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Effects of magnesium sulfate on cardiac conduction and refractoriness in humans
Insights
Magnesium administration significantly impacts cardiac electrophysiology, increasing sinus node recovery and atrioventricular node conduction times. This study systematically evaluated magnesium
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Magnesium is empirically used for arrhythmias.
- Systematic human studies on magnesium's cardiac electrophysiologic effects are lacking.
Purpose of the Study:
- To determine the electrocardiographic and electrophysiologic effects of magnesium in humans.
- To evaluate magnesium's impact on cardiac conduction and refractoriness.
Main Methods:
- 10 patients with normal baseline serum magnesium received 6g IV magnesium sulfate followed by 1g/hr infusion.
- Electrocardiographic and electrophysiologic parameters were measured.
- Serum magnesium levels were monitored.
Main Results:
- Serum magnesium increased significantly (2.0 to 5.4 mg/dl).
- No significant changes in heart rate, QRS, QT, or QTc intervals.
- Significant increases in sinus node recovery time, AV node conduction time, and AV node refractory periods.
Conclusions:
- Magnesium administration alters cardiac conduction and refractoriness.
- Findings provide a systematic evaluation of magnesium's electrophysiologic effects in humans.
Abstract:
Magnesium has been used empirically for several decades in the treatment of atrial and ventricular arrhythmias in patients with normal and decreased serum magnesium levels. However, a systematic evaluation of the effects of magnesium on cardiac conduction and refractoriness in humans has not been described. In this study, the electrocardiographic and electrophysiologic effects of magnesium were determined in 10 patients with normal baseline serum magnesium and other electrolyte levels. Six grams of magnesium sulfate was administered intravenously over 6 minutes followed by a continuous infusion of 1 additional gram over 1 hour. Serum magnesium levels rose significantly from a baseline of 2.0 +/- 0.2 to 5.4 +/- 0.4 mg/dl (p less than 0.001). No significant change occurred in heart rate at rest, or in duration of the QRS complex or QT or QTc intervals during sinus rhythm. There were significant increases in sinus node recovery time (1,000 +/- 211 to 1,106 +/- 223 ms, p less than 0.01) and corrected sinus node recovery time (279 +/- 87 to 336 +/- 104 ms, p less than 0.05). Significant increases occurred in atrioventricular (AV) node conduction time during sinus rhythm (82 +/- 22 to 97 +/- 17 ms, p less than 0.02), in the atrial paced cycle length at which AV node Wenckebach block occurred (350 +/- 46 to 419 +/- 65 ms, p less than 0.01) and in the AV node relative refractory period (397 +/- 27 to 422 +/- 18 ms, p less than 0.05), functional refractory period (395 +/- 41 to 415 +/- 33 ms, p less than 0.05) and effective refractory period (306 +/- 67 to 338 +/- 38 ms, p less than 0.05).