01Approach to the Critical Patient/attcp48

Immediate stabilization

›Airway and breathing priorities

›Airway protection status

›Depressed mental status or coma

›Seizure activity

›If unable to protect airway, early intubation

›Oxygen saturation

›SpO2 target greater than 94%

›Bronchospasm screen if wheezing present

›Respiratory depression

›Slowed rate in severe toxicity

›Prepare for bag-mask ventilation

›Circulation priorities

›Hemodynamic instability thresholds

›HR less than 50 bpm symptomatic

›SBP less than 90 mmHg

›MAP less than 65 mmHg

›Continuous cardiac monitor and 12-lead ECG immediately

›QRS width greater than 120 ms signals propranolol sodium channel blockade

›QT prolongation signals sotalol potassium channel blockade

›Two large-bore IV lines and cardiac monitoring

›Point-of-care glucose immediately

›Isotonic crystalloid bolus for hypotension

Key early actions and escalation triggers

›Graduated antidote sequence

›Atropine first for symptomatic bradycardia

›0.5 to 1 mg IV; often insufficient as monotherapy

›Maximum 3 mg IV total

02History/hx62

Ingestion details

›Agent characterization

›Specific beta-blocker agent if known

›Propranolol: sodium channel blockade, lipid soluble, CNS penetrating

›Sotalol: potassium channel blockade, QT prolongation, torsades risk

›Labetalol or carvedilol: alpha-1 antagonism, vasodilatory shock pattern

›Atenolol, nadolol, sotalol: water-soluble, renally cleared

›Formulation type

›Immediate-release: peak toxicity within 1 to 2 hours

›Sustained-release: peak toxicity delayed several hours; prolonged course

›Estimated dose and pill count

›Access to other patient medications

›Intentional versus accidental exposure

Co-ingestants and context

›High-risk co-ingestants

›Calcium channel blockers

›Synergistic bradycardia and hypotension

›Dramatically worsens outcomes

›Other AV-nodal blocking agents

›Digoxin, clonidine

›Amplified conduction suppression

›Sedatives and alcohol

›CNS depression compounded

›Airway protection risk increased

›Intent and access

›Intentional ingestion

›Suicidal ideation assessment

›Prior overdose attempts

03Physical Exam/exam42

Vital signs

›Vital sign snapshot

›Heart rate

›Bradycardia often less than 50 bpm

›Junctional or escape rhythm possible

›Blood pressure

›SBP less than 90 mmHg in significant toxicity

›Distributive pattern with alpha-blocking agents

›Temperature

›Hypothermia in severe cases

›Respiratory rate

›Respiratory depression in comatose patients

›Tachypnea if bronchospasm or metabolic acidosis

Cardiovascular and perfusion exam

›Cardiac findings

›Heart rate regularity and rhythm

›Bradycardia or AV block pattern

›S3 gallop if cardiogenic shock developing

›Jugular venous distension

›Elevated in cardiogenic shock

›Peripheral perfusion

›Cool and clammy skin

›Prolonged capillary refill: indicator of poor perfusion

›Mottled extremities in severe shock

Neurologic exam

›Mental status

›Level of consciousness

›Lethargy to coma spectrum

04Differential Diagnosis/ddx40

Life-threatening mimics

›Calcium channel blocker overdose

›ICD-10 T46.1

›Similar bradycardia and hypotension

›CCB toxicity more often causes hyperglycemia versus hypoglycemia in beta-blocker toxicity

›More prominent vasodilatory shock pattern

›Digoxin toxicity

›ICD-10 T46.0

›Bradycardia and AV block

›Hyperkalemia: distinguishing feature

›Bidirectional VT and regularized atrial fibrillation patterns

›Clonidine or central alpha-2 agonist overdose

›ICD-10 T46.5

›Bradycardia, hypotension, miosis, CNS depression

›No hypoglycemia

›Organophosphate poisoning

›ICD-10 T60.0

›Bradycardia with full cholinergic toxidrome

›SLUDGE findings: salivation, lacrimation, urination, defecation, GI upset, emesis

