Calcium channel blocker toxicity

Learning objectives

Calcium channel blockers (CCBs) are used to treat hypertension, supraventricular tachycardia, vasospasm, and migraine headaches
Ingestion of excessive CCB agents is one of the most potentially lethal prescription drug overdoses
Overdoses of immediate-release CCBs are characterized by rapid progression to hypotension, bradydysrhythmia, and cardiac arrest
Overdoses of extended-release formulations result in delayed onset of dysrhythmias, shock, sudden cardiac collapse, and bowel ischemia
Symptoms occur within six hours after ingestion, although some forms of medication do not start until after 24 hours
Calcium channel blockers target the L-type voltage-gated calcium channels and these are predominant in the following sites and roles:
- Depolarization of the sinoatrial node (SA) and impulse propagation through the atrioventricular node (AV).
Three main classes of CCBs:
- Phenylalkylamines (verapamil)
- Benzothiazepines (diltiazem)
- Dihydropyridines (nifedipine, amlodipine, felodipine, isradipine, nicardipine, nimodipine)

Complications from toxicity	Complications from treatment
Refractory cardiogenic and distributive shock	Multiorgan failure from calciphylaxis with overaggressive calcium infusion
Acute Respiratory Distress Syndrome	Hypokalemia and Hypoglycemia
Severe hypoperfusion and resultant end-organ injury like ischemic bowel, myocardial infarction, acute tubular necrosis, limb necrosis	Acute Respiratory Distress Syndrome hypertriglyceridemia, pancreatitis, and fat overload syndrome with lipid emulsion therapy
Pulseless electrical activity with cardiac arrest (PEA)	Nausea, vomiting, ileus, and Hypokalemia with glucagon
	Arterial and venous thrombosis and limb ischemia with interventions like ECMO