cardiac output falls to approximately two- 

 thirds normal and the right atrial pressure rises im- 

 mediately from —2 mm Hg to + 2 mm Hg. How- 

 ever, within approximately 30 sec to 1 min, circulatory 

 reflexes, especially pressoreceptor reflexes, cause a) the 

 cardiac output curve to rise to that depicted by the 

 solid curve, and b) the venous return curve to shift 

 to the solid venous return curve. These two curves 

 equate at point B which depicts the final effects of 

 opening the chest on cardiac output, that is, only a 

 little decrease in cardiac output (22) but a con- 

 siderable rise in right atrial pressure. One might 

 immediately ask, therefore: Does opening the chest 

 have any significant detrimental effect on the circu- 

 lation? The answer to this is very definitely "yes", 

 for the following reasons: In order for the venous re- 

 turn and cardiac output to recompensate essentially 

 to normal, strong circulator)- reflexes will have been 

 set into play. Thus, an animal with his chest open 

 has already utilized a major share of his circulatory 

 reflex power simply to compensate for opening the 

 chest. Now, the reserve reflex power left to compen- 



sate for other circulatory stresses, such as hemorrhage, 

 has been greatly reduced. Therefore, it can be said 

 that the '"circulatory reserve'' has been considerably 

 reduced as a result of the opened chest. This analysis, 

 therefore, explains why the cardiac outputs of open- 

 chest animals are normally only slightly below those 

 of normal animals, but it also explains why animals 

 and human beings under these conditions can with- 

 stand far less circulatory stress than can the normal 

 (42). 



EFFECT OF MYOCARDIAL DAMAGE ON VENOUS RETURN, 

 CARDIAC OUTPUT, AND RIGHT ATRIAL PRESSURE. Figure 



1 8 illustrates the progressive changes that occur in 

 the circulation following sudden acute myocardial 

 damage to both sides of the heart approximately 

 equally. The short dashed curves illustrate normal 

 equilibrium conditions. Then, suddenly, the heart 

 becomes severely damaged as a result of acute myo- 

 cardial infarction, reducing the cardiac output curve 

 to that depicted by the long dashes. As a result, the 

 new equilibrium point is now approximately one- 

 third normal, and the right atrial pressure has risen 

 to +4 mm Hg. However, these conditions do not 

 obtain for a prolonged period of time because auto- 

 nomic reflexes, mainly sympathetic, cause immediate 

 compensations within the next 30 sec to 2 min (2-4,40, 

 80, 152). At the end of this period, the sympathetic 

 stimulation will have increased the cardiac output 



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o -4 44 +8 +12 



RIGHT ATRIAL PRESSURE (mm Hg) 



fig. 17. Effect of opening the chest on the venous return 

 and cardiac output curves, showing by point A the immediate 

 effect and point B the effect after circulatory reflexes ensue. 



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1600 



1200 



800 



400 



"4 +4 + 8 +12 + I6 



RIGHT ATRIAL PRESSURE (mm Hg) 



fig. 18. Effect of acute myocardial infarction and subse- 

 quent stages of recovery on the cardiac output and venous 

 return curves. The sequence of events is explained in the text. 



