The Annals of Thoracic Surgery, Vol 31, 117-120, Copyright © 1981 by The Society of Thoracic Surgeons
Intramyocardial electrical and metabolic activity during hypothermia and potassium cardioplegia
B Brandt 3d, JV Richardson, P O'Bryan and JL Ehrenhaft
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.
