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Medical Toxicology

Beta-Blocker Toxicity

Manage suspected beta-blocker toxicity as a time-critical cardiotoxic poisoning: identify conduction delay, shock, hypoglycemia, seizures, and coingestants; initiate resuscitation and monitored antidotal therapy; and escalate refractory cardiogenic shock promptly to high-dose insulin and advanced critical care.

Clinical question: How should clinicians evaluate and treat hemodynamically significant beta-blocker toxicity?

First Minutes

Identify the unstable beta-blocker overdose phenotype

Treat cardiovascular compromise before defining the exact agent or ingested dose.

Prioritize airway, breathing, and circulation in any suspected beta-blocker poisoning. The immediately dangerous phenotype is bradycardia with hypotension or shock; serial blood-pressure measurements and continuous cardiac monitoring are indicated after exposures capable of cardiovascular toxicity. BMJToxidromes and a general approach to poisoningScienceDirectManagement of Beta-Adrenergic Blocker Poisoning - ScienceDirect

Obtain a 12-lead ECG after intentional ingestion or exposure to a poison capable of dysrhythmia. Specifically assess rhythm and conduction intervals: QRS prolongation indicates sodium-channel blockade and is associated with dysrhythmia, seizures, and fatality. Propranolol toxicity can present with altered mentation, seizures, and ventricular dysrhythmias because of sodium-channel blockade. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect

Measure bedside glucose immediately in altered sensorium or seizure. Treat documented hypoglycemia with oral glucose when safe or dextrose-containing intravenous fluids when enteral treatment is unsafe. Glucose abnormalities may also help distinguish beta-blocker toxicity from calcium-channel blocker toxicity, although neither routine laboratory testing nor a single metabolic pattern confirms either diagnosis. BMJToxidromes and a general approach to poisoningjaccBRASH Syndrome Following Coronary Angiography - JACCScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect

Clinical patterns that change initial priorities in suspected beta-blocker toxicity. BMJToxidromes and a general approach to poisoningNEJMTreatment of Calcium-Channel–Blocker Intoxication with Insulin Infusion | New England Journal of MedicineScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect
FindingInterpretationImmediate next action
Bradycardia with hypotension or shockHemodynamically significant cardioactive poisoning; beta-blocker and calcium-channel blocker toxicity can overlap. BMJToxidromes and a general approach to poisoningNEJMTreatment of Calcium-Channel–Blocker Intoxication with Insulin Infusion | New England Journal of MedicineContinuous monitoring, repeated blood pressure assessment, IV resuscitation, and prompt antidotal escalation if instability persists. BMJToxidromes and a general approach to poisoningScienceDirectManagement of Beta-Adrenergic Blocker Poisoning - ScienceDirect
Prolonged QRS, ventricular dysrhythmia, or seizureSuggests sodium-channel blockade; propranolol is a key beta-blocker exposure associated with this phenotype. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirectTreat as severe cardiotoxic poisoning in a monitored critical-care setting while addressing hemodynamic instability. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect
Altered mental status or seizure with low bedside glucoseHypoglycemia is an immediately reversible contributor to neurologic dysfunction. BMJToxidromes and a general approach to poisoningGive oral glucose if safe or IV dextrose-containing fluid if not. BMJToxidromes and a general approach to poisoning
Hyperglycemia, metabolic acidosis, and shockSupports severe calcium-channel blocker effect or mixed beta-blocker/calcium-channel blocker ingestion; calcium-channel blockade causes hypoinsulinemia, hyperglycemia, acidosis, and shock. NEJMTreatment of Calcium-Channel–Blocker Intoxication with Insulin Infusion | New England Journal of MedicineEvaluate for calcium-channel blocker coingestion and use a shock strategy that includes calcium and high-dose insulin when indicated. NEJMTreatment of Calcium-Channel–Blocker Intoxication with Insulin Infusion | New England Journal of Medicineacep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEP

Targeted Evaluation

Order tests that identify reversible toxicity and coingestion

Testing should guide resuscitation and identify competing toxicologic syndromes, not delay treatment.

