Overview
Calcium Channel Blocker Overdose
Topic Overview
Summary
Calcium channel blocker (CCB) overdose causes profound cardiovascular toxicity including bradycardia, hypotension, and cardiogenic shock. Non-dihydropyridines (verapamil, diltiazem) primarily affect the heart, while dihydropyridines (amlodipine, nifedipine) cause vasodilation. Treatment includes IV calcium, high-dose insulin euglycaemic therapy (HIET — first-line for severe toxicity), IV fluids, vasopressors, and in refractory cases, lipid emulsion and extracorporeal support.
Key Facts
- Mechanism: L-type calcium channel blockade → ↓cardiac contractility, ↓conduction, vasodilation
- Features: Bradycardia, hypotension, cardiogenic shock, hyperglycaemia
- Treatment: IV calcium, high-dose insulin (HIET), IV fluids, vasopressors
- Verapamil/diltiazem: More cardiotoxic (bradycardia, AV block)
- Amlodipine: More vasodilation, prolonged duration
Clinical Pearls
Hyperglycaemia is a clue to CCB overdose — insulin-mediated glucose uptake is impaired
High-dose insulin is the most effective treatment for severe CCB toxicity
HIET: Insulin 1 unit/kg bolus, then 0.5-1 unit/kg/hr — monitor glucose and K+
Why This Matters Clinically
CCB overdose can cause refractory shock that does not respond to conventional resuscitation. HIET is the most important treatment but is often under-dosed or delayed.
Visual Summary
Visual assets to be added:
- CCB mechanism of action
- Dihydropyridine vs non-dihydropyridine comparison
- CCB overdose management algorithm
- HIET dosing protocol
Epidemiology
Incidence
- Increasing (common antihypertensives)
- Significant mortality in severe cases
Demographics
- Adults taking CCBs (accidental or intentional)
- Elderly at higher risk
Common CCBs
| Class | Examples | Main Effect |
|---|---|---|
| Non-dihydropyridine | Verapamil, diltiazem | Cardiac (negative inotropy, chronotropy, dromotropy) |
| Dihydropyridine | Amlodipine, nifedipine, felodipine | Peripheral vasodilation |
Pathophysiology
Mechanism
- Blockade of L-type calcium channels
- Reduced calcium influx into cardiac and vascular smooth muscle
- ↓Cardiac contractility (negative inotropy)
- ↓Heart rate (negative chronotropy)
- ↓AV node conduction (negative dromotropy)
- Vasodilation (dihydropyridines)
Why Hyperglycaemia
- Calcium needed for insulin release from pancreas
- CCB blocks calcium influx → ↓insulin secretion → hyperglycaemia
- Also reduces cellular glucose uptake
Why High-Dose Insulin Works
- Improves cardiac myocyte glucose uptake and metabolism
- Positive inotropic effect (independent of calcium channels)
- Improves myocardial contractility
Clinical Presentation
Cardiovascular
Metabolic
Neurological
Timeline
Red Flags
| Finding | Significance |
|---|---|
| Hypotension unresponsive to fluids | Cardiogenic shock |
| HR under 40 | Severe toxicity |
| AV block | Verapamil/diltiazem |
| Hyperglycaemia | Supports diagnosis |
Bradycardia (especially verapamil/diltiazem)
Common presentation.
Hypotension
Common presentation.
Cardiogenic shock
Common presentation.
AV block
Common presentation.
Reflex tachycardia (dihydropyridines — may mask toxicity initially)
Common presentation.
