Treatment Options for Bradyarrhythmias Caused by Cardiac Glycoside Overdose

Bradyarrhythmias resulting from cardiac glycoside toxicity, particularly digoxin poisoning, require prompt and appropriate intervention. In cases where patients develop bradycardia due to digoxin toxicity, atropine is commonly administered to inhibit vagal stimulation, which can reflexively increase heart rate. This medication is especially effective in mild to moderate cases where the patient remains hemodynamically stable.

Managing Severe Conduction Disturbances

When patients exhibit more severe manifestations such as third-degree atrioventricular (AV) block or even ventricular standstill, pharmacological treatment may be insufficient. In such situations, the implantation of a temporary pacemaker is often necessary to stabilize cardiac function and maintain adequate cardiac output until the toxic effects subside.

Eliminating Excess Cardiac Glycosides

In cases of overdose, it is crucial to limit further absorption of the drug. Patients should discontinue the medication immediately and may benefit from gastrointestinal decontamination techniques such as gastric lavage, especially if the ingestion was recent. Diuretics can also be used to enhance renal clearance of the drug. For severe toxicity, advanced interventions like plasma exchange or hemoperfusion may be required to effectively remove accumulated cardiac glycosides from the bloodstream.

Assessing and Monitoring Mild Toxicity

Cardiac toxicity is a well-known complication of cardiac glycoside overdose, often presenting as bradyarrhythmias. In less severe instances—where patients exhibit findings such as sinus bradycardia, prolonged PR interval, or second-degree AV block (either Mobitz Type I or II)—and where there is no significant hemodynamic compromise or severe hypotension, aggressive treatment may not be necessary. In these cases, close monitoring and supportive care are typically sufficient.

Pharmacological and Device-Based Interventions

However, if bradycardia becomes symptomatic or leads to hemodynamic instability, atropine remains the first-line pharmacologic agent. In situations where atropine proves ineffective, the next step often involves the placement of a temporary pacemaker to provide rhythm support while the body metabolizes and clears the toxic levels of the drug.