Obtain serum electrolytes and renal function in suspected clinically important poisoning, and measure lactate when shock or end-organ hypoperfusion is suspected. Renal function and lactate do not establish the diagnosis of beta-blocker toxicity, but they define organ injury and perfusion deficit that should drive ICU-level monitoring and escalation. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect

In intentional or potentially toxic exposure, obtain quantitative acetaminophen and salicylate concentrations; add a digoxin concentration when digoxin coingestion is plausible. Obtain pregnancy testing when appropriate because it changes imaging, medication, and disposition decisions. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect

Use targeted studies for alternate toxidromes: blood gas for pH and serum lactate in severe poisoning; serum osmolality when toxic alcohol exposure is suspected; and co-oximetry when carbon monoxide exposure or methemoglobinemia is possible. These tests are phenotype-directed rather than routine confirmation studies for beta-blocker exposure. BMJToxidromes and a general approach to poisoning

Initial testing for suspected beta-blocker toxicity and the action each result supports. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect
TestWhen to obtainActionable result
Point-of-care glucoseImmediately for altered sensorium or seizure; before high-dose insulin. BMJToxidromes and a general approach to poisoningPubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfTreat hypoglycemia promptly; establish a baseline before insulin-based therapy. BMJToxidromes and a general approach to poisoningPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
12-lead ECG and serial ECGsAll intentional ingestions or possible dysrhythmogenic exposures. BMJToxidromes and a general approach to poisoningQRS prolongation identifies sodium-channel blocker physiology associated with seizure and fatal dysrhythmia risk. BMJToxidromes and a general approach to poisoning
Electrolytes and renal functionClinically important ingestion, shock, or planned high-dose insulin therapy. BMJToxidromes and a general approach to poisoningPubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfCorrect and monitor electrolyte disturbances; potassium must be checked before high-dose insulin. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Lactate and blood gasShock, acidosis, or suspected end-organ hypoperfusion. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirectUse abnormal values to identify severity and follow resuscitation response. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect
Acetaminophen, salicylate, and selective digoxin concentrationsIntentional ingestion or plausible coingestion. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirectTreat coingestions using their specific toxicologic pathways rather than attributing all findings to beta-blockade. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect

Hemodynamic Support

Treat bradycardia and shock while preparing antidotal therapy

Escalate on perfusion and electrical instability, not on reported tablet count alone.

Provide immediate supportive resuscitation for hypotension, bradycardia, or shock. If hemodynamic compromise persists after IV fluids and atropine, use glucagon as a beta-blocker-directed antidotal therapy; refractory cases should progress promptly to high-dose insulin euglycemia treatment rather than repeated ineffective temporizing measures. ScienceDirectManagement of Beta-Adrenergic Blocker Poisoning - ScienceDirectPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Glucagon has a physiologic rationale in impending or actual shock from beta-blocker overdose, but its optimal dose and clinical efficacy are uncertain. Anticipate vomiting and hyperglycemia; hypocalcemia has also been reported. In a controlled physiologic study, glucagon doses as high as 50 micrograms/kg produced hemodynamic effects, with nausea lasting less than 30 minutes when present. AHA JournalsHigh‐Dose Glucagon Has Hemodynamic Effects Regardless of ...acep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Give IV calcium as an adjunct for hypotension after beta-blocker overdose, particularly when calcium-channel blocker coingestion is possible. Calcium chloride 1-5 g IV, or an equivalent calcium gluconate dose, may be followed by an infusion; calcium is not a substitute for escalation to high-dose insulin when shock persists. acep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Use vasopressors as supportive therapy when perfusion remains inadequate, recognizing that the inotropic response to high-dose insulin may be delayed 15-60 minutes. Vasopressor selection should follow the dominant bedside hemodynamic abnormality rather than a fixed toxicology protocol. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Escalation approach for hemodynamically significant beta-blocker poisoning. ScienceDirectManagement of Beta-Adrenergic Blocker Poisoning - ScienceDirectPubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedacep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Clinical stateTreatment stepMonitoring or limitation
Bradycardia or hypotension without established refractory shockIV fluids and atropine; consider IV calcium, especially with suspected calcium-channel blocker coingestion. acep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPPubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfContinuous cardiac monitoring and repeated blood-pressure measurement are required. BMJToxidromes and a general approach to poisoning
Impending or established shock attributed to beta-blockadeUse glucagon as a beta-blocker-directed therapy. acep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPPubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfExpect vomiting and hyperglycemia; efficacy and optimal dosing are uncertain. acep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Shock refractory to fluids, atropine, and glucagonInitiate high-dose insulin euglycemia therapy with dextrose support. PubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfCheck potassium and glucose before therapy; provide vasopressors during delayed inotropic effect. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Persistent perfusion failure despite antidotal and vasoactive treatmentManage in critical care with urgent advanced hemodynamic support consideration. ScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirectScienceDirectHigh dose insulin for beta-blocker and calcium channel-blocker poisoningacep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPSevere calcium-channel blocker poisoning literature supports extracorporeal life support as an escalation option; decisions require toxicology and critical-care expertise. acep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEP

Refractory Shock

Use high-dose insulin euglycemia therapy safely

High-dose insulin is an inotropic rescue therapy for poison-induced cardiogenic shock.

For beta-blocker toxicity with shock refractory to fluids, atropine, and glucagon, administer regular insulin 1 U/kg IV bolus followed by a continuous infusion of 1-10 U/kg/h. Earlier protocols used a 0.5 U/kg bolus followed by 0.5-1 U/kg/h, but published treatment recommendations increased to the 1 U/kg bolus and 1-10 U/kg/h regimen. PubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Administer 0.5 g/kg IV dextrose with the insulin bolus unless glucose exceeds 400 mg/dL, then continue dextrose support to maintain glucose 100-200 mg/dL. Initiate a 10% dextrose infusion and give 50% dextrose IV boluses as needed. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Measure glucose and potassium before insulin. Check glucose every 30 minutes initially for up to 4 hours; high-dose insulin can cause profound hypoglycemia and hypokalemia, which may worsen cardiotoxicity. Titrate insulin to hemodynamic response while maintaining euglycemia and correcting clinically important electrolyte abnormalities. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Do not judge high-dose insulin failure in the first several minutes: its inotropic effect may be delayed 15-60 minutes, and vasopressors may be needed during that interval. Experimental models and accumulated case experience support high-dose insulin in severe beta-blocker and calcium-channel blocker poisoning, but controlled human trial evidence remains limited. PubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

High-dose insulin euglycemia therapy protocol for refractory beta-blocker shock. PubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
PhaseActionTarget or safety check
EligibilityUse after shock remains refractory to fluids, atropine, and glucagon. PubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfConfirm that cardiovascular toxicity, rather than isolated asymptomatic ingestion, is driving treatment. ScienceDirectManagement of Beta-Adrenergic Blocker Poisoning - ScienceDirectPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
BaselineMeasure glucose and potassium before insulin. PubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfPrepare IV dextrose and continuous cardiac monitoring. BMJToxidromes and a general approach to poisoningPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
BolusRegular insulin 1 U/kg IV plus 0.5 g/kg IV dextrose. PubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedPubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfWithhold the dextrose bolus if glucose is greater than 400 mg/dL. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
InfusionContinue regular insulin at 1-10 U/kg/h. PubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedTitrate to hemodynamic response while providing dextrose. PubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Glucose monitoringCheck glucose every 30 minutes initially for up to 4 hours. PubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfMaintain glucose 100-200 mg/dL using 10% dextrose infusion and 50% dextrose boluses as needed. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Electrolyte monitoringFollow potassium during therapy. PubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfDetect and treat hypokalemia, which can potentiate cardiotoxicity. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Escalation

Escalate refractory cardiotoxicity and monitor for delayed deterioration

Disposition follows electrical instability, perfusion failure, treatment intensity, and coingestion risk.

