Prospective evaluation of parenteral magnesium sulfate in the treatment of patients with reentrant AV supraventricular tachycardia

This study prospectively assessed the electrophysiologic effects of parenteral magnesium sulfate administration on paroxysmal atrioventricular (AV) reentrant supraventricular tachycardia and the efficacy of magnesium to terminate these arrhythmias. Eleven normomagnesemic patients, seven with orthodromic reentrant supraventricular tachycardia that used an accessory AV pathway, and four with typical AV nodal reentry were examined. All patients had a history of sustained supraventricular tachycardia requiring pharmacologic therapy or electrical cardioversion for termination of tachycardia. After baseline electrophysiologic study, including documentation of sustained supraventricular tachycardia that was reproducibly induced, parenteral magnesium sulfate (a bolus of 0.3 mEq/kg of elemental magnesium infused over a 10-minute period followed by a maintenance infusion of 0.2 mEq/kg/hr) was administered during sustained supraventricular tachycardia. The serum magnesium concentration increased from (mean±standard deviation) 1.9±0.2 mg/dl to 4.0±0.6 mg/dl (p=0.0001). Except for flushing and mild diaphoresis during infusion of the magnesium sulfate bolus, and dry heaves in one patient, there were no untoward effects or significant changes in systolic blood pressure. During administration of magnesium, the tachycardia cycle length increased from 319±39 msec to 348±43 msec (p=0.0001). Slowing of the tachycardia occurred predominantly in the antegrade limb of the circuit at the level of the AV node with the AH interval increasing from 171±66 msec to 197±68 msec (p=0.0001), whereas there was no significant change in the HV interval (43±3 msec to 43±4 msec, p=NS) or the VA interval (106±43 msec to 110±47 msec, p=NS) during tachycardia. In two patients the tachycardia terminated spontaneously. However, termination of supraventricular tachycardia in these patients was the result of three- and four-beat runs of spontaneous nonsustained ventricular tachycardia. Administration of magnesium did not suppress the inducibility of supraventricular tachycardia in any patient or significantly influence the effective refractory periods of the right atrium, AV node, accessory pathway, or right ventricle. Thus in normomagnesemic patients with reentrant paroxysmal supraventricular tachycardia, parenterally administered magnesium sulfate increases the tachycardia cycle length by slowing the antegrade limb of the reentrant circuit at the level of the AV node. Although it slows the tachycardia, magnesium sulfate is only rarely effective in terminating supraventricular tachycardia.