ECG Topic - Toxicology

Last Updated 1/2/25

Learning Objectives

1. Learn a systematic approach to the ECG in patients with suspected or confirmed poisoning
2. Identify ECG findings and pathophysiologic mechanisms in specific cardiotoxic poisonings

Basic Approach

Follow these 7 steps:

Additional Tips

• ECG findings may change over the course of a poisoning so perform serial ECGs
• ECG features are used to direct treatment
• Compare to a pre-poisoning ECG if available

Algorithms based on Rate and Rhythm

Source: Yates C, Manini AF. Utility of the electrocardiogram in drug overdose and poisoning: theoretical considerations and clinical implications. Curr Cardiol Rev. 2012 May;8(2):137-51. doi: 10.2174/157340312801784961. PMID: 22708912; PMCID: PMC3406273.

Based on clinical findings and sinus rhythm

Bradycardia

Tachycardia

Sodium Channel Blockade

ECG findings & pathophysiology

• Blockade of fast sodium channels → delayed influx of Na and prolonged phase 0 → QRS widening


• Right-sided conduction is more sensitive to Na channel blockade → terminal R in avR and/or right axis deviation
• The left side finishes depolarizing while the right side lags (hence the rightward terminal shift).

Terminal R wave in aVR

• Defined as R > 3mm in avR or R/S ratio > 0.7 in avR

Sodium channel blockade can also result in a Brugada-type pattern

Based on studies in TCA toxicity, a QRS > 100 ms is associated with an increased risk of seizures, and QRS ≥ 160 ms significantly raises the risk of ventricular dysrhythmias.

Common Culprits: TCAs, Class 1A/1C/2/4 antiarrhythmics, diphenhydramine, antimalarials, cocaine, etc.

Example 1

Beta Blocker + Calcium Channel Blocker Toxicity

Beta-blocker toxicity

• Mechanism: Decreased inotropy & chronotropy via cAMP inhibition → ↓ intracellular calcium
• ECG findings: Sinus bradycardia, AV blocks, fascicular blocks, junctional rhythms
• Special Cases:
1. Propranolol (Class I effect) → Na+ channel blockade → QRS widening, terminal R in aVR
2. Sotalol (Class III effect) → K+ channel blockade → QTc prolongation, risk of Torsades de Pointes

Calcium channel blocker toxicity

• ECG findings: similar as beta-blocker
• Key Differences
• CCBs → inhibit insulin release (calcium-dependent) → hyperglycemia
• Beta-blockers → inhibit counterregulatory hormones → euglycemia or hypoglycemia

Example 1

Example 2

Drug Induced QTc Prolongation

QT/QTc prolongation results from K+ channel blockade, prolonging cardiac myocyte repolarization.

A long list of medications can prolong the QTc, but key offenders include:

• Antipsychotics
• Antiarrhythmics (Class 1a, 1c, and 3)
• Antidepressants (including TCAs and bupropion)
• Methadone
• Antihistamines
• Macrolides
• Antiemetics

Always calculate the QT yourself. You can also use a QT nomogram—which plots uncorrected QT vs. heart rate—to gauge Torsades de Pointes (TdP) risk, especially at lower heart rates. Though not externally validated, one retrospective study showed 96.9% sensitivity in predicting TdP. A point above the line indicates an increased risk of TdP.

Example 1

For the following tox cases with prolonged QT/QTc, is there an increased TdP risk?

Example 2

Example 3

What’s the rate and rhythm here?

Digoxin

Mechanism of action

1. Increased Intracellular Calcium and Inotropy
• Digoxin inhibits the Na⁺/K⁺ ATPase (sometimes called the “sodium–potassium exchanger”), reducing sodium efflux from the cell.
• The resulting higher intracellular sodium level leads to less activity of the Na⁺/Ca²⁺ exchanger (which normally pumps Ca²⁺ out of the cell), thereby increasing intracellular calcium.
• This elevated calcium enhances cardiac contractility (positive inotropy).
2. Effect on Conduction (Vagal Tone)
• Digoxin increases vagal tone, which slows the sinoatrial (SA) and atrioventricular (AV) nodal conduction (negative chronotropy and negative dromotropy).
• Clinically, this can help control ventricular rate in certain arrhythmias such as atrial fibrillation.

Typical ECG changes

• “Salvador Dalí Mustache” ST-Segment Changes
• Digoxin can produce a characteristic downsloping, scooped ST segment on ECG.
• Some describe this as resembling the curved mustache of surrealist painter Salvador Dalí.
• These ST-segment changes can appear in patients who have therapeutic (non-toxic) levels of digoxin and may be asymptomatic.

Toxic ECG findings

• Digoxin toxicity can cause various arrhythmias, including:
• Ventricular fibrillation (VF)
• Premature ventricular contractions (PVCs)
• AV block (of any degree)
• Junctional rhythms
• Bidirectional Ventricular Tachycardia
• A rare but classic arrhythmia associated with digoxin toxicity is bidirectional VT, characterized by a 180° shift in the QRS axis on every other beat.
• When you see bidirectional VT, digoxin toxicity is high on the differential diagnosis list.

Let’s take a break and recall the 7 step approach to ECG in Tox

Practice ECGs

Zoom-In Instructions

Desktop: click ECG for full image Mobile: click 📷 for full image

Assume all cases are presenting with toxic ingestion

ECG 1 (📷)

ECG 2 (📷)

ECG 3 (📷)

ECG 4 (📷)

ECG 5 (📷)

ECG 6 (📷)

ECG 7 (📷)

ECG 8 (📷)

ECG 9 (📷)

ECG 10 (📷)

Sources

1. Chan A, Isbister GK, Kirkpatrick CM, Duffull SB. Drug-induced QT prolongation and torsades de pointes: evaluation of a QT nomogram. QJM. 2007;100(10):609-615. doi:10.1093/qjmed/hcm072. PMID: 17881416
2. Douglas T. Kings County EM Conference Lecture. December 1, 2021. Video.

Available at: https://www.youtube.com/watch?v=ZIT2oEAAhR8&ab_channel=KingsofCountyEM

3. Life in the Fast Lane (LITFL).

Available at: https://litfl.com.

4. Yates C, Manini AF. Utility of the electrocardiogram in drug overdose and poisoning: theoretical considerations and clinical implications. Curr Cardiol Rev. 2012;8(2):137-151. doi:10.2174/157340312801784961. PMID: 22708912; PMCID: PMC3406273.

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