Beta blocker

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Anna Lee

First posted June 2006

Pharmacology

• Competitive ß antagonists

  • indirectly decrease cAMP production, and hence decrease Ca influx through the L-type Ca channel. Interruption of calcium fluxes leads to cardiovascular dysfunction and metabolic abnormalities

  • ß1 receptors in heart

  • ß2 receptors in bronchial tree and blood vessels

• Heterogeneous group of drugs with different channel selectivity, lipid solubility, membrane stabilizing activity and intrinsic sympathomimetic activity

  • Selectivity lost with overdose (eg metoprolol, atenolol, esmolol)

  • ß blockers with intrinsic sympathomimetic activity theoretically safer in overdose (eg pindolol)

  • ß blockers with high lipid solubility cause more adverse CNS effects, and a higher volume of distribution makes extracorpeal removal less effective (eg Carvedilol, propanolol)

  • ß blockers with membrane stabilizing activity associates with higher risk of seizure and TCA-like cardiac toxicity – QRS widening (eg propranolol, acebutolol, pindolol)

Clinical features

• Depend on drug type, amount and timing of overdose, other drugs ingested and comorbidity.

• Clinical features usually present within 4 h of ingestion, can be delayed for 6-12 hours for sustained released formulation

Cardiovascular

• hypotension,

• bradycardia & heart block

• congestive cardiac failure

• ECG - bradycardia, 1st AV block, intraventricular conduction delays, QT prolongation

Respiratory

• bronchospasm

CNS

• lethargy, stupor, coma

• seizures (especially following propranolol OD, particularly if QRS duration >100msec)

Metabolic

• Hyperglycemia, hypokalaemia, hypocalcemia and lactate acidosis ; hypoglycaemia rarely encountered

Complications of end-organ ischemia

• renal failure, myocardial infarction, bowel infarction, stroke

Management

Supportive

• Preadministration of atropine before intubation to blunt vagally mediated bradycardia associated with laryngoscopy

• Cautious fluid resuscitation – beware fluid overload in view of negative inotropic effects of ß blockers

• Atropine for bradycardia

Management of hypotension

• For refractory hypotension, invasive monitoring is recommended to guide therapy

• Catecholamines:

  • Isoprenaline for low HR

  • Dobutamine, Epinephrine for low contractility

  • Nor-epinephrine, Vasopressin for low peripheral vascular resistance

• Calcium chloride 0.4ml/k/h

• Glucagon 5-10mg iv followed by infusion 1-5mg/h for resistant hypotension (no human study)

• Phosphodiesterase inhibitors as 2nd line treatment for bradycardia

• Insulin and glucose infusion (no studies in ß blocker toxicity)

• Non-pharmacological treatment

  • Transvenous pacing

  • IABP

  • Extra Corporeal Life Support (in case report only)

Management of other complications

• Salbutamol for bronchospasm

• Benzodiazepine for seizure

• Sodium bicarbonate for widened QRS complex

• Ventricular arrhythmia associated with prolonged QT interval can be treated with Mg and lidocaine; correct hypokalaemia and hypocalaemia

Elimination

GI decontamination

• life saving measures take precedence

• induced emesis contraindicated because of risk of sudden cardiovascular collapse

• gastric lavage within 60 min of ingestion may be helpful

• ± activated charcoal

Extracorporeal elimination

In case reports only

Further reading

Mokhlesi B et al. Adult toxicology in critical care. Chest 2003; 123:897-922

Christopher R et al. Pharmacology, Pathophysiology and Management of Calcium Channel Blocker and B-Blocker Toxicity. Toxicol Rev 2004; 23 (4): 223-238

©Charles Gomersall, October, 2009 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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