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Digoxin Toxicity

PGI Silan
Digoxin Toxicity
• Harrisons Principles of IM
• Chap. 450 Poisoning and Drug
Overdose
• Physiologic depression
• Sympatholytic/
Parasympathomimetic
• Decreased pulse, blood pressure,
respiratory rate, temperature,
and neuromuscular activity
• Cardiac arrhythmias and
conduction disturbances
Digoxin
• Cardiac glycoside
• MOA: Inhibition of cardiac Na+, K+-ATPase membrane pump
• Metabolism: 60%-kidneys, 40%-liver
• Clinical Uses:
• Heart Failure – positive inotropic effect (Increased Ca → Increased
cardiac contractility)
• Atrial Fibrillation – parasympathomimetic effect → rate control
• Has a narrow therapeutic window
• Minimum effective concentration is about 1 ng/mL (Pt: 1.23 ng/mL)
Digoxin Toxicity
• Clinical Features:
• Gastrointestinal, psychiatric, and visual symptoms
• Atrioventricular block with or without concomitant
supraventricular tachyarrhythmia
• Ventricular tachyarrhythmias
• Hyperkalemia in acute poisoning
• Toxicity occurs at lower drug levels in chronic poisoning than in acute
poisoning.
Digoxin Toxicity
• Diagnosis:
• Labs – Hyperkalemia in acute poisoning (>5.5 mEq/L)
• ECG – Downsloping ST depression (Salvador Dali sign), flattened,
inverted, or biphasic T waves, shortened QT interval
• Toxicologic analysis

Salvador Dali sign


Digoxin Toxicity
• Treatment:
• Digoxin-specific antibody fragments (Digibind) – for
hemodynamically compromising dysrhythmias, Mobitz II or third-
degree atrioventricular block and hyperkalemia.
• Temporizing measures which include:
• Atropine, Dopamine, Epinephrine, and External cardiac pacing –
for bradydysrhythmias
• Magnesium, Lidocaine, or Phenytoin – for ventricular
tachydysrhythmias.
• Internal cardiac pacing and cardioversion can increase ventricular
irritability and should be reserved for refractory cases.
References:
• Harrisons Principles of Internal Medicine 20E
• Katzung and Trevor’s Pharmacology Examination and Review 11E
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816869/
• https://litfl.com/digoxin-effect-ecg-library/

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