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Management of calcium channel antagonist overdose
Steven D Salhanick1, Michael W Shannon
1Children's Hospital, Boston, Massachusetts 02115, USA. steven.salhanick@TCH.harvard.edu
Insights
Calcium channel antagonist overdose is lethal, causing shock, hyperglycemia, and acidosis. Aggressive treatment with gut decontamination, calcium salts, glucagon, and insulin is critical for survival.
Area of Science:
- Cardiology
- Toxicology
- Pharmacology
Background:
- Calcium channel antagonists treat hypertension and tachyarrhythmias.
- Overdose is life-threatening, impacting cardiac and vascular function.
- Toxicity results in vasodilatation, bradycardia, shock, hyperglycemia, and acidosis.
Purpose of the Study:
- To outline the pathophysiology of calcium channel antagonist overdose.
- To detail aggressive therapeutic strategies for managing overdose.
- To provide guidance on patient evaluation and observation.
Main Methods:
- Review of the mechanism of action of calcium channel antagonists.
- Description of overdose symptoms and complications.
- Outline of decontamination and antidote therapies.
- Discussion of supportive care and monitoring.
Main Results:
- Calcium channel antagonists block L-type calcium channels, leading to decreased vascular tone and cardiac contractility.
- Overdose causes significant hemodynamic compromise and metabolic disturbances.
- Specific antidotes like calcium, glucagon, and insulin are effective.
- Supportive measures are crucial when antidotes are insufficient.
Conclusions:
- Aggressive management, including decontamination and specific antidotes, is essential for calcium channel antagonist overdose.
- Insulin therapy shows promise for improving cardiac function and survival.
- Careful patient monitoring and evaluation are vital for successful outcomes.
Abstract:
Calcium channel antagonists are used primarily for the treatment of hypertension and tachyarrhythmias. Overdose of calcium channel antagonists can be lethal. Calcium channel antagonists act at the L-type calcium channels primarily in cardiac and vascular smooth muscle preventing calcium influx into cells with resultant decreases in vascular tone and cardiac inotropy and chronotropy. The L-type calcium channel is a complex structure and is thus affected by a large number of structurally diverse antagonists. In the setting of overdose, patients may experience vasodilatation and bradycardia leading to a shock state. Patients may also be hyperglycaemic and acidotic due to the blockade of L-type calcium channels in the pancreatic islet cells that affect insulin secretion. Aggressive therapy is warranted in the setting of toxicity. Gut decontamination with charcoal, or whole bowel irrigation or multiple-dose charcoal in the setting of extended-release products is indicated. Specific antidotes include calcium salts, glucagon and insulin. Calcium salts may be given in bolus doses or may be employed as a continuous infusion. Care should be exercised to avoid the administration of calcium in the setting of concomitant digoxin toxicity. Insulin administration has been used effectively to increase cardiac inotropy and survival. The likely mechanism involves a shift to carbohydrate metabolism in the setting of decreased availability of carbohydrates due to decreased insulin secretion secondary to blockade of calcium channels in pancreatic islet cells. Glucose should be administered as well to maintain euglycaemia. Supportive care including the use of phosphodiesterase inhibitors, adrenergic agents, cardiac pacing, balloon pump or extracorporeal bypass is frequently indicated if antidotal therapy is not effective. Careful evaluation of asymptomatic patients, including and electrocardiogram and a period of observation, is indicated. Patients ingesting a nonsustained-release product should be observed in a monitored setting for 12 hours, while those who ingest a sustained-release preparation should be observed for no less than 24 hours. Charcoal should be given to the asymptomatic patient with a history of calcium channel antagonist overdose.