• Generic stem/suffix: No shared suffix; recognized by name as the only cardiac glycoside still in common clinical use.
• Prototype / key drugs: Digoxin (Lanoxin) — used for heart failure (symptom control, not mortality benefit) and rate control in atrial fibrillation/flutter.
• Pharmacologic class: Cardiac glycoside · Therapeutic class: Antiarrhythmic / inotropic agent for heart failure and atrial fibrillation

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• "Digoxin makes the heart squeeze more, beat less" → the two-part mechanism (stronger + slower) in one line.
• "Low K, high dig-toxicity" → the potassium-competition rule that explains most toxicity cases.
• Early toxicity: GI first, then eyes, then rhythm — nausea/anorexia → visual changes (halos, yellow-green tint) → dysrhythmias, the classic progression.

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Picture it: The sodium-potassium pump is the cell's "reset switch," keeping sodium out and potassium in after every heartbeat — digoxin partially jams that switch, and the downstream effect is more calcium and a stronger squeeze.

The player(s): The Na⁺/K⁺-ATPase pump and the AV node, in cardiac muscle cells.

Its normal job(s): The pump maintains the normal sodium/potassium gradient after each contraction; the AV node paces conduction from the atria to the ventricles, moderated by vagal tone.

Normal numbers: Therapeutic digoxin level 0.5–2.0 ng/mL; normal potassium 3.5–5.0 mEq/L; normal adult resting HR 60–100 bpm.

Bottom line: The sodium-potassium pump and the AV node are the two levers digoxin pulls — one makes the heart squeeze harder, the other makes it beat slower.

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The move: Digoxin partially inhibits the Na⁺/K⁺-ATPase pump, which indirectly increases intracellular calcium (via the sodium-calcium exchanger) and strengthens contraction; it also increases vagal tone, slowing AV node conduction and heart rate.

How it works:

• Na⁺/K⁺-ATPase inhibition → more intracellular sodium → less sodium-calcium exchange → more intracellular calcium — because calcium drives the strength of contraction, this is a positive inotropic effect.
• Increased vagal tone → slowed AV conduction — because this separate effect on the AV node makes digoxin useful for ventricular rate control in atrial fibrillation/flutter, independent of its inotropic action.

What It's For (Indications)

• Heart failure with reduced ejection fraction — symptom/hospitalization benefit, not proven mortality benefit; add-on after guideline-directed therapy.
• Atrial fibrillation/flutter — ventricular rate control, especially when other agents aren't tolerated.

Bottom line: Digoxin's two effects — stronger contraction and slower AV conduction — come from two separate mechanisms on two separate targets, which is why it can help both heart failure and atrial fibrillation.

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Classic & Testable Side Effects

• Early toxicity: anorexia, nausea, vomiting — often the very first sign. → Nurse: ask about appetite/GI symptoms at every check, especially in patients with risk factors.
• Visual disturbances (blurred vision, halos around lights, yellow-green tint to vision) — a classic, testable early-to-mid toxicity sign. → Nurse: ask specifically about vision changes.
• Confusion, especially in older adults — can be an early or atypical sign of toxicity.
• Dysrhythmias (bradycardia, PVCs, heart block) — the late, dangerous stage. → Nurse: continuous ECG monitoring in a patient with suspected toxicity.

Numbers to Know (thresholds + action)

• Hold for apical HR <60 bpm (adult) and notify the provider. → Nurse: check the apical pulse for a full minute before every dose.
• Therapeutic level 0.5–2.0 ng/mL; toxicity risk rises above this, and even within it if potassium is low. → Nurse: draw levels as ordered, and always interpret alongside the potassium.
• Monitor potassium closely — hypokalemia increases toxicity risk at any digoxin level. → Nurse: correct low potassium promptly in patients on digoxin.

Contraindications & Interactions

• Ventricular fibrillation, second/third-degree heart block (without a pacemaker) — because digoxin would worsen the underlying conduction problem.
• Diuretics that cause hypokalemia (loop, thiazide) — because low potassium sharply raises toxicity risk; monitor levels closely when combined.
• Amiodarone, verapamil, and several other drugs raise digoxin levels via drug interactions — because reduced clearance/altered protein binding increases exposure.

Bottom line: Digoxin toxicity has a recognizable order — GI symptoms first, then visual changes, then dysrhythmias — and hypokalemia is the single biggest risk multiplier along the way.

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Nursing Care — In Priority Order

1. Check apical pulse for a full minute before every dose; hold and notify for HR <60 bpm (adult) (Safety).
2. Monitor digoxin level and serum potassium (and magnesium/renal function) (Safety) — because hypokalemia/hypomagnesemia and renal impairment both raise toxicity risk.
3. Assess for early toxicity signs at every visit: appetite/GI symptoms, vision changes, confusion (Assessment) — because these precede the dangerous dysrhythmias.
4. Continuous ECG monitoring if toxicity is suspected (Circulation).
5. Verify potassium-altering drugs (diuretics) and known drug interactions (amiodarone, verapamil) before administration (Safety).

Antidote / Rescue

• Digoxin Immune Fab (Digibind/DigiFab) for life-threatening toxicity — see the dedicated Digoxin Immune Fab guide.
• For mild toxicity: hold the dose, correct potassium, monitor.

Patient Teaching

• Check your own pulse before each dose and hold/call the provider if it's slower than instructed (Safety/Adherence).
• Report nausea, loss of appetite, vision changes (halos, color changes), or confusion right away (Safety) — early toxicity signs.
• Don't double up on a missed dose; call the provider if more than one dose is missed (Adherence).
• Tell every provider you're on digoxin before starting a new medication (Safety) — because of significant interaction potential.

🚨 When to Hold / Report

• Apical HR <60 bpm (adult) — hold, notify.
• Any early toxicity sign (GI symptoms, visual changes, confusion) in an at-risk patient — notify, check level and potassium.
• New dysrhythmia on the monitor — notify immediately, prepare for possible Digoxin Immune Fab.

Bottom line: The nurse's core safeguard is the apical pulse check before every dose — it's the single fastest bedside catch for a drug whose therapeutic and toxic doses sit close together.

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Don't Confuse

Escalate Now

• Apical HR <60 bpm before a dose → hold, notify.
• New dysrhythmia with suspected toxicity → notify immediately, prepare Digoxin Immune Fab.
• Severe hyperkalemia in acute massive overdose → urgent treatment, consider Digoxin Immune Fab.