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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



with progressive deterioration of the right myocardium 

 from pulmonary artery stenosis, the changes in 

 coronary flow and oxygen usage per minute and per 

 beat may be in the same direction (increase) as those 

 described for the nonfailing right myocardium, but of 

 lesser magnitude (see section on Valvular Disease). 

 If the heart failure is severe enough, extravascular 

 compression can become dominant over any active 

 coronary dilatation from metabolic processes, and 

 coronary flow and oxygen usage may be normal or 

 decrease, with the oxygen extraction at times reaching 

 go per cent (153)- The coronary circulation in the 

 heart, failing with severe aortic stenosis, undergoes 

 similar changes (Gregg, unpublished data). When 

 acute heart failure and chronic congestive failure 

 simulating the human condition are induced by 

 surgical complete heart block, changes in left coronary 

 flow and ventricular oxygen consumption also rather 

 closely parallel alterations in the reduced left ventricu- 

 lar work (355). In each instance, the mechanical 

 efficiency of the myocardium drops, the total energy 

 of liberation (oxygen consumption) being fairly well 

 maintained, but the work falls off. The isolated 

 mammalian heart or heart-lung is also characterized 

 by deterioration of mechanical efficiency and on the 

 same basis (74, 243). In chronic left heart failure 

 due to rheumatic, arteriosclerotic, and hypertensive 

 heart disease, the coronary circulation apparently 

 responds by a slight increase in oxygen usage through 

 maintenance of the left coronary flow and an in- 

 creased coronary A-V oxygen difference. This 

 corresponds with the changes indicated for the right 

 heart in an early stage of failure. As is true for the 

 heart-lung or isolated heart, such hearts have con- 

 siderable difficulty in transforming released energy 

 into realizable work. Studies of the coronary circula- 

 tion in high-output failure from excessive transfusion 

 or a chronic aorta-caval fistula are not available. In 

 the anesthetized open-chest dog, however, an acute 

 arteriovenous fistula sufficient to increase cardiac 

 output and cardiac work causes considerable aug- 

 mentation of stroke coronary flow and stroke coronary 

 oxygen even in the presence of a sizeable decrease in 

 arterial blood pressure (389). 



When acute heart failure induced by pulmonary 

 artery constriction has advanced to the stage where 

 systemic blood pressure is low, left ventricular size is 

 small, right ventricular size is large, and release of 

 the constriction does not restore ventricular working 

 capacity, then the use of arterial transfusion with a 

 pump temporarily promotes functional recovery of 

 the heart (increase in arterial and coronary perfusion 



pressure, coronary flow, cardiac output, cardiac work, 

 and myocardial vigor, decrease in cardiac size and 

 coronary A-V oxygen difference). Veno-arterial 

 pumping accentuates and makes more permanent 

 these beneficial changes. Since an increase in coronary 

 flow invariably precedes recovery of the heart, it 

 suggests that it is a primary stimulus through an 

 effect on myocardial metabolism for increased 

 ventricular performance and decrease in heart 

 size (14). 



Postmortem specimens from human patients may 

 show myocardial edema (increased water, Na and CI 

 content per unit of myocardium) in the presence of 

 congestive heart failure, acute infarction, and ischemic 

 areas. Very often, however, previous drug administra- 

 tion, together with agonal and postmortem changes, 

 makes interpretation difficult. The isolated dog heart 

 does not develop edema when directly perfused from 

 a donor dog, but increased myocardial water content 

 is found after acute cardiac injury (over-distended 

 ventricle), excessive perfusion pressure, increased 

 coronary venous pressure, and by perfusion with 

 blood from a disposable bag oxygenator system. It 

 occurs spontaneously in the failing heart-lung prepa- 

 ration and in chronic heart failure produced experi- 

 mentally by thoracocaval constriction, pulmonary 

 stenosis, and tricuspid insufficiency, separately or 

 together. The mechanism or mechanisms involved are 

 unknown, but in these chronic preparations, elevation 

 of right atrial pressure seems to be a major pathogenic 

 factor in its formation. Whether its presence con- 

 tributes to abnormal cardiac function or whether its 

 prevention or reversal is a therapeutic objective in 

 the management of heart disease is a moot question 

 (3 2 9. 409 )• 



Hemorrhagic Slunk 



Standardized oligemic shock in dogs is characterized 

 during the hypotensive phase by a decrease in 

 cardiac output, systemic blood pressure, cardiac 

 work, stroke volume and stroke work, and by an 

 increase in heart rate and an adequate central venous 

 pressure. Coronary flow and coronary resistance 

 are greatly decreased but the coronary flow fraction 

 of cardiac output is increased (102). Coronary flow is 

 generally greater and the resistance generally less than 

 can be accounted for by a simple decline in arterial 

 blood pressure (281). At the same time, the oxygen 

 uptake decreases and the coronary arteriovenous 

 oxygen difference is generally unchanged (166). The 

 coronary response to sustained hypotension through 