Cardiac causes

›Acute myocardial infarction with cardiogenic shock

›ICD-10 I21

›Bradycardia from inferior MI with AV block

›No toxicologic history

›Sick sinus syndrome or high-degree AV block

›ICD-10 I49.5 or I44

›No ingestion history

›Baseline conduction disease context

05Laboratory Tests/lt47

Immediate bedside testing

›Point-of-care glucose

›Hypoglycemia common and immediately treatable

›Treat without awaiting formal labs

›Serial monitoring mandatory during high-dose insulin therapy

Core metabolic panel

›Basic metabolic panel

›Potassium

›Baseline before insulin therapy

›Monitor every 1 hour during high-dose insulin infusion

›Calcium

›Baseline ionized calcium before calcium therapy

›Magnesium level for sotalol toxicity

›Renal function

›Creatinine for water-soluble agent clearance assessment

›Guides hemodialysis consideration for atenolol, sotalol, nadolol

›Glucose

›Serial every 15 to 30 minutes during high-dose insulin therapy

Toxicology screen

›Co-ingestant screen

›Acetaminophen level

›Mandatory for all intentional ingestions

›Salicylate level

›Rule out as co-ingestant

›Ethanol level

›Compounding CNS depression

›Digoxin level

›If on digoxin or digoxin toxicity in differential

06Diagnostic Tests/dt56

Scoring Systems

›Toxicity severity stratification

›Mild toxicity

›Asymptomatic bradycardia

›Normotensive and alert

›Immediate-release formulation with limited dose

›Moderate toxicity

›Symptomatic bradycardia

›Mild hypotension responsive to fluids and atropine

›Altered mentation without coma

›Severe or life-threatening toxicity

›Refractory hypotension not responsive to vasopressors

›Cardiogenic shock

›Seizures, coma, cardiac arrest

›QRS greater than 120 ms or QTc greater than 500 ms

›Clinical utility of scoring

›Severity guides escalation to high-dose insulin or ECMO

›AHA 2025 guidelines recommend early HDIET initiation for life-threatening toxicity

›Do not wait for complete pharmacologic failure before ECMO referral

MRI

›MRI role in beta-blocker toxicity

›Limited acute utility

›Not indicated for hemodynamic assessment

›Availability constraints in unstable patients

›Possible indication

›Altered mental status with unclear structural brain cause after stabilization

›Post-arrest neurologic assessment

›Contraindications

07Disposition/dispo44

ICU admission indications

›Mandatory ICU criteria

›Hemodynamic instability

›Vasopressor requirement

›Refractory bradycardia or AV block

›Pharmacologic antidote requirement

›High-dose insulin infusion

›Glucagon infusion

›Calcium infusion

›Altered mental status or seizures

›Airway monitoring

›Seizure recurrence risk

›Dysrhythmia requiring active management

›Wide QRS necessitating sodium bicarbonate

›QT prolongation with torsades risk

Monitored bed or observation criteria

›Observation minimum duration

›Immediate-release formulations

›Minimum 6 hours of monitoring

›Requires stable vitals, normal ECG, normal glucose, no symptoms

›Sustained-release formulations

›Minimum 12 to 24 hours of monitoring

›Delayed peak toxicity mandates extended observation

Discharge and psychiatric disposition

›Discharge criteria

›Stable hemodynamics for full observation period

›HR greater than 50 bpm without support

›SBP greater than 90 mmHg without support

08Treatment/t115

GI decontamination

›Activated charcoal

›Indication window

›Within 1 to 2 hours of ingestion

›Airway must be protected before administration

›Dosing

›1 g/kg orally or via nasogastric tube, maximum 50 g

›Single dose; no evidence for multi-dose in beta-blocker toxicity

›Whole-bowel irrigation

›Sustained-release formulation ingestion

›Polyethylene glycol solution 1 to 2 L/hour orally or via NGT

›Continue until rectal effluent clear

›Protect airway throughout

Atropine

›First-line for symptomatic bradycardia

›Dosing

›0.5 to 1 mg IV bolus; repeat every 3 to 5 minutes

›Maximum 3 mg IV total

›Limitations

›Often insufficient as monotherapy for significant toxicity

›Do not delay other antidotes if inadequate response

›Contraindication note

›Caution in heart transplant patients: may cause paradoxical heart block

High-dose insulin therapy

›AHA 2025 recommended early for life-threatening toxicity

›Mechanism

›Shifts myocardial metabolism to carbohydrate utilization

›Positive inotropy independent of adrenergic receptors

›Bolus dose

›1 unit/kg IV regular insulin bolus

›Administer with concurrent dextrose if glucose less than 5.5 mmol/l

›Infusion

›1 to 10 units/kg/hour continuous infusion

›Titrate up every 10 to 15 minutes for hemodynamic effect

›Glucose co-administration

›D10W infusion concurrent at 100 to 250 mL/hour

›Titrate to maintain glucose 5.5 to 10 mmol/l

›Monitoring during therapy

›Glucose every 15 to 30 minutes initially

›Potassium every 1 hour; replace aggressively to maintain greater than 3.0 mmol/l

