Beta blockers

β1

• Heart
• Kidneys
  • β1 blockade of the juxtaglomerular cells → ↓ renin release → ↓ angiotensin II conversion → ↓ H₂O resorption → ↓ BP t

Tip

• Beta-1 agonists can result in increased renin release → hypokalemia
• Beta-2 agonists can increase the activity of the Na-K-ATPase pump → hypokalemia (transient)

Beta blocker overdose

Epidemiology/Risk Factors

History of depression/suicidality, accidental pediatric ingestion, or dosing error. Access to common agents (metoprolol, atenolol, propranolol).

Clinical Presentation

• Cardiovascular: Bradycardia, hypotension (cardiogenic shock), conduction delays (AV block).
• Pulmonary: Bronchospasm/wheezing (if non-selective agent like propranolol is used). c
• Neurologic: Altered mental status, seizures (especially propranolol due to Na+ channel blocking effects).
• Metabolic: Hypoglycemia (beta-blockers blunt glycogenolysis and mask hypoglycemic symptoms).

Diagnosis

• Clinical: Diagnosis is based on history and toxidrome (Bradycardia + Hypotension).
• ECG: Sinus bradycardia, PR prolongation (1st degree block), or advanced AV blocks.
• Bedside Glucose: Mandatory to rule out hypoglycemia.
• Labs: Electrolytes, renal function, toxicology screen (though usually not detectable on standard urine tox).

Management

Treatment follows a strict hierarchy based on response.

• Initial Stabilization:
  • ABCDEs.
  • IV Fluids (Isotonic saline) for hypotension.
  • IV Atropine for symptomatic bradycardia.
• Specific Antidote (Next Best Step):
  • If refractory to fluids/atropine → IV Glucagon. c
  • Mechanism: Increases intracellular cAMP directly (bypassing the beta receptor) to increase heart rate and contractility.
• Refractory Cases:
  • High-Dose Insulin + Glucose (HDI): Emerging as a preferred therapy for severe toxicity.
  • IV Calcium: Often attempted if co-ingestion of Calcium Channel Blockers is suspected.
  • Lipid Emulsion Therapy: “Lipid sink” to sequester lipophilic drugs (e.g., propranolol).
  • Vasopressors: Norepinephrine or Epinephrine.

Key Associations/Complications

• Propranolol: Highly lipophilic → enters CNS → higher risk of Seizures and QRS widening (Na+ channel blockade). Treat QRS widening with Sodium Bicarbonate.
• Sotalol: Potassium channel blockade → QT prolongation → Risk of Torsades de Pointes.
• Differential Diagnosis:
  • Calcium Channel Blocker (CCB) Overdose: Presentations are nearly identical (Bradycardia/Hypotension).
  • Differentiation: CCB overdose typically causes Hyperglycemia (blocks insulin release); BB overdose causes Hypoglycemia or normal glucose.