Clinical Commander

All dossiers
cardio.cardiogenic-shock.bb-overdose.v1

Cardiogenic shock — Beta-blocker overdose (HIE-first toxicologic CS)

cardiologyacuteadultacuteinpatienttransitionoutpatient

Phase E variant of cardio.cardiogenic-shock.core.v1 — narrowed to acute beta-blocker (BB) overdose presenting with hemodynamic collapse / cardiogenic shock. Pathophysiology: massive β1/β2 receptor blockade → bradycardia + AV block + hypotension + reduced inotropy → CS. Lipophilic agents (propranolol prototype) cross BBB → seizures / AMS; propranolol additionally has Na-channel blocking (membrane-stabilising) effect → QRS widening + ventricular arrhythmia. Sotalol additionally has class III activity → QT prolongation + torsades. Per AACT 2017 PMID 29022414. Treatment pivots from generic CS bundle: HIGH-DOSE INSULIN-EUGLYCEMIA THERAPY (HIE) is FIRST-LINE inotropic strategy — regular insulin 1 U/kg IV bolus → 0.5–2 U/kg/h infusion + D10W titrated to euglycemia 100–250 (Engebretsen 2011 PMID 21626672 — HIE > standard pressors in BB/CCB OD). GLUCAGON 5–10 mg IV bolus → 5–10 mg/h infusion (anti-emetic pre-treatment — vomiting universal at therapeutic dose). CALCIUM gluconate 3 g IV q5 min (max ~12 g) — especially for concurrent CCB co-ingestion. SODIUM BICARBONATE 1–2 mEq/kg IV bolus for QRS widening (propranolol Na-channel block — analogous to TCA OD pathway). LIPID EMULSION 20% (1.5 mL/kg bolus → 0.25 mL/kg/min infusion) for severe lipophilic OD (Levine 2014 PMID 25498415). AVOID (relatively): standard ACLS dosing of epinephrine alone (often inadequate due to receptor blockade — combine with HIE + glucagon); pure α-agonists (phenylephrine) less effective; transvenous pacing capture often poor (bridge with isoproterenol + epinephrine + HIE during attempt). MCS: VA-ECMO if refractory CS despite all of above (toxicologic CS reversible if bridged 24–48 h until drug clearance). HEMODIALYSIS for water-soluble + low-Vd agents (atenolol, nadolol, sotalol) — propranolol / metoprolol NOT dialyzable. Concurrent BB + CCB co-ingestion is the HIGHEST-MORTALITY phenotype — synergistic toxicity (combined β + Ca-channel blockade); prophylactic VA-ECMO team activation. Sotalol OD uniquely combines BB physiology (HIE pathway) with class III QT prolongation → Mg + overdrive pacing + emergent hemodialysis. Psychiatric inpatient admission post medical clearance for intentional OD (mandatory safety planning + lethal-means counseling per SAMHSA). Inherits parent CS framework (vasopressor / MCS escalation, MDT activation); specialises for BB-specific toxicologic pharmacology (HIE FIRST-LINE inotropy, glucagon for chronotropy, calcium for synergistic CCB co-ingestion, bicarbonate for propranolol QRS, lipid emulsion for severe lipophilic OD, hemodialysis for water-soluble agents). 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.ccb-overdose.v1).

Entry points (4)

  • history
    Intentional β-blocker ingestion + bradycardia + hypotension — BB OD with shock physiology; HIE pathway
    intentional_bb_ingestion_with_bradycardia_hypotension
  • symptom
    Altered mental status / seizure with known β-blocker exposure — suspect propranolol (lipophilic, BBB penetrant)
    altered_mental_status_with_known_bb_use
  • imaging
    ECG bradycardia + AV block ± QRS widening (propranolol Na-channel effect) post-BB ingestion → bicarbonate + HIE pathway
    ecg_bradycardia_av_block_qrs_widening_post_bb_od
  • history
    Concurrent BB + CCB ingestion — synergistic toxicity; severe CS requires HIE + calcium + glucagon + early MCS planning
    co_ingestion_bb_plus_ccb_synergistic_shock