›Phosphate monitoring with prolonged infusion

Vasopressors

›First-line for hypotension

›Norepinephrine

›Starting dose 0.05 to 0.1 mcg/kg/min IV

›Titrate to MAP greater than 65 mmHg

›Escalate rapidly as needed

›Epinephrine

›Starting dose 0.05 to 0.1 mcg/kg/min IV

›Useful when both inotropic and vasopressor effect needed

›Titrate to hemodynamic targets

›Note: vasopressor response may be blunted due to receptor blockade

›Non-adrenergic strategies essential as concurrent therapy

Glucagon

›Mechanism

›Activates adenylyl cyclase independently of beta receptors

›Bypasses blocked adrenergic receptors

›Positive chronotropic and inotropic effects

›Dosing

›Bolus 2 to 10 mg IV over 3 to 5 minutes

›Anticipate vomiting: protect airway

›Infusion if response to bolus

›1 to 15 mg/hour continuous infusion

›Titrate to effect

›Limitations

›Tachyphylaxis with prolonged use

›Limited supply in many pharmacies; anticipate early

Intravenous calcium

›Mechanism

›Increases extracellular calcium; partially overcomes beta-blocker cardiovascular depression

›Particularly useful with concurrent CCB exposure

›Dosing options

›Calcium chloride 2 g IV (10 mL of 10% solution)

›Higher elemental calcium per gram than gluconate

›Central line preferred; tissue necrosis with extravasation

›Calcium gluconate 6 g IV if no central access

›Peripheral administration safer

›Infusion if response

›20 to 40 mg/kg/hour of calcium chloride; titrate to blood pressure

›Monitor ionized calcium level during infusion

›Target ionized calcium 1.5 to 2.0 mmol/l

Sodium bicarbonate

›Propranolol-specific: sodium channel blockade

›Indication

›QRS greater than 120 ms attributable to propranolol

›Ventricular dysrhythmia from sodium channel blockade

›Dosing

›1 to 2 mEq/kg IV bolus

›Repeat as needed targeting serum pH 7.45 to 7.55

›Infusion option

›150 mEq sodium bicarbonate in 1 L D5W; run at 150 to 250 mL/hour

›Monitor serum pH every 1 to 2 hours

Sotalol-specific management

›QT prolongation management

›IV magnesium sulfate

›2 g IV over 10 to 15 minutes for torsades de pointes

›May repeat 2 g dose once

›Overdrive pacing

›Transvenous or transcutaneous pacing for recurrent torsades

›Target rate 90 to 110 bpm to suppress ectopy

›Avoid QT-prolonging agents

›Amiodarone contraindicated

›Fluoroquinolones and antipsychotics avoid

›Hemodialysis consideration for sotalol

›Water-soluble; dialyzable

›Renal impairment with severe toxicity

›Prolonged or refractory toxicity despite pharmacotherapy

Intravenous lipid emulsion

›Expert consensus advises against routine use

›AHA 2025 recommendation

›Risk of abrupt cardiac arrest reported after administration in oral beta-blocker overdose

›Benefit-risk ratio unfavorable in most beta-blocker toxicity cases

›May be considered only in extremis when all else has failed

›Toxicology or poison control guidance recommended before use

VA-ECMO

›Refractory cardiogenic shock

›Initiate cannulation process early

›Do not wait for cardiac arrest if trajectory is deteriorating

›AHA 2025 supports ECMO as rescue therapy

›ECMO cannulation

›Venoarterial configuration for cardiogenic shock

›Cardiology or cardiac surgery team involvement

›Bridge to recovery

›Beta-blocker toxicity is often reversible with time

›ECMO supports until drug clearance

09Special Populations/sp56

Pregnancy

›Pregnancy-specific considerations

›Beta-blocker toxicity risk to fetus

›Fetal bradycardia and hypoglycemia from placental transfer

›Continuous fetal monitoring when viable gestation

›Obstetrics consultation early

›Antidote safety in pregnancy

›High-dose insulin: generally safe; monitor fetal glucose

›Glucagon: limited data; use for life-threatening maternal toxicity

›Atropine: crosses placenta; fetal tachycardia may occur

›GI decontamination

›Activated charcoal: safe if airway protected

›Avoid whole-bowel irrigation in third trimester if risks outweigh benefit

›Vasopressors

›Norepinephrine preferred over epinephrine when possible

›Maintain uteroplacental perfusion

›Imaging

›Avoid CT unless clinical necessity clear

›POCUS for hemodynamic assessment preferred

Geriatric

›Older adult considerations

›Pharmacokinetic changes

›Reduced renal clearance; water-soluble agents accumulate

›Higher risk with atenolol, sotalol, nadolol in renal impairment

›Presentation differences

›Baseline bradycardia may mask initial toxicity severity

›Delirium as primary symptom of severe toxicity

›Falls and syncope as presenting events

10Background/b59

Epidemiology

›Incidence and exposure data

›Poison center data

›Beta-blockers among the most common cardiovascular drug overdoses

›10-year German poison center analysis of 2,967 cases: no fatalities in single-substance beta-blocker exposures in adults

