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Calcium channel blocker poisoning

Calcium channel blocker poisoning
Fermin Barrueto, Jr, MD, MBA, FACHE
Section Editor:
Andrew Stolbach, MD, MPH, FAACT, FACMT, FACEP
Deputy Editor:
Jonathan Grayzel, MD, FAAEM
Literature review current through: Feb 2023. | This topic last updated: May 18, 2022.

INTRODUCTION — Calcium channel blockers (CCBs) are used in the treatment of hypertension, angina pectoris, cardiac arrhythmias, and other disorders. These medications are available in both immediate-release and extended-release preparations; the latter are in wide clinical use (figure 1) [1].

The potential toxicity of these agents is substantial and is often underappreciated by the public. As an example, over 9500 cases of CCB intoxication, caused by intentional or unintentional overdose, were reported to poison centers in the United States during 2002 [2]. Although only 16 percent of all cardiovascular drug exposures were due to CCBs, this class accounted for 38 percent of deaths [2].

The management of CCB intoxication will be reviewed here. A summary table to facilitate emergency management is provided (table 1). An overview of the major side effects of CCBs is presented separately. (See "Major side effects and safety of calcium channel blockers".)

PATHOPHYSIOLOGY — Calcium channel blockers (CCBs) can be divided into two major categories based upon their predominant physiologic effects: dihydropyridines, which preferentially block the L-type calcium channels in the vasculature; and non-dihydropyridines, such as verapamil and diltiazem, which selectively block L-type calcium channels in the myocardium [1,3].

L-type calcium channels are responsible for myocardial contractility and vascular smooth muscle contractility; they also affect conducting and pacemaker cells. Dihydropyridines (including nifedipine, amlodipine, felodipine, nicardipine, nisoldipine, isradipine, and lacidipine) are potent vasodilators that have little negative effect upon cardiac contractility or conduction at standard doses. In contrast, verapamil and diltiazem are relatively weak vasodilators but have a depressive effect on cardiac conduction and contractility [3].

Dihydropyridine intoxication generally results in arterial vasodilation and reflex tachycardia, whereas diltiazem and verapamil toxicity cause peripheral vasodilation, decreased cardiac inotropy, and bradycardia [4]. However, as the dose is increased, this selectivity can be lost, and dihydropyridine CCBs (including nifedipine and amlodipine) may affect the myocardium and conducting system, resulting in decreased inotropy and bradycardia.

PHARMACOKINETICS — Most calcium channel blockers (CCBs) are highly protein bound, have a large volume of distribution, and are metabolized in the liver. As the dose is increased, the rate of CCB clearance decreases, prolonging the half-life [5]. Extended-release preparations slowly release the drug from a matrix to facilitate once-daily dosing. In overdose, this property makes absorption unpredictable and prolongs the duration of toxicity.


History — Whenever possible, determine the time of ingestion as well as the type, amount, and preparation (immediate or sustained release) of drug ingested. The identity of the drug ingested will help predict toxicity, and the type of preparation will help determine the appropriate approach to gastrointestinal decontamination. Patients ingesting more than 5 to 10 times the usual dose can develop signs of severe intoxication.

It is important to clarify whether the ingestion was accidental or intentional and to assess the patient for suicidality; however, this determination is often made after resolution of the acute episode. (See "Suicidal ideation and behavior in adults".)

Physical examination — Vital sign abnormalities include hypotension, which may be seen in any calcium channel blocker (CCB) overdose, and bradycardia, which usually is seen only in verapamil or diltiazem overdose. However, bradycardia may also be seen with severe dihydropyridine (eg, nifedipine) poisoning. Jugular venous distension, pulmonary crackles, and other signs of heart failure may be noted in some cases [6]. Despite hypotension, CCB-poisoned patients may maintain a surprisingly clear mental status, possibly due to the neuroprotective effects of CCBs. However, neurologic status may deteriorate precipitously once cerebral perfusion becomes critically diminished.


Electrocardiogram — An electrocardiogram (ECG) should be obtained in patients with known or suspected calcium channel blocker (CCB) intoxication [7]. ECG changes associated with CCB intoxication include PR interval prolongation and any bradydysrhythmia.

