Master Acute Digoxin Toxicity with Picmonic for Medicine

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Digoxin's mechanism of action is the inhibition of the sodium/potassium ATPase pump. In the heart, this results in increased calcium concentrations in myocytes, as well as increased vagal tone. Adverse drug reactions to digoxin are relatively common due to a narrow therapeutic index. Hyperkalemia is seen in acute toxicity. Patients with pre-existing hypokalemia, however, are particularly vulnerable to side effects since digoxin normally competes with K+ ions for the same binding site on the Na/K ATPase pump. The increased vagal tone causes cholinergic symptoms like nausea, vomiting, and diarrhea due to increased gastrointestinal motility. Eye involvement can include blurry yellow and green vision, with halos around each point of light. Cardiac effects can involve a range of arrhythmias secondary to increased intracellular calcium, such as bradycardia, bigeminy and ventricular tachycardia or fibrillation. The combination of increased atrial arrhythmias with inhibited AV conduction (like paroxysmal atrial tachycardia with AV block) is highly suggestive of acute digoxin toxicity. Electrocardiogram changes include a prolonged PR interval, QT interval shortening, ST segment scooping and T wave inversion.

9 KEY FACTS

In digoxin toxicity, hyperkalemia is common due to paralysis of the Na/K ATPase pump. This can be a life threatening issue that must be quickly addressed when managing digoxin toxicity.

Common adverse effects include cholinergic symptoms like nausea, vomiting, and diarrhea due to increased gastrointestinal motility.

Common adverse effects include disturbance of color vision involving mostly yellow and green. Additionally, digoxin can cause generalized blurry vision as well as seeing a halo around each point of light.

Increased intracellular calcium can cause arrhythmias including bigeminy and ventricular tachycardia or fibrillation. The combination of increased atrial arrhythmias and inhibited AV conduction like paroxysmal atrial tachycardia with AV block is commonly said to be pathognomonic of digoxin toxicity.

Digoxin use can lead to bradycardia, which is a disorder of the heart rate in which it beats too slowly.

While normal digoxin use can cause certain EKG changes, an elongated PR interval is specifically associated with digoxin toxicity.

Digoxin use can cause shortening of the QT interval on EKG, which is thought to be related to increased calcium and increased ionotropy of the heart.

Digoxin can cause a characteristic scooping of the ST-T complex in which the ST segments and T waves are fused together making it impossible to tell where one ends and the other begins. Scooping can occur even when digoxin is in the therapeutic range.

T wave inversion is a common EKG finding in digoxin use, even when the levels are within a therapeutic range.

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