BLOOD SUPPLY TO THE HEART 



1559 



spinal anesthesia or injection of procaine and Etamon 

 is similar (168). With partial or complete restoration 

 to normal systemic blood pressure by reinfusion 

 (intra-arterial and intravenous routes are equally 

 effective) (56, 361), coronary flow is greater and flow 

 resistance is less than at an equivalent arterial blood 

 pressure in the preshock state. 



The fact that early in the hypotensive phase neither 

 ventricular end-diastolic pressure nor atrial pressure 

 rises indicates that the functional capacity of the 

 heart is adequate for the work performed. However, 

 that myocardial depression or failure is partially 

 responsible for the hemorrhagic shock syndrome is 

 suggested by different observations, a) After prolonged 

 hypotension, there may be evident cardiac dilatation 

 and elevated left and right atrial pressures with the 

 heart eventually proceeding to ventricular fibrillation 

 or standstill (331). With spontaneous cardiovascular 

 decay after reinfusion, the atrial pressure may be at a 

 normal or elevated level despite large cardiac output 

 reduction (402). b) During prolonged oligemic 

 hypotension, as the animal starts to take up blood 

 from the reservoir to maintain its falling blood 

 pressure, the atrial pressure may rise to very high 

 levels (163). Gross and microscopic evidence of 

 myocardial injury appears in both reversible and 

 irreversible shock. Such myocardial depression could 

 be caused by an insufficient coronary flow during 

 either the hypotensive or the post-hemorrhagic 

 periods. The high coronary flow during the restora- 

 tion period would seem to preclude an inadequate 

 coronary flow as an adequate explanation. During 

 the hypotensive period, the actual coronary flow is 

 greatly curtailed. The problem is whether the 

 associated sizeable reduction in coronary resistance 

 is sufficient to permit enough blood to reach the 

 myocardium to prevent it from failing. In some 

 instances, at least, this loss of myocardial contrac- 

 tility is consequent upon an insufficient coronary 

 flow, since the relation of atrial pressure to cardiac 

 size can be reversed by increasing left coronary flow 

 mildly with a pump, without change in either the 

 hypotension or blood volume (331). 



The work just discussed has been largely restricted 

 to studies in experimental animals exposed to anes- 

 thesia, surgery, and varying amounts of traumatic 

 insult. More proper studies might be conducted in 

 intact conscious dogs; this is possible with methodology 

 now available. This type of study has been made with 

 the use of modified and improved electromagnetic 

 flowmeters which were chronically implanted on the 

 left coronary artery as well as the aorta and various 



systemic arteries (159). The experiments confirm 

 previous findings that, of all the arterial beds, only 

 the coronary shows a decreased vascular resistance 

 during hemorrhagic irreversible shock, and add new 

 information regarding the compensatory behavior of 

 the left coronary vascular bed. The coronary pressure- 

 flow ratio moderately increases during hemorrhage, 

 progressively decreases during the hypotensive period 

 as the coronary flow increases spontaneously, and is 

 temporarily restored during the reinfusion. During 

 the irreversible period, in which the coronary flow is 

 fairly well maintained, the pressure-flow ratio again 

 drops. The resistance, however, to coronary flow is 

 somewhat less during the period of spontaneous decay 

 than during the initial hypotensive period. These 

 pressure-flow changes may have their explanation in 

 certain characteristic changes in the coronary flow 

 pattern. The phasic flow pattern, initially some dis- 

 tance above the zero flow line throughout the cardiac 

 cycle, moves closer to the zero flow line during 

 hemorrhage, and backflow may appear during 

 systole. The magnitude of the flow pattern, however, 

 increases, indicating increased vigor of contraction. 

 As the hypotensive period progresses, flow is re- 

 established in systole and increased somewhat in 

 diastole. Following reinfusion, and late in the period 

 of spontaneous hemodynamic decay, the flow pattern 

 may resemble somewhat the prevailing aortic pres- 

 sure pulse with the systolic flow equal to or exceeding 

 the diastolic flow. The mechanisms whereby coronary 

 systolic flow is thus preferentially enhanced are not 

 known. 



Hypothermia 



The circulatory and metabolic adjustments of the 

 heart during hypothermia have been partially 

 explored (87). When the body temperature is dropped 

 from 37 C to 20-28 C, by immersion hypothermia or 

 by cooling the systemic arterial blood flow, the 

 associated changes that occur which tend to reduce 

 the coronary flow are a diminution in blood and 

 muscle temperatures, cardiac output, heart rate, 

 cardiac work, and oxygen usage by the heart, an 

 increased blood viscosity and a greatly lengthened 

 period of ventricular systole. The coronary A-V 

 oxygen difference remains about normal or decreases 

 (103, 128, 175, 180, 322). Opposing these factors are 

 the relaxation of the major coronary vessels, which is 

 known to occur with hypothermia, and dilatation of 

 the coronary bed caused by the hypotension per se 

 (25, 177). As a resultant of these determinants, 