Serum glucose — A finger stick blood glucose measurement may reveal hyperglycemia, which is caused by inhibition of calcium-mediated insulin release; however, this elevation is rarely clinically significant, except for diagnostic purposes [8,9]. The presence of hyperglycemia in a nondiabetic patient may help to distinguish CCB from beta blocker poisoning.

Additional testing — We recommend testing for acetaminophen or salicylate in suicidal patients to exclude these ingestions [7]. Serum electrolytes, blood urea nitrogen (BUN), creatinine, calcium, and glucose concentrations should be assessed. A chest radiograph should be obtained if there are any signs of pulmonary edema, hypoxia, or respiratory distress. (See "General approach to drug poisoning in adults".)

DIAGNOSIS — The diagnosis of calcium channel blocker (CCB) poisoning is made clinically on the basis of the history and clinical findings. Typically there is a history of overdose combined with hypotension. Overdose with dihydropyridine CCBs (eg, nifedipine) causes hypotension coupled with reflex tachycardia, although severe toxicity may result in hypotension and bradycardia. Overdose with verapamil or diltiazem causes the dangerous combination of hypotension and bradycardia. Other findings may include signs of heart failure (eg, pulmonary crackles or jugular venous distension). CCB-poisoned patients may maintain a surprisingly clear mental status in the setting of hypotension. Electrocardiogram changes associated with CCB poisoning include PR interval prolongation and any bradydysrhythmia. The presence of hyperglycemia in a nondiabetic patient may help to distinguish CCB from beta blocker poisoning. (See "Beta blocker poisoning".)


Initial resuscitation — Circulation is the main focus of the treatment of calcium channel blocker (CCB) exposures. Hypotension and bradycardia can be profound and refractory even to maximal treatment. Intravenous (IV) fluids are the initial therapy for hypotension, and atropine the initial treatment for bradycardia, but both may be insufficient.

CCB-poisoned patients may maintain a clear mental status despite hypotension and bradycardia. However, clinicians need to reassess these patients frequently, as precipitous deterioration is common, and many will eventually require intubation and mechanical ventilation.

Approach to the selection of specific therapies — Although it is ideal to institute treatments individually to assess their success or failure, this is often not possible in patients who are severely poisoned with CCBs, especially verapamil or diltiazem. These patients are frequently moribund on presentation, but even when initially well-appearing may deteriorate rapidly and disastrously. Our suggested approaches to therapy, based upon the severity of clinical signs, are described below; a summary table to facilitate emergency management is provided (table 1). Studies of therapies for CCB poisoning consist primarily of case series and animal studies, and thus, the approaches to treatment that we describe below are based upon limited evidence and our clinical experience [10].

Severely symptomatic patients — Our suggested approach to patients manifesting signs of severe CCB poisoning (profound hypotension and/or bradycardia) consists of multiple simultaneous interventions, including all of the following treatments [4,11]:

Stabilization of the airway as necessary (avoid induction agents that exacerbate hypotension)

Additional IV boluses of isotonic crystalloid

IV calcium salts

IV glucagon

IV high-dose insulin and glucose

IV vasopressor (eg, norepinephrine)

IV lipid emulsion therapy

Dosing for each of these therapies is provided below. (See 'Specific medical therapies' below.)

Mildly symptomatic patients — Our suggested approach to patients with mild hypotension or bradycardia begins with IV boluses of isotonic crystalloid and atropine, respectively. However, these therapies often do not reverse the cardiotoxic effects of CCB poisoning. In such cases, we add the following treatments in succession based upon patient response. As an example, we begin treatment with a calcium salt if IV crystalloid is ineffective, but if hypotension resolves following treatment with a calcium salt, we do not proceed to IV glucagon or any other treatment.

IV boluses of isotonic crystalloid

IV calcium salts

IV glucagon

IV high-dose insulin and glucose

IV vasopressor (eg, norepinephrine)

IV lipid emulsion therapy

A period of 15 minutes is reasonable to determine the effectiveness of a specific therapy before proceeding to the next treatment. Dosing for each of these therapies is provided below. (See 'Specific medical therapies' below.)

Asymptomatic patients — Some patients with an isolated immediate-release CCB overdose remain asymptomatic (primarily those with dihydropyridine [eg, nifedipine] poisoning) and may be discharged after a period of observation of six to eight hours, unless the overdose was intentional. We recommend observing patients who ingest sustained-release medications for at least 24 hours. (See 'Disposition' below.)

