|
First Article
"The Role of Magnesium in Cardiac Arrhythmias", Keller, Peter K. and Aronson, Ronald S., Progress in Cardiovascular Diseases, May/June 1990;32(6):433-448. (Address: Ronald S. Aronson, M.D., Department of Medicine, Division of Cardiology, Albert Einstei
n College of Medicine, Forchheimer Building, Room G42, 1300 Morris Park Avenue, Bronx, NY 10461, U.S.A.) ______________________
Magnesium deficiency leads to arrhythmias by reduced activity of the magnesium dependent Na-K-ATPase with consecutive intracellular K- deficiency, decreased resting membrane potential and increased Digitalis toxicity. Indications for parenteral magnesiu
m therapy for arrhythmias include ventricular tachycardia, torsades de pointes, intractable ventricular tachycardia and fibrillation, ventricular tachyarrhythmias with digitalis toxicity, multifocal atrial tachycardia and paroxysmal atrial tachycardia.
Magnesium may also be of benefit in acute myocardial infarction and prevention of sudden death in coronary heart disease. 6225
"Possible Use of Magnesium in The Clinical Treatment of Cardiac Arrhythmias", Antoni, D.H., Magnesium Research, 1988;1(½):104, 10th Hohenheim Magnesium Symposium. (Address: D.H. Antoni, Medicinische Klinik I, Stadt. K.H. Munchen-Bogenhausen, Federal Re
public of Germany)
Magnesium activates sodium-potassium adenosine triphosphate which helps maintain resting membrane potential. Magnesium deficiency is associated with a loss of intracellular potassium, increased intracellular sodium and cell excitability. Increased intr
acellular sodium causes a sodium-calcium exchange which increases the chances of depolarization and repetitive arrhythmias. The RDA for magnesium is 5 mg/kg. Hypomagnesemia occurs in those receiving loop or thiazide diuretics. Thirty-seven of CHF patien
ts on diuretics were found to be deficient in magnesium and 38-42% of patients receiving diuretic therapy who were hypokalemic were also hypomagnesemic. Magnesium repletion is usually neglected while physicians pay attention to potassium repletion. There
is an association between low magnesium levels and increased cardiac mortality and sudden death. There is also an association with sudden death and low magnesium in the soil and water supplies. Potassium repletion in long term diuretic patients who hav
e ventricular ectopy have not necessarily resulted in the normalization of intracellular levels of potassium until magnesium sulfate was administered. The ability to maintain the potassium gradient is dependent on the presence of magnesium. This possibly
may be the reason for sudden death in hypertensive patients on long term diuretic therapy. Magnesium works well to suppress ventricular arrhythmias in Digitalis toxicity due to its ability to counteract the inhibitory effect of Digitalis on sodium-pota
ssium adenosine triphosphate. Digitalis therapy increases intracellular calcium and has an inotropic effect. Magnesium levels should be routinely assessed in patients receiving digitalis therapy. Intravenous magnesium should be a routine therapy for digi
talis toxicity with ventricular arrhythmias. Torsades de pointes is a life threatening ventricular arrhythmia effectively treated with magnesium. Two to 4 gram boluses of magnesium sulfate followed by 3 to 20 mg/min for the next 7 to 48 hours has been d
ocumented to have a very positive benefit in this condition. Low potassium, magnesium and high levels of calcium have been found in infarcted areas and transient low magnesium levels have been seen in acute myocardial infarction. Myocardial infarction
and congestive heart failure patients frequently have low magnesium levels. In 342 patients with acute myocardial infarction there was an increased frequency of ventricular ectopy with hypomagnesemia. In acute myocardial infarction a single bolus of magn
esium sulfate reduced ventricular arrhythmias from 35 to 50% in the following four hours. The authors support the routine use of magnesium in acute myocardial infarction. The authors encourage the supplementation of magnesium chloride in any suspected ca
se of hypomagnesemia even though serum levels may be normal because intracellular levels may be abnormal. In patients with digitalis toxicity, torsades de pointes or complicated acute myocardial infarction magnesium chloride administration is recommended
regardless of blood magnesium levels. They suggest an oral preparation containing both potassium and magnesium. 8669
"Suppression of Ventricular Arrhythmias by Magnesium", Tzivoni, Dan, M.D. and Keren, Andre, M.D., The American Journal of Cardiology, June 1, 1990;65:1397-1399. (Address: Dan Tzivoni, M.D., The Heiden Department of Cardiology, Bikur Cholim Hospital, P.
