Toxicologic ECG Patterns

Most drug and poison ECG patterns come from three electrical effects. Sodium-channel blockers slow the fast phase 0 upstroke of the ventricular action potential. The result: the QRS widens and conduction slows. Digoxin inhibits the Na⁺/K⁺-ATPase pump. That shortens ventricular repolarization, and you see it as the scooped ST segment and flattened T wave. It also raises vagal tone and ectopic activity at the AV node and ventricle. Beta-blockers and calcium channel blockers slow SA and AV nodal conduction. That gives you bradycardia, AV block and hypotension.

Drugs that block the rapid delayed rectifier potassium current prolong repolarization. The QT interval gets longer. Then a pause or a second hit can trigger polymorphic VT, torsades de pointes. Electrolyte losses, bradycardia and ischemia add to that risk. Here's the key: the ECG is the fastest bedside clue to which mechanism is active, so read the QRS, the ST segment, the rate and the QTc before you name the drug.

Start with a stable, averaged rhythm strip, and check it against the baseline 12-lead if you have one. The thresholds below are toxicity cut-offs, not normal limits. That difference matters at the bedside.

1. Choose the widest QRS: measure every limb lead and V1–V2; use the widest complex as the QRS duration.
2. Measure aVR: look for a terminal R wave of 3 mm or more, which signals sodium-channel block.
3. Measure QTc: average several beats in lead II or V5–V6, and correct with Fridericia when the rate is outside the usual range.
4. Look at the ST segment and T wave: note scooped, down-sloping ST depression and flattened or inverted T waves.
5. Check the rate and rhythm: note bradycardia, AV block, junctional rhythm, PVCs or VT.

Sodium-channel blockers slow conduction through the ventricles. The list includes tricyclic and tetracyclic antidepressants, class I antiarrhythmics, diphenhydramine and cocaine. The QRS widens first. As it widens, the risk of seizures and ventricular arrhythmias climbs with it.

ECG Criteria

• Maximal limb-lead QRS of 100 ms or more: in the Boehnert-Lovejoy tricyclic cohort, no patient with a QRS under 100 ms had seizures or ventricular arrhythmias, and seizures occurred at 100 ms or more.
• QRS of 160 ms or more: ventricular arrhythmias occurred only at this width or more in the same cohort.
• Terminal R wave in aVR of 3 mm or more (the terminal 40 ms of the QRS): in the Liebelt cohort of 79 patients, this predicted seizures or arrhythmias with a sensitivity of 81%, close to the 82% for a QRS over 100 ms, and a positive predictive value of 43% against 35% for the QRS. It is a small cohort, so treat aVR as a risk marker, not a cut-off.
• Terminal 40 ms rightward axis (terminal R in aVR, terminal S in I): the quick bedside clue; it does not replace the QRS measurement.

Causes

Clinical Significance

• Seizures, hypotension and ventricular arrhythmias are the main risks. The serum drug level did not predict them in the Boehnert-Lovejoy cohort. The QRS did.
• Trend the QRS after every intervention. Narrowing after bicarbonate is the response you want.

Look-Alikes

• Hyperkalemia widens the QRS too. Check K⁺ and see the Electrolyte ECG page.
• Bundle branch block gives you a wide QRS without any toxicity. See the QRS Complex page.

Digoxin pushes intracellular calcium and sodium up, and it turns vagal tone up. The toxic picture is arrhythmias, AV conduction block and a characteristic repolarization pattern. The kidneys do most of the clearing. Lose renal function and the risk climbs.

ECG Criteria

• Scooped ST segment: down-sloping ST depression, a “reverse tick” appearance, with flattened or inverted T waves. On its own this is a digoxin effect (exposure), not toxicity.
• Increased U-wave amplitude alongside the ST changes.
• Rhythms that indicate toxicity (per Andrews 2023 and Hack 2025): atrial tachycardia with block, bidirectional VT, accelerated junctional rhythm, regularized atrial fibrillation (a regular, slow rhythm suggests complete AV dissociation with a junctional escape), and frequent PVCs with sinus bradycardia.
• QT shortening is a digoxin effect; it is not a toxicity criterion by itself.
• Arrhythmias and AV block: bradycardia, all degrees of AV block, PVCs and ventricular tachycardia are the dangerous forms.
• Signs of life-threatening toxicity: VT or VF, asystole or symptomatic high-degree AV block (or atropine-resistant bradycardia), serum K⁺ above 5.5 mEq/L in adults (above 6 in children) with progressing toxicity (FDA label), or above 6.5 mmol/L per the 2023 European consensus. Protocols differ, and Fab should not wait for a digoxin level in an unstable patient. Hypotension with end-organ dysfunction also qualifies.

Causes

Clinical Significance

• The serum digoxin level does not reliably predict toxicity. Toxicity can happen at levels in the usual therapeutic range. So decide on the clinical picture and the ECG first.
• Hyperkalemia from digoxin toxicity is itself a life-threatening sign. Get the K⁺ early.