Gastrointestinal decontamination — Orogastric lavage may be necessary in patients who present within one to two hours of a potentially dangerous ingestion (greater than 5 to 10 times the standard dose). Note that vagal stimulation from orogastric lavage may exacerbate CCB-induced hypotension and bradycardia [12]. Orogastric lavage is a difficult procedure that is rarely performed, and we recommend that clinicians who are considering it first consult a poison control center or medical toxicologist.

Activated charcoal (AC) should be administered to patients with CCB overdose, even if they are asymptomatic. AC is maximally effective if administered within one hour of ingestion, but patients with delayed presentation after CCB exposure may still benefit. Charcoal should be withheld in patients with a depressed mental status who may not be able to protect their airway, unless endotracheal intubation is performed first. AC is given as a single dose of 1 g/kg for children up to the adult dose of 50 g. (See "Gastrointestinal decontamination of the poisoned patient" and "Enhanced elimination of poisons".)

Whole bowel irrigation (WBI) may be implemented in the setting of known or strongly suspected ingestion of a sustained-release or extended-release preparation [13]. If the history is in doubt, WBI may be delayed until the patient develops signs or symptoms of toxicity. If ingestion of sustained-release or extended-release preparation is certain, particularly if the drug is verapamil or diltiazem, WBI should be started even in the asymptomatic patient. WBI involves the administration of polyethylene glycol/electrolyte lavage solution by mouth at a rate of 2 L per hour for adults (up to 500 mL per hour in children) until the rectal effluent is clear [14,15]. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Whole bowel irrigation'.)

Specific medical therapies

Atropine — Atropine should be administered to any patient with symptomatic bradycardia; however, it is often ineffective after significant CCB exposure [16]. Atropine is administered in a dose of 0.5 to 1.0 mg IV every two to three minutes to a maximum of 3 mg. Pediatric dosing is 0.02 mg/kg IV, with a minimum dose of 0.1 mg to avoid the paradoxical bradycardia that may result from very small doses of this medication. (See "Primary drugs in pediatric resuscitation", section on 'Atropine'.)

Intravenous calcium — Calcium salts are often used to overcome the cardiovascular effects of CCBs. However, treatment with calcium salts is often ineffective. This is because CCB poisoning interferes with both the serum concentration and the intracellular handling of calcium.

Calcium gluconate may be administered via peripheral or central venous access; calcium chloride is more irritating and should be administered via central venous access if possible. In adults, calcium chloride, 10 to 20 mL of a 10 percent solution, can be administered over 10 minutes; if no effect is noted, the dose can be repeated up to four times approximately every 20 minutes. If calcium gluconate is used, the dose must be adjusted (30 to 60 mL of 10 percent calcium gluconate), as calcium gluconate has only one third the calcium of calcium chloride [17].

A high-dose continuous infusion of calcium has been used anecdotally with success [18-20]; we believe a reasonable infusion is 0.5 mEq of calcium/kg per hour (or 0.2 to 0.4 mL/kg per hour of 10 percent calcium chloride; or 0.6 to 1.2 mL/kg per hour of 10 percent calcium gluconate). Close monitoring of the serum or ionized calcium concentration (measurements every two hours) and serial electrocardiograms (ECGs) are necessary to avoid clinically significant hypercalcemia, which has been reported with intensive calcium therapy [21]. (See "Clinical manifestations of hypercalcemia" and "Treatment of hypercalcemia".)

Glucagon — Glucagon increases intracellular levels of cyclic adenosine monophosphate (AMP) and, in animal models, has been shown to increase heart rate in CCB toxicity [22]. However, it has minimal effects on the mean arterial pressure. Glucagon has been effective in treating human cases of CCB toxicity [23-25].

The dosing regimen for glucagon in the treatment of CCB poisoning has not been established in human clinical trials. For the adult patient, an initial 5 mg IV bolus is a reasonable start and may be repeated twice at 10-minute intervals. A glucagon infusion can be started at the total dose at which a response is noted. Nausea and vomiting are common side effects of glucagon administration.

Vasopressors — The ideal vasopressor in CCB poisoning would be a direct-acting agent with positive inotropy, positive chronotropy, and vasoconstrictive effects. Based on these criteria, we believe that norepinephrine is the initial vasopressor of choice. We start the infusion at a rate of 2 mcg per minute but titrate rapidly upwards with the goal of achieving a mean arterial pressure of 65 mmHg. Check the blood pressure every few minutes, increasing the infusion liberally (one reasonable approach is 10 mcg per minute increments) if hypotension persists.