›Deaths occurred with co-ingestions such as bisoprolol plus verapamil

›Intentional versus unintentional

›Intentional overdose associated with higher doses and co-ingestants

›Pediatric exposures usually unintentional; single-pill toxicity possible

›Mortality and morbidity

›Isolated beta-blocker overdose: low fatality rate with modern management

›Propranolol and sotalol carry highest morbidity and mortality among class

›CCB co-ingestion dramatically increases mortality risk

Pathophysiology

›Receptor-level mechanisms

›Beta-1 receptor blockade

›Decreased heart rate via SA node suppression

›Decreased AV node conduction velocity

›Reduced myocardial contractility

›Beta-2 receptor blockade

›Bronchospasm in reactive airway disease

›Inhibition of hepatic glycogenolysis contributing to hypoglycemia

›Inhibition of glucagon-stimulated glycogenolysis

›Additional channel effects by agent

›Propranolol: sodium channel blockade causing QRS widening and seizures

›Sotalol: potassium channel blockade causing QRS-independent QT prolongation and torsades de pointes

›Labetalol and carvedilol: alpha-1 antagonism causing vasodilatory shock

›Cardiovascular toxicity cascade

11Patient Discharge Instructions/pdi34

copy discharge instructions

›Home care after beta-blocker ingestion

›Full observation period completed before discharge

›You were monitored for heart rate, blood pressure, blood sugar, and heart rhythm

›You are safe to go home based on stable results throughout observation

›Activity

›Rest at home for the remainder of the day

›No driving or operating machinery for 24 hours

›Do not drink alcohol

›Warning signs: return to emergency immediately

›Heart or circulation

›Feeling your heart beating very slowly or irregularly

›Fainting or nearly fainting

›Chest pain or pressure

›Feeling cold, clammy, or extremely weak

›Brain and nervous system

›Confusion, unusual drowsiness, or loss of consciousness

›Seizure

›Breathing

›Shortness of breath at rest

›Wheezing or difficulty breathing

›Blood sugar

›Shaking, sweating, confusion suggesting low blood sugar

›Psychiatric and safety follow-up

›Mandatory psychiatric or mental health follow-up arranged

›Attend all scheduled appointments

›Contact crisis line if thoughts of self-harm recur

›Medication safety

12References/r27

Guidelines and key sources

›AHA 2025 Guidelines

›Cao D, Arens AM, Chow SL et al. Part 10: Adult and Pediatric Special Circumstances of Resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025.

›Primary reference for high-dose insulin, ECMO, and vasopressor recommendations in beta-blocker toxicity

›AHA 2023 Focused Update

›Lavonas EJ, Akpunonu PD, Arens AM et al. 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning. Circulation. 2023.

›Activated charcoal and decontamination guidance; antidote escalation framework

›ACC/AHA/HRS 2018 Bradycardia Guideline

›Kusumoto FM, Schoenfeld MH, Barrett C et al. 2018 ACC/AHA/HRS Guideline on The Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. Heart Rhythm. 2019.

›Drug-induced bradycardia algorithm; pacing indications

Systematic reviews and clinical studies

›Rotella JA, Greene SL, Koutsogiannis Z et al. Treatment for Beta-Blocker Poisoning: A Systematic Review. Clinical Toxicology. 2020.

›Evidence synthesis for high-dose insulin, glucagon, calcium, and lipid emulsion

›High-dose insulin: best hemodynamic evidence among antidotes

›ILE: insufficient evidence to recommend in beta-blocker overdose

›Hu Y, Mujahid K, Ahsan A et al. Effectiveness of Treatments for Propranolol Toxicity: A Systematic Review. European Journal of Clinical Pharmacology. 2026.

›Propranolol-specific evidence for combined insulin, vasopressors, bicarbonate, and ECMO

›Lauterbach M. Clinical Toxicology of Beta-Blocker Overdose in Adults. Basic and Clinical Pharmacology and Toxicology. 2019.

›Agent-specific pharmacokinetics; dialysis evidence for water-soluble agents

Additional references

›Suarez F, Koyfman A, Long B. Pearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity. The Journal of Emergency Medicine. 2026.

›Emergency department approach; pitfall avoidance

›Graudins A, Lee HM, Druda D. Calcium Channel Antagonist and Beta-Blocker Overdose: Antidotes and Adjunct Therapies. British Journal of Clinical Pharmacology. 2016.

›Antidote mechanisms and practical dosing guidance

›Tisdale JE, Chung MK, Campbell KB et al. Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association. Circulation. 2020.

›Sotalol QT prolongation and torsades management framework

›ICD-10 coding

›T44.7: poisoning by beta-adrenoreceptor antagonists, initial encounter

Evidence & Review

Evidence & Review