Digoxin (Cardiac Glycoside)
Common brand names: Lanoxin, Digitek, Cardoxin
Three nutrients listed against this medication. The most severe is marked critical.
At a glance
One of the three is marked well documented. The other two carry their own evidence levels.
At a glance
- MagnesiumCritical · Well documented
- PotassiumCritical · Traditionally cited, limited evidence
- CalciumModerate · Traditionally cited, limited evidence
Color shows how serious each listed effect is. The label beside it shows how strong the evidence is. The cards below explain each one and show its evidence.
Nutrients it can lower
Mechanism, Magnesium and digoxin compete for the same Na+/K+-ATPase pump. Low magnesium sensitizes the heart to digoxin toxic arrhythmogenic effects. Most digoxin toxicity involves concurrent magnesium or potassium depletion.
Common signs, Nausea, visual disturbances, potentially fatal arrhythmias at toxic levels
Br J Clin Pharmacol (1991): in 81 hospital patients on digoxin, those with clinical digoxin toxicity had significantly lower serum and monocyte magnesium than those without.
Magnesium glycinate was used at 300–400 mg daily; drug levels and serum magnesium are monitored monthly.
Mechanism, Digoxin and potassium compete for Na+/K+-ATPase. Hypokalemia is THE classic precipitant of digoxin toxicity. A potassium of 3.0 mEq/L can convert therapeutic digoxin to toxic.
Common signs, Nausea/vomiting, confusion, yellow-green visual halos, potentially fatal ventricular arrhythmia
Brater and Morrelli (Clinical Pharmacology and Therapeutics, 1977; PMID PubMed ID: the permanent number the US National Library of Medicine gives a published paper. Each one links to that paper's record on PubMed. 872493): digoxin toxicity occurred in patients with total-body potassium depletion despite normal serum potassium, so a normal serum value does not exclude the depletion.
Trials targeted potassium of 4.0 to 5.0 mEq/L under physician monitoring. Potassium beyond diet alongside digoxin belongs under medical guidance.
Mechanism, Hypercalcemia from any cause potentiates digoxin toxicity, so calcium status matters on this drug. The older teaching that intravenous calcium is absolutely contraindicated in digitalized patients rests on 1930s case reports and animal work at extreme calcium concentrations; a retrospective series of digoxin-toxic patients found no life-threatening dysrhythmia within an hour of intravenous calcium and no mortality difference. Acute management of digoxin toxicity and hyperkalemia is toxicology-level care, not a calcium rule. Oral calcium requires care and monitoring.
Common signs, Arrhythmia risk at both extremes of calcium, requires careful monitoring
An interaction, not a depletion: rapid IV calcium can worsen digoxin toxicity ('stone heart'). A monitoring caution only.
Normal dietary calcium intake is maintained. Calcium supplements are separated from digoxin by at least 2 hours, and calcium status is monitored because hypercalcemia potentiates digoxin toxicity.
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Disclosure
These statements have not been evaluated by the Food and Drug Administration. Any grade on this page describes the strength of published human trial evidence in the populations studied. It is not a recommendation for any individual and is not medical advice. Starting, stopping or changing any supplement or medication is a decision for your physician.
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