Modes of induced cardiac arrest: hyperkalemia and hypocalcemia - literature review

Abstract

The entry of sodium and calcium play a key effect on myocyte subjected to cardiac arrest by hyperkalemia. They cause cell swelling, acidosis, consumption of adenosine triphosphate and trigger programmed cell death. Cardiac arrest caused by hypocalcemia maintains intracellular adenosine triphosphate levels, improves diastolic performance and reduces oxygen consumption, which can be translated into better protection to myocyte injury induced by cardiac arrest.

Sevoflurane Versus Total Intravenous Anesthesia for Isolated Coronary Artery Bypass Surgery With Cardiopulmonary Bypass: A Randomized Trial

“…Cardioplegia and optimization of hemodynamics traditionally are used to minimize complications. 4,5 Recent findings suggest that volatile anesthetics provide a cardioprotective effect with pharmacologic mechanisms of action that are only partially related to the anesthetic effects on the myocardial oxygen balance. 6 The molecular mechanisms for the implementation of the cardioprotective effect of halogenated anesthetics are similar to those that contribute to ischemic preconditioning.…”

Resetting of Cardiac Ventricular Tachycardia Storm with Intravenous Potassium Chloride: A Case Report

“…The IV correction of potassium deficiency is by its administration as an intravenous solution at different concentrations. Potassium chloride shouldn't be administered via IV push/bolus since uptake by the cardiomyocytes is limited by saturation of its receptors [7], and pooling of the injected potassium in the plasma can cause a transient hyperkalemia which may lead to cardiac arrest [8]. It also has an irritant and painful effect as a bolus which may cause chemical phlebitis [9].…”

Mecanismos das alterações eletrocardiográficas na hiperpotassemia / Mechanisms of electrocardiographic changes in hyperkalemia

“…Quanto maior o potencial de repouso, menor será a velocidade de condutância. Consequentemente, essa redução na velocidade prolonga o tempo da fase zero do potencial de ação, sendo demonstrado no eletrocardiograma como alargamento do complexo QRS 3,8 .…”