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• The beta blocker toxicity depends on the protein binding, lipid solubility, Na channel blockade , partial agonist, receptor selectivity of the drug.

• Primary organ affected in beta blocker toxicity is CVS and hallmark is bradycardia with hypotension.

• Lipid soluble , drugs like propranolol can cross BBB and produce mental status depression, seizures, coma.

• Cardioselective drugs have less side effect, whereas non selective drugs can cause bronchospasm.

• Drugs like labetalol which has both α & β blocking effect can lead to exaggerated hypotension.

• Drugs with partial agonist activity leads to hypotension and tachycardia initially.

• Beta blockers with Na channel blockade leads to wide complex bradycardia.

• Sotalol is unique drug with ability to block K+ channel , this leads to prolongation of QT interval and leads to VT, VF ,VPC, Torsades depointes.

Clinical Feature

Cardiac

• Hypotension

• Bradycardia

• Conduction delays & blocks

• Ventricular dysarrythmia

• Asystole

• Decreased contractility

CNS

• Depressed mental status

• Coma

• Psychosis

• Seizures

Pulmonary

• Bronchospasm

Diagnosis

• ECG

• RFT, ABG, B. Glucose

• SpO2

• BP Monitoring

Management

GI Deontamination

• Activated charcoal may be of benefit if it is given within 1-2 hrs.

• Whole bowel irrigation may be beneficial.

Glucagon

• First line agent in acute beat blocker toxicity .

• Glucagon produced in pancreatic alpha cells from proglucagon.

• It is thought to activate myocardial adenyl cyclase independent of the beta receptor.

• Effect is seen within 1-2 min , reach a peak in 5-7 min & have a duration of action of 10-15 min.

• Bolus dose of glucagon is 0.05- .15mg/kg

• Continous infusion: 1-10mg/h

Adrenergic Receptor Agonist

• Adrenaline, Noradrenaline, Dopamine, Isoproterenol are used routinely.

• Noradrenaline is most effective due to its ability to increase heart rate and Blood pressure.

Hyperinsulinemia Euglycemia therapy

• Insulin facilitates myocardial utilization of glucose the desired substance during stress.

• Dose : 1U/kg IV bolus followed by 0.5-1.0 U/kg /h

• 0.5 gm/kg boluse glucose , followed by infusion.

• Blood glucose to be monitored every 20 to 30min until euglycemia is achieved later every hrly.

• Adverse effect : Hypoglycemia, hypokalemia

• Normally the heart uses free fatty acids as its primary energy source but during stress it switches to using carbohydrate to maintain metabolism

Calcium

• They improve depression of myocardium via positive inotropic action.

• Adverse effect : Hypercalcemia, conduction blocks, worsening bradycardia

• Recommended dose : 0.6ml/kg given over 5-10min followed by continuous infusion 0.6-1.5ml/kg/h.

Sodium Bicarbonate

• To treat severe metabolic acidosis & wide QRS dysarrythmia secondary to Na + channel blockade.

• Rapid bolus 2-3 mEql/kg.

Phosphodiesterase inhibitor

• It can be used as an alternate to glucagon .

• They prevent break down of cyclical adenosine monophosphate thereby maintaing intracellular calcium.

• Milrinone dose : 0.5mcg/kg/min

Sotalol toxicity

• Magnesium sulphate & Lidocaine are used to treat sotalol toxicity.

Updated on 2/2/2015

Reference : Tintinalli