Magnesium deficiency alters the threshold for epinephrine-induced arrhythmias during halothane or sevoflurane anesthesia in the rat.

OBJECTIVE

To determine the effect of chronic magnesium (Mg2+) deficiency on the relative arrhythmogenicity of halothane and sevoflurane in the rat.

DESIGN

Prospective, randomized, nonblinded study.

SETTING

University laboratory.

PARTICIPANTS

Male Sprague-Dawley rats (n = 48).

INTERVENTIONS: Rats were maintained on a Mg2+-deficient or control diet for 14 days, at which time they were anesthetized with halothane or sevoflurane, a tracheostomy was performed, and the lungs were ventilated to maintain normocapnia. Catheters were inserted into a femoral vein and carotid artery. Lead II of the electrocardiogram was monitored to determine the threshold for epinephrine-induced arrhythmias.

MEASUREMENTS AND MAIN

RESULTS

Chronic Mg2+ deficiency significantly decreased the dose of epinephrine required for arrhythmias (ADE). The reduction in the ADE was approximately one third during halothane anesthesia (p < 0.05) and one fifth during sevoflurane anesthesia (p < 0.001). Infusion of magnesium sulphate completely reversed the reduction in ADE. In normomagnesemic rats, the halothane ADE was significantly less than the sevoflurane ADE (mean difference = 6.0 microg/kg, 95% confidence interval of the difference = 3.6 to 8.4 microg/kg) (p < 0.005). Mg2+ deficiency significantly attenuated the difference between the halothane ADE and the sevoflurane ADE (mean difference in the Mg2+-deficient group = 0.6 microg/kg, 95% confidence interval of the difference = -0.2 to 1.5 microg/kg).

CONCLUSION

Chronic Mg2+ deficiency decreased the threshold for epinephrine-induced arrhythmias and attenuated differences between the arrhythmogenic potential of halothane and sevoflurane, suggesting that arrhythmias are as likely to develop with sevoflurane as with halothane in the presence of coexisting magnesium deficiency and elevated catecholamines.