ECG criteria
- Sinus bradycardia: HR <60 bpm, sometimes pronounced (<40 bpm)
- Prolonged PQ (PR) interval >200 ms — slowed AV conduction
- Second-degree AV block (Mobitz type I or II) or complete third-degree AV block
- QRS complex widening: normal duration is typically <110 ms, 110–119 ms is an intermediate value requiring attention, ≥120 ms is marked widening; the dynamics of QRS width compared to the baseline ECG are also important; most characteristic of propranolol and certain β-blockers with membrane-stabilizing (sodium-channel blocking) activity; requires the exclusion of co-ingestion and hyperkalemia
- QTc prolongation — particularly with sotalol (potassium channel blockade, IKr), risk of torsades de pointes
- Nodal (junctional) or idioventricular escape rhythm during sinus node depression
- Low blood pressure in the setting of bradycardia without compensatory tachycardia (unlike other causes of shock)
- Asystole or pulseless electrical activity in the terminal stage of severe intoxication
What it looks like on ECG
The baseline and most frequent sign is sinus bradycardia: sinus rhythm (P wave before each QRS, positive in lead II), decreased HR, which can drop below 40 bpm in severe intoxication. The PQ (PR) interval lengthens to over 200 ms, progressing to a second-degree AV block, and in severe poisoning, to a complete third-degree AV block with AV dissociation and an escape junctional or idioventricular rhythm.
The width of the QRS complex depends on the specific drug. Normal QRS duration is typically <110 ms; values of 110–119 ms are considered intermediate — they may already reflect intraventricular conduction disturbances and require attention, while ≥120 ms represents clear widening. When assessing toxic effects, not only the absolute figure is important, but also the dynamics of the QRS width compared to the patient's baseline ECG. Most cardioselective beta-blockers (metoprolol, bisoprolol, atenolol) do not widen the QRS — their effect is realized solely through the depression of automaticity and AV conduction. Propranolol is the most well-known example of a drug with an additional quinidine-like (membrane-stabilizing, sodium-channel blocking) effect: at toxic concentrations, it can widen the QRS, which is visible in any lead and easiest to evaluate in V1 and II. Acebutolol is mentioned as a drug with similar activity, but the clinical significance of this effect in overdose is less typical and less well described. Carvedilol and sotalol are not classified as typical sodium-channel blocking β-blockers — a wide QRS is not characteristic of their overdose as a leading sign; if it does occur, another cause must be sought (co-ingestion, hyperkalemia, another sodium-channel blocking toxicrome).
Sotalol separately blocks potassium channels (IKr, class III according to Vaughan Williams), thus causing prolongation of the QT interval (corrected QTc) with the risk of polymorphic ventricular tachycardia (torsades de pointes) — this is its primary and clinically most significant ECG risk, rather than QRS widening. Table of typical findings:
| Drug | Bradycardia | Wide QRS | QT prolongation |
|---|---|---|---|
| Metoprolol, atenolol, bisoprolol | Yes | No | No |
| Propranolol | Yes | Yes (sodium-channel blocking effect) | Sometimes |
| Sotalol | Yes | Usually no / not a leading sign | Yes, markedly |
Upon progression — junctional escape rhythm, idioventricular rhythm, asystole.
Mechanism
Beta-blockers competitively block β1-adrenoceptors of the sinus node, AV node, and myocardium, reducing the influence of catecholamines. At therapeutic doses, this dose-dependently decreases sinus node automaticity and AV conduction velocity. At toxic doses, the blockade becomes nearly complete, sinus node automaticity drops sharply, and the AV node conducts with a long delay or is blocked entirely.
At toxic concentrations, propranolol additionally blocks fast sodium channels of cardiomyocytes — like quinidine or tricyclic antidepressants — slowing ventricular depolarization and widening the QRS; this is the main mechanism of toxic wide QRS among beta-blockers. Sotalol is structured differently: it is a relatively hydrophilic drug with predominantly renal elimination, lacking a clinically significant sodium-channel blocking effect; its toxicity is associated with potassium channel blockade (IKr), which slows repolarization and prolongs the QT interval, creating a substrate for torsades de pointes. The depression of myocardial inotropic function along with bradycardia leads to a drop in cardiac output and cardiogenic shock.
Causes
- Intentional overdose with suicidal intent (the most common cause of severe intoxication)
- Accidental overdose in children
- Therapeutic dose in the setting of renal or hepatic impairment (reduced clearance)
- Drug interactions enhancing the effect of the beta-blocker
- Co-administration with calcium channel blockers, digoxin, or other drugs depressing AV conduction
- Overdose of beta-blocker eye drops (timolol) in children or the elderly
Differential diagnosis
Calcium channel blocker poisoning — clinically and on the ECG, it is very similar (bradycardia, AV block, hypotension). Differentiation is based on medical history, clinical presentation, glucose and electrolyte levels, renal function, and ECG dynamics: beta-blockers can cause both hypoglycemia and hyperglycemia, whereas CCBs more frequently (though not always) present with hyperglycemia due to the blockade of calcium-dependent insulin secretion. A trial response to calcium or glucagon is not used as a definitive diagnostic test.
Digoxin poisoning — also presents with bradycardia and AV block, but ventricular extrasystoles, accelerated junctional rhythm, and scooping ST-segment depression are characteristic. The concentration of digoxin in the blood helps confirm exposure, but does not resolve the issue by itself: interpretation requires taking into account the time since ingestion, potassium levels, renal function, and the clinical picture.
Autonomic (vasovagal) bradycardia — no QRS widening, no history of drug intake, resolves quickly.
Hyperkalemia — also widens the QRS and slows conduction, but adds tall peaked T waves and P wave flattening; differentiated by potassium levels.