In patients who remain hypotensive at maximal doses of an initial vasopressor, we suggest the addition of a second vasopressor. Invasive hemodynamic monitoring (with a pulmonary artery catheter) or echocardiography may point to a selective failure of inotropy or vascular resistance, thus helping to refine the choice of catecholamine and the titration rate. We believe that such information is particularly important to guide the choice of a second agent. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults" and "Echocardiographic assessment of the right heart".)

Patients with profound CCB toxicity may require higher doses of vasopressors than those typically used in the treatment of severe sepsis or other causes of shock. In one series, patients with severe diltiazem or verapamil toxicity received vasopressor doses as high as 100 mcg per minute of norepinephrine, 150 mcg per minute of epinephrine, and 100 mcg/kg per minute for dopamine [26]. However, the arrhythmogenic effects of these drugs become more prominent at higher doses; thus, the risk of such high doses, particularly with multiple agents, may outweigh the benefits. (See "Use of vasopressors and inotropes".)

Insulin and glucose — High-dose insulin therapy has positive inotropic effects in patients with CCB toxicity. Its effectiveness and safety have been noted in animal models and case reports [27-30].

Relative hypoglycemia and hypokalemia must be corrected prior to initiating high-dose insulin therapy. For patients with a serum glucose concentration below 150 mg/dL (8.25 mmol/L), we administer 50 mL of 50 percent dextrose (D50W) IV. In young children, the initial dose of dextrose is 0.25 g/kg body weight, usually given as 2.5 mL/kg of 10 percent dextrose solution (see "Approach to hypoglycemia in infants and children", section on 'Treatment'). For patients with a serum potassium concentration below 3 mEq/L (3 mmol/L), we administer 20 mEq of potassium IV.

We initiate high-dose insulin therapy with a bolus of 1 unit/kg of regular, short-acting insulin given IV. Following this bolus, we begin a continuous infusion at 0.5 units/kg per hour IV and titrate upwards until hypotension is corrected or a maximum dose of 10 units/kg per hour is reached. One approach is to increase the infusion rate by 50 percent every 20 minutes until either target is met. High doses of insulin may be necessary and are appropriate in some cases, and the accepted range is 1 to 10 units/kg per hour given IV of regular, short-acting insulin. Even higher doses may be given under the direction of a medical toxicologist or poison control center.

CCB overdose often causes hyperglycemia that is refractory to high-dose insulin. Therefore, not all patients require supplemental dextrose. If necessary, euglycemia can be maintained by means of a continuous IV infusion of 5 to 10 percent dextrose. A reasonable initial rate for such an infusion is 0.5 to 1 g of dextrose/kg per hour. Titration of the dextrose infusion and additional boluses of 50 percent dextrose are provided based upon serum glucose measurements (finger stick glucose), which are obtained every 15 to 30 minutes until the concentration is stable and every hour thereafter until several hours after therapy is complete.

The serum potassium concentration is measured every 30 minutes until it is stable, and every one to two hours thereafter. Supplementation is given as necessary to maintain a potassium concentration in the low normal range. Magnesium replacement is often needed in hypokalemic patients. (See "Clinical manifestations and treatment of hypokalemia in adults".)

A hemodynamic response to high-dose insulin therapy is delayed for 30 to 60 minutes; therefore, simultaneous implementation of other therapies to support the patient's pulse and blood pressure are generally required.

Animal studies of CCB toxicity have shown improved survival associated with hyperinsulinemia/euglycemia therapy compared with calcium, epinephrine, or glucagon [27,31]. Clinical experience with this approach is limited [28,29]; in one case series of four verapamil-poisoned patients, hyperinsulinemia/euglycemia therapy improved blood pressure and ejection fraction without changing heart rate [29]. High-dose insulin therapy is also used in beta blocker poisoning. (See "Beta blocker poisoning".)

