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Cardiac Glycoside Plant Poisoning (Oleander, Foxglove): An ICU Nurse's Guide

⚕️ Medical Disclaimer: This content is for educational purposes only and is intended for licensed healthcare professionals. It does not constitute medical advice and should not replace clinical judgment, facility protocols, or physician orders. Always verify medications, doses, and procedures with your institution's guidelines.

Part of the ICU Emergencies Hub — browse every related guide in one place.

This article was created with AI assistance.

Updated July 2026  |  More ICU nursing guides →

Several common garden and wild plants contain cardiac glycosides — the same class of molecule as the drug digoxin. Oleander (every part, including the smoke from burning it and water that flowers have sat in), foxglove (the original source of digitalis), lily-of-the-valley, and yellow oleander seeds can all produce a poisoning that behaves like a massive digoxin overdose. Patients arrive after a suicide attempt, an herbal remedy, a foraging mistake, or a curious child, and the ICU nurse's job is to recognize the toxidrome, respect the potassium, and know why the definitive antidote is the same one used for digoxin.

Scope note: Educational overview for licensed ICU and ED nurses — not a treatment protocol. Antidote dosing, pacing decisions, and toxicology consultation belong to the provider and your regional Poison Control Center. Follow your facility's protocols and orders.

What cardiac glycosides do

Cardiac glycosides poison the sodium-potassium pump (Na/K-ATPase) on every cell. In heart muscle this increases contractility but also makes the heart electrically irritable and slows conduction through the AV node. Systemically, blocking the pump keeps potassium from moving back into cells, so serum potassium rises. That rise is the single most useful number in acute poisoning: a high and climbing potassium in an acutely poisoned patient signals severe toxicity and a worse prognosis. The clinical picture blends gastrointestinal, cardiac, and sometimes neurologic and visual features.

SystemWhat you see
GI (early)Nausea, vomiting, abdominal pain
CardiacBradycardia, heart block, junctional rhythms, ectopy, and paradoxically both slow and fast dysrhythmias
MetabolicHyperkalemia in acute poisoning (a key severity marker)
Neuro / visualConfusion, weakness, classically yellow-green vision and halos (more in chronic)

The rhythm can be almost anything

Cardiac glycoside toxicity is famous for producing nearly every dysrhythmia in the book, but the theme is increased automaticity plus depressed conduction. Bradycardia, various degrees of AV block, junctional escape rhythms, and ventricular ectopy are common; bidirectional ventricular tachycardia, though rare, is nearly pathognomonic. The nurse keeps the patient on continuous telemetry, has atropine ready for symptomatic bradycardia, and anticipates that a poisoned heart may not respond to the usual measures until the antidote is on board.

The calcium fear: In most hyperkalemia, IV calcium stabilizes the cardiac membrane and is reflexive. In cardiac glycoside poisoning, giving calcium has traditionally been feared to worsen the already calcium-overloaded, glycoside-poisoned myocardium — the so-called "stone heart." The evidence is debated, but the practical point for the nurse is clear: do not reach for IV calcium on your own in a glycoside-poisoned patient with hyperkalemia. The definitive treatment for both the rhythm and the potassium is the antidote, not calcium.

Digoxin immune Fab is the antidote

Because plant cardiac glycosides are structurally similar to digoxin, digoxin immune Fab (the antibody fragment marketed as DigiFab, historically Digibind) binds and neutralizes many of them and is the treatment of choice for serious plant-glycoside poisoning with life-threatening dysrhythmias or significant hyperkalemia. Two caveats the nurse should hold: a serum digoxin assay may turn mildly positive from the cross-reacting plant toxin but does not reliably measure the true toxin level, so it cannot be used to titrate the way it would for a digoxin overdose; and empiric dosing is often needed because the ingested amount is unknown. As the Fab neutralizes the glycoside, the Na/K pump recovers and the potassium can fall, so potassium must be rechecked frequently to avoid overcorrection.

Your role in one line: Continuous telemetry, atropine and pacing ready, watch the potassium as the severity dial, keep IV calcium out of your own hands, and expect digoxin immune Fab — then recheck potassium as the antidote works.

Decontamination and supportive care

Activated charcoal may be given early to a patient with an intact, protected airway after a recent ingestion, on the provider's order. Beyond that, care is supportive and cardiac-focused: correct magnesium (low magnesium worsens the dysrhythmias), manage bradyarrhythmias, and prepare for transcutaneous or transvenous pacing if the heart block is severe and not responding. For the potassium-lowering measures used alongside the antidote, see hyperkalemia emergency treatment; note the calcium caveat above overrides the usual reflex. For the rhythm the nurse fears with QT-related toxins, see torsades de pointes.

Plant glycoside versus the drug digoxin

The nurse who already knows digoxin toxicity has most of the framework, but two differences matter. First, the dose is unknown and often large in a deliberate ingestion, so poisoning tends to be more severe than a slow drug accumulation. Second, the digoxin level is unreliable, so treatment decisions lean on the clinical picture, the potassium, and the ECG rather than a number. For the drug-toxicity comparison, see digoxin.

What the ICU nurse monitors

Monitor continuous telemetry and 12-lead ECGs, serial potassium and magnesium, renal function, and mental status, and track the response to digoxin immune Fab including the potassium fall as the pump recovers. Keep atropine and pacing capability immediately available, keep Poison Control engaged, and remember that a rising potassium is your loudest alarm. Related toxic-exposure guides: amatoxin mushroom poisoning and caustic ingestion.

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