Cardiogenic shock — Calcium channel blocker overdose (HIE-first toxicologic CS)
Phase E variant of cardio.cardiogenic-shock.core.v1 — narrowed to acute calcium channel blocker (CCB) overdose presenting with hemodynamic collapse / cardiogenic shock. Pathophysiology depends on subclass: dihydropyridines (DHP — amlodipine, nifedipine) selective vascular L-type Ca block → vasodilation → distributive shock; non-dihydropyridines (non-DHP — diltiazem, verapamil) myocardial L-type Ca block → bradycardia + AV block + neg inotropy → cardiogenic shock; severe / mixed phenotype at high doses. Per AACT 2017 PMID 29022414 + St-Onge meta PMID 27767299. Treatment FIRST-LINE: HIGH-DOSE INSULIN-EUGLYCEMIA THERAPY (HIE) — same regimen as BB OD: regular insulin 1 U/kg IV bolus → 0.5–2 U/kg/h infusion + D10W titrate to euglycemia 100–250 (HIE > standard pressors per St-Onge meta PMID 27767299 and Engebretsen PMID 21626672). CALCIUM gluconate 3 g IV q5 min (max ~12 g) or calcium chloride 10% 1 g via central — CCB-specific antagonism (CORE therapy in CCB OD vs adjunct in BB OD); titrate to ionized Ca >2.0 (avoid >3.0). GLUCAGON less effective in CCB than BB (no β-blockade defect; trial dose only). LIPID EMULSION 20% (1.5 mL/kg bolus → 0.25 mL/kg/min infusion) for amlodipine / verapamil (lipophilic; Levine 2014 PMID 25498415). METHYLENE BLUE 1–2 mg/kg IV bolus over 5 min for refractory amlodipine vasoplegia (NO-cGMP pathway). AVOID (relatively): pure vasoconstrictors alone (phenylephrine) — bradycardia + AV block + neg inotropy of non-DHP CCB OD need inotropy + chronotropy, not just vasoconstriction; β-agonists LESS helpful (calcium channels primary defect; β-receptor pathway intact); methylene blue AVOID with serotonergic drugs (serotonin syndrome risk). MECHANICAL: VA-ECMO if refractory CS despite all of above (toxicologic CS reversible if bridged 24–72 h until drug clearance; amlodipine longer due to t½ 30–50 h); transvenous pacing for symptomatic bradycardia (capture often acceptable in CCB OD vs poor in BB OD). WHOLE-BOWEL IRRIGATION especially important for sustained-release CCB (verapamil-SR, diltiazem CD) — polyethylene glycol 1.5–2 L/h until rectal effluent clear; HEMODIALYSIS generally NOT effective (most CCBs high Vd + protein-bound); CRRT for AKI from sustained shock. Concurrent CCB + BB co-ingestion is the HIGHEST-MORTALITY phenotype — synergistic toxicity; prophylactic VA-ECMO team activation. Sustained-release CCB ingestions can have delayed decompensation 4–8 h post-ingestion — admit and observe at least 24 h. Psychiatric inpatient admission post medical clearance for intentional OD (mandatory safety planning + lethal-means counseling per SAMHSA — esp removal of long-acting amlodipine from home). Inherits parent CS framework (vasopressor / MCS escalation, MDT activation); specialises for CCB-specific toxicologic pharmacology (HIE FIRST-LINE inotropy, calcium CORE antagonism, lipid emulsion for lipophilic agents, methylene blue + vasopressin for vasoplegic phenotype, whole-bowel irrigation for sustained-release formulations, prolonged MCS bridge for amlodipine long t½). Status INTEGRATED until terminology + RxNav-validated drug codes are reconciled. Authored 2026-05-15 by shard-06-cardio-acute as Phase E wave 18 toxicologic CS variant (paired with cardio.cardiogenic-shock.bb-overdose.v1).
