The Annals of Thoracic Surgery, Vol 43, 373-379, Copyright © 1987 by The Society of Thoracic Surgeons
Electrical activity in the heart during hyperkalemic hypothermic cardioplegic arrest: site of origin and relationship to specialized conduction tissue
TB Ferguson Jr, LS Smith, PK Smith, RJ Damiano and JL Cox
Previous studies from this laboratory have shown that low-amplitude
electrical activity (LEA) may occur during standard hyperkalemic
hypothermic cardioplegic arrest and be undetected by routine monitoring
techniques. The present study was designed to elucidate the
electrophysiological nature of LEA. Ten dogs were monitored continuously
during standard cardioplegic arrest using a 32-channel data acquisition
system. In 7 animals (Part I), electrophysiological mapping of the lower
right atrial septum during arrest was performed. The initial site of
activation of LEA was consistently recorded from the region of the lower
atrial septum prior to atrial or ventricular electrical activation. The
site of origin of LEA was thus localized to the anatomical region of the
atrial septum containing the atrioventricular nodal conduction tissue. In
Part II, the electrophysiological mechanism of LEA was investigated in the
remaining 3 animals utilizing an intrinsic property of specialized
conduction tissue. Inclusion of a calcium channel-blocking agent in
standard cardioplegic solution completely prevented the development of LEA
in all 3 animals, which is in contrast to findings in previous studies
using standard cardioplegic solution alone. These data suggest that LEA may
be related to calcium-mediated activation of specialized conduction tissue.
This mechanism of activation may explain why LEA cannot be detected by the
intraoperative monitoring techniques routinely employed.
