Digoxin
A cardiac glycoside that slows and strengthens the heartbeat; used in heart failure and atrial fibrillation.
Digoxin increases the force of myocardial contraction (positive inotropy) by inhibiting the sodium-potassium ATPase pump, and slows conduction through the AV node (negative chronotropy) by enhancing vagal tone. It has a narrow therapeutic index (0.5–2 ng/mL), making toxicity monitoring essential.
On the exam, digoxin is almost always a toxicity question. The therapeutic level is a razor-thin 0.5–2 ng/mL, and several conditions push a “normal” level into the toxic range — most importantly hypokalemia (so a patient taking both digoxin and furosemide is the classic high-risk pairing), along with hypomagnesemia, hypercalcemia, and the declining renal function of older adults, since digoxin is excreted by the kidneys.
Learn the toxicity timeline. The earliest signs are GI and visual — anorexia, nausea, vomiting, and the hallmark yellow-green halos or blurred vision — while serious toxicity shows up as bradycardia and AV block. The antidote is digoxin immune Fab (DigiFab). Before each dose, take the apical pulse for a full minute and hold for a rate below 60 bpm, then check the most recent potassium: correcting low potassium is often the first step when toxicity is suspected, because it relieves symptoms and helps prevent dysrhythmias.
Source: ATI Pharmacology for Nursing Care, 10th ed.
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