Key Point
- ECG as a Critical Diagnostic Tool: The ECG is often the first and most reliable clue in toxicology. Early recognition of drug-induced conduction disturbances or arrhythmias can guide life-saving interventions.
- 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 (≥100 ms): hallmark of ventricular conduction delay, correlates with risk of VT/VF. The wider the QRS, the higher the risk of life-threatening arrhythmias.
- QT Prolongation: increases risk of torsades de pointes.
- R wave in aVR > 3 mm: specific marker of severe sodium channel blockade.
- Treatment: sodium bicarbonate (bolus and infusion) is first-line and life-saving.
Classic example: TCA overdose
- Wide QRS, rightward axis (dominant R in aVR).
- Sinus tachycardia common due to anticholinergic effect.
- Severity is QRS-dependent: >160 ms strongly predicts seizures/VT.
Beta-Blocker & Calcium Channel Blocker Overdose
- Bradycardia and Hypotension: cardinal findings.
- AV Block & PR Prolongation: especially in CCB toxicity.
- Treatment:
- Glucagon (BB),
- Calcium salts (CCB),
- High-dose insulin therapy for refractory shock.
Digoxin Toxicity
- Downsloping ST (“dig effect”): baseline marker of use, not toxicity.
- Arrhythmias: atrial tachycardia with block, PVCs, bidirectional VT.
- PR Prolongation: vagal effect, but exaggerated prolongation suggests toxicity.
- Treatment: digoxin-specific antibody (Digibind) if unstable or life-threatening.
Opioid Overdose
- Primarily a respiratory emergency.
- Secondary ECG changes: bradycardia, asystole, or hypoxia-driven arrhythmias.
- Management: airway + naloxone.
Cocaine & Other Sympathomimetics
- Mechanism: intense adrenergic surge + sodium channel blockade.
- ECG Findings: sinus tachycardia, QT prolongation, ST changes, wide QRS.
- Complications: MI, stroke, aortic dissection, VT/VF.
- Treatment: benzodiazepines, nitrates, CCBs for vasospasm. Avoid β-blockers.
KEY CLINICAL PEARLS:
- 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.
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