Beta-Blocker & Calcium Channel Blocker Toxicity

Beta-blocker (BB) and calcium channel blocker (CCB) poisoning is shock caused by a drug. Both drug classes block the pathways that drive heart rate, contractility, conduction and systemic vascular resistance (SVR). Hypotension, bradycardia, low SVR and cardiogenic shock are the signs of both poisonings.

Beta-1 blockade slows the heart and weakens it. Beta-2 blockade limits vasodilation. CCBs block L-type calcium channels in the myocardium, the conduction tissue and the vascular smooth muscle. That cuts contractility, AV conduction and vascular tone. One patient can have both effects, and a co-ingestion can add to them.

• Common causes: Intentional overdose, co-ingestions, and interactions between BB or CCB and other drugs. A 2025 educational review also lists tricyclic antidepressants, clonidine, lithium, ethanol and opioids. Each can cause hypotension and bradycardia, mimicking BB or CCB toxicity or adding to it
• Therapeutic-dose accumulation: Toxicity can happen without an overdose. When clearance falls, the drug builds up. Renally cleared drugs such as sotalol are dosed by creatinine clearance, so reduced kidney function raises the risk
• Shock mechanism: Low cardiac output from poor contractility and bradycardia. Add low SVR, which both drug classes can cause
• Clinical course: The course can run from hypotension to high-grade AV block, cardiogenic shock, periarrest and cardiac arrest. Severe cases need escalating support, and early toxicology input

The first-line, refractory and rescue steps here come from the 2017 CCB consensus. The beta-blocker data come from the high-dose insulin literature and a 2025 educational review. Drug details live on the linked medication pages.

Typical Presentation

• Beta-blocker: Bradycardia, hypotension, AV block and cardiogenic shock. Drowsiness can occur, and severe cases can progress to altered mental status. Hypoglycemia can also occur with beta-blocker overdose
• Calcium channel blocker: Hypotension and shock. Non-dihydropyridine agents add bradycardia and conduction block. Dihydropyridine agents mainly cause vasodilation. See the subclass table.
• Exposure clue: A known or suspected ingestion, a pill count that does not add up, or an unexplained shock picture in a patient taking one of these drugs

Calcium Channel Blocker Subclasses

Beta-Blocker Agent Clues

• Sotalol: QT prolongation and torsades de pointes. Check the QTc. Correct hypokalemia and hypomagnesemia, and avoid other QT-prolonging drugs. For overdose torsades, the sotalol label lists magnesium sulfate, pacing and cardioversion (see Magnesium Sulfate)
• Propranolol: Lipophilic, and also a sodium-channel blocker. A wide QRS is a warning sign. Get toxicology input on sodium-channel treatment (see Sodium Bicarbonate)
• Hypoglycemia (any beta-blocker): Check glucose early, then repeat it. Hypoglycemia is a listed presentation of beta-blocker overdose

Red Flags

• Hypotension with mean arterial pressure below 65 mmHg, or systolic BP below 90 mmHg with poor perfusion
• Bradycardia with high-grade AV block, or any new conduction block on the ECG
• Cardiogenic shock: poor perfusion with a weak pulse, pulmonary edema or documented myocardial dysfunction
• Altered mental status, drowsiness or seizures; cardiac arrest or periarrest. Check glucose and treat seizures per protocol

This is a clinical diagnosis, built on the exposure history and the hemodynamics. Start treatment alongside the work-up. Lab results should not hold up first-line therapy.

• Digoxin toxicity: Bradycardia and AV block. The calcium chloride label says to avoid calcium with digoxin unless it is needed. If it is needed, monitor the ECG and calcium. Sort it out with the digoxin exposure history
• Sepsis or other vasodilatory shock: Fever, a source of infection and rising lactate. The drug exposure history and bradycardia point toward BB or CCB
• Acute coronary syndrome with cardiogenic shock: Ischemic ST changes on the 12-lead ECG and a troponin rise. Poisoning and ischemia can coexist, so keep the ischemia work-up going
• Other drug causes: Clonidine, opioids, tricyclic antidepressants, lithium and ethanol (see Toxidromes). What separates them is the toxidrome pattern, such as pupils, respiratory rate and sedation

1. Scene and history: identify the drug names, tablet strengths and amount, time of ingestion and any other pills in the home. Bring all containers.
2. Airway and breathing: keep the airway open and suction secretions. Drowsy or bradycardic patients are at risk of aspiration; position them to protect the airway and give oxygen per protocol.
3. Circulation: keep the patient supine with the legs raised if hypotensive. Do not let the patient walk or stand. BLS does not treat hypotension from these drugs; call for ALS early.
4. Monitoring: pulse, blood pressure, SpO₂, mental status and, if available, a rhythm strip. Record changes with times.
5. Do not give medicines by mouth or induce vomiting unless a toxicologist or poison center directs it.
6. Notify and transport: call the poison center at 1-800-222-1222 and transport to a facility that can give ALS and toxicology care.

