Mechanism of Action

Cardiac glycoside with one of the narrowest therapeutic windows in cardiology (0.5–2.0 ng/mL). It inhibits the myocardial sodium-potassium ATPase pump, raising intracellular calcium to strengthen contraction (positive inotrope) while slowing AV-node conduction via vagal tone (negative chronotrope) — stronger, slower beats. Toxicity can occur even WITHIN the therapeutic range when potassium is low, renal function declines, or an interacting drug is added.

Sub-therapeutic

Therapeutic window

Toxic

0.5

ng/mL

Common Medications

digoxinPrototype

single high-yield agent; no class suffix

Indications

heart failure with reduced EF

improves contractility

atrial fibrillation rate control

slows ventricular response; does NOT convert to sinus rhythm

Side Effects

EarlyProgresses →

anorexia

loss of appetite is often the FIRST toxicity clue

nausea

vomiting

diarrhea

Late / Severe

yellow-green halos Hallmark

xanthopsia — classic visual sign of digoxin toxicity

blurred vision

confusion

CNS sign, especially in older adults

fatigue

Contraindications & Interactions

Interactions

hypokalemia Hallmark

potentiates toxicity even at therapeutic levels — the #1 NCLEX setup; potassium competes for the same binding site

loop diuretics

furosemide depletes potassium → dangerous synergy

thiazide diuretics

deplete potassium

renal impairment

drug accumulates — renally cleared

amiodarone

raises digoxin level — reduce dose

Contraindications

electrical cardioversion

can trigger refractory ventricular fibrillation in digoxin toxicity; use lowest energy only if unavoidable

IV calcium

potentiates cardiotoxicity

Administration & Monitoring

count apical pulse for 60 seconds

full minute before every dose

hold dose and notify providerHoldHR < 60

check serum potassium before dosehold if K+ < 3.5 mEq/L

correct hypokalemia first

check serum digoxin level0.5–2.0 ng/mL

draw STAT if toxicity suspected

continuous cardiac monitoring

telemetry in suspected toxicity

antidote: digoxin immune Fab

Digibind/DigiFab for life-threatening dysrhythmias, instability, or level > 10 ng/mL

expect digoxin level to rise after Fab

assay reads bound + free drug — NOT worsening toxicity

Patient Teaching

count pulse for a full minute before each dose

apical, 60 seconds

hold the dose if pulse < 60

and call the provider

report yellow or green halos

report nausea or loss of appetite

earliest toxicity clue

do not double a missed dose

do not stop abruptly

keep potassium-rich diet as advised

low potassium triggers toxicity, especially on a loop diuretic

Report Nowescalate immediately

bradycardiaHR < 60

hold and notify provider; hallmark cardiac sign of toxicity

heart block

new AV block from enhanced vagal tone / conduction delay

ventricular dysrhythmias

PVCs, ventricular tachycardia / fibrillation

serum digoxin > 2.0 ng/mL> 2.0 ng/mL

hyperkalemiaK+ >5.0 mEq/L

acute toxicity causes hyperkalemia via Na+/K+-ATPase inhibition; unpredictable during Fab therapy

Clinical Pearl

No potassium, no digoxin — hypokalemia is the setup, toxicity is the punchline. Before every dose you need three numbers: apical pulse (hold < 60), potassium (hold < 3.5), and the digoxin level. And after Digibind, the level lies — it goes UP because the lab reads bound drug too, so trust the monitor, not the number.