Entry points (4)
- historyIntentional CCB ingestion + bradycardia + AV block + hypotension — non-DHP (diltiazem / verapamil) cardiogenic phenotype; HIE pathwayintentional_ccb_ingestion_with_bradycardia_av_block_hypotension
- historyAmlodipine OD with vasoplegic shock refractory to norepinephrine — DHP distributive phenotype; HIE + methylene blue + vasopressin pathwayamlodipine_overdose_with_vasoplegia_refractory_ne
- imagingECG bradycardia + 1st/2nd/3rd-degree AV block in known or suspected CCB OD — non-DHP toxicity; calcium + HIE + pacing planningecg_bradycardia_av_block_post_ccb_od
- historyConcurrent CCB + BB ingestion — highest-mortality synergistic toxicity; activate VA-ECMO team prophylacticallyco_ingestion_ccb_plus_bb_synergistic_shock
Required inputs (15)
- agerequireddemographic • used at CONTEXTPediatric single-tablet CCB ingestion (esp amlodipine, verapamil-SR) catastrophic; geriatric polypharmacy compounds toxicity
- weightrequireddemographic • used at TREATMENTHIE dosing weight-based (insulin 1 U/kg bolus → 0.5–2 U/kg/h); calcium gluconate 3 g per dose; lipid emulsion 1.5 mL/kg bolus
- sbprequiredvital • used at RED_FLAGSSCAI 2022 baseline + vasopressor titration; persistent SBP <90 despite HIE + pressors → MCS escalation
- hrrequiredvital • used at RED_FLAGSBradycardia (HR <60) + AV block hallmark of non-DHP OD; reflex tachycardia possible in early DHP OD before vasoplegia decompensates
- temperaturerequiredvital • used at CONTEXTHypothermia common in severe CCB OD; warm to ≥36°C before pronouncement of refractoriness
- glucoserequiredlab • used at INITIAL_WORKUPCCB OD impairs pancreatic insulin release (Ca-dependent) → HYPERGLYCEMIA at presentation (distinguishes from BB OD which causes hypoglycemia); during HIE, target euglycemia 100–250 with D10W
- potassiumrequiredlab • used at INITIAL_WORKUPInsulin shifts K intracellularly during HIE — replace aggressively (K target ≥4.0); hourly during HIE infusion
- calcium_ionizedrequiredlab • used at TREATMENTTrack ionized Ca during high-dose calcium therapy; target ionized Ca >2.0 (avoid hypercalcemia toxicity > 3.0)
- lactaterequiredlab • used at RISK_STRATIFICATIONSCAI 2022 staging + perfusion marker; CardShock prognostication (Harjola PMID 26333869)
- creatininerequiredlab • used at CONTEXTeGFR for supportive drug dosing (most CCBs NOT dialyzable due to high Vd + protein binding); CRRT for AKI from sustained shock
- troponinrequiredlab • used at INITIAL_WORKUPDifferentiate primary toxic CS from ischemia-precipitated shock; modest elevations common from low-flow
- ecgrequiredimaging • used at INITIAL_WORKUPBradycardia + AV block (non-DHP); usually preserved sinus + normal PR (DHP); QRS narrow (no Na-channel effect, distinct from propranolol BB OD); QT typically not prolonged
- echorequiredimaging • used at INITIAL_WORKUPReduced contractility (non-DHP cardiogenic phenotype) vs hyperdynamic + low SVR (amlodipine vasoplegic phenotype) — distinguishes management focus; serial echo to track HIE inotropic recovery
- agent_dose_time_of_ingestionrequiredhistory • used at CONTEXTIdentify specific CCB (amlodipine = long t½ + vasoplegia; verapamil = highest mortality + bradycardia; diltiazem intermediate; sustained-release formulations have delayed peak); dose in mg/kg; coingestants
- co_ingestion_screenrequiredhistory • used at CONTEXTConcurrent BB / TCA / opioid / EtOH; BB co-ingestion is the highest-mortality phenotype — early VA-ECMO planning
12-phase flow (11)
- 1FRAMERecognize CCB OD as toxicologic CS — Ca-channel blockade defeats standard pressors; HIE + calcium + lipid emulsion + methylene blue (DHP) are pillars; standard NE / vasopressin alone often inadequateinputs: ecg, sbpadvance: CCB OD with shock physiology confirmed
- 2ENTRYActivate poison control (1-800-222-1222) + medical toxicology + CS team; secure airway if AMS; IV access × 2 large-bore + arterial line + central line if shock; identify agent + dose + time of ingestion + sustained-release formulationinputs: sbp, hr, agent_dose_time_of_ingestionadvance: Tox + CS team activated + airway secured + access in place
- 3CONTEXTSpecific agent (amlodipine = long t½ vasoplegia; verapamil = highest mortality; diltiazem intermediate; sustained-release formulations delayed peak), dose in mg/kg, time of ingestion, co-ingestants (BB synergistic), psych history, prior cardiac diseaseinputs: weight, temperature, creatinine, co_ingestion_screenadvance: Agent + co-ingestants + dosing weight documented
