Beta-Blocker Poisoning, Emergency Medicine

Basics

Description

Normal Physiology

Cardiovascular: β1-receptors:
- ATP converted to cAMP by adenyl cyclase with stimulation of β-receptors.
- cAMP activates protein kinase, which phosphorylates proteins of the sarcoplasmic reticulum.
- Sarcoplasmic reticulum releases calcium.
- Excitation-contraction coupling occurs.
Effects of β-blockers:
- Cardiovascular:
  - Decreased excitation/contraction
  - Membrane stabilizing activity
  - Sodium channel blockade causes a prolongation of the QRS complex (with some agents).
  - Prolongation of QTc interval leading to ventricular dysrhythmias (with some agents)
  - Intrinsic sympathomimetic activity
  - Partial agonist properties (with some agents)
- Neurologic:
  - CNS effects with the lipophilic agents (propranolol, metoprolol, labetalol)

Diagnosis

Signs and Symptoms

Cardiovascular:
- Hypotension
- Bradycardia
- Cardiac conduction delays
- Heart block
- Heart failure
- Electrical mechanical dissociation
- Loss of β-selectivity in overdose settings
Neurologic:
- Coma
- Seizures
Pulmonary:
- Bronchospasm
- Pulmonary edema
Metabolic:
- Hypoglycemia

History

Inquire about risk of medication error.
Inquire about risk of suicidal ideation with intent.
Inquire about possible exposure to medications with a pediatric patient.

Physical Exam

Hypotension
Bradycardia
Dysrhythmias

Essential Workup

With unknown ingestion: Suspect β-blocker poisoning with bradycardia/hypotension.
ECG:
- Conduction delays
- 1st-, 2nd-, or 3rd-degree heart block
- Bradycardia

Diagnosis Tests & Interpretation

Lab

CBC
Electrolytes, BUN, creatinine, glucose
Toxicology screen if coingestants suspected

Differential Diagnosis

Calcium-channel blocker toxicity
Clonidine toxicity
Digitalis toxicity
Acute myocardial infarction with heart block

Treatment

Pre-Hospital

Transport pills and pill bottles when overdose suspected.

Initial Stabilization/Therapy

ABCs:
- Airway protection as indicated by mental status
- Supplemental oxygen as needed
- 0.9% NS IV access
- Close hemodynamic monitoring
Naloxone and thiamine if altered mental status
Bedside glucose determination, treat hypoglycemia with D50W
Treat prolonged seizures with benzodiazepines

Ed Treatment/Procedures

Goals

Heart rate >60 beats per minute
Systolic BP >90 mm Hg
Adequate urine output
Improving level of consciousness

GI Decontamination

Syrup of ipecac: Contraindicated in the prehospital and ED setting.
Consider lavage with Ewald tube if ingestion within 1 hr:
- Propranolol may cause esophageal spasm producing difficulty with passage and removal of gastric lavage tube.
Activated charcoal helpful especially in the presence of coingestants.

Bradycardia/Hypotension

Atropine:
- Initial agent
- Low success rate
Glucagon:
- Initial drug of choice for β-blocker-induced hemodynamic instability
- Administer if atropine does not increase heart rate.
- Promotes cAMP production through a receptor site other than the β-receptor
- May cause nausea and vomiting
- Mix with NS or D5W
IV fluids:
- Administer cautiously in the hypotensive patient
- Swan-Ganz catheter or central venous pressure (CVP) monitoring to help follow volume status
Amrinone:
- Selective phosphodiesterase inhibitor
- Indirectly increases cAMP leading to increased inotropy
- Use in conjunction with glucagon to treat symptomatic sustained bradycardia.
Vasopressor agents:
- Initiate when symptomatic hypotension/bradycardia persists after atropine/glucagon.
- Use invasive monitoring to help guide therapy.
- Utility may be limited owing to β-blockade:
  - Higher doses may be required.
- Isoproterenol (nonselective β-agonist):
  - Titrate for BP and heart rate.
- Epinephrine (potent α- and β-receptor agonist):
  - BP increases as a result of direct myocardial stimulation, increase in heart rate, and vasoconstriction.
  - Use if no BP response with isoproterenol
- High-dose dopamine
Sodium bicarbonate:
- In theory, this is used if there is evidence of prolongation of QRS >100 ms owing to some of the β-blockers also causing sodium channel blockade leading to a prolonged QRS.
- Not routinely administered for all β-blocker toxicities
Electrical pacing: When other treatment options have failed