Doses vary by protocol; follow local protocols and medical direction. Everything below rests on the 2017 CCB consensus and the high-dose insulin literature. Tags mark anything beyond BLS scope.

• Access and monitoring (Paramedic/RN/CCT): two large-bore IV or IO lines, continuous ECG and pulse oximetry, BP every 5 min. A 12-lead ECG when feasible, with QRS width and QTc. IO access is an option when IV access fails.
• Fluids: crystalloid 10–20 mL/kg over 10–15 min, and keep going only while the patient is fluid-responsive. Suspect myocardial dysfunction? Use smaller aliquots. Reassess lungs and point-of-care ultrasound after each one. Stop for pulmonary edema or no response.
• Calcium for CCB toxicity (Paramedic/RN/CCT): calcium chloride 10%, 1–2 g (10–20 mL) IV slowly every 10–20 min, or an infusion of 20–40 mg/kg/hr (0.2–0.4 mL/kg/hr of 10%). Calcium chloride goes in no faster than 1 mL/min, through a central or deep vein as its label directs. For peripheral access, calcium gluconate is the choice: 10%, 3–6 g (30–60 mL) every 10–20 min, or 60–120 mg/kg/hr (0.6–1.2 mL/kg/hr). It irritates peripheral veins less. Only a peripheral line in an emergency? Use calcium gluconate and check the site often. See Calcium Chloride and Calcium Gluconate.
• High-dose insulin for BB or CCB shock (RN/CCT, per protocol): regular insulin 1 unit/kg IV bolus, then 1 unit/kg/hr, with dextrose as needed to hold euglycemia. Only non-responders get titrated toward 10 units/kg/hr, and toxicology makes that call. See Insulin and Dextrose.
• Glucagon for BB toxicity (off-label, per toxicology): The 2017 CCB consensus does not recommend glucagon. The label covers only hypoglycemia and radiology, so no dose is given here. A 2025 educational review calls it a short bridge while insulin takes effect. Give an antiemetic and protect the airway. The label warns the patient may vomit on waking. Contraindicated in pheochromocytoma and insulinoma. See Glucagon.
• Vasopressors (Paramedic/RN/CCT): Norepinephrine is the preferred choice for vasodilatory shock, titrated to a MAP of 65 mmHg (Norepinephrine). Shock with a cardiogenic component gets epinephrine (Epinephrine IV). Dobutamine is an option once myocardial dysfunction is confirmed (Dobutamine). Dopamine is not suggested. Vasopressin alone is discouraged.
• Sotalol QT prolongation or torsades (Paramedic/RN/CCT): give magnesium sulfate per protocol, correct potassium, avoid other QT-prolonging drugs, and use pacing or cardioversion for unstable torsades, as the sotalol label directs. See Magnesium Sulfate.
• Atropine for symptomatic bradycardia or AV block: 0.5 mg IV every 3–5 min for a few doses if needed, the dose the 2017 CCB consensus suggests. Don't expect much from it. Bradycardia protocols often use a larger dose, so follow local protocol. See Atropine.
• Transcutaneous pacing: Attempt it first for unstable bradycardia or high-grade AV block. Capture problems are common, so treat the shock in parallel. See Transcutaneous Pacing.
• Lipid emulsion (refractory shock or periarrest only): 20% lipid emulsion 1.5 mL/kg IV bolus, repeated up to twice as needed until stable, then 0.25 mL/kg/min for 30–60 min. The FDA maximum is 12.5 mL/kg per 24 hours. Write down the total volume and tell the receiving team. Draw labs at least 6 hours after stopping. Use only with toxicology or medical direction (see Pitfalls).
• Cardiac arrest from CCB or BB poisoning: Run the current AHA ACLS algorithm. Add IV calcium for CCB exposure, and lipid emulsion. Call for VA-ECMO if it is available.

1. Toxicology and poison center now: Early involvement shapes every later step. Activated charcoal may be considered up to one hour after ingestion if the airway is protected. The 2017 CCB consensus notes that a benefit after one hour cannot be excluded. That consensus does not recommend whole bowel irrigation. It defers decontamination to the EAPCCT and AACT position statement.
2. Start high-dose insulin euglycemia therapy (HIET) with first-line calcium and vasopressors: Check glucose and potassium first. Regular insulin 1 unit/kg IV bolus, then 1 unit/kg/hr, is the proposed regimen in the 2017 CCB consensus. Give dextrose as needed to hold euglycemia. Use a D50 bolus only for low glucose, per protocol. A 2025 educational review describes a pre-insulin D50 push. Insulin is an ISMP high-alert medication. Confirm the concentration in units/mL, and have a second clinician double-check the bolus and infusion.
3. Titrate for response: Incremental increases up to 10 units/kg/hr rest only on case series. Reserve the upper range for patients who do not respond to first-line therapy, with myocardial dysfunction documented first where possible.
4. Glucose and potassium: Watch glucose and K⁺ at the interval set by protocol, during therapy and after stopping. The 2017 consensus names hypoglycemia, hypokalemia and volume overload as the risks of high-dose insulin.
5. Refractory shock: Lipid emulsion goes in for refractory shock or periarrest if it has not already been given. Add VA-ECMO when cardiogenic shock is present and the center offers it.
6. Hemodialysis: Hydrophilic beta-blockers such as atenolol can be cleared with help from hemodialysis. Discuss it with toxicology.
7. Observation and disposition: An asymptomatic patient after a potentially toxic CCB ingestion above a single therapeutic dose needs about 24 hours of hospital observation, per the 2017 consensus. Extended-release products can delay toxicity. Set the observation period for beta-blocker and extended-release exposures with toxicology and the poison center. Admit to ICU or a step-down unit with continuous monitoring when the patient is on vasoactive infusions, insulin infusions or pacing.

