Hypokalemia during the cooling phase of therapeutic hypothermia and its impact on arrhythmogenesis

BackgroundMild to moderate therapeutic hypothermia (TH) has been shown to improve survival and neurological outcome in patients resuscitated from out-of-hospital cardiac arrest (OHCA) with ventricular fibrillation (VF) as the presenting rhythm. This approach entails the management of physiological variables which fall outside the realm of conventional critical cardiac care. Management of serum potassium fluxes remains pivotal in the avoidance of lethal ventricular arrhythmia.MethodsWe retrospectively analyzed potassium variability with TH and performed correlative analysis of QT intervals and the incidence of ventricular arrhythmia.ResultsWe enrolled 94 sequential patients with OHCA, and serum potassium was followed intensively. The average initial potassium value was 3.9 ± 0.7 mmol l−1 and decreased to a nadir of 3.2 ± 0.7 mmol l−1 at 10 h after initiation of cooling (p < 0.001). Eleven patients developed sustained polymorphic ventricular tachycardia (PVT) with eight of these occurring during the cooling phase. The corrected QT interval prolonged in relation to the development of hypothermia (p < 0.001). Hypokalemia was significantly associated with the development of PVT (p = 0.002), with this arrhythmia being most likely to develop in patients with serum potassium values of less than 2.5 mmol l−1 (p = 0.002). Rebound hyperkalemia did not reach concerning levels (maximum 4.26 ± 0.8 mmol l−1 at 40 h) and was not associated with the occurrence of ventricular arrhythmia. Furthermore, repletion of serum potassium did not correlate with the development of ventricular arrhythmia.ConclusionsTherapeutic hypothermia is associated with a significant decline in serum potassium during cooling. Hypothermic core temperatures do not appear to protect against ventricular arrhythmia in the context of severe hypokalemia and cautious supplementation to maintain potassium at 3.0 mmol l−1 appears to be both safe and effective.