Required inputs (14)

  • agerequired
    demographic • used at CONTEXT
    Pediatric BB OD (single-tablet ingestion of long-acting propranolol) catastrophic; geriatric polypharmacy compounds toxicity
  • weightrequired
    demographic • used at TREATMENT
    HIE 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
  • sbprequired
    vital • used at RED_FLAGS
    SCAI 2022 baseline + vasopressor titration; persistent SBP <90 despite HIE → MCS escalation
  • hrrequired
    vital • used at RED_FLAGS
    Bradycardia (HR <60) + AV block hallmark; may be capture-failure on transvenous pacing due to receptor blockade
  • temperaturerequired
    vital • used at CONTEXT
    Hypothermia common in severe BB OD; warm to ≥36°C before pronouncement of refractoriness
  • glucoserequired
    lab • used at INITIAL_WORKUP
    BB OD impairs glycogenolysis → hypoglycemia (esp pediatric); during HIE, target euglycemia 100–250 mg/dL with D10W titration
  • potassiumrequired
    lab • used at INITIAL_WORKUP
    Insulin shifts K intracellularly during HIE — replace aggressively (K target ≥4.0); hourly during HIE infusion
  • lactaterequired
    lab • used at RISK_STRATIFICATION
    SCAI 2022 staging + perfusion marker; CardShock prognostication (Harjola PMID 26333869)
  • creatininerequired
    lab • used at CONTEXT
    eGFR for water-soluble BB clearance (atenolol/nadolol — hemodialysis option) + supportive drug dosing
  • troponinrequired
    lab • used at INITIAL_WORKUP
    Differentiate primary toxic CS from ischemia-precipitated arrhythmia / shock
  • ecgrequired
    imaging • used at INITIAL_WORKUP
    Bradycardia + AV block (1st/2nd/3rd-degree); QRS widening with propranolol (Na-channel block — bicarbonate response); QT prolongation with sotalol (class III)
  • echorequired
    imaging • used at INITIAL_WORKUP
    Confirms reduced contractility; rules out structural / ischemic mimics; serial echo to track HIE inotropic recovery
  • agent_dose_time_of_ingestionrequired
    history • used at CONTEXT
    Identify specific BB (propranolol most dangerous — lipophilic + Na-channel effect; sotalol → torsades); dose in mg/kg; coingestants (CCB synergistic)
  • co_ingestion_screenrequired
    history • used at CONTEXT
    Concurrent CCB / TCA / opioid / EtOH; CCB co-ingestion is the highest-mortality phenotype

12-phase flow (11)

