The cardiac manifestations of CCB toxicity are essentially an extension of their therapeutic effects. Extracardiac effects of CCB’s include lethargy, confusion, seizures (rare), hyperglycemia and lactic acidosis from hypoperfusion. However, in overdose, the selectivity of specific agents may be lost. Nifedipine and other dihydropyridines act preferentially on vascular smooth muscle, resulting in vasodilation their effect on cardiac conduction is insignificant in therapeutic doses. Diltiazem is similar in action to verapamil but produces less cardiac depression at therapeutic doses. Different CCBs have varying degrees of effect on these physiologic functions: verapamil has depressive effects predominantly on SA/AV nodal conduction and myocardial contractility. The results include decreased rate of firing of the sinus node pacemaker, decreased rate of conduction through the AV node, decreased cardiac contractility, and decreased vascular tone. What are the treatment options for CCB toxicity?ĬCBs block intracellular entry of calcium by binding L-type calcium channels located primarily in cardiac and vascular smooth muscle.When can a patient be safely medically cleared?.What decontamination procedures should be performed for acute CCB overdose?.
What is the pathophysiology of CCB poisoning and what are the typical presenting symptoms and signs?.He was transferred to psychiatry on hospital day # 4.
Intravenous drugs were eventually weaned and the patient recovered with no further events. Finally, a transvenous pacemaker was inserted, with subsequent normalization of his heart rate and blood pressure. A bolus of insulin and dextrose were also administered with minimal effect as dopamine and norepinephrine were started. Glucagon, 5 mg IV, and calcium chloride (total of 5 ampules of 10% solution) had no effect on his hemodynamics, nor did transcutaneous pacing. Atropine had no effect on his heart rate of 40 bpm and intravenous fluids did not improve his blood pressure of 70/40 mmHg.
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