Toxicologic Emergencies

Key Points

ECG as a Critical Diagnostic Tool: In toxicological emergencies, the ECG is a powerful tool that can reveal the effects of various drug toxicities, particularly those involving sodium channel blockers.
Sodium Channel Blocker Toxicity: This class of drugs can cause life-threatening arrhythmias, often detectable through specific ECG changes such as QRS widening and prolonged QT intervals.
Early Recognition Saves Lives: Identifying these ECG changes early allows for prompt intervention, including the use of sodium bicarbonate, which can reverse the cardiotoxic effects and prevent deterioration.

Sodium Channel Blocker Toxicity:

QRS Widening: One of the hallmark signs of sodium channel blocker toxicity is a widened QRS complex (≥ 100 ms), which indicates impaired ventricular conduction. The wider the QRS, the higher the risk of life-threatening arrhythmias.
Prolonged QT Interval: Sodium channel blockers can also prolong the QT interval, increasing the risk of Torsades de Pointes and other dangerous arrhythmias.
R-Wave in aVR: An R wave greater than 3 mm in lead aVR is another specific sign of sodium channel blocker toxicity and correlates with the severity of the toxicity.

Tricyclic Antidepressant (TCA) Overdose:

Widened QRS Complex: Similar to other sodium channel blockers, TCAs cause QRS widening, which is directly related to the severity of the overdose.
Rightward Axis Deviation: TCAs may also cause rightward axis deviation, seen as a dominant R wave in aVR, indicative of severe toxicity.
Sinus Tachycardia: Often present due to the anticholinergic effects of TCAs, sinus tachycardia can further complicate the clinical picture.

Beta-Blocker and Calcium Channel Blocker Overdose:

Bradycardia: Both beta-blockers and calcium channel blockers can cause significant bradycardia, leading to hypotension and shock.
AV Block: These overdoses can result in various degrees of atrioventricular (AV) block, ranging from first-degree AV block to complete heart block.
Prolonged PR Interval: A prolonged PR interval is common and should raise suspicion of beta-blocker or calcium channel blocker toxicity, especially in the context of hypotension.

Digoxin Toxicity:

Downsloping ST Depression: The classic “scooped” appearance or “digoxin effect” in the ST segment, typically in the lateral leads, is a hallmark of digoxin use, but when exaggerated, it can indicate toxicity.
Various Arrhythmias: Digoxin toxicity can cause a range of arrhythmias, including atrial tachycardia with block, ventricular ectopy, and bidirectional ventricular tachycardia.
Prolonged PR Interval: Digoxin toxicity may also lead to a prolonged PR interval due to increased vagal tone.

Other Drug-Induced Toxicities:

Cocaine and Sympathomimetics: These can cause tachycardia, QT prolongation, and an increased risk of arrhythmias, particularly in the setting of myocardial ischemia.
Opioid Overdose: While primarily a respiratory depressant, opioid overdose may lead to hypoxia-induced arrhythmias, bradycardia, or asystole. Look for hypoxia-induced ECG changes.

Here are some important toxicities & topics to consider:

QRS Widening is a Red Flag: In any suspected drug overdose, a widened QRS complex on the ECG should prompt immediate consideration of sodium channel blocker toxicity, and sodium bicarbonate therapy should be initiated.
aVR Lead as a Diagnostic Tool: Pay close attention to the aVR lead in cases of sodium channel blocker or TCA overdose. A prominent R wave in aVR is a strong indicator of severe toxicity.
Bradycardia and Hypotension: In the context of beta-blocker or calcium channel blocker overdose, bradycardia coupled with hypotension is a critical finding. Early intervention with glucagon, calcium, or high-dose insulin therapy may be required.
Digoxin Effect vs. Toxicity: Distinguish between the therapeutic “digoxin effect” on the ECG and signs of toxicity, which may require digoxin-specific antibody therapy.
Rapid Action for Reversal: Drug-induced toxicological emergencies require rapid recognition and prompt treatment. Sodium bicarbonate for sodium channel blocker toxicity, glucagon for beta-blocker overdose, and digoxin-specific antibodies for digoxin toxicity can be life-saving.
Continuous Monitoring: In all toxicological emergencies, continuous ECG monitoring is essential to detect and respond to life-threatening arrhythmias as they develop.