Drug Mnemonic

Digoxin

Antiarrhythmic • Na/K ATPase Blocker • Heart Failure
May 11, 2026

A story built from the name digoxin itself - so the mechanism of action, key side effects, and the way Step 1 actually tests it stick on the first read.

RxMnemonic Antiarrhythmic
Digoxin
Antiarrhythmic • Na/K ATPase Blocker • Heart Failure
DIG = dig + OX = ox +IN = in
Separate digoxin into DIG - OX - IN. Imagine an ox (OX) digging (DIG) in (IN) its hind legs and refusing to continue pulling a cart. It's decreasing its heart rate since it's not moving, but increasing its contractility since it's digging in its hind legs, as if ready to lunge. The ox is saying K Nah, to signify how digoxin blocks Na/K ATPase and has yellow eyes, a side effect of digoxin toxicity.
Digoxin pharmacology mnemonic illustration
Antiarrhythmic DIG = dig | OX = ox | IN = in
HOW STEP TESTS IT
1
Digoxin inhibits Na/K ATPase, causing intracellular sodium to accumulate. The cell normally uses the Na/Ca antiporter to pump calcium out by bringing sodium in, but with sodium already high inside, this exchanger slows down. Calcium stays trapped inside the cell, increasing contractility. Digoxin also increases vagal tone, slowing heart rate.
2
Side Effects: Digoxin is renally excreted - anything that impairs kidney function, including NSAIDs or aminoglycosides, can cause toxicity even at a normal dose. Toxicity presents with yellow-green vision, bradycardia, and heart block.
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Practice Question

A 68-year-old woman with chronic heart failure is stable on digoxin. She is started on ibuprofen for knee osteoarthritis. Two weeks later, her digoxin level is significantly elevated. What is the mechanism?

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Pharmacology Summary

Digoxin: Mechanism, Uses & High-Yield Facts for USMLE Step 1

Digoxin is a cardiac glycoside that inhibits Na/K ATPase, raising intracellular sodium and slowing the Na/Ca antiporter — trapping calcium inside cardiomyocytes and increasing contractility. It also increases vagal tone, slowing the ventricular rate in atrial fibrillation. Digoxin is renally cleared, so anything that reduces GFR — NSAIDs, aminoglycosides, hypokalemia — can push a therapeutic dose into the toxic range. Toxicity classically presents with yellow-green visual changes, bradycardia, and heart block.

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