Admit patients requiring continuous cardiac monitoring, serial ECGs, vasopressors, glucagon, calcium infusion, or high-dose insulin to a monitored critical-care setting. Serial ECGs are particularly important after exposure to cardiotoxins because conduction delay and dysrhythmia can evolve after the initial assessment. BMJToxidromes and a general approach to poisoning

When shock persists despite fluids, atropine, glucagon, calcium, vasopressors, and high-dose insulin, obtain urgent multidisciplinary critical-care and toxicology support for advanced circulatory support. Extracorporeal life support is described as an escalation therapy in severe cardioactive poisoning literature, particularly for calcium-channel blocker poisoning; its use in a beta-blocker or mixed overdose should be individualized to reversible toxic cardiogenic shock and local capability. ScienceDirectHigh dose insulin for beta-blocker and calcium channel-blocker poisoningacep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEP

Treat concomitant poisonings in parallel. Acetaminophen, salicylate, and digoxin measurements are specifically useful in intentional ingestion or suspected coingestion, and calcium-channel blocker coingestion should be suspected when hyperglycemia, metabolic acidosis, and profound shock accompany bradycardia or conduction delay. BMJToxidromes and a general approach to poisoningNEJMTreatment of Calcium-Channel–Blocker Intoxication with Insulin Infusion | New England Journal of MedicineScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect

Disposition triggers in beta-blocker toxicity. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirectPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Disposition levelTriggerRequired capabilities
Resuscitation bay or monitored emergency careInitial bradycardia, hypotension, altered mental status, seizure, or suspected dysrhythmogenic ingestion. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirectImmediate glucose testing, 12-lead and serial ECGs, continuous cardiac monitoring, repeated blood-pressure assessment, and IV resuscitation. BMJToxidromes and a general approach to poisoning
Intensive careVasopressor requirement, high-dose insulin therapy, persistent shock, conduction abnormality, ventricular dysrhythmia, or seizures. ScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirectPubMedBeta-Blocker Toxicity - StatPearls - NCBI BookshelfFrequent glucose and potassium testing, continuous monitoring, vasoactive therapy, and toxicology/critical-care collaboration. PubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf
Advanced shock centerRefractory toxic cardiogenic shock despite antidotal and vasoactive therapies. ScienceDirectHigh dose insulin for beta-blocker and calcium channel-blocker poisoningacep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEPCapacity for advanced mechanical circulatory support evaluation and multidisciplinary critical care. ScienceDirectHigh dose insulin for beta-blocker and calcium channel-blocker poisoningacep[PDF] T H E 2 0 1 7 L L S A L IT E R A T U R E R E V IE W - ACEP

Common questions

When should high-dose insulin be started in beta-blocker toxicity?

Start high-dose insulin euglycemia therapy when shock remains refractory to IV fluids, atropine, and glucagon. Use regular insulin 1 U/kg IV followed by 1-10 U/kg/h with dextrose support, glucose checks every 30 minutes initially, and potassium surveillance. PubMedHigh-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning - PubMedPubMedBeta-Blocker Toxicity - StatPearls - NCBI Bookshelf

Does a normal initial ECG exclude severe beta-blocker poisoning?

No. Obtain serial ECGs after cardiotoxin exposure because conduction abnormalities and dysrhythmias may evolve. Escalate monitoring based on clinical instability, not a single normal tracing. BMJToxidromes and a general approach to poisoning

What laboratory tests should accompany suspected intentional beta-blocker overdose?

Obtain glucose, electrolytes, renal function, and ECG evaluation; measure acetaminophen and salicylate concentrations, and obtain a digoxin concentration when coingestion is plausible. Add lactate and blood gas testing when shock or acidosis is present. BMJToxidromes and a general approach to poisoningScienceDirectPearls and Pitfalls for the Emergency Clinician: Beta Blocker and Calcium Channel Blocker Toxicity - ScienceDirect

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