The role of magnesium in cardiac arrhythmias

T HE RELATIONSHIP between electrolyte deficiencies and the development and prevention of cardiac arrhythmias has been a subject of continued interest in the medical literature. Studies have suggested a correlation between certain electrolyte deficiencies, such as hypokalemia, and the occurrence of arrhythmias and sudden death.le6 Recent interest, however, has focused on magnesium (Mg) deficiency and its role in this area. Interest in Mg may be related to the recognition of the extensive role this cation plays in a multitude of human physiological processes. Mg is the second most abundant intracellular cation in the human body and is involved in over 300 different enzymatic reactions including: glucose use; the synthesis of fat, protein, and nucleic acids; the metabolism of adenosine triphosphate (ATP); muscle contraction; and some membrane transport systems. Effects of Mg on atrioventricular (AV) nodal conduction, the transmembrane potential, and arrhythmias have also been postulated.‘*7-12 Total body Mg stores approximate 1,000 mmol/L with 1% present extracellularly, 60% present in skeletal tissue, and 39% present intracellularly.’ A normal homeostatic level of Mg is maintained via a balance between gastrointestinal absorption and renal excretion. Gastrointestinal net absorption is approximately 35% to 40% of an orally administered load and occurs almost exclusively via the small intestine. Mg loss occurs primarily via renal excretion and averages only 3% to 5% of a filtered load. Over 65% of Mg reabsorption occurs in the thick ascending limb of Henle and, depending on the Mg concentration in plasma, excretion may range from 10 to 5,000 mg over a 24-hour period.274F7,97’0*‘3-15 Despite the apparent ability of the human body to maintain Mg homeostasis through intestinal and renal processes, Mg deficient states occur and are being increasingly recognized. Two studies have documented the prevalence of Mg deficiency in hospitalized patients.‘6-‘8 In one study the prevalence of hypomagnesemia was determined in 2,300 patients in a Veteran’s Administration hospital.16*” When hypomagnesemia was defined as a serum Mg concentration less than 1.25 mEq/L the prevalence of hypomagnesemia was 6.9%. In another study Wong et all8 determined serum magnesium levels in 621 samples of randomly selected hospitalized patients and found hypomagnesemia (< 1.2 mEq/ L) in 11%. The causes of hypomagnesemia are many and varied and include: nutritional causes secondary to prolonged parenteral fluid administration, starvation with metabolic acidosis, protein-calorie malnutrition, Kwashiorkor, or alcoholism; intestinal causes secondary to chronic diarrhea or a malabsorption syndrome; renal causes secondary to disease-related states such as renal tubular acidosis, the diuretic phase of acute tubular necrosis, chronic glomerulonephritis, chronic pyelonephritis, or familial and sporadic renal Mg losses; drug-related causes secondary to diuretics, antibiotic therapy including gentamicin, tobramyocin, ticarcillin, carbenicillin, or amphoteritin B, antineoplastic drugs including cisplatin and cyclosporine; endocrine and metabolic causes including primary and secondary aldosteronism, hyperthyroidism, excessive lactation, pregnancy, hypercalcemia, primary hyperparathyroidism, uncontrolled diabetes mellitus with glucosuria, and acute intermittent porphyria; and congenital causes including maternal diabetes, maternal hyperparathyroidism, maternal hypothyroidism and exchange transfusions.7’9”0~1’7’7*‘9’20 In light of the multitude of etiologies of hypomagnesemia and its prevalence in hospitalized patients, it is possible that reduced Mg often goes undetected by the unsuspecting physician. The symptoms of hypomagnesemia are as varied as its causes, yet these may often be absent or vague. 9*21 Documented manifestations include: neuromuscular symptoms including tremor, myoclonic jerks, convulsions, Chvostek sign, Trous-