Key Points
- Use the highest‑yield diagnostic test early; do not let testing delay time‑critical therapy.
- Set objective targets (hemodynamic, neurologic, respiratory) and reassess frequently.
- Plan definitive source control or disease‑specific therapy when indicated; document follow‑up and patient education.
Algorithm
- Airway/IV access; start cardiac monitoring and frequent labs.
- Give calcium salts; start vasopressors for hypotension.
- Initiate HIE: bolus insulin then infusion with dextrose; monitor glucose and electrolytes closely.
- Consider lipid emulsion for lipophilic agents; add pacing/atropine for severe bradycardia.
- Consult toxicology; escalate to ECMO in refractory cardiogenic shock.
Clinical Synopsis & Reasoning
Severe hypotension/bradycardia from CCB toxicity requires airway protection, calcium salts, vasopressors, and **high‑dose insulin euglycemia therapy (HIE)** with dextrose and electrolyte monitoring; add lipid emulsion for lipophilic agents and consider ECMO for refractory shock.
Treatment Strategy & Disposition
Stabilize ABCs. Initiate guideline‑concordant first‑line therapy with precise dosing and continuous monitoring. Escalate to advanced/procedural interventions based on explicit failure criteria. Define ICU, step‑down, and ward disposition triggers; involve specialty teams early.
Epidemiology / Risk Factors
- Risk varies by comorbidity and precipitants; see citations for condition‑specific data.
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| ECG, glucose, electrolytes, VBG/ABG | Baseline severity | Bradycardia, hyperglycemia, acidosis | Trend frequently |
| Serum drug levels (limited utility) | Adjunct | Rarely changes management | — |
| Point‑of‑care ultrasound | Hemodynamics | Cardiogenic vs vasoplegic shock | Guide therapy |
Pharmacology
| Medication/Intervention | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Calcium chloride 20 mg/kg IV (central) or gluconate 30 mg/kg IV | Calcium | Minutes | Membrane stabilization/inotropy | Transient benefit |
| High‑dose insulin: 1 U/kg IV bolus → 1–10 U/kg/h infusion + dextrose | Metabolic inotrope | Minutes‑hours | Improves contractility/uses carbohydrate metabolism | Frequent glucose/K+/Mg monitoring |
| Norepinephrine ± epinephrine | Vasopressors | Minutes | Treat vasoplegia and hypotension | Titrate to MAP |
| Lipid emulsion 20%: 1.5 mL/kg bolus → 0.25 mL/kg/min 30–60 min | Lipid sink | Minutes | Lipophilic CCBs | Interferes with labs/CPR |
| Glucagon (limited efficacy) | cAMP mediator | Minutes | Adjunct in β‑blocker overlap | Nausea/vomiting |
Prognosis / Complications
- Outcome depends on timeliness of diagnosis and definitive therapy; monitor for complications.
Patient Education / Counseling
- Provide red‑flag education, adherence guidance, and explicit return precautions; arrange timely specialty follow‑up.
References
- Clinical Toxicology reviews on CCB overdose and HIE — Link