Type-2 MI (demand ischemia, no plaque rupture)
Encounter flow
12/12 authoredCanonical 12-phase frame with authored status for this dossier.
Frame
Confirm type-2 MI per 4th UDMI 2018 PMID 30153967 — hsTn rise from supply-demand mismatch (sepsis, anemia, tachyarrhythmia, hypoxia, hypotension, severe HTN, drug toxicity) WITHOUT ischemic ECG, WITHOUT clinical ACS syndrome, WITHOUT plaque-rupture imaging
Type-2 vs type-1 distinction documented; trigger identified
Patient inputs (13)
Type-2 MI commoner in elderly + multimorbid; comorbidity-driven prognosis per DeFilippis PMID 30689349
Tachyarrhythmia trigger identification; rate control is primary therapy
Sepsis screening — most common type-2 trigger
Hypoxia trigger identification (e.g., COPD exacerbation, severe pneumonia, PE)
Known obstructive CAD changes management — selective cath if ongoing ischemia post-trigger correction per ACC/AHA 2025
0/1-h or 0/3-h ESC 2023 algorithm — pattern in type-2 typically slow rise/plateau without sharp peak; distinguishes from type-1 acute coronary thrombus
Hgb identifies anemia trigger; WBC for sepsis trigger; platelets for HIT/DIC
Sepsis / shock screening — drives source-control timing
Baseline kidney function — many type-2 triggers (sepsis, hypotension) cause concurrent AKI per KDIGO 2026
Confirm absence of ischemic ECG; detect sinus tachycardia / AF with RVR / strain pattern (PE)
Pneumonia, edema, PTX, dissection screen — many trigger sources
Hypotension itself a trigger (decreases coronary perfusion); also gates whether this is type-2 vs type-1 with cardiogenic shock
Sympathomimetic toxicity is a type-2 trigger; cocaine chest pain has unique workflow per AHA 2008
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Severity triggers (5)
- informationallife_threateningseptic_shock_with_type2_miSeptic shock + hsTn rise — type-2 MI driven by sepsis; sepsis bundle is primary therapy per SSC 2026Trigger could not be auto-evaluated — needs clinician judgement.
- informationalseveresevere_anemia_with_type2_miHgb <7 (or <8 with cardiac symptoms) + hsTn rise — type-2 MI driven by anemiaTrigger could not be auto-evaluated — needs clinician judgement.
- informationalseveretachyarrhythmia_demand_ischemiaAF with RVR / SVT / sustained VT with HR >150 + hsTn rise — type-2 MI from rate-driven demand ischemiaTrigger could not be auto-evaluated — needs clinician judgement.
- informationalseverereclassification_to_type1_acsNew dynamic ECG OR clinical ACS syndrome appears during type-2 admission — pathology now suggests type-1 plaque ruptureTrigger could not be auto-evaluated — needs clinician judgement.
- informationalseverecocaine_or_methamphetamine_chest_painCocaine or methamphetamine use with chest pain + hsTn rise — sympathomimetic toxicity drives type-2 MI; AVOID β-blockerTrigger could not be auto-evaluated — needs clinician judgement.
Workflow calculators
Run this disease's risk and dosing calculators inline.
Recommended regimen
Type-2 MI trigger-targeted therapy — antithrombotic only if known obstructive CAD per ACC/AHA 2025; treat the trigger primarily per 4th UDMI 2018 PMID 30153967- aspirincomorbidity specificantiplatelet_cox181 mg daily • PO • daily IF known obstructive CAD; otherwise NO antiplatelet for type-2 MI alonetriggers: type_2_mi_with_known_obstructive_cadACC/AHA 2025 — treat trigger primarily; antiplatelet only if obstructive CAD known. Type-2 MI 1-yr mortality 37% vs type-1 28% but driven by comorbidity not by deferred antithrombotic per DeFilippis PMID 30689349rxcui 1191
- atorvastatincomorbidity specificstatin_high_intensity40-80 mg daily • PO • daily IF known obstructive CAD or independent ASCVD indicationtriggers: type_2_mi_with_known_cad, independent_ascvd_indicationPROVE-IT PMID 15007110 — benefit established in type-1 ACS; type-2 use depends on CAD status not on type-2 event itself per ACC/AHA 2025rxcui 83367
- metoprolol_tartratecomorbidity specificbeta_blocker_cardioselective5 mg IV q5 min × 3 if AF with RVR + stable; OR PO 25 mg BID • IV/PO • titrate to HR <110triggers: af_with_rvr_demand_ischemia, sympathomimetic_trigger_excluding_cocaineRate control for tachyarrhythmia trigger; AVOID in cocaine-induced (unopposed alpha) per AHA 2008 cocaine chest pain pathwayrxcui 6918
