A 79-year-old man sits forward on the stretcher, pale and queasy, repeatedly asking whether the room has “gone yellow.” His daughter says he has eaten little for a week and has been weaker, but he denies chest pain or syncope. The monitor shows a slow, irregular rhythm while his blood pressure drifts downward. The next decision is still unmade.

— What’s your move? Read on.

Before you read
  • How much should a serum digoxin level influence treatment?
  • When is digoxin immune Fab indicated?

When to Think of It

Think of it with new nausea, anorexia, delirium, weakness, visual disturbances, bradycardia, AV block, atrial tachycardia with block, or ventricular dysrhythmia in a patient taking digoxin—especially with CKD, dehydration, low body mass, or a recent medication change.

Sick or Not Sick

The key call is stable toxicity versus toxicity with a life-threatening rhythm, hemodynamic instability, or dangerous hyperkalemia. Do not wait for a “toxic” serum level if the patient is unstable.

The First Fifteen Minutes

  • Place on continuous ECG monitoring, obtain IV access, serial ECGs, glucose, electrolytes, magnesium, renal function, and a digoxin level drawn at least 6–8 hours after the last dose when possible. The level supports—but does not override—the clinical picture.
  • Symptomatic bradycardia or high-grade AV block → atropine 1 mg IV, repeat every 3–5 minutes to a maximum of 3 mg, because vagolysis may improve nodal conduction.
  • Life-threatening dysrhythmia, hemodynamic instability, or significant digoxin-associated hyperkalemia → digoxin immune Fab IV; use the package/institutional or toxicology protocol because chronic toxicity often needs fewer vials than acute massive ingestion. A common estimate is number of 40-mg vials = serum level (ng/mL) × weight (kg) ÷ 100; if the level is unavailable in a critically ill adult, an empiric 10 vials IV is commonly used.
  • Ventricular dysrhythmia while Fab is being obtained → lidocaine 1–1.5 mg/kg IV, then 0.5–0.75 mg/kg IV every 5–10 minutes to a maximum of 3 mg/kg, because it suppresses ventricular automaticity with relatively little AV-nodal effect.
  • Severe hyperkalemia with ECG changes while awaiting Fab → regular insulin 10 units IV plus dextrose 25 g IV, because intracellular potassium shift buys time; Fab is the definitive treatment for digoxin-mediated potassium toxicity.
  • If hypotension persists → cautious 0.9% saline 500–1,000 mL IV, reassessing for heart failure or renal failure, because perfusion may improve renal clearance and drug distribution. Avoid reflexive large-volume resuscitation in pulmonary edema.

Definitive Care & Disposition

Stop digoxin and review interacting drugs, renal function, and potassium/magnesium abnormalities. Consult medical toxicology or poison control early. Admit patients with symptomatic toxicity, ECG abnormalities, renal dysfunction, electrolyte abnormalities, or Fab treatment; ICU care is appropriate for unstable rhythms, shock, need for pacing, or repeated Fab. Digoxin levels can remain misleading after Fab because total measured digoxin includes bound drug; follow clinical status, ECG, potassium, and renal function.

How This One Kills

The dangerous error is dismissing nausea, weakness, or visual symptoms because the digoxin level is “therapeutic,” while progressive AV block or ventricular dysrhythmia develops in a patient with reduced renal clearance.
The Differential — What Else Looks Like This
  • Beta-blocker or calcium-channel blocker toxicity — marked hypotension with hypoglycemia or hyperglycemia patterns and no characteristic digoxin-associated visual/GI syndrome; confusing them may delay Fab and appropriate antidotes.
  • Acute coronary syndrome — ischemic symptoms and regional ECG changes rather than diffuse conduction toxicity; mislabeling toxicity can delay reperfusion.
  • Hypokalemia or hypomagnesemia alone — electrolyte abnormality may amplify digoxin effects but does not explain the entire syndrome; missing the drug accumulation allows recurrence.
  • Intracranial or metabolic delirium — altered mentation without the rhythm pattern; anchoring on digoxin can miss another lethal process.

The Second-Day Story

Older adults may have only anorexia, falls, fatigue, confusion, or “failure to thrive,” with no reported visual change or vomiting. Chronic toxicity can occur at apparently acceptable serum concentrations because tissue effect depends on timing, renal clearance, electrolytes, and individual sensitivity. Look for a new bradyarrhythmia or AV block, compare with an old ECG, review the medication list and renal trend, and treat the patient—not an isolated number.
Back to Our Patient
Back to the 79-year-old man: his anorexia, yellow-tinged vision, renal dysfunction, slow irregular rhythm, and new AV block make chronic digoxin toxicity recognizable despite an initially nondiagnostic concentration. Because his blood pressure is falling and the rhythm is unstable, he is the “sick” branch: monitoring, IV access, ECG/electrolyte assessment, atropine for symptomatic bradycardia, and urgent digoxin immune Fab are initiated with toxicology guidance. He is admitted to the ICU, digoxin is stopped, and potassium, renal function, ECG, and clinical status guide further Fab rather than the post-Fab serum level.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 79-year-old man on digoxin with one week of anorexia, weakness, nausea, and yellow visual distortion, now with hypotension and a new slow irregular rhythm. He has CKD and poor oral intake, with no chest pain, focal neurologic deficit, or fever. ECG shows bradycardia with AV conduction disease, and labs show renal dysfunction with an abnormal potassium; the digoxin level was drawn at an appropriate post-dose interval but will not determine treatment alone. I’m concerned for symptomatic chronic digoxin toxicity with hemodynamic instability. I’ve placed him on continuous monitoring, given atropine for symptomatic bradycardia, and am contacting toxicology to administer digoxin immune Fab, with ICU admission and serial ECG, potassium, glucose, and renal monitoring.”

Study Directive

Draw the ECG and electrolyte patterns of digoxin toxicity from memory. Practice calculating Fab dose from weight and serum level, then verify the calculation against your institutional protocol or Lexicomp/UpToDate. Review five ECGs for digoxin-associated AV block, atrial tachycardia with block, and bidirectional ventricular tachycardia.

Recent Literature