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Serum electrolytes and catecholamines after cardioversion from ventricular tachycardia and atrial fibrillation
D M Salerno1, A Katz, D N Dunbar
1Department of Medicine, Hennepin County Medical Center, University of Minnesota, Minneapolis.
Insights
Hypokalemia and hypomagnesemia occur after ventricular tachycardia cardioversion due to hormonal responses. This electrolyte shift into cells is linked to insulin release triggered by hypotension during the arrhythmia.
Area of Science:
- Cardiology
- Endocrinology
- Electrolyte Physiology
Background:
- Hypokalemia is observed post-cardioversion for ventricular fibrillation and tachycardia.
- The role of hormonal responses to hemodynamic stress in electrolyte changes requires elucidation.
Purpose of the Study:
- To investigate the hypothesis that hormonal responses to hemodynamic stress from arrhythmias trigger potassium level changes.
- To compare electrolyte and hormone levels in patients undergoing different cardiac procedures.
Main Methods:
- Comparison of serum electrolytes and hormones in three patient groups.
- Analysis of changes after cardioversion from induced ventricular tachycardia versus normal programmed stimulation or atrial fibrillation cardioversion.
Main Results:
- A decrease in serum potassium and magnesium was observed after cardioversion from induced ventricular tachycardia.
- No significant electrolyte changes were noted after normal programmed stimulation or atrial fibrillation cardioversion.
- Hormonal changes preceded electrolyte shifts: norepinephrine and epinephrine rose first, followed by glucose, then insulin.
Conclusions:
- Hypotension during ventricular tachycardia likely stimulates the observed hormonal and electrolyte changes.
- Electrolyte decrease is attributed to insulin-mediated glucose uptake, causing potassium and magnesium to shift into cells.
Abstract:
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.