• Destination: An ED or ICU with toxicology support. If cardiogenic shock is refractory and the center offers VA-ECMO, go there. Arrange early transfer rather than waiting for deterioration.
• Infusions: Run insulin and dextrose on a pump. Confirm the bag concentration in units/mL and the units/hr setting, not only the mL/hr. Calcium chloride infusions go through a central or deep vein, per its label. Check the site at each rate change.
• Delayed onset: Toxicity can appear hours after a stable early course. Extended-release and large exposures need observation before any clearance. A normal first set of vital signs does not end the risk.
• Monitoring in transit: Keep the monitor on: continuous ECG, BP, SpO₂ and mental status. Check glucose at each rate change and at the interval set by protocol. Potassium comes at the next lab draw. Keep transcutaneous pacing pads on for patients with unstable bradycardia.
• Labs drawn during lipid therapy: Lipids can interfere with some lab tests. Draw labs at least 6 hours after stopping the infusion.
• Handoff essentials: agent, dose and time of ingestion, including any extended-release product; insulin bolus and rate in units/kg/hr with bag concentration; last glucose and potassium with times; calcium doses; vasopressor doses; pacing settings; total lipid volume in mL/kg; and the poison center or toxicology contact.

• Pediatrics: The 2017 CCB consensus says its recommendations can reasonably be applied to children, because pediatric evidence is scarce. No pediatric calcium, insulin or HIET doses are given here. Weight-based dosing depends on protocol, so call the poison center early and use medical direction. Beta-blockers can cause hypoglycemia. Check glucose early. See Weight-Based Dosing and Pediatric Vital Signs.
• Pregnancy: No specific adjustment for BB or CCB poisoning in pregnancy is established in the sources reviewed. Stabilize the patient first. Bring the obstetric team in early, and call the poison center for drug-specific advice.
• Older Adults: Reduced reserve and polypharmacy raise the risk of severe toxicity. Check for duplicate or unintended prescriptions.
• Renal Impairment: Hydrophilic beta-blockers such as atenolol can be removed by hemodialysis. Renally cleared drugs such as sotalol are dosed by creatinine clearance. For CCB poisoning, no specific adjustment is established.
• Hepatic Impairment: No specific adjustment is established. Triglycerides need monitoring during lipid emulsion, per the label.
• Obesity: The sources give per-kilogram doses without naming a dosing weight. Use the dosing weight set by local protocol and toxicology.
• Patients on Beta-Blockers: Glucagon can cause a transient rise in pulse and blood pressure. In coronary artery disease, that rise may need treatment.

• Error: Trusting atropine or glucagon alone. They often fail in severe poisoning. Start calcium, high-dose insulin and vasopressors in parallel.
• Error: Starting insulin without serial glucose checks and a dextrose plan, even when glucose is normal or low. Hypoglycemia, hypokalemia and volume overload are the risks named by the 2017 consensus.
• Error: Pushing calcium chloride fast, or running it through a small peripheral vein. The label caps the rate at 1 mL/min, directs a central or deep vein, and forbids IM or subcutaneous use because of tissue injury. For peripheral access, use calcium gluconate and check the site.
• Error: Giving calcium to a patient on digoxin with no clear need. The label advises avoiding the combination, and monitoring the ECG and calcium levels if it is needed.
• Error: Giving lipid emulsion routinely. The 2017 consensus reserves it for refractory shock or periarrest. The FDA label covers parenteral nutrition only. It says to stop the infusion if triglycerides exceed 400 mg/dL in adults, and it warns of fat overload syndrome and pancreatitis.
• Error: Giving glucagon to a patient with pheochromocytoma or insulinoma. Both are contraindications. Pheochromocytoma can cause a dangerous rise in blood pressure. Insulinoma can cause hypoglycemia.
• Error: Relying on pacing with no vasopressor or insulin plan. Capture problems are common. Pacing does not replace shock treatment.
• Error: Clearing a patient early because the first vital signs are normal after an extended-release or large exposure. Observe for about 24 hours in hospital, and involve toxicology before discharge.