Digoxin toxicity 5 mark answer
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Digoxin Toxicity
Definition & Mechanism
Digoxin has a narrow therapeutic index (therapeutic range: 0.5-2.0 ng/mL; toxic: >2.5 ng/mL). Toxicity results from excessive inhibition of the Na+/K+-ATPase pump in myocardial cells:
- Na+/K+-ATPase is blocked → intracellular Na+ rises → Na+/Ca2+ exchanger fails → intracellular Ca2+ accumulates
- Excess Ca2+ causes delayed afterdepolarizations → triggered arrhythmias, increased automaticity
- Simultaneously, vagal tone is increased → SA and AV nodal depression
- At toxic doses, Na+/K+-ATPase is paralysed → K+ cannot enter cells → hyperkalemia (levels up to 13.5 mmol/L reported)
(Rosen's Emergency Medicine, p. 2929)
Precipitating Factors (Increased Risk)
| Category | Factors |
|---|---|
| Electrolyte disturbances | Hypokalemia, hypomagnesemia, hypercalcemia, alkalosis |
| Renal impairment | Reduced digoxin clearance |
| Cardiac conditions | Heart failure, ischemic heart disease, myocarditis |
| Drug interactions | Amiodarone, verapamil, quinidine, erythromycin, nifedipine (all raise serum digoxin) |
| Other drugs | Beta-blockers, Ca2+ channel blockers, class IA antiarrhythmics (synergistic bradycardia) |
(Rosen's Emergency Medicine, p. 2930)
Clinical Features
Acute vs. Chronic Toxicity
| Feature | Acute | Chronic |
|---|---|---|
| History | Intentional/accidental overdose | Elderly on diuretics; renal insufficiency |
| GI | Nausea, vomiting, abdominal pain, anorexia | Nausea, vomiting, diarrhea |
| CNS | Headache, dizziness, confusion, coma | Fatigue, weakness, delirium prominent |
| Cardiac | Bradyarrhythmias, AV block | Almost any arrhythmia; ventricular arrhythmias common |
| Electrolytes | Hyperkalemia | Normal/low/high K+ |
| Digoxin level | Markedly elevated | Minimally elevated or "therapeutic" |
(Tintinalli's Emergency Medicine, p. 1309)
Cardiac Manifestations (Arrhythmias)
Nonspecific:
- PVCs (especially bigeminal/multiform)
- AV block (all degrees)
- Sinus bradycardia, SA block/arrest
- Atrial fibrillation with slow ventricular response
- Ventricular tachycardia/fibrillation
More specific (not pathognomonic):
- Bidirectional ventricular tachycardia (hallmark - very few drugs cause this)
- Paroxysmal atrial tachycardia (PAT) with block (atrial rate 150-200/min)
- Non-paroxysmal junctional tachycardia (70-130/min)
- AF with slow, regular ventricular rate (complete AV dissociation)
(Rosen's Emergency Medicine, p. 2930)
Non-cardiac (Extracardiac) Features
- GI: Anorexia, nausea, vomiting, diarrhea, abdominal pain (often earliest symptoms)
- Visual: Blurred or snowy vision, chromatopsia (yellow-green halos), photophobia, diplopia, scotomata
- Neurological: Dizziness, headache, confusion, delirium, hallucinations, paresthesias, seizures
- General: Weakness, fatigue, malaise
(Rosen's Emergency Medicine, p. 2930)
ECG Findings (at therapeutic levels - do not indicate toxicity):
- "Scooped" ST-segment depression
- T-wave flattening or inversion
- QT interval shortening
- Increased U-wave amplitude
(Tintinalli's Emergency Medicine, p. 1309)
Diagnosis
- Clinical composite - no single test confirms/excludes diagnosis
- Serum digoxin level: sample at least 6 hours post-ingestion (distribution phase complete)
- In acute toxicity, serum K+ is a better indicator of end-organ toxicity than digoxin level
- In chronic toxicity, serum K+ and digoxin levels are less reliable
- Note: Digoxin-like immunoreactive substances (e.g., in neonates, renal failure) can give false-positive levels
(Tintinalli's Emergency Medicine, p. 1310)
Treatment
General
- Discontinue digoxin immediately
- IV access + continuous cardiac monitoring
- Activated charcoal (1 g/kg PO) if awake, alert, within 1 hour of ingestion
- Correct precipitating factors: hypoxia, hypovolaemia, electrolyte imbalance
Specific Arrhythmia Management
- Bradyarrhythmias: Atropine 0.5-1.0 mg IV (temporizing); transcutaneous pacing if refractory
- Ventricular arrhythmias: IV magnesium sulfate (counteracts ventricular irritability)
- Avoid: Calcium salts (controversial; historically associated with "stone heart"); class IA antiarrhythmics
Specific Antidote - Digoxin-Specific Antibody Fragments (Digibind / Digoxin Fab)
Indications:
- Progressive, haemodynamically significant bradydysrhythmias
- Life-threatening ventricular arrhythmias
- Serum K+ >5.0 mEq/L in acute toxicity
- Should be used before pacing or antiarrhythmic drugs
Dosing:
- Chronic poisoning: 1 vial (often sufficient)
- Acute poisoning: 2 vials (most patients)
- Unknown amount + cardiac arrest: 10 vials IV bolus
- Exact dose based on total body load of digoxin
Important: Hyperkalemia in acute digoxin toxicity is best treated with Fab fragments, NOT insulin/glucose/bicarbonate (these do not reduce mortality).
(Rosen's Emergency Medicine, p. 2929; Tintinalli's Emergency Medicine, p. 1310)
Summary Mnemonic: "Dig Tox"
- D - Decreased K+ (hypokalemia precipitates); hyperkalemia occurs in acute toxicity
- I - Increased vagal tone → bradycardia/AV block
- G - GI symptoms (earliest: nausea, vomiting)
- T - Triggered arrhythmias (PAT with block, bidirectional VT)
- O - Ophthalmologic (yellow-green halos)
- X - antidote = digoXin Fab (Digibind)
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