Experimental Treatment Options

Consult with local poison center
High-dose insulin:
- Promotes more efficient myocardial metabolism
- Hypoglycemia commonly seen in β-blocker overdose, will require frequent monitoring of glucose concentration
- Perform in consultation with local poison center
IV fat emulsion therapy (20% intralipid)

Enhanced Elimination

Hemodialysis helpful with water-soluble β-blocking agents:
- Nadolol
- Atenolol
- Sotalol
IV fat emulsion (20% Intralipid):
- Potential treatment in the future

Medication

Activated charcoal: 1 g/kg PO
Amrinone: Loading dose 0.75 mg/kg; maintenance drip 2-20 μg/kg/min; titrate for effect
Atropine: 0.5 mg (peds: 0.02 mg/kg) IV; repeat 0.5-1 mg IV (peds: 0.04 mg/kg)
Dopamine: 2-20 μg/kg/min IV
Dextrose: D50W 1 ampule (50 mL or 25 g; peds: D25W 2-4 mL/kg) IV
Epinephrine: 2 μg/min (peds: 0.01 mg/kg [0.1 mL/kg 1:10,000]); titrate to effect
Glucagon: 3-5 mg IV over 1-2 min (peds: 0.03-0.1 mg/kg) bolus followed by 70 μg/kg/h infusion
Insulin (regular insulin): 1 IU/kg bolus IV followed by 0.5-1 IU/kg/h titrated to clinical response (be sure to supplement with dextrose)
Isoproterenol: 5 μg/min IV and titrate for heart rate effect
Norepinephrine: Start 2-4 μg/min IV, titrate up to 1-2 μg/kg/min IV
Sodium bicarbonate: 1 mEq/kg IVP

First Line

IV fluids
Glucagon
Vasopressor agents

Second Line

Sodium bicarbonate
Hemodialysis

Follow-Up

Disposition

Admission Criteria

ICU admission for decreased level of consciousness or hemodynamic instability (bradycardia, conduction delays, hypotension)
Observation and monitoring for 24 hr for long-acting or sustained-release preparations owing to the potential delay in symptoms

Discharge Criteria
Asymptomatic 8-10 hr after ingestion of short- or immediate-release preparation �

Follow-Up Recommendations

Psychiatric evaluation for all suicidal patients
Poison prevention guidance for parents of pediatric accidental ingestion

Pearls and Pitfalls

Consider β-blocker toxicity in patients who present with hypotension and bradycardia.
Wide complex QRS dysrhythmias should be treated with sodium bicarbonate.

Additional Reading

Harvey �MG, Cave �GR. Intralipid infusion ameliorates propranolol-induced hypotension in rabbits. J Med Toxicol. 2008;4:71-76.
Pfaender �M, Casetti �PG, Azzolini �M, et al. Successful treatment of a massive atenolol and nifedipine overdose with CVVHDF. Minerva Anestesiol. 2008;74:97-100.
Shepherd �G. Treatment of poisoning caused by β-adrenergic and calcium-channel blockers. Am J Health Sys Pharm. 2006;63:1828-1835.

Codes

ICD9

971.3 Poisoning by sympatholytics [antiadrenergics] �

ICD10

T44.7X1A Poisoning by beta-adrenocpt antagonists, accidental, init
T44.7X4A Poisoning by beta-adrenocpt antagonists, undetermined, init
T44.7X5A Adverse effect of beta-adrenoreceptor antagonists, initial encounter
T44.7X2A Poisoning by beta-adrenocpt antagonists, self-harm, init

SNOMED

241762008 Poisoning by beta-adrenergic blocking drug
292419005 beta-adrenoceptor blocking drug adverse reaction (disorder)
242260002 Accidental overdose of beta-adrenergic blocking drug (disorder)

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