Why the study?
Does potassium-induced cardiac arrest increase SGOT levels in patients undergoing open-heart surgery?
Does potassium-induced cardiac arrest increase SGOT levels in patients undergoing open-heart surgery?
Potassium-induced cardiac arrest is the primary driver of marked SGOT elevation following open-heart surgery.
Answers are grounded in this paper and cite their sources.
Potassium arrest-associated transaminase rises should not yet alter protocols; hypothesis-generating for randomized trials on myocardial protection.
Serial SGOT levels have been obtained on a group of 85 patients. Total body per-fusion and intracardiac repair was employed in 80, while the remaining five, acting as a control group, underwent general thoracic procedures. Transaminase values have been correlated with induced cardiac arrest, type of operation, duration and rate of perfusion, age and postoperative course. The study indicates that the chief factor associated with marked SGOT elevation is potassium-induced cardiac arrest. Compared with nonarrested cases, its use doubled or tripled transaminase levels in all types of open-heart operations.
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Quinn et al. (1960) studied this question.
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