The mechanism by which hyperinsulinemia-euglycemia therapy exerts its effects remains unclear. CCBs appear to disrupt fatty acid metabolism and create relative insulin resistance within the myocardium, and it is possible that this state of carbohydrate dependence and insulin resistance is overcome with high-dose insulin [32,33]. In addition, calcium is needed to facilitate exocytosis of insulin from the beta-islet cells of the pancreas. CCBs block the influx of calcium and prevent insulin release from the beta-islet cells. High-dose insulin therapy may compensate for this impaired secretion of insulin.

Lipid emulsion therapy — Lipid emulsions are the fats used in total parenteral nutrition (TPN). Initially used to treat overdoses of local anesthetics such as bupivacaine, IV lipid emulsion (ILE) is being studied as a potential therapy for poisonings from multiple lipophilic medications.

We suggest consultation with a medical toxicologist or poison control center to determine whether ILE therapy is appropriate for the patient with CCB poisoning. The dosing protocol most widely reported consists of an IV bolus of 1.5 mL/kg of a 20 percent lipid emulsion solution delivered over one minute to patients with hemodynamic instability or cardiac arrest [34-36]. If there is no response, the same dose may be repeated every three to five minutes for a total of three bolus doses.

Following the initial bolus, an infusion is started at a rate of 0.025 mL/kg per minute until hemodynamic recovery occurs. This infusion rate is lower than the 0.25 mL/kg per minute rate typically used for local anesthetic toxicity [37]. In the setting of CCB overdose, re-bolus of the initial 1.5 mL/kg dose if there is not sufficient response and the lower-rate infusion of 0.025 mL/kg per minute are both in line with expert opinion. The maximum ILE dosing is 12.5 mL/kg in a 24-hour span.

Possible adverse effects from standard ILE treatment include hypertriglyceridemia, fat embolism, infection, and hypersensitivity reactions. Although these and other potential complications from ILE treatment have been reported, further study is needed to determine the risk of complications from circumscribed treatment in the setting of acute overdose.

ILE therapy interferes with some laboratory measurements and may affect therapeutic drug monitoring [38,39]. As examples, serum glucose concentrations when determined by colorimetric testing and serum magnesium concentrations become inaccurate following the administration of ILE, while creatinine and lipase become unmeasurable. Potassium and troponin-I are not affected. Centrifugation of blood samples substantially reduces any interference.

Studies of ILE therapy are preliminary. Systematic reviews of lipid emulsion therapy for acute poisoning have found the overall quality of studies supporting this treatment to be low or very low, but included human case reports provide some evidence of benefit in patients with toxicity from verapamil, beta blockers, some tricyclic antidepressants, bupivacaine, chlorpromazine, and some antidysrhythmics (eg, flecainide) [40-42]. ILE may have a useful role in the treatment of patients who are hemodynamically unstable from such poisonings [34,35,43,44].

Several mechanisms are theorized to account for the effectiveness of ILE. The first is that the emulsion acts as a "lipid sink," surrounding a lipophilic drug molecule and rendering it ineffective. The second is that the fatty acids from the ILE provide the myocardium with a ready energy source, thereby improving cardiac function [36]. In addition, there is a possible "lipid shuttle" effect wherein the toxin is encapsulated and then transported to the liver and/or kidney for metabolism.

Phosphodiesterase inhibitors — Phosphodiesterases inhibitors, such as inamrinone (formerly known as amrinone) increase cyclic AMP levels by preventing intracellular degradation of cyclic AMP. Although there are reports of successful treatment with inamrinone in combination with glucagon after amlodipine poisoning [45], phosphodiesterase inhibitors may exacerbate hypotension and should not be used routinely. We recommend that inamrinone not be considered unless therapy with a readily titratable vasopressor has been instituted, a pulmonary artery catheter is in place to help guide management, and the clinician is in direct consultation with a medical toxicologist or poison control center. (See "Use of vasopressors and inotropes".)

Other phamacologic treatments — Some have proposed levosimendan as a treatment for CCB poisoning [46]. However, studies of levosimendan are limited, and we do not recommend its use for this purpose. Levosimendan sensitizes the calcium channels and promotes the influx of calcium into the cell. Theoretically, this would appear beneficial in a CCB overdose, but results from animal models are conflicting, and the drug has some phosphodiesterase activity which may exacerbate hypotension [47-50].

Invasive treatments including transvenous pacing — A transvenous pacemaker can be inserted to assist with electrical conduction. However, pacing does not counteract the negative inotropic effects of these drugs, and successful capture may not correct the patient's hypotension [51]. If there are no contraindications, an intraaortic balloon pump may help correct intractable hypotension [52]. (See "Temporary cardiac pacing" and "Intraaortic balloon pump counterpulsation".)

