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Patient handout

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

PRODUCTION

1. Your condition

This handout is for cardiogenic shock — beta-blocker overdose (hie-first toxicologic cs). Your care team identified this based on: intentional β-blocker ingestion + bradycardia + hypotension — bb od with shock physiology; hie pathway.

Other reasons your team may use this plan: altered mental status / seizure with known β-blocker exposure — suspect propranolol (lipophilic, bbb penetrant); ecg bradycardia + av block ± qrs widening (propranolol na-channel effect) post-bb ingestion → bicarbonate + hie pathway; concurrent bb + ccb ingestion — synergistic toxicity; severe cs requires hie + calcium + glucagon + early mcs planning.

2. Your medications

Take these medications exactly as prescribed. Do not stop or change a dose without talking to your provider.

MedicationStarting doseHowWhenWhat it does
insulin regular1 U/kg IV bolus → 0.5–2 U/kg/h continuous infusion (HIE)IVcontinuous; titrate up if persistent hypotension, no upper limit set in OD literature beyond 10 U/kg/h has been reportedEngebretsen 2011 PMID 21626672 — HIE > standard pressors in BB/CCB OD; restores myocyte glucose oxidation and provides direct positive inotropy independent of β-receptor signalling; FIRST-LINE in toxicologic CS
glucagon5–10 mg IV bolus → 5–10 mg/h continuous infusionIVcontinuousAACT 2017 PMID 29022414 — bypasses β-receptor and stimulates myocardial cAMP via glucagon receptor; pre-treat with anti-emetic (ondansetron 8 mg IV) — vomiting universal at therapeutic dose; tachyphylaxis common after 24 h
calcium gluconate3 g IV q5 min × max ~12 g (then titrate to ionized Ca >2.0)IVq5 min initial then q4–6 h titrateAugments intracellular Ca; especially helpful for concurrent CCB co-ingestion (synergistic toxicity); calcium chloride 10% 1 g via central line is alternative — 3× more elemental Ca per gram
sodium bicarbonate1–2 mEq/kg IV bolus then infusion to keep arterial pH 7.50–7.55IVbolus + continuous infusionTreats propranolol Na-channel blockade (membrane-stabilising effect — analogous to TCA OD); bolus repeat q5 min until QRS narrows; continuous infusion to maintain alkalemia (target pH 7.50–7.55)
intralipid 20%1.5 mL/kg IV bolus over 1 min → 0.25 mL/kg/min infusion × 30–60 min (max ~10 mL/kg total)IVbolus may repeat × 2 q5 min then continuousLevine 2014 PMID 25498415 — lipid sink for lipophilic agents (propranolol most lipophilic; metoprolol intermediate; atenolol/nadolol hydrophilic — limited value for hydrophilic BBs); rescue therapy in shock or arrest
norepinephrine0.05–0.5 µg/kg/min IV titrate MAP ≥65IVcontinuousSOAP-II PMID 20200382 — first-line vasopressor in generic CS; in BB OD often inadequate alone (β blockade) — combine with HIE; doses required often supraphysiologic
epinephrine0.05–0.5 µg/kg/min IV titrateIVcontinuousAdjunct when NE alone fails; partial β-receptor override at high doses; AVOID as monotherapy without HIE — receptor blockade defeats standard ACLS dosing
isoproterenol2–10 µg/min IV titrate to HR 60–80IVcontinuousβ-1 chronotropic bridge during pacing capture-failure (common in severe BB OD due to receptor blockade); transvenous pacing remains preferred definitive bridge to HIE recovery
atropine0.5–1 mg IV q3–5 min × max 3 mgIVq3–5 minAHA 2020 ACLS bradycardia algorithm; usually inadequate in severe BB OD (receptor blockade defeats vagolysis); transient bridge to HIE / pacing
magnesium sulfate2 g IV bolus then 2 g/h infusionIVcontinuous if torsadesAHA 2020 ACLS — first-line for torsades regardless of serum Mg; SOTALOL OD specifically prone to QT prolongation + torsades (class III effect); combine with overdrive pacing if bradycardia-dependent
ondansetron8 mg IV before glucagon bolusIVq8 h while on glucagon infusionPre-treatment for glucagon-induced vomiting (universal at 5–10 mg dose); aspiration risk in obtunded patient
activated charcoal1 g/kg PO/NG if airway protected, ingestion <1 h (<2 h for sustained-release)PO/NGone-timeGI decontamination per AACT/EAPCCT — limited evidence; AVOID if ileus / obtundation without intubation

Plan: BB overdose with CS — HIE-first toxicologic pillars (insulin-euglycemia + glucagon + calcium + bicarbonate + lipid emulsion); pressors as adjuncts; VA-ECMO if refractory

3. When to call your provider

Contact your care team if any of the following happen:

  • Recurrent suicidal ideation → ED + involuntary hold
  • Inadvertent BB exposure → ED
  • Progressive conduction / contractile disease → cardiology + EP

4. When to seek emergency care

Call 911 or go to the nearest emergency room right away if you have:

  • Symptomatic bradycardia (HR <40 + hypotension or AMS) despite glucagon + atropine + isoproterenol bridge in BB OD — start HIE if not already running + transvenous pacing (capture often poor) + early MCS planning(life-threatening)
  • Propranolol OD with QRS widening >120 ms — Na-channel (membrane-stabilising) effect; analogous to TCA OD; maximize bicarbonate + lipid emulsion; pre-arrest harbinger(life-threatening)
  • Refractory shock / pre-arrest despite HIE + glucagon + calcium + bicarbonate + lipid emulsion in severe lipophilic BB OD (esp propranolol) — emergent VA-ECMO bridge(life-threatening)
  • Intentional BB OD with concurrent CCB ingestion — highest mortality phenotype; synergistic toxicity (combined β + Ca-channel blockade); prophylactic VA-ECMO team activation; psych safety planning post medical clearance(life-threatening)
  • Sotalol OD with QTc >500 ms ± polymorphic VT — class III effect; Mg + overdrive pacing + emergent hemodialysis (sotalol is dialyzable; low Vd)(life-threatening)

5. Follow-up

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

6. Sources

Guideline: AACT 2017 BB Toxicity Expert Consensus (PMID 29022414); Engebretsen 2011 HIE in BB/CCB OD (PMID 21626672); SCAI 2022 CS staging (Naidu PMID 35718438); ACMT HIE position statement; AHA 2020 ACLS

  1. pubmed.ncbi.nlm.nih.gov/29022414
  2. pubmed.ncbi.nlm.nih.gov/21626672
  3. pubmed.ncbi.nlm.nih.gov/25498415