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cardio.hypertensive-emergency.cocaine-sympathetic-crisis.v1

Cocaine / sympathomimetic hypertensive crisis (alpha-driven HTN + tachycardia + coronary vasospasm)

cardiologyacuteadultacuteinpatienttransitionoutpatient
Start encounter →Print handoutPRODUCTION

Phase E variant of cardio.hypertensive-emergency.core.v1 — narrowed to cocaine / sympathomimetic-driven HTN crisis. Inherits HTN-emergency framework + workup arc from parent; specializes for toxidrome-aware pharmacology: benzodiazepine FIRST for sympatholysis (AHA 2008 Class I), then NTG, then phentolamine for alpha-reversal (Boehrer 1993), then CCB. AVOID β-blocker monotherapy in acute cocaine period — Lange NEJM 1989 + AHA 2008 + ACC/AHA 2025 ACS Class III (unopposed alpha vasoconstriction with worsened HTN + coronary vasospasm). Concurrent rule-out for cocaine MI (6% rate per Hollander NEJM 2008), aortic dissection (4-5× risk), ICH, Takotsubo. Long-term SUD treatment integration (matrix model + contingency management); β-blocker safe AFTER cocaine clearance. Manifest pointer reuses cardio.hypertensive-emergency.core.v1 manifest. Design-brief pointer reuses parent (cocaine-specific differences documented inline). Status INTEGRATED until terminology + RxNav-validated drug codes are reconciled. Authored 2026-05-14 by shard-06-cardio-acute as part of HTN emergency Phase E variant batch (wave 8).

Entry points (3)

  • history
    Cocaine, methamphetamine, MDMA, or sympathomimetic use within 24-72 h + SBP ≥180 / DBP ≥120 (AHA 2008 PMID 18391116; Hollander NEJM 2008 PMID 18172180)
    cocaine_or_sympathomimetic_use_within_24h
  • symptom
    Hypertensive crisis + tachycardia + diaphoresis + agitation + dilated pupils + chest pain — sympathomimetic toxidrome
    sympathetic_crisis_constellation
  • imaging
    ECG ischemia/STEMI pattern in setting of acute cocaine/stimulant use — cocaine-associated ACS pathway
    ecg_ischemia_with_stimulant_history

Required inputs (12)

  • agerequired
    demographic • used at CONTEXT
    Younger patients overrepresented; older users have higher coronary disease prevalence + worse outcomes (Hollander NEJM 2008)
  • sbprequired
    vital • used at RED_FLAGS
    Defines crisis threshold; drives titration of phentolamine + nitroglycerin
  • dbprequired
    vital • used at RED_FLAGS
    Component of MAP; DBP >120 supports emergency criterion + alpha-overdrive severity
  • heart_raterequired
    vital • used at RED_FLAGS
    Sympathetic-driven tachycardia + risk of demand ischemia; HR >120 plus HTN drives benzo-first decision
  • temperaturerequired
    vital • used at RED_FLAGS
    Hyperthermia (>40 C) signals sympathomimetic toxidrome severity / serotonin syndrome overlap → aggressive cooling
  • stimulant_exposure_historyrequired
    history • used at CONTEXT
    Confirms sympathomimetic etiology — cocaine/meth/MDMA/MAOI-tyramine/pseudoephedrine — drives AVOID list (no β-blocker monotherapy)
  • chest_pain_assessmentrequired
    symptom • used at INITIAL_WORKUP
    Cocaine-associated MI in up to 6% of cocaine-chest-pain ED visits (Hollander NEJM 2008 PMID 18172180); drives troponin + ECG cascade
  • ecg_12_leadrequired
    imaging • used at INITIAL_WORKUP
    STEMI pattern, ischemia, QTc prolongation, demand ischemia from tachycardia all relevant
  • troponinrequired
    lab • used at INITIAL_WORKUP
    Cocaine-associated MI rate up to 6%; serial troponin q3-6h × 2 to rule out (Hollander NEJM 2008)
  • urine_drug_screenrequired
    lab • used at INITIAL_WORKUP
    Confirms cocaine (3-d window for benzoylecgonine), amphetamine class, fentanyl/opioid co-ingestion
  • creatininerequired
    lab • used at INITIAL_WORKUP
    Rhabdomyolysis + AKI common in stimulant toxidrome → drives volume resuscitation + drug dosing
  • creatine_kinaserequired
    lab • used at INITIAL_WORKUP
    Rhabdomyolysis screen — common in stimulant + hyperthermia + agitation; CK >5000 → aggressive IV fluids

12-phase flow (10)

