Effect of Prolonged Periods of Anoxia on Atrioventricular Conduction and Cardiac Muscle

Abstract

The return of A-V conduction according to the electrocardiogram, the ability to maintain the blood pressure, the cardiac muscle ATP, the coronary venous pH, lactic acid, and potassium were studied to delineate the effects on the heart of prolonged periods of anoxia in dogs maintained on an extracorporeal circulation. Myocardial anoxia for 100 minutes was the limit for return of A-V conduction in all dogs in these experiments. Only 2 of 5 hearts anoxic for 120 minutes, and 1 of 3 hearts anoxic for 150 minutes regained A-V conduction. One heart subjected to anoxia for 165 minutes did not show A-V conduction on reperfusion of the coronary arteries. The dogs whose hearts were subjected to periods of anoxia longer than 100 minutes could not maintain the blood pressure on removal from the extracorporeal circulation. This was due to the development of an unusual firmness of the left ventricular muscle, usually appearing after 90 minutes of anoxia and progressing to involve the entire heart. This firmness was not reversible on reperfusion of the heart. Since A-V conduction and speed of conduction returned in some of these firm hearts, it was concluded that there was earlier permanent damage to the myocardial muscle than to the conduction system during anoxia. Cardiac muscle ATP values were not definitely changed after 30 minutes of anoxia, but were decreased and regenerated on reperfusion of the heart after 60 minutes of anoxia. The low levels of ATP did not return toward normal on reperfusion of the heart after 90 and 120 minutes of myocardial anoxia. Additional experiments on anoxic hearts of nonperfused dogs also demonstrated the marked decrease in ATP levels. In both types of studies, the earliest onsets of firmness showed some correlation with low ATP levels. The high lactic acid levels and low pH values of the coronary venous blood found after long periods of anoxia may be related to the failure of ATP regeneration and to the onset of firmness in these hearts. Potassium arrest of hearts subjected to anoxia showed no difference in the return of A-V conduction, in the ability to maintain blood pressure on removal from the extracorporeal circulation, in the onset or degree of myocardial firmness, nor in the levels of cardiac muscle ATP, coronary venous pH, and lactic acid, from the anoxic, nonarrested hearts. The variability of the effect of anoxia on A-V conduction and myocardial muscle of different hearts by the parameters measured in this study is stressed.