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Management of Calcium Channel Blocker Overdoses

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Management of Calcium Channel Blocker Overdoses REVIEWS Management of Calcium Channel Blocker Overdoses Sundeep Shenoy, MD, FACP1*, Shilpa Lankala, MD2, Sasikanth Adigopula, MD, MPH, FACP3 1Division of Inpatient Medicine, University of Arizona, Tucson, Arizona; 2Division of Hospital Medicine, Banner Good Samaritan Hospital, Phoenix, Arizona; 3Division of Cardiology, Advanced Heart Failure, Mechanical Circulatory Support and Heart Transplantation, University of California, Los Angeles, Los Angeles, California. Calcium channel blockers (CCBs) are some of the most have been tried and have been successful. However, the commonly used medications in clinical practice to treat evidence for these are limited to case reports and case hypertension, angina, cardiac arrhythmias, and some series. We take this opportunity to review the various cases of heart failure. Recent data show that CCBs are treatment options in the management of CCB overdoses the most common of the cardiovascular medications with a special focus on high-dose insulin therapy as the noted in intentional or unintentional overdoses.1 Novel emerging choice for initial therapy in severe overdoses. treatment approaches in the form of glucagon, high-dose Journal of Hospital Medicine 2014;9:663–668. VC 2014 insulin therapy, and intravenous lipid emulsion therapies Society of Hospital Medicine The 2011 National Poison Data System (NPDS) of high serum concentrations of either CCB class, how- the American Association of Poison Control Centers ever, selectivity is lost, and patients may presents with reported that among the top 25 categories associated bradycardia, hypotension, and decreased cardiac with mortality, cardiovascular medications were sec- contractility.7,8 ond to sedatives/hypnotics/antipsychotics in terms of CCBs show good oral bioavailability and undergo the number of deaths resulting from overdose. More- first-pass metabolism. During an overdose, the over, of cardiovascular medications, Calcium channel enzymes involved in hepatic oxidation can become blockers (CCBs) were the most common agents associ- oversaturated, which reduces the effects of first-pass ated with mortality.1,2 The 2012 NPDS report showed metabolism, resulting in increased quantities of the a similar trend, with cardiovascular drugs ranking active drug reaching the systemic circulation and a among the top causes of overdoses, with an additional prolonged half-life.7 In addition, CCBs are highly pro- approximately 4614 cases in comparison to 2011.3 In tein bound and have large volumes of distribution.9 light of emerging strategies for the management of Calcium enters cells through specific channels and CCB overdoses, we sought to review the pathophysiol- regulates various cell processes. In myocardial cells, ogy of CCB overdose and its management. calcium affects excitation-contraction coupling and potential action generation in the sinoatrial node. Sim- PATHOPHYSIOLOGY OF CCB OVERDOSE ilarly, in the pancreas, calcium facilitates the release CCBs are widely used in the management of various of insulin. CCB overdose can result in inhibition of conditions such as hypertension, angina pectoris, insulin secretion from the pancreas and a state of atrial fibrillation, and other cardiac arrhythmias. hypoinsulinemia and insulin resistance.10 Mtabolic 4 CCBs block L-type receptors on the cell surface. acidosis is a common presentation noted in several Based on their predominant physiological effect, CCBs published case reports.11 Metabolic acidosis represents have been classified as dihydropyridines and nondihy- a combination of insulin dysregulation with ketoaci- dropyridines (Table 1). Dihydropyridine overdose gen- dosis and hypoperfusion with lactic acidosis. In addi- erally results in vasodilation with resultant tion, because CCBs block the entry of calcium into 5 hypotension and reflex tachycardia. In comparison, the mitochondria,12,13 and because calcium is required nondihydropyridine overdose generally results in bra- for the normal enzymatic activity of the Krebs cycle, 6 dycardia and decreased cardiac contractility. With CCB overdose leads to lactic acid build-up from its direct effects on aerobic metabolism.14 The clinical picture of CCB overdose is further *Address for correspondence and reprint requests: Sundeep Shenoy, complicated by the switch in the mechanism of adeno- MD, Assistant Professor of Medicine, Division of Inpatient Medicine, Uni- sine triphosphate (ATP) generation in the myocardium versity of Arizona, 1501 N. Campbell Avenue, Tucson, AZ 85724-5212; Telephone: 520-626-5797; Fax: 520-626-5721; E-mail: from free fatty acid oxidation to carbohydrate metab- [email protected] olism.15 In response to this stress, the liver increases Additional