A 64-year-old man presents with nausea, vomiting, and weakness. He states that his wife made him come in when he fainted today while attempting to stand up. He otherwise states he has noticed some visual changes, including noting a yellow tint to objects. He has a history of heart failure with reduced ejection fraction, obesity, diabetes, hypertension, acute coronary syndrome, atrial fibrillation, and peripheral vascular disease. His temperature is 98.5°F (36.9°C), blood pressure is 153/91 mmHg, pulse is 40/min, respirations are 15/min, and oxygen saturation is 97% on room air. Physical exam reveals a frail man who is unable to ambulate secondary to lightheadedness. His neurological exam is otherwise non-focal. An ECG is performed as seen in Figure A. Which of the following is the most likely etiology of this patient’s symptoms?
Amiodarone
Digoxin
Diltiazem
Procainamide
Digoxin
This patient with a history of heart failure with reduced ejection fraction and atrial fibrillation is presenting with nausea, vomiting, visual changes, bradycardia, and premature ventricular complexes, which are concerning for digoxin toxicity. Note that digoxin can be given in patients with poor cardiac function and atrial fibrillation; thus it is a plausible home medication for this patient.

Digoxin is a cardiac glycoside that is used in conditions such as heart failure with reduced ejection fraction and atrial fibrillation. While it does not lower mortality, it may reduce symptoms of heart failure. Digoxin toxicity classically presents with gastrointestinal symptoms (nausea/vomiting), blurred vision or yellow halos, and cardiac dysrhythmias. While there is a myriad of dysrhythmias, digoxin can cause bradycardia, atrioventricular block, and premature ventricular contractions. ST-segment scooping can be seen with digoxin use both in toxicity but also with regular therapeutic use. Toxicity is treated with anti-digoxin antibodies.

Patocka et al review digoxin toxicity. They note that this medication has a narrow therapeutic range and recommend close monitoring. Toxicity depends on severity and can be treated with anti-digoxin antibodies.

Figure/Illustration A is an ECG demonstrating bradycardia and premature ventricular complexes (red circles). This is consistent with digoxin toxicity.

Incorrect Answers:
Answer A: Amiodarone is an antidyshythmic agent with toxicities including bradycardia, heart block, a prolonged QT interval, hepatitis, interstitial lung disease, hypothyroidism, corneal deposits and optic neuropathy. This patient could use amiodarone for his atrial fibrillation, but the visual disturbances are more typical of digoxin toxicity.

Answer C: Diltiazem is a calcium channel blocker that would cause hypotension, bradycardia, and hyperglycemia. Treatment would involve immediate administration of calcium and vasopressors such as epinephrine. Other treatments in severe toxicity may include glucagon, dextrose, and insulin (to increase cardiac contractility).

Answer D: Procainamide is the preferred antidysrhythmic in tachydysrhythmias associated with Wolff Parkinson White syndrome. It may cause drug-induced lupus and other dysrhythmias in overdose but would not cause this patient’s constellation of symptoms. Procainiamide is used rarely for atrial fibrillation and is only available for intravenous infusion in the US.

Answer E: Propranolol toxicity would present with bradycardia, hypotension, confusion, seizures, and hypoglycemia. Treatment is centered on glucagon, calcium, and vasopressors such as epinephrine. In severe toxicity, lipid emulsion therapy and insulin/dextrose should be administered.

Bullet Summary:
Digoxin toxicity may present with nausea, vomiting, visual changes, bradycardia, and premature ventricular complexes.