Clinical Examination
Vital Signs
- Bradycardia (or tachycardia with dihydropyridines)
- Hypotension
- Normal or increased respiratory rate
Cardiovascular
- Weak pulse
- Hypoperfusion signs
- Pulmonary oedema (cardiogenic shock)
Skin
- Warm, flushed (vasodilation — dihydropyridines)
- Cold, clammy (shock)
Investigations
Blood Tests
| Test | Finding |
|---|---|
| Glucose | Elevated (hyperglycaemia) |
| Potassium | Monitor (for HIET) |
| Lactate | Elevated if shock |
| U&E | Baseline |
| ABG | Metabolic acidosis (late) |
ECG
| Finding | Agent |
|---|---|
| Sinus bradycardia | All |
| AV block (1st, 2nd, 3rd degree) | Verapamil, diltiazem |
| Junctional rhythm | |
| QT prolongation | Less common |
Other
- Paracetamol, salicylate (co-ingestion)
- Echo (if cardiogenic shock)
Classification & Staging
By Agent
| Class | Agents | Main Effect |
|---|---|---|
| Non-dihydropyridine | Verapamil, diltiazem | Cardiac toxicity predominant |
| Dihydropyridine | Amlodipine, nifedipine | Peripheral vasodilation predominant |
By Severity
| Severity | Features |
|---|---|
| Mild | Mild bradycardia, minor hypotension |
| Moderate | Symptomatic hypotension, AV block |
| Severe | Cardiogenic shock, refractory hypotension |
Management
Initial Resuscitation
| Action | Details |
|---|---|
| Airway | Protect if reduced GCS |
| Oxygen | |
| IV access | Large bore |
| Continuous ECG | Essential |
| Monitor glucose hourly | For HIET |
Decontamination
- Activated charcoal: Consider if within 1-2 hours (especially sustained-release)
- Whole bowel irrigation: Consider for sustained-release
IV Calcium — First-Line
| Agent | Dose |
|---|---|
| Calcium gluconate 10% | 60 mL IV (30 mL if calcium chloride) |
| Or calcium chloride 10% | 30 mL IV (more irritant — central line preferred) |
| Repeat | Every 15-20 min up to 3-4 doses |
| Infusion | 10-20 mL/hr calcium gluconate |
High-Dose Insulin Euglycaemic Therapy (HIET) — Key Treatment
| Step | Details |
|---|---|
| Bolus | Insulin 1 unit/kg IV |
| Infusion | 0.5-1 unit/kg/hr (may need up to 10 units/kg/hr) |
| Dextrose | 50% dextrose bolus if glucose under 14; then 10-20% dextrose infusion |
| Monitor glucose | Hourly; target 10-14 mmol/L |
| Monitor K+ | Replace if under 3.0 |
Vasopressors
| Agent | Notes |
|---|---|
| Noradrenaline | First-line vasopressor |
| Adrenaline | If noradrenaline fails |
| May need high doses |
IV Lipid Emulsion
| Indication | Notes |
|---|---|
| Lipophilic CCBs | Verapamil, diltiazem |
| Dose | 1.5 mL/kg 20% lipid bolus, then 0.25 mL/kg/min |
| Later rescue | After HIET |
Other Treatments
- Glucagon: Less effective than for beta-blockers
- Atropine: Often ineffective
- Pacing: If severe bradycardia
Extracorporeal Support
- VA-ECMO for refractory shock
- Consider early in severe cases
Complications
Cardiac
- Cardiogenic shock
- Cardiac arrest
- Death
Metabolic
- Hypoglycaemia (from HIET — monitor closely)
- Hypokalaemia (from HIET)
- Metabolic acidosis
Other
- Bowel ischaemia (prolonged shock)
- Multi-organ failure
Prognosis & Outcomes
Prognosis
- Good if treated early with HIET
- Higher mortality with sustained-release, delayed presentation
Mortality
- 5-10% with treatment
- Higher with verapamil
Evidence & Guidelines
Key Guidelines
- TOXBASE (UK National Poisons Information Service)
- AACT/EAPCCT Position Statement
Key Evidence
- HIET is most effective treatment for severe CCB toxicity
- Lipid emulsion is a rescue therapy
Patient & Family Information
What is CCB Overdose?
Calcium channel blockers are blood pressure medications. Taking too many can dangerously slow the heart and lower blood pressure.
Symptoms
- Feeling faint or dizzy
- Slow heartbeat
- Confusion
- Collapse
Treatment
- Medications to support the heart (calcium, insulin, blood pressure drugs)
- Intensive care monitoring
- Sometimes a heart support machine is needed
Resources
References
Key Reviews
- Graudins A, et al. Treatment of beta-blocker and calcium channel blocker overdose. Br J Clin Pharmacol. 2016;81(3):453-461. PMID: 26551696
- St-Onge M, et al. Expert consensus recommendations for the management of calcium channel blocker poisoning in adults. Crit Care Med. 2017;45(3):e306-e315. PMID: 27749343
Guidelines
- TOXBASE. Calcium Channel Blocker Poisoning Management. 2023.