# 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?

Updated: 2026-09-15T23:59:13.192096+00:00

## What matters in practice
- Obtain bedside glucose and a 12-lead ECG early; repeat ECGs and use continuous cardiac monitoring when cardioactive poisoning may cause bradycardia, hypotension, conduction delay, or dysrhythmia. [1]
- Check electrolytes, renal function, and lactate to define end-organ hypoperfusion; obtain acetaminophen, salicylate, and digoxin concentrations when intentional ingestion or relevant coingestion is possible. [1][11]
- Use glucagon for impending or established shock from beta-blocker overdose, recognizing that vomiting and hyperglycemia are common adverse effects and that its optimal dosing and efficacy remain uncertain. [20][23]
- For shock refractory to fluids, atropine, and glucagon, initiate high-dose insulin euglycemia therapy with regular insulin 1 U/kg IV bolus followed by 1-10 U/kg/h infusion, with dextrose support and intensive glucose and potassium monitoring. [19][23]
- Do not wait for laboratory confirmation to treat severe beta-blocker poisoning; diagnosis is clinical, and propranolol-associated altered mental status, seizures, or ventricular dysrhythmia should heighten concern for sodium-channel blockade. [11][13]

## 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. [1][13]

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. [1][11]

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. [1][6][11]
- Move to a monitored resuscitation setting for bradycardia, hypotension, conduction delay, dysrhythmia, seizure, altered mental status, or rising lactate. [1][11]
- Elicit the exact agent, formulation, time of ingestion, possible calcium-channel blocker or digoxin coingestion, and access to other cardiotoxic drugs; mixed cardioactive ingestion increases morbidity and mortality risk. [11][13]
- Consider non-toxicologic causes of bradycardia when the exposure history is uncertain, including hypothyroidism, obstructive sleep apnea, and increased vagal tone from vomiting. [4]

*Clinical patterns that change initial priorities in suspected beta-blocker toxicity. [1][2][11]*

| Finding | Interpretation | Immediate next action |
| --- | --- | --- |
| Bradycardia with hypotension or shock | Hemodynamically significant cardioactive poisoning; beta-blocker and calcium-channel blocker toxicity can overlap. [1][2] | Continuous monitoring, repeated blood pressure assessment, IV resuscitation, and prompt antidotal escalation if instability persists. [1][13] |
| Prolonged QRS, ventricular dysrhythmia, or seizure | Suggests sodium-channel blockade; propranolol is a key beta-blocker exposure associated with this phenotype. [1][11] | Treat as severe cardiotoxic poisoning in a monitored critical-care setting while addressing hemodynamic instability. [1][11] |
| Altered mental status or seizure with low bedside glucose | Hypoglycemia is an immediately reversible contributor to neurologic dysfunction. [1] | Give oral glucose if safe or IV dextrose-containing fluid if not. [1] |
| Hyperglycemia, metabolic acidosis, and shock | Supports severe calcium-channel blocker effect or mixed beta-blocker/calcium-channel blocker ingestion; calcium-channel blockade causes hypoinsulinemia, hyperglycemia, acidosis, and shock. [2] | Evaluate for calcium-channel blocker coingestion and use a shock strategy that includes calcium and high-dose insulin when indicated. [2][20] |

## 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. [1][11]

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. [1][11]

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. [1]
- Repeat ECGs after cardiotoxin exposure rather than relying on a single initial tracing, particularly when conduction delay or dysrhythmia is present. [1]
- Trend renal function, electrolytes, glucose, and lactate during shock because evolving renal injury, metabolic disturbance, or inadequate perfusion changes the need for ongoing critical-care support. [1][11]
- Do not use absence of a confirmatory beta-blocker concentration to exclude clinically important poisoning; beta-blocker toxicity remains a clinical diagnosis. [11][13]

*Initial testing for suspected beta-blocker toxicity and the action each result supports. [1][11]*

| Test | When to obtain | Actionable result |
| --- | --- | --- |
| Point-of-care glucose | Immediately for altered sensorium or seizure; before high-dose insulin. [1][23] | Treat hypoglycemia promptly; establish a baseline before insulin-based therapy. [1][23] |
| 12-lead ECG and serial ECGs | All intentional ingestions or possible dysrhythmogenic exposures. [1] | QRS prolongation identifies sodium-channel blocker physiology associated with seizure and fatal dysrhythmia risk. [1] |
| Electrolytes and renal function | Clinically important ingestion, shock, or planned high-dose insulin therapy. [1][23] | Correct and monitor electrolyte disturbances; potassium must be checked before high-dose insulin. [23] |
| Lactate and blood gas | Shock, acidosis, or suspected end-organ hypoperfusion. [1][11] | Use abnormal values to identify severity and follow resuscitation response. [1][11] |
| Acetaminophen, salicylate, and selective digoxin concentrations | Intentional ingestion or plausible coingestion. [1][11] | Treat coingestions using their specific toxicologic pathways rather than attributing all findings to beta-blockade. [1][11] |

## 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. [13][23]

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. [10][20][23]

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. [20][23]