Poisoning with tricyclic antidepressants and other sodium channel blockers — QRS widening is similar, and a prominent terminal R wave in aVR reflects sodium channel blockade in both cases (this sign is also possible in severe propranolol intoxication, meaning it does not differentiate between TCAs and propranolol on its own). Differentiation is performed based on the history of specific drug ingestion, concomitant clinical manifestations (anticholinergic syndrome in TCAs), and toxicological assessment rather than a single ECG sign.
Clinical significance and management
Severe beta-blocker intoxication is dangerous due to refractory bradycardia, cardiogenic shock, and asystole, especially with wide QRS (sodium-channel blocking effect of propranolol) or QT prolongation (sotalol, risk of torsades de pointes).
The physician needs: continuous ECG monitoring, assessment of heart rate, QRS width, and QTc dynamics, support according to the ABC algorithm. In symptomatic bradycardia, atropine is permissible, but its effect is often limited. In hypotension and shock, intensive support should not be delayed — high-dose hyperinsulinemic-euglycemic therapy and vasopressors are considered early; glucagon can be used, but the evidence base is limited. Intravenous calcium is not a specific beta-blocker antidote, but it can be considered as an adjunctive measure in refractory hypotension or conduction abnormalities — especially if calcium channel blocker co-ingestion or mixed poisoning cannot be ruled out; data on its efficacy in isolated beta-blocker poisoning are limited, and it does not replace primary shock management. In refractory shock, extracorporeal support (ECMO) is considered. For bradyarrhythmias refractory to medications, temporary cardiac pacing is used.
In clinically significant QRS widening presumably related to the sodium-channel blocking effect (typical of propranolol), a toxicologist is consulted and intravenous sodium bicarbonate is considered with monitoring of pH, sodium, and hemodynamics; this approach is not automatically transferred to isolated sotalol poisoning, where the QRS is usually unaffected.
In sotalol intoxication with QT prolongation, the drug and other QT-prolonging agents should be discontinued first, and potassium and magnesium levels corrected. If torsades de pointes occurs, IV magnesium is administered immediately (regardless of baseline magnesium levels) along with defibrillation for hemodynamic instability; for recurrent torsades, temporary pacing or increasing heart rate to shorten the QT interval is considered.
Common interpretation errors
- Mistaking bradycardia for "simple vagotonia" without considering the history of drug intake
- Failing to assess QRS width and missing the sodium-channel blocking effect of propranolol, including intermediate widening of 110–119 ms and progressive widening over time
- Mistakenly expecting QRS widening in sotalol overdose and failing to measure QTc, thereby missing the risk of torsades de pointes
- Confusing it with calcium channel blocker poisoning without considering the clinical picture, glucose, and electrolytes
- Failing to notice the progression of AV block from first-degree to complete during serial monitoring
1. Which ECG sign is most characteristic of beta-blocker poisoning regardless of the specific agent?
Beta-1 receptor blockade suppresses sinus node automaty and AV conduction regardless of whether the drug has additional membrane-stabilizing or potassium-blocking effects.
2. QRS complex widening in beta-blocker overdose is most likely with the intake of:
Propranolol has an additional quinidine-like effect with sodium channel blockade, which widens the QRS, unlike cardioselective drugs.
3. What additional ECG risk does sotalol overdose carry compared to most other beta-blockers?
Sotalol blocks IKr potassium channels, delaying repolarization and prolonging QTc, which creates a risk of polymorphic ventricular tachycardia (torsades de pointes), unlike QRS widening, which is not characteristic of sotalol.
Frequently asked questions
How to distinguish beta-blocker poisoning from calcium channel blocker poisoning?
The ECG presentation is similar—bradycardia, AV block, hypotension. Differentiation is based on history, clinical picture, glucose, electrolytes, renal function, and ECG dynamics: beta-blockers can cause both hypo- and hyperglycemia, whereas CCBs more frequently present with hyperglycemia, though this is not an absolute sign. A trial dose of calcium or glucagon is not considered a definitive diagnostic test.
Is beta-blocker poisoning dangerous?
Yes, severe overdose can lead to refractory bradycardia, cardiogenic shock, asystole. Propranolol is especially dangerous due to sodium-channel-blocking QRS widening; sotalol due to pronounced QT prolongation and the risk of torsades de pointes.
Do all beta-blockers widen the QRS in overdose?
No. QRS widening is most characteristic of overdose with propranolol and certain beta-blockers with membrane-stabilizing activity. With sotalol, the leading ECG sign is QT prolongation rather than QRS widening; if a wide QRS does occur, an additional cause should be sought. Cardioselective beta-blockers (metoprolol, bisoprolol, atenolol) in overdose cause bradycardia and AV block, but typically do not widen the QRS.
Why is sotalol overdose more dangerous than other beta-blockers?
In addition to beta-blockade, sotalol blocks potassium channels (Vaughan Williams class III), which prolongs the QT interval and increases the risk of polymorphic ventricular tachycardia (torsades de pointes). This is the main additional danger of sotalol, unlike propranolol, where the risk is more related to QRS widening.
Can calcium be administered in beta-blocker poisoning?
Calcium is not a specific antidote for beta-blockers, but it can be considered as an adjunctive measure in refractory hypotension or conduction disturbances, including isolated severe intoxication, although data on its efficacy are limited. Its use is particularly justified if concomitant calcium channel blocker intoxication cannot be ruled out. Calcium does not replace the primary treatment for shock—fluid resuscitation, vasopressors, and high-dose insulin euglycemic therapy.
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Related terms
More in "Pharmacology and Toxicology"
Sources
- Goldberger A. Clinical Electrocardiography: A Simplified Approach
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.