- 4RED_FLAGSAmlodipine vasoplegia refractory to NE (DHP distributive phenotype — methylene blue + vasopressin); diltiazem AV block requiring pacing (non-DHP cardiogenic phenotype); HIE failure → ECMO triggers (lactate not clearing, SBP unsupportable); suicide risk + repeated OD (psych safety planning)inputs: sbp, hr, glucoseactions: cardiogenic_shock, wide_complex_tachadvance: Acute hemodynamic + electrical derangements managed + co-ingestion screened
- 5INITIAL_WORKUPECG (bradycardia, AV block — usually narrow QRS); STAT echo (cardiogenic vs distributive phenotype distinction — drives MCS strategy); BMP + Mg + ionized Ca + glucose + lactate + ABG; troponin (rule out ischemic mimic); APAP + salicylate level (universal coingestant screen); EtOH; tox screen; serum / urine drug screen; serum drug level if assay available (rare)inputs: ecg, echo, glucose, potassium, calcium_ionized, lactate, troponinactions: cardiogenic_shock, wide_complex_tach, panel.cardiac, panel.renaladvance: Baseline labs + ECG + echo + co-ingestion labs documented
- 6BRANCHING_WORKUPGI decontamination — activated charcoal 1 g/kg PO if airway protected + ingestion <1 h (or <2 h for sustained-release); WHOLE-BOWEL IRRIGATION especially important for sustained-release CCB (verapamil-SR, diltiazem CD) — polyethylene glycol 1.5–2 L/h until rectal effluent clear; hemodialysis generally NOT effective (most CCBs high Vd + protein-bound); CRRT for AKI from sustained shockinputs: ecgadvance: Decontamination decision + dialysis triage documented
- 7RISK_STRATIFICATIONSCAI 2022 stage; SOFA / CardShock score; agent-specific risk (verapamil = highest mortality; amlodipine = vasoplegia challenge); refractoriness to first-line (HIE + calcium) → MCS / VA-ECMO triage; vasoplegia phenotype → methylene blue trialinputs: sbp, lactateadvance: SCAI stage + agent-specific severity + MCS triage assigned
- 8TREATMENTPILLAR THERAPY: HIE — regular insulin 1 U/kg IV bolus → 0.5–2 U/kg/h infusion + D10W titrate to euglycemia 100–250 (St-Onge meta PMID 27767299); CALCIUM gluconate 3 g IV q5 min × max ~12 g (or CaCl2 10% 1 g via central line — 3× more elemental Ca per gram) — CCB-specific antagonism; trial GLUCAGON 5–10 mg IV (less effective than for BB OD); LIPID EMULSION 20% 1.5 mL/kg bolus → 0.25 mL/kg/min infusion for amlodipine / verapamil (lipophilic). PRESSORS: norepinephrine titrate MAP ≥65 (combine with HIE); add vasopressin 0.04 U/min for vasoplegia; consider METHYLENE BLUE 1–2 mg/kg IV bolus for refractory amlodipine vasoplegia (NO-cGMP pathway). PACING: transvenous if symptomatic brady refractory (capture acceptable in CCB OD). MCS: VA-ECMO if refractory CS despite all of above (SCAI D/E)inputs: sbp, lactate, glucose, calcium_ionized, weightactions: cardiogenic_shockadvance: HIE + calcium + lipid (if lipophilic) + pressors + methylene blue (if vasoplegic) + MCS plan all in place
- 9DISPOSITIONCICU at MCS-capable center; transfer if MCS not available locally; Toxicology + Cardiology + Psych comanagement; psychiatric admission post-medical clearance for intentional ODadvance: CICU bed assigned + tox + psych comanagement + MCS pathway documented
- 10MONITORINGContinuous telemetry; A-line; central line; serial ECG q4–6 h (track conduction); glucose q1h during HIE (D10W titration; target 100–250); K hourly (insulin shifts intracellularly — replace aggressively to ≥4.0); ionized Ca q4–6 h (target >2.0; avoid >3.0 toxicity); Mg q4–6 h; lactate q2–4 h until clearing; UOP hourly; serial echo q12–24 h to track inotropic recovery + distinguish persistent cardiogenic vs distributive phenotypeinputs: glucose, potassium, calcium_ionized, lactateactions: panel.cardiac, panel.renaladvance: Monitoring cadence + HIE + calcium titration loop established
- 11FOLLOWUPPsychiatric inpatient admission post-medical clearance for intentional OD (mandatory safety planning); Toxicology + Cardiology follow-up at 1–4 wks; outpatient SSRI / mood stabilizer review with psychiatry; medic-alert documentation for severe CCB-sensitivity if therapeutic re-introduction needed; family education on lethal-means counseling (esp removal of long-acting CCBs from home)advance: Psych admission + safety plan + outpatient cardiology + toxicology follow-up scheduled