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. [23]
- Give glucagon with readiness for emesis and airway deterioration in patients with depressed consciousness. [20][23]
- Treat fluids, atropine, glucagon, calcium, vasopressors, and high-dose insulin as components of an escalating strategy; do not interpret transient heart-rate improvement alone as adequate shock reversal. [13][15][23]
- Consult a poison center or medical toxicologist early for any patient with shock, QRS prolongation, seizures, ventricular dysrhythmia, or need for high-dose insulin. [11][13]

*Escalation approach for hemodynamically significant beta-blocker poisoning. [13][19][20][23]*

| Clinical state | Treatment step | Monitoring or limitation |
| --- | --- | --- |
| Bradycardia or hypotension without established refractory shock | IV fluids and atropine; consider IV calcium, especially with suspected calcium-channel blocker coingestion. [20][23] | Continuous cardiac monitoring and repeated blood-pressure measurement are required. [1] |
| Impending or established shock attributed to beta-blockade | Use glucagon as a beta-blocker-directed therapy. [20][23] | Expect vomiting and hyperglycemia; efficacy and optimal dosing are uncertain. [20][23] |
| Shock refractory to fluids, atropine, and glucagon | Initiate high-dose insulin euglycemia therapy with dextrose support. [23] | Check potassium and glucose before therapy; provide vasopressors during delayed inotropic effect. [23] |
| Persistent perfusion failure despite antidotal and vasoactive treatment | Manage in critical care with urgent advanced hemodynamic support consideration. [11][12][20] | Severe calcium-channel blocker poisoning literature supports extracorporeal life support as an escalation option; decisions require toxicology and critical-care expertise. [20] |

## 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. [19][23]

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. [23]

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. [23]

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. [19][23]
- Before initiation: obtain glucose and potassium, establish continuous cardiac monitoring, and prepare a dextrose infusion. [23]
- Initial regimen: regular insulin 1 U/kg IV plus 0.5 g/kg IV dextrose unless glucose is greater than 400 mg/dL; begin insulin infusion at 1 U/kg/h. [19][23]
- Titration range: 1-10 U/kg/h according to hemodynamic response. [19]
- Early monitoring: glucose every 30 minutes for up to 4 hours; maintain 100-200 mg/dL and monitor potassium for hypokalemia. [23]
- Bridge support: use vasopressors when needed because improvement in contractility can take 15-60 minutes. [23]

*High-dose insulin euglycemia therapy protocol for refractory beta-blocker shock. [19][23]*

| Phase | Action | Target or safety check |
| --- | --- | --- |
| Eligibility | Use after shock remains refractory to fluids, atropine, and glucagon. [23] | Confirm that cardiovascular toxicity, rather than isolated asymptomatic ingestion, is driving treatment. [13][23] |
| Baseline | Measure glucose and potassium before insulin. [23] | Prepare IV dextrose and continuous cardiac monitoring. [1][23] |
| Bolus | Regular insulin 1 U/kg IV plus 0.5 g/kg IV dextrose. [19][23] | Withhold the dextrose bolus if glucose is greater than 400 mg/dL. [23] |
| Infusion | Continue regular insulin at 1-10 U/kg/h. [19] | Titrate to hemodynamic response while providing dextrose. [19][23] |
| Glucose monitoring | Check glucose every 30 minutes initially for up to 4 hours. [23] | Maintain glucose 100-200 mg/dL using 10% dextrose infusion and 50% dextrose boluses as needed. [23] |
| Electrolyte monitoring | Follow potassium during therapy. [23] | Detect and treat hypokalemia, which can potentiate cardiotoxicity. [23] |

## 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. [1]

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. [12][20]

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. [1][2][11]
- ICU-level monitoring is indicated for shock, vasopressor need, high-dose insulin infusion, seizures, ventricular dysrhythmia, or ECG conduction abnormalities. [1][11][23]
- Continue serial glucose and potassium surveillance while high-dose insulin and dextrose are being administered. [23]
- Before discharge from any intentional ingestion, ensure toxicologic reassessment and psychiatric safety evaluation after medical stabilization; intentional exposure also mandates assessment for occult coingestions. [1][11]

*Disposition triggers in beta-blocker toxicity. [1][11][23]*

| Disposition level | Trigger | Required capabilities |
| --- | --- | --- |
| Resuscitation bay or monitored emergency care | Initial bradycardia, hypotension, altered mental status, seizure, or suspected dysrhythmogenic ingestion. [1][11] | Immediate glucose testing, 12-lead and serial ECGs, continuous cardiac monitoring, repeated blood-pressure assessment, and IV resuscitation. [1] |
| Intensive care | Vasopressor requirement, high-dose insulin therapy, persistent shock, conduction abnormality, ventricular dysrhythmia, or seizures. [11][23] | Frequent glucose and potassium testing, continuous monitoring, vasoactive therapy, and toxicology/critical-care collaboration. [23] |
| Advanced shock center | Refractory toxic cardiogenic shock despite antidotal and vasoactive therapies. [12][20] | Capacity for advanced mechanical circulatory support evaluation and multidisciplinary critical care. [12][20] |

## 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. [19][23]

### 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. [1]

### 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. [1][11]

## References
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## Editorial note

Prepared from cited clinical literature using Astra's research workflow. Verify recommendations against current guidance and patient-specific factors.