Look-Alikes

• Ischemic ST depression is usually not scooped, and it appears in a coronary territory. See the ST and T Wave page.

Beta-blockers and calcium channel blockers, especially diltiazem and verapamil, suppress conduction through the SA and AV nodes. In overdose they can cause profound bradycardia, AV block and hypotension. It can come on within minutes of a large ingestion, or take hours.

ECG Criteria

• Sinus bradycardia, junctional rhythm or AV block, from first degree to complete heart block.
• A narrow QRS in most cases, so the QRS width alone will not flag the toxic pattern.
• Hypotension that does not respond to fluids, with a slow ventricular rate.

Causes

Clinical Significance

• Bradycardia and hypotension can progress fast. The AV block may be complete, and the QRS may stay narrow. So do not take comfort from the rhythm.
• Atropine has limited effect in this poisoning. Plan the escalation with the antidote and vasopressor steps in the Bedside Management section.
• Propranolol also blocks sodium channels. Expect QRS widening and seizures along with the bradycardia. Sotalol prolongs the QT and can cause torsades.

Torsades is polymorphic VT that twists around the baseline, and a pause often sets it off. Know the two numbers. A QTc of 500 ms or more is high risk. So is a rise of 60 ms or more from baseline. That makes a bradycardia drug, or a pause after a QT-prolonging drug, a common trigger.

ECG Criteria

• QTc of 500 ms or more, or a rise of 60 ms or more from the baseline QTc.
• Polymorphic VT with a long QT: the QRS amplitude waxes and wanes around the baseline.
• Pauses or bradycardia that leave a long QT exposed to an early beat.

Causes

• Drugs that prolong the QT. See the drug list on the QT Interval page.
• Hypokalemia, hypomagnesemia and hypocalcemia, and bradycardia or pauses from any cause.

Clinical Significance

• Torsades can degenerate to VF, and the worst setup is a pause, a long QT and a low K⁺ or Mg²⁺.
• Stop the offending drug. Fix the electrolytes before you lean on rate control.

Wide QRS in a poisoned patient? It may not be the toxin. Hyperkalemia, a bundle branch block or a ventricular paced beat can all do it. The table separates the common mimics.

Artifact & Lead Misplacement

• Reversed limb leads change the aVR and lead I pattern. Confirm the lead labels on a repeat tracing.
• Shivering, cable motion or transport vibration can look like VT or torsades. Check the pulse and the SpO₂ waveform.
• Precordial electrodes placed too high change the QRS shape in V1–V2.

Normal Variants

• Digoxin can scoop the ST with no toxicity at all. Read the finding with the level, the electrolytes and the rhythm.

Every drug dose on this page sits in this section. Doses vary by protocol; follow local protocols and medical direction.

Stability and Actions

Therapy and Doses

Follow local protocols and online medical direction.

Pediatrics

• Dose by weight, capped at the adult dose. See the Weight-Based Dosing page.
• Sodium bicarbonate is 1–2 mEq/kg, never above the adult single dose. Digoxin immune Fab: acute ingestion with unknown amount 10–20 vials (watch volume under 20 kg); chronic toxicity with unknown level 1 vial under 20 kg and 6 vials at 20 kg or more (label).
• Magnesium for torsades is 25–50 mg/kg, capped at 2 g. Calcium chloride for calcium channel block: 10–20 mg/kg is a protocol-dependent starting point; verify with the poison center. Insulin infusion and glucagon doses for toxicity are not established here: consult toxicology.
• Pediatric QRS and QTc norms depend on age. For heart rate limits, check the Vital Signs page.

Other Populations

• Renal impairment: digoxin accumulates. Expect a longer toxicity course and a lower K⁺ tolerance.
• Older adults: more QT-prolonging drugs, and less renal reserve. Review the medication list before the ECG-based decision.
• Pregnancy: treat the emergency first. Discuss magnesium and bicarbonate with the obstetric and toxicology teams.

1. Identify the toxin or the likely class from the history, the drug list and the timing.
2. Measure the widest QRS and the aVR terminal R; these decide whether sodium-channel block is present.
3. Measure the QTc and look for pauses or polymorphic VT; check K⁺, Mg²⁺ and Ca²⁺ at the same time.
4. Look for scooped ST depression and arrhythmia; if present, treat as possible digoxin toxicity and check the level.
5. Assess rate and AV conduction; bradycardia with hypotension suggests a beta-blocker or calcium channel blocker.
6. Give the first-line antidote or electrolyte for the pattern, using the doses in Bedside Management.
7. Repeat the ECG after each intervention and document the QRS, the QTc and the rhythm.

Common Pitfalls

• Treating 100 ms as a normal value. Or treating the normal limit of 110 ms as a safe ceiling.
• Trusting the serum digoxin level over the ECG and electrolytes.
• Giving epinephrine or isoproterenol for digoxin bradyarrhythmia with no expert input.
• Reaching for amiodarone or procainamide in torsades.
• Missing hypokalemia or hypomagnesemia after bicarbonate or insulin.