Supporting Information may be found in the online version of glucose production via glycogenolysis. With concomi- this article. tant hypoinsulinemia10 and relative insulin resistance, Received: March 11, 2014; Revised: July 1, 2014; Accepted: July 8, intracellular glucose transport is disturbed, with a 2014 2014 Society of Hospital Medicine DOI 10.1002/jhm.2241 resultant decrease in ATP production that quickly Published online in Wiley Online Library (Wileyonlinelibrary.com). leads to myocardial dysfunction and cardiogenic An Official Publication of the Society of Hospital Medicine Journal of Hospital Medicine Vol 9 | No 10 | October 2014 663 Shenoy et al | Management of CCB Overdoses TABLE 1. The Most Commonly Used Calcium dycardia, hyperglycemia, and persistent hypotension, Channel Blockers with signs of hypoperfusion usually manifested as altered mental status, clinically defines a severe Dihydropyridine Short-acting agents: nifedipine overdose. Longer-acting formulations: felodipine, isradipine, nicardipine, nifedipine, nisoldipine, amlodipine* Nondihydropyridine Verampamil and diltiazem MANAGEMENT APPROACH Maintenance of the airway and circulation is of pri- NOTE: mary importance in CCB overdose cases (Table 2). *Longer-acting agents generally have little cardio depressant activity, with amlodipine having the least.6 Hypotension and bradyarrhythmias are noted in cases of severe overdose, and some patients might require endotracheal intubation and mechanical ventilation shock. The resultant clinical state of acidosis, hyper- very early in their management. The initial treatment glycemia, and insulin deficiency is similar to diabetic strategy typically consists of the use of intravenous ketoacidosis.11,14 A presentation of symptomatic bra- crystalloids and gastrointestinal (GI) decontamination; atropine is reserved for symptomatic bradycardia. Some patients may also require transcutaneous and transvenous pacing early and emergently due to com- TABLE 2. Treatment Options of Calcium Channel plete cardiovascular collapse. Therefore, having a Blocker Overdose medical toxicologist or a regional poison control Initial resuscitation measures expert involved from the time of initial management Intravenous hydration with crystalloids, colloids. is advised, especially for cases of severe overdose or Gastrointestinal decontamination consumption of extended-release preparations. Activated charcoal 1 g/kg body weight in hemodynamically stable patients who can protect their airways.1 Best administered within 2 hours. However, in poisoning from extended release preparations, it can be used beyond the 2-hour window. GI Decontamination Anecdotally, WBI has been utilized in calcium channel blocker overdose. In cases of severe overdose, patients may present with However, it is not the recommended approach, especially in patients who are hemodynamically lethargy from hypotension and poor cerebral flow, unstable. Atropine and the risk for aspiration and pneumonitis should be Reserved for bradycardia; 0.5 mg every 3–5 minutes, not to exceed a total of 3 mg or strongly considered in these patients if GI decontami- 0.04 mg/kg (per ACLS protocol). nation is considered. GI decontamination is best in Sodium bicarbonate cases where the patient is hemodynamically stable and 1–2 mEq/kg boluses of hypertonic sodium bicarbonate when QRS widening is noted on the 46 presents early to the emergency department (ED), ECG. For severe acidosis or persistent ECG changes, a sodium bicarbonate drip can be initi- 7,9 ated with 150 mEq sodium preferably within 2 hours ; early use might decrease bicarbonate in 1 L D W to run at about 100–125 mL per hour.46 drug absorption and enterohepatic circulation, thus 5 16 Following intravenous hydration and GI decontamination (hyperinsulinemia-euglycemia therapy) lowering the drug levels. However, in cases in which or vasopressors are usually initiated as resuscitation measures. the drug consumed was an extended-release prepara- Agents used to reverse the calcium channel blocker poisoning tion, GI decontamination is beneficial even when the Hyperinsulinemia-euglycemia therapy (refer to Table 33). 17 Glucagon patient presents late to the ED. GI decontamination Initiated at 0.05–0.15 mg/kg as bolus dosing, with a repeat dosing in 3–5 minutes. An intrave- is typically achieved using activated charcoal (1 g/kg nous infusion can be initiated following this.1 body weight) or by performing whole bowel irrigation Calcium salts (WBI) with polyethylene glycol.9 However, there is A bolus of 0.3 mEq/kg of calcium can be administered as intravenously over 5–10 minutes very little evidence that either approach changes the (0.6 mL/kg of 10% calcium gluconate solution or 0.2 mL/kg of 10% calcium chloride solution). overall outcome, and WBI can be potentially harmful If beneficial response noted, an infusion
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