In overdose, β blockers inhibit both β1 and β2 adrenoceptors; selectivity, if any, is lost at high dosage. The most toxic β blocker is propranolol. As little as two to three times the therapeutic dose can cause serious toxicity. This may be because propranolol in high doses may cause sodium channel blocking effects similar to those seen with quinidine-like drugs, and it is lipophilic, allowing it to enter the CNS .
Bradycardia and hypotension are the most common manifesta-tions of toxicity. Agents with partial agonist activity (eg, pindolol) can cause tachycardia and hypertension. Seizures and cardiac conduction block (wide QRS complex) may be seen with propranolol overdose.
General supportive care should be provided as outlined earlier. The usual measures used to raise the blood pressure and heart rate, such as intravenous fluids, β-agonist drugs, and atropine, are gener-ally ineffective. Glucagon is a useful antidote that—like β agonists—acts on cardiac cells to raise intracellular cAMP but does so independent of β adrenoceptors. It can improve heart rate and blood pressure when given in high doses (5–20 mg intravenously).