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Intraop MI — Type 1 vs Type 2 Management
TEXTCrisis Management · 6 min read
The intraop MI that matters most is the one nobody recognized — periop mortality is twice out-of-hospital MI because bleeding constraints limit the standard playbook.
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3 min read6 sectionsType 1 vs Type 2 — Universal Definition framework
Type 2 is myocardial injury from oxygen demand/supply mismatch WITHOUT acute plaque event — tachycardia, hypotension, hypoxia, anemia, vasospasm, hypertensive crisis.
Intraop MI is predominantly Type 2: the stress + sympathetic discharge + anemia + hypotension + reversal of antiplatelet/anticoagulant therapy combine to push a marginal coronary bed into ischemia.
Distinguishing them changes management: Type 1 needs urgent revascularization, Type 2 needs correction of the upstream driver.
Recognition — intraop signs
ST depression >1 mm or new ST elevation >1 mm in two contiguous leads = ischemia until proven otherwise.
New T-wave inversion, ventricular ectopy, new arrhythmia, or unexplained hemodynamic instability are softer signs.
TEE if available: new regional wall motion abnormality is the most sensitive intraop marker — appears before ECG changes.
Troponin (high-sensitivity) drawn intraop