  1. 1FRAME
    Cocaine / sympathomimetic HTN crisis = alpha-adrenergic-driven vasoconstriction + tachycardia + coronary vasospasm + risk of MI/stroke/aortic dissection. Pharmacology pivot: BENZODIAZEPINE FIRST for sympatholysis; AVOID β-blocker monotherapy (unopposed alpha → worse HTN + vasospasm — Lange NEJM 1989 PMID 2522592; AHA 2008 PMID 18391116; ACC/AHA 2025 ACS Class III). Route to parent engine for shared HTN-emergency arc; this dossier owns the toxidrome-aware pharmacology + ACS rule-out.
    inputs: sbp, dbp, heart_rate, stimulant_exposure_history
    advance: sympathomimetic etiology confirmed by history or UDS
  2. 2ENTRY
    Recognize toxidrome (HTN + tachy + diaphoresis + agitation + dilated pupils + hyperthermia); ECG within 10 min if chest pain; benzo-first sympatholysis
    inputs: age, sbp, temperature
    advance: IV access + cardiac monitor + benzo administered if agitated
  3. 3CONTEXT
    Stimulant exposure timeline + dose + coingestants (alcohol → cocaethylene; opioids → fentanyl-laced supply; MAOI; SSRI → serotonin syndrome overlap); prior CV history; prior MI on cocaine
    inputs: age
    advance: context complete
  4. 4RED_FLAGS
    Concurrent STEMI/ACS → cocaine-associated MI pathway (PCI safe; thrombolytics historically debated due to ICH risk in cocaine HTN — but generally permitted if PCI unavailable per AHA 2008); aortic dissection (cocaine increases risk 4-5×); ICH (cocaine + HTN drives ICH risk); hyperthermia >40 C → aggressive cooling + benzo; rhabdomyolysis + AKI → IV fluids
    inputs: sbp, temperature, chest_pain_assessment
    actions: htn_emergency, cocaine_chest_pain, acs_pathway
    advance: RED flags screened + life-threats addressed
  5. 5INITIAL_WORKUP
    ECG q15 min × 1h if chest pain; serial troponin q3-6h × 2; UDS; CMP + Mg + CK; CXR (aortic disease, pulm edema); CT head if neuro deficit; CT angio chest if dissection concern (cocaine HTN is dissection risk factor)
    inputs: ecg_12_lead, troponin, urine_drug_screen, creatinine, creatine_kinase
    actions: panel.cardiac, panel.renal
    advance: workup documented + ACS/dissection/ICH ruled in/out
  6. 6BRANCHING_WORKUP
    If STEMI → cath lab (cocaine-associated MI is treated like standard ACS but β-blocker still avoided acutely); if dissection → CTA chest + emergent CT surgery + parent aortic-dissection HTN engine; if ICH → CT head + neuro pathway
    advance: syndrome-specific pathway activated
  7. 7TREATMENT
    STEP 1: Benzodiazepine IV (lorazepam 1-2 mg or diazepam 5-10 mg, repeat q5-10 min) — sympatholytic + reduces HTN + reduces tachy + treats agitation/seizure (AHA 2008 Class I PMID 18391116). STEP 2: If BP still elevated — nitroglycerin IV (5-200 mcg/min titrate) for vasodilation + coronary vasodilation. STEP 3: Phentolamine 1-5 mg IV q5-15 min — pure alpha-blocker reverses cocaine alpha-vasoconstriction + reverses coronary vasospasm (Boehrer Am J Med 1993 PMID 8390052). STEP 4: CCB acceptable — verapamil 5-10 mg IV or diltiazem (Negus Circulation 1994). LABETALOL is debated — mixed alpha-beta blocker theoretically OK but small β-effect may cause unopposed alpha; AHA 2008 says reasonable but not first-line; AVOID pure β-blockers (metoprolol, esmolol, propranolol) — Lange NEJM 1989 documented propranolol potentiates coronary vasoconstriction.
    inputs: sbp, dbp, heart_rate
    advance: IV agent titrated to SBP <160; sympathetic features improving; agitation controlled
  8. 8DISPOSITION
    ICU / monitored bed for q15 min BP + telemetry; repeat ECG q4h × 12-24 h; serial troponin × 2; observation 6-12 h minimum if cocaine chest pain rule-out per Hollander pathway
    advance: monitored bed assigned + ACS rule-out complete
  9. 9MONITORING
    Continuous ECG + telemetry; q15-30 min BP; serial troponin q3-6h × 2; CK q6h if rhabdomyolysis; UOP; mental status
    inputs: sbp, heart_rate
    actions: panel.cardiac
    advance: BP at target + ACS ruled out + sympathetic features resolved
  10. 10FOLLOWUP
    Substance use disorder counseling + treatment (matrix model for stimulant, contingency management evidence-based per Stitzer 2010); cardiology follow-up if MI occurred (high-risk for recurrent cocaine-MI); echo if Takotsubo suspected (cocaine is precipitant); BP regimen if persistent HTN; opioid agonist therapy if fentanyl-laced supply suspected; harm reduction
    advance: SUD treatment booked + cardiology follow-up + BP regimen if needed