Intramyocardial electrical and metabolic activity during hypothermia and potassium cardioplegia

Hypothermic potassium cardioplegia is widely used to reduce myocardial metabolism as a means of myocardial protection. To investigate the efficacy of intramyocardial electrical activity as an indicator of myocardial metabolism, 12 dogs were placed on cardiopulmonary bypass and myocardial oxygen consumption, partial pressure of carbon dioxide (PCO2) in the coronary sinus, myocardial temperature, and intramyocardial and surface electrocardiograms were measured. The hearts were fibrillated and cooled to 15 degrees C. In Group 1 (6 dogs), potassium cardioplegia was given at 15 degrees C. In Group 2 (6 dogs), it was given at 25 degrees C. Maximum coronary sinus PCO2 and oxygen consumption occurred at 36 degrees C and gradually decreased, but there was still evidence of metabolic activity and intramyocardial electrical activity at 15 degrees C. When cardioplegia was given at 15 degrees C, all electrical activity ceased and there was a further significant reduction in metabolic activity (coronary sinus PCO2 and oxygen consumption). In Group 2 similar findings were found at 25 degrees C, and there was no further reduction in metabolic activity at 15 degrees C. These data indicate that: (1) myocardial metabolic activity is lowest when there is electrical quiescence as measured with an intramyocardial electrode; (2) potassium arrest and hypothermia are both necessary to achieve electrical quiescence; and (3) in the potassium-arrested heart, lowering temperature from 25 degrees to 15 degrees C does not result in a further reduction of metabolic activity.