O. Box 492, Jerusalem, Israel 91002)
____________________
This is a clinical review article reporting the role of magnesium in the prevention and treatment of arrhythmias. Magnesium stimulates the sodium-potassium-ATPase pump which regulates intracellular and extracellular potassium levels. Magnesium administra
tion to hypokalemic individuals reduces ventricular ectopic beats by normalization of membrane potential and enhancing repolarization. The risks to hypomagnesemia include chronic alcoholism, malabsorption, long term nasogastric suction, renal dysfunction
and medications such as thiazide diuretics, digitalis, and aminoglycosides. Those who have inflammation of the bowel resulting in diarrhea or ulcerative colitis are susceptible to magnesium loss. Magnesium has been used at a dose of 5.4 mEq/hr/24 hrs (1
mEq Mg = 0.5 mmol Mg = 12.3 mg Mg) in acute myocardial infarction immediately upon admission and decreased ventricular arrhythmias significantly (1 mEq Mg = 0.5 mmol Mg = 12.3 mg Mg). It is quoted as having "virtually zero toxicity". In ventricular fibr
illation magnesium could possibly be an excellent first line agent. Magnesium can be used in unresponsive ventricular tachycardia to cardioversion or lidocaine therapy. The treatment is magnesium sulfate 2 gms (4 mL of 50%) over 1-5 minutes in combinati
on with other antiarrhythmic agents. Magnesium can also be used for tricyclic antidepressant overdose as a first line antiarrhythmic agent and also for torsades de pointes. In torsades de pointes magnesium sulfate 2 gms (4 mL of 50%) IV push is given fol
lowed by 1-2 gm/min. For stable patients 2 gm/20 minutes followed by 2 gm/hr. It is excellent for life threatening digitalis induced arrhythmias and can be given after Digoxin immune fab (ovine, Digibind) and lidocaine in a 2 gm IV push over 1-2 minutes
then at a dosage of 2 gm/hr. Check magnesium levels every four hours. For premature ventricular contractions 2 gm/20 minutes initially and then at 2 gm/hr. Magnesium should be given along with potassium for hypokalemia. Magnesium is necessary to assist p
otassium's movement into the muscle cells. Even though serum potassium levels rose with potassium administration in one study, muscle biopsies showed no improvement. Do not rely on serum magnesium levels. Only 1% of total body magnesium is found in the s
erum. Ultra filtration levels are probably more accurate. Risk of inducing hypermagnesemia is low except in cases of renal insufficiency or failure, and in patients receiving magnesium cathartics. 10356
"Practical Briefings: Clinical News You Can Put Into Your Practice Now. Ventricular Arrhythmias and Magnesium", Patient Care, October 15, 1990;16-20. (Address: Corey M. Slovis, MD, Dept. of Emergency Medicine, University of Rochester School of Medicine a
nd Dentistry Medical Center, Rochester, NY 14642/Patient Care, 680 Kinderkamack Road, Oradell, NJ 07649, U.S.A.)
Magnesium and Cardiomyopathy
Ten patients, seven men between 56 and 78 years of age who had ischemic dilated cardiomyopathy who were normomagnesemic, and who had severe ventricular arrhythmias, were given magnesium sulfate in 9% NaCl in an infusion of 50 mg/min/60 minutes two times
daily for seven days. In all patients there was an antiarrhythmic effect with marked reduction in premature ventricular contractions and coupling as well as runs of ventricular tachycardia which disappeared by the 5th day. Heart rate QTc intervals remain
ed normal. These infusions did not raise serum magnesium levels immediately post infusion. No side effects were noted. The authors conclude magnesium infusions are an effective antiarrhythmic drug for short and middle term control of severe ventricular a
rrhythmias in ischemic dilated cardiomyopathy. 10174
|