BLOOD SUPPLY TO THE HEART 



1557 



and decreased systemic blood pressure, cardiac index, 

 and cardiac work index. In small groups of human 

 subjects, a normal or decreased coronary blood flow 

 has been reported (216). In a large group of females, 

 the above systemic changes have been found to be 

 associated with a decrease in left ventricular coronary 

 blood flow, increased coronary oxygen extraction, 

 and decreased left ventricular oxygen utilization per 

 unit of myocardium, as compared with normal 

 females but not as compared with normal males 

 (321). This depression of the left coronary circulation 

 in the presence of a lowered activity of the left 

 ventricle would be expected. Acceptance of these 

 data, although in line with those previously reported 

 in the intact dog (118), should possibly be deferred 

 until previous work indicating that the left coronary 

 circulation in the female is maintained at a con- 

 siderably higher level than in the male (320) is 

 confirmed. 



mitral insufficiency. Mitral regurgitation has been 

 experimentally produced in the open-chest dog by 

 permitting blood to flow externally from the left 

 ventricular apex through a flowmeter into the left 

 atrium during systole. Such controlled regurgitant 

 flows, up to three times the resting cardiac output, 

 are tolerated with only slight or mild alterations of 

 effective cardiac output, aortic, left atrial and left 

 ventricular pressures, total peripheral resistance, and 

 the effective left ventricular function curves (45). In 

 anesthetized open-chest dogs, acute mitral insuffi- 

 ciency of variable severity, produced by means of an 

 umbrella-type valve spreader so as to allow a partial 

 or incomplete return of the aortic flow to its control 

 level, results in a moderate increase in coronary blood 

 flow and myocardial oxygen usage and a reduced 

 efficiency. Presumably, the left ventricle expends a 

 significant amount of energy in regurgitating blood 

 into the left atrium during mitral insufficiency (388). 

 No comparable studies of this nature are available in 

 humans. 



aortic coarctation. With simulation of clinical 

 coarctation by acute mechanical constriction of the 

 thoracic aorta just beyond the left subclavian artery, 

 venous return to the heart by way of the inferior vena 

 cava is decreased but compensatory flow through 

 various branches of the aortic arch may increase, 

 with a resultant maintained cardiac output and 

 elevated left ventricular work load. With greater 

 aortic constriction, the net cardiac output decreases, 

 causing the cardiac work to decrease. In either case, 

 the coronary dilatation and increased flow arise in 



large part from active changes in the bore of the 

 coronary bed related to the metabolic demands, and, 

 in part, passively from the increased blood pressure 

 and moderately decreased heart rate (90, 207). The 

 cardiac oxygen consumption is increased much more 

 by this augmentation of pressure work than with an 

 equal increase of volume work following transfusion 

 (335). No chronic studies of aortic coarctation have 

 been made because, owing to development of col- 

 lateral circuits, the aorta may be first partially and 

 then completely constricted at the arch without 

 permanent development of hypertension proximal to 

 the occlusion. In human coarctation not much 

 change is reported in coronary flow and oxygen 

 uptake, but this might be expected because systemic 

 pressure is only mildly elevated (31). However, if true, 

 the deviation might be explained by the fact that in 

 these hearts, which are hypertrophied, there are 

 fewer capillaries per unit of muscle to carry the oxygen 

 and flow. 



Hypertensive Cardiovascular Disease 



An exception to the general picture of coronary 

 compensation to increased systemic stress appears to 

 be the response of the chronically hypertensive heart. 

 In essential hypertension, with a normal cardiac 

 output and elevated systemic blood pressure, the 

 coronary flow and oxygen consumption per 100 g 

 myocardium are unaltered while coronary resistance 

 increases. This increased resistance is shared with the 

 renal and cerebral circulations. Since these hearts are 

 generally hypertrophied, total coronary flow and 

 oxygen usage are probably increased. This deviation 

 is explainable if it is assumed that such hearts with 

 known coronary artery disease have an increased 

 amount of perfused fibrotic tissue (31, 316). 



Heart Failure 



Although the underlying mechanisms for various 

 types of heart failure may be different, the basic 

 hemodynamic manifestations of cardiac failure are 

 similar from causes such as congestive heart failure, 

 anemia, anoxia, hemorrhagic shock, myocardial 

 infarction, hyperthyroidism, and beriberi. Experi- 

 mentally, such hearts exhibit depressed Starling or 

 ventricular function curves (increased ratio of end- 

 diastolic ventricular volume or ventricular filling 

 pressure to stroke work), and show the characteristic 

 optimum beyond which further stretching reduces 

 the force of contraction and leads to myocardial 

 failure. In acute heart failure in the open-chest dog, 