  1. 1FRAME
    Recognize BB OD as toxicologic CS — receptor blockade defeats standard ACLS; HIE + glucagon + calcium + lipid emulsion + bicarbonate are the pillars; standard epinephrine alone often inadequate
    inputs: ecg, sbp
    advance: BB OD with shock physiology confirmed
  2. 2ENTRY
    Activate 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
    inputs: sbp, hr, agent_dose_time_of_ingestion
    advance: Tox + CS team activated + airway secured + access in place
  3. 3CONTEXT
    Specific agent (propranolol = lipophilic + Na-channel; sotalol = class III + QT; atenolol/nadolol = hydrophilic + dialyzable), dose in mg/kg, time of ingestion, co-ingestants (CCB synergistic), psych history, prior cardiac disease
    inputs: weight, temperature, creatinine, co_ingestion_screen
    advance: Agent + co-ingestants + dosing weight documented
  4. 4RED_FLAGS
    Refractory bradycardia / AV block (HR <40 + symptomatic; pacing capture-failure common); QRS widening (propranolol Na-channel block — needs bicarbonate); QTc >500 (sotalol — torsades risk); coma / seizure (propranolol BBB penetration); concurrent CCB co-ingestion (highest mortality phenotype); hypoglycemia (BB impairs glycogenolysis)
    inputs: sbp, hr, glucose
    actions: cardiogenic_shock, wide_complex_tach
    advance: Acute hemodynamic + electrical derangements managed + co-ingestion screened
  5. 5INITIAL_WORKUP
    ECG (bradycardia, AV block, QRS, QT); STAT echo (LVEF + structural rule-out); BMP + Mg + 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 (esp sotalol — dialyzable)
    inputs: ecg, echo, glucose, potassium, lactate, troponin
    actions: cardiogenic_shock, wide_complex_tach, panel.cardiac, panel.renal
    advance: Baseline labs + ECG + echo + co-ingestion labs documented
  6. 6BRANCHING_WORKUP
    GI decontamination — activated charcoal 1 g/kg PO if airway protected + ingestion <1 h (or <2 h for sustained-release formulation); whole-bowel irrigation for sustained-release sotalol / metoprolol XL; hemodialysis for atenolol / nadolol / sotalol (water-soluble + low Vd) if refractory or sotalol-induced torsades
    inputs: ecg
    advance: Decontamination + dialysis decision documented
  7. 7RISK_STRATIFICATION
    SCAI 2022 stage; SOFA / CardShock score; agent-specific risk (propranolol QRS widening = severe; sotalol QTc >500 = torsades risk; CCB co-ingestion = highest mortality); refractoriness to first-line (HIE + glucagon + calcium) → MCS / VA-ECMO triage
    inputs: sbp, lactate
    advance: SCAI stage + agent-specific severity + MCS triage assigned
  8. 8TREATMENT
    PILLAR THERAPY: HIE — regular insulin 1 U/kg IV bolus → 0.5–2 U/kg/h infusion + D10W titrate to euglycemia 100–250; CALCIUM gluconate 3 g IV q5 min (max ~12 g); GLUCAGON 5–10 mg IV bolus → 5–10 mg/h infusion (pre-treat with anti-emetic — vomiting universal); SODIUM BICARBONATE 1–2 mEq/kg IV bolus for QRS widening (propranolol); LIPID EMULSION 20% 1.5 mL/kg bolus → 0.25 mL/kg/min infusion for severe lipophilic OD (esp propranolol). PRESSORS: norepinephrine titrate MAP ≥65 (combine with HIE — alone often inadequate); epinephrine if NE inadequate. PACING: transvenous if symptomatic brady refractory to drugs (capture often poor — bridge with HIE + drugs). MCS: VA-ECMO if refractory CS despite all of above (SCAI D/E)
    inputs: sbp, lactate, glucose, potassium, weight
    actions: cardiogenic_shock
    advance: HIE + glucagon + calcium + bicarbonate (if QRS) + lipid (if severe lipophilic) + pressors + MCS plan all in place
  9. 9DISPOSITION
    CICU at MCS-capable center; transfer if MCS not available locally; Toxicology + Cardiology + Psych comanagement; psychiatric admission post-medical clearance for intentional OD
    advance: CICU bed assigned + tox + psych comanagement + MCS pathway documented
  10. 10MONITORING
    Continuous telemetry; A-line; central line; serial ECG q4–6 h (track QRS, QT, conduction); glucose q1h during HIE (D10W titration; target 100–250); K hourly (insulin shifts intracellularly — replace aggressively to ≥4.0); Mg q4–6 h; lactate q2–4 h until clearing; UOP hourly; serial echo q12–24 h to track inotropic recovery
    inputs: glucose, potassium, lactate
    actions: panel.cardiac, panel.renal
    advance: Monitoring cadence + HIE titration loop established
  11. 11FOLLOWUP
    Psychiatric 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 BB-sensitivity if therapeutic re-introduction needed; family education on lethal-means counseling
    advance: Psych admission + safety plan + outpatient cardiology + toxicology follow-up scheduled