Extracorporeal membrane oxygenation — There are several case reports of patients with severe CCB poisoning who survived following treatment with extracorporeal membrane oxygenation (ECMO) [53-55]. We believe that ECMO should be considered a last resort and on a case-by-case basis in conjunction with guidance from a poison control center or medical toxicologist. An example of a case potentially amenable to ECMO might involve a child with severe poisoning who is hemodynamically unstable and for whom standard therapies have been ineffective. (See "Extracorporeal membrane oxygenation (ECMO) in adults".)

Extracorporeal removal — CCBs are highly protein bound; therefore, extracorporeal removal by hemodialysis is not effective. The lack of effectiveness is supported by the available clinical evidence [56].

Disposition — A patient who ingests or claims to have ingested an immediate-release CCB but remains asymptomatic after six to eight hours may be considered medically cleared. If the CCB preparation was a sustained- or extended-release preparation, admission and cardiac monitoring for 24 hours is warranted. In the symptomatic patient, continuous hemodynamic monitoring is required until the patient does not require any pharmacologic assistance to maintain blood pressure. If multiple agents are being utilized, invasive monitoring with a pulmonary artery catheter should be strongly considered to help guide therapy. If an intentional overdose is known or suspected, psychiatric evaluation is needed.


Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Treatment of acute poisoning caused by specific agents other than drugs of abuse" and "Society guideline links: General measures for acute poisoning treatment".)


Life-threatening poisoning and emergency management table – Severe calcium channel blocker (CCB) poisoning is life threatening, and management is often challenging. Patients may be moribund at presentation, and those who are not may deteriorate precipitously. A summary table to facilitate emergency management is provided (table 1). Diltiazem and verapamil are the most cardiotoxic of the CCBs, although any of these agents can be dangerous when large doses are ingested.

Clinical features – Patients ingesting more than 5 to 10 times the usual dose may develop signs of severe intoxication, including drowsiness and confusion. Vital sign abnormalities may include hypotension and bradycardia. Jugular venous distension, pulmonary crackles, and other signs of heart failure may be noted. (See 'Clinical features' above.)

Electrocardiogram (ECG) manifestations of poisoning – ECG changes associated with CCB intoxication may include PR interval prolongation, sinus tachycardia (with dihydropyridine agents), and any bradydysrhythmia (with diltiazem, verapamil, or massive dihydropyridine ingestion). A finger stick blood glucose measurement may reveal hyperglycemia. (See 'Laboratory evaluation and other diagnostic testing' above.)

Overview of management – Treatment varies according to the severity of symptoms and may include gastrointestinal decontamination, possibly including gastric lavage, and the administration of intravenous (IV) calcium, glucagon, catecholamines, and high-dose insulin therapy. Intralipid therapy may be of benefit in critically ill, hemodynamically unstable patients resistant to standard medical therapies. A transvenous pacemaker, intraaortic balloon pump, and extracorporeal membrane oxygenation are treatment options for the severely poisoned. A summary table to facilitate emergency management is provided (table 1). (See 'Initial resuscitation' above and 'Approach to the selection of specific therapies' above.)

Management of severe poisoning – For patients with severely symptomatic CCB poisoning, we suggest simultaneous treatment with all of the following therapies (Grade 2C). Dosing is provided in the text and the table summarizing emergency management (table 1). Severe CCB poisoning can be difficult to manage, and consultation with a medical toxicologist or regional poison control center is prudent (see 'Severely symptomatic patients' above and 'Specific medical therapies' above):

Stabilization of the airway as necessary (avoid induction agents that exacerbate hypotension)

IV boluses of isotonic crystalloid

IV calcium salts (see 'Intravenous calcium' above)

IV glucagon (see 'Glucagon' above)

IV high-dose insulin and glucose (see 'Insulin and glucose' above)

IV vasopressor (norepinephrine) (see 'Vasopressors' above)

IV lipid emulsion therapy (see 'Lipid emulsion therapy' above)

Management of mild poisoning – A suggested treatment approach for patients with mild hypotension or bradycardia caused by CCB toxicity is provided in the text. (See 'Mildly symptomatic patients' above.)

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