Why the study?
Does cardioversion from induced ventricular tachycardia cause changes in serum electrolytes and hormones compared to normal programmed stimulation or cardioversion from stable atrial fibrillation?
Does cardioversion from induced ventricular tachycardia cause changes in serum electrolytes and hormones compared to normal programmed stimulation or cardioversion from stable atrial fibrillation?
Cardioversion from induced ventricular tachycardia leads to hypokalemia and hypomagnesemia, likely driven by a catecholamine and insulin-mediated intracellular shift of electrolytes secondary to hemodynamic stress.
Electrolyte shifts after induced VT cardioversion may warrant monitoring; leaves open applicability to spontaneous clinical VT.
We have observed hypokalemia after cardioversion from spontaneous out-of-hospital ventricular fibrillation and induced ventricular tachycardia. To test the hypothesis that the hormone response to the hemodynamic stress of the arrhythmia initiated the change in potassium, we compared the electrolytes and hormones in three groups of patients. We observed a decrease in serum potassium and magnesium after cardioversion from ventricular tachycardia induced by programmed stimulation, but not after normal programmed stimulation of the ventricle or after cardioversion from stable atrial fibrillation. These changes were preceded first by a rise in norepinephrine and epinephrine, then a rise in glucose, followed by a rise in insulin. The stimulus for these changes was probably the hypotension associated with ventricular tachycardia. The sequence of changes suggests that the decrease of potassium and magnesium after ventricular tachycardia was due to a shift of the electrolytes into cells, related to the insulin-mediated movement of glucose from the blood into cells.
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Salerno et al. (1993) studied this question.
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