- diltiazemcomorbidity specificcalcium_channel_blocker_non_dhp0.25 mg/kg IV bolus → 5-15 mg/h infusion • IV • continuous titrate to HR <110triggers: af_with_rvr_when_bb_contraindicated, cocaine_associated_tachycardia_with_cautionRate control alternative when β-blocker contraindicated; 2024 AHA AF guidelinerxcui 3443
- norepinephrinecomorbidity specificvasopressor0.05-0.5 µg/kg/min titrate MAP ≥65 • IV • continuoustriggers: septic_shock_trigger, distributive_shockSOAP-II first-line vasopressor; restoring perfusion corrects demand-supply mismatch driving type-2 MIrxcui 7512
outpatient playbook — drug actions (3)
- 1. optimise comorbidity GDMTper comorbidity • PO • as scheduledtrigger: Comorbidity optimisationComorbidity drives type-2 mortality per DeFilippis PMID 30689349
- 2. add aspirin 81 + statin if stress test confirms obstructive CADaspirin 81 + atorvastatin 40-80 • PO • dailytrigger: Newly identified obstructive CADACC/AHA 2025 secondary prevention if CAD confirmed
- 3. address trigger recurrence preventionrate control for AF (BB / NDCCB) / iron supplementation / preventive abx if recurrent UTI / inhaler optimisation if COPD • PO/SC • as scheduledtrigger: Trigger pattern identifiedPrevent recurrent demand ischemia via underlying disease control
Auto-drafted A&P note
outpatientSubjective
- Possible entry pathways: hsTn rise/fall in patient with sepsis, severe anemia, tachyarrhythmia, hypoxia, hypotension, severe HTN, or drug toxicity (4th UDMI 2018); hsTn elevation WITHOUT ischemic ECG and without clinical ACS syndrome — supports type-2 vs type-1; Sepsis or septic shock with hsTn rise — most common type-2 trigger; treat sepsis bundle first per SSC 2026.
Objective
- No vitals, labs, or imaging entered for this encounter.
Assessment
**Type-2 MI (demand ischemia, no plaque rupture)** (cardio.nstemi.type2.v1). Phenotype framing: Type-2 MI vs type-1 NSTEMI (plaque rupture) vs Takotsubo vs myocarditis vs strain (PE, severe HTN) per 4th UDMI 2018 PMID 30153967 Scope: Confirm type-2 MI per 4th UDMI 2018 PMID 30153967 — hsTn rise from supply-demand mismatch (sepsis, anemia, tachyarrhythmia, hypoxia, hypotension, severe HTN, drug toxicity) WITHOUT ischemic ECG, WITHOUT clinical ACS syndrome, WITHOUT plaque-rupture imaging No severity triggers fired against current inputs.
Plan
Regimen axis: **Type-2 MI trigger-targeted therapy — antithrombotic only if known obstructive CAD per ACC/AHA 2025; treat the trigger primarily per 4th UDMI 2018 PMID 30153967**. 1. aspirin 81 mg daily PO daily IF known obstructive CAD; otherwise NO antiplatelet for type-2 MI alone (antiplatelet_cox1, comorbidity specific) — ACC/AHA 2025 — treat trigger primarily; antiplatelet only if obstructive CAD known. Type-2 MI 1-yr mortality 37% vs type-1 28% but driven by comorbidity not by deferred antithrombotic per DeFilippis PMID 30689349 2. atorvastatin 40-80 mg daily PO daily IF known obstructive CAD or independent ASCVD indication (statin_high_intensity, comorbidity specific) — PROVE-IT PMID 15007110 — benefit established in type-1 ACS; type-2 use depends on CAD status not on type-2 event itself per ACC/AHA 2025 3. metoprolol_tartrate 5 mg IV q5 min × 3 if AF with RVR + stable; OR PO 25 mg BID IV/PO titrate to HR <110 (beta_blocker_cardioselective, comorbidity specific) — Rate control for tachyarrhythmia trigger; AVOID in cocaine-induced (unopposed alpha) per AHA 2008 cocaine chest pain pathway 4. diltiazem 0.25 mg/kg IV bolus → 5-15 mg/h infusion IV continuous titrate to HR <110 (calcium_channel_blocker_non_dhp, comorbidity specific) — Rate control alternative when β-blocker contraindicated; 2024 AHA AF guideline 5. norepinephrine 0.05-0.5 µg/kg/min titrate MAP ≥65 IV continuous (vasopressor, comorbidity specific) — SOAP-II first-line vasopressor; restoring perfusion corrects demand-supply mismatch driving type-2 MI Setting playbook (outpatient) — Long-term type-2 MI surveillance — outpatient cardiology with stress test or CCTA result; comorbidity optimisation; transition to chronic disease management 6. optimise comorbidity GDMT per comorbidity PO as scheduled — Comorbidity optimisation (Comorbidity drives type-2 mortality per DeFilippis PMID 30689349) 7. add aspirin 81 + statin if stress test confirms obstructive CAD aspirin 81 + atorvastatin 40-80 PO daily — Newly identified obstructive CAD (ACC/AHA 2025 secondary prevention if CAD confirmed) 8. address trigger recurrence prevention rate control for AF (BB / NDCCB) / iron supplementation / preventive abx if recurrent UTI / inhaler optimisation if COPD PO/SC as scheduled — Trigger pattern identified (Prevent recurrent demand ischemia via underlying disease control) Non-pharmacologic actions: - Reinforce daily BP + symptom log - Cardiac rehab if CAD confirmed - Smoking cessation reinforcement - Mediterranean / DASH diet counseling if CAD or HTN AVOID / contraindication checks: - Antiplatelet not routine in type2 mi without known obstructive cad (ACC/AHA 2025) - Beta blocker block if cocaine induced (AHA 2008 — unopposed alpha) - Beta blocker block if cardiogenic shock (ACC/AHA 2025) - Transfuse to mint threshold (Carson NEJM 2023 — restrictive Hgb 7 8 in cardiac disease)
Monitoring
Regimen monitoring: - Trend hsTn to peak then normalisation (confirms trigger correction) - Serial lactate q2-4 h if shock trigger - Continuous ECG to detect new ischemic changes that would re-classify to type-1 - Hgb q12 h if anemia trigger; transfuse to MINT threshold per Carson NEJM 2023 - Trigger-specific (cultures + source control for sepsis; toxicology for drug; thyroid for storm) Setting (outpatient) monitoring: - BMP at week 4 - Lipid panel — if obstructive CAD, target LDL <70 (or <55 very-high-risk) - A1c at 3 mo if newly diagnosed DM2 - Trigger-specific (Hgb trend, AF rhythm, HF NYHA) Follow-up plan: Outpatient cardiology + stress test or CCTA if recovers — to detect underlying obstructive CAD that contributed to demand-supply ischemia. Optimise comorbidities (sepsis recovery, HF, CKD, DM) - Close-out criterion: Outpatient cardiology + stress workup booked Monitoring phase: Serial hsTn to confirm trigger correction normalises trend; trend lactate, vitals, trigger-specific markers; re-screen ECG for new ischemic changes that would re-classify to type-1
Disposition
Current setting: outpatient — Long-term type-2 MI surveillance — outpatient cardiology with stress test or CCTA result; comorbidity optimisation; transition to chronic disease management Disposition criteria: - Formal handoff to chronic CAD engine if obstructive CAD confirmed; otherwise long-term comorbidity management with cardiology surveillance Escalation triggers (move to higher acuity): - Recurrent chest pain → ED for serial hsTn + ECG - Recurrent trigger → trigger-specific re-eval - Stress test positive for obstructive CAD → cardiology + cath consideration
Earlier-Return Triggers
Return-precaution thresholds (watch for): - [LIFE_THREATENING] Septic shock + hsTn rise — type-2 MI driven by sepsis; sepsis bundle is primary therapy per SSC 2026 - [SEVERE] Hgb <7 (or <8 with cardiac symptoms) + hsTn rise — type-2 MI driven by anemia - [SEVERE] AF with RVR / SVT / sustained VT with HR >150 + hsTn rise — type-2 MI from rate-driven demand ischemia
Citations
- 4th Universal Definition of MI 2018 (Thygesen Circulation 2018, PMID 30153967); 2025 ACC/AHA ACS Guideline (Rao); ESC 2023 NSTE-ACS Guideline (Byrne, PMID 37622670) [PMID:30153967](https://pubmed.ncbi.nlm.nih.gov/30153967/) - Cited evidence (PMID 30689349) [PMID:30689349](https://pubmed.ncbi.nlm.nih.gov/30689349/) - Cited evidence (PMID 37622670) [PMID:37622670](https://pubmed.ncbi.nlm.nih.gov/37622670/) - Cited evidence (PMID 34669377) [PMID:34669377](https://pubmed.ncbi.nlm.nih.gov/34669377/) - Cited evidence (PMID 19720857) [PMID:19720857](https://pubmed.ncbi.nlm.nih.gov/19720857/) Last reconciled with current guidelines: 2026-05-14.
- 4th Universal Definition of MI 2018 (Thygesen Circulation 2018, PMID 30153967); 2025 ACC/AHA ACS Guideline (Rao); ESC 2023 NSTE-ACS Guideline (Byrne, PMID 37622670) — PMID:30153967
- Cited evidence (PMID 30689349) — PMID:30689349
- Cited evidence (PMID 37622670) — PMID:37622670
- Cited evidence (PMID 34669377) — PMID:34669377
- Cited evidence (PMID 19720857) — PMID:19720857