Cardiovascular Toxicity of Beta Blockers and Calcium Channel Blockers

Introduction to Toxicity

The American College of Cardiology and Circulation journal report that beta blocker and calcium channel blocker poisoning can produce potentially fatal systemic cardiovascular effects due to their negative chronotropic and inotropic effects, as well as vasodilation 1, 2

Patients with beta blocker and calcium channel blocker poisoning may present with severe hypotension, bradycardia, conduction disorders (including various degrees of AV block), refractory cardiogenic shock, and cardiovascular collapse in severe cases 2, 3

Calcium channel blocker poisoning is often associated with significant hyperglycemia due to complex metabolic alterations, although this fact is not directly cited, a related fact is: the American Heart Association and Circulation journal report that these poisonings can cause hyperglycemia, acidosis, and electrolyte disturbances 2, 3

The American Heart Association recommends that treatment for these poisonings be based on counteracting the pathophysiological mechanisms, including the use of intravenous calcium to increase extracellular calcium, improve cardiac contractility, and heart rate 3
The American College of Cardiology suggests that glucagon can be used to activate hepatic adenylate cyclase, promote glycogenolysis, increase AMPc through a beta-receptor independent pathway, and improve cardiac contractility and heart rate 1, 2
High-dose insulin therapy can improve glucose utilization by the myocardium, has a positive inotropic effect, and improves hemodynamic parameters 3

In severe cases, aggressive and multimodal treatment may be required, including the use of ECMO in refractory situations, as reported by the American Heart Association and Circulation journal 3