Management of Calcium Channel Blocker Poisoning
Calcium channel blocker poisonings are the leading cause of death from cardiovascular medication-related overdoses (Mowry et al. Clin Toxicol (Phila) 52(10):1032–1283, 2014; Shenoy et al. J Hosp Med 9(10):663–668, 2014). Clinical effects in the poisoned p
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Management of Calcium Channel Blocker Poisoning David M. Black and Robert W. Shaffer
Introduction Calcium channel blocker poisonings are the leading cause of death from cardiovascular medication-related overdoses [1, 2]. Clinical effects in the poisoned patient may include hypotension, bradycardia, atrioventricular conduction disturbances, pulmonary edema, stroke, bowel ischemia, altered mental status, and cardiac arrest. Many immediate and sustained-release preparations exist, hence pharmacokinetics are highly variable. Calcium channel blockers are generally lipophilic and highly-protein bound, rendering traditional extracorporeal elimination methods such as hemodialysis largely ineffective.
D.M. Black Emergency Medicine, University of Michigan Health System, Ann Arbor, MI, USA R.W. Shaffer (*) Department of Emergency Medicine, University of Michigan Health System, Ann Arbor, MI, USA e-mail: [email protected]
Dihydropyridines Nicardipine Nifedipine Isradipine Amlodipine Felodipine Nimodopine Nisoldipine Nitrendipine Non-Dihydropyridines Verapamil Diltiazem Bepridil
Calcium channel blockers act at L-type calcium channels and are generally divided into two unique pharmacologic classes based on their preferred sites of action. Dihydropyridine (i.e. nifedipine, amlodipine) overdoses primarily cause hypotension with reflex tachycardia through their peripheral vasodilatory effects on vascular smooth muscle. The toxicity from non-dihydropyridines (i.e. verapamil, diltiazem), tends to be more severe owing to their primary effects on the myocardium [3]. This may lead to bradydysrhythmias, depressed myocardial contractility, and circulatory collapse [4]. It should be noted that in severe poisonings from either class, this selectivity may be lost [2]. The management of hemodynamically unstable patients with calcium channel blocker toxicity
© Springer International Publishing Switzerland 2017 R.C. Hyzy (ed.), Evidence-Based Critical Care, DOI 10.1007/978-3-319-43341-7_7
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can be quite challenging, and responses to therapeutic interventions can be variable. Traditional therapies include intravenous fluid resuscitation, and the administration of calcium salts, glucagon, and vasopressor agents. Refractory bradycardia and atrioventricular nodal blocks may necessitate the use of atropine and temporary pacemakers. More contemporary treatment strategies including the use of intravenous lipid emulsions and high-dose insulin euglycemic therapy have shown great promise.
Case Presentation A 47 year old female with a history of depression and chronic migraine headaches was brought to the emergency department by her spouse immediately following a witnessed intentional ingestion of approximately sixty 120 mg sustained-release verapamil tablets. On arrival, she was alert and oriented. Vital signs were as followed: pulse 62, blood pressure 95/62, respiratory rate 16, temperature 37.2, and pulse oximetry 99 % on room air. Her EKG showed normal sinus rhythm with normal intervals. IV access was established and a liter of no
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