i54" 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



the metabolic needs accumulated during the anoxic 

 period. The large increase in systolic as well as dia- 

 stolic flow within the first few seconds, before there is 

 time for a change in myocardial contractility, in- 

 dicates that massive active vasodilation has taken 

 place which overcomes systolic flow resistance. With 

 a longer period of occlusion, there must be considered 

 the possibility of flow through arteriovenous shunts 

 and through vessels probably near the epicardial 

 surface, whose surrounding myocardium is now "tired" 

 and does not so strongly oppose flow. 



The oxygen consumption during myocardial re- 

 active hyperemia is measured by determining the 

 left coronary artery blood flow (rotameter) and the 

 difference in oxygen saturation of the arterial and 

 coronary sinus blood (measured continuously with 

 an optical densitometer). The theoretical oxygen 

 "debt" (control oxygen consumption X duration of 

 left coronary artery occlusion) is overpaid for 15- and 

 30-sec but slightly underpaid for 10-sec occlusions 

 (67). The rate of oxygen consumption during the 

 increased blood flow period is greater than in the 

 control state, showing that the myocardium has been 

 stimulated to take up more oxygen. The basic hy- 

 pothesis governing the calculation of the oxygen 

 "debt" in these studies is somewhat erroneous, for the 

 oxygen in the blood in the coronary vascular bed 

 during arterial occlusion, the metabolic rate during 

 the circulatory stasis, and changes in cardiac work are 

 not considered. As further evidence that the myo- 

 cardium develops an oxygen deficit, i.e., that 

 anaerobic metabolism occurs, it has been found that 

 lactic acid increases in the coronary sinus blood, 

 often in comparison to pyruvic acid levels following 

 the period of anoxia (67). These observations have 

 been confirmed in the unanesthetized dog with the 

 aid of chronically implanted (3-14 days postoperative) 

 electromagnetic flowmeters and coronary sinus 

 sampling tubes (280). 



The contracting myocardium can withstand much 

 shorter periods of arterial occlusion and oxygen 

 deficit than resting skeletal muscle, and repays its 

 oxygen "debt" with an increased blood flow but with a 

 decreased A-V oxygen difference. 



Heart Rate 



Early reports indicated that myocardial oxygen 

 usage increases in the heart-lung and isolated heart 

 when heart rate spontaneously changes or when it is 

 increased by warming the sinus node or by driving the 

 heart electrically, but the evidence was conflicting 



concerning the effect of rhythm of the heart on coro- 

 nary blood flow. In the above preparations, increase 

 in heart rate either increases, decreases, or does not 

 affect coronary flow do). More recent investigations 

 with somewhat better techniques and methodologies 

 confirmed this finding of correlation of oxygen usage 

 with heart rate in these preparations and showed a 

 higher energy cost of external work at the faster heart 

 rate (369). The oxygen observations were extended 

 to the empty heart beating in the open-chest dog 

 (249). In the latter preparation, electrically induced 

 ventricular tachycardia after section of the bundle of 

 His (23, 236, 355) or electrically induced auricular 

 tachycardia at rates somewhat higher than those 

 naturally occurring generally increases aortic blood 

 pressure, cardiac output, and cardiac work, while the 

 stroke volume and stroke work decrease (225). 

 Simultaneously, minute coronary flow and oxygen 

 usage increase, coronary resistance decreases, oxygen 

 extraction is unchanged, but the coronary flow and 

 oxygen consumption per beat decrease (23). Com- 

 parable results were obtained in normal human 

 subjects with atropine-induced cardio-acceleration 

 (137) and in the anesthetized closed-chest dog with 

 electrically induced auricular tachycardia, except 

 that systemic blood pressure, cardiac output, and 

 cardiac work did not rise (256). Since acceleration of 

 of the heart means proportionally greater time per 

 beat and per minute in systole than in diastole, and 

 since in systole coronary flow is less than in diastole, 

 it would be anticipated that increased heart rate per 

 se should reduce coronary flow. Since it does not, it 

 must be that increased flow is due to arteriolar dilata- 

 tion resulting from the increased metabolic activity. 

 Actual measurements indicate that as heart rate 

 increases, extravascular resistance rises but intra- 

 vascular resistance falls to a greater extent, indicating 

 a fall in net coronary resistance (236). The same trend 

 of flow and oxygen usage per beat and per minute 

 also occurs at the faster heart rate when minute 

 cardiac work is held constant or when comparisons 

 are made at the same level of stroke work. This means 

 that cardiac acceleration can augment the energy 

 metabolism of the myocardium without manifesta- 

 tion of the extra energy as work (23, 225). Data on 

 alteration in the coronary circulation following a 

 naturally occurring change in heart rate are limited 

 to the observation of increased coronary flow with 

 increased heart rate (92). Hence, the value of these 

 observations in relation to natural changes in heart 

 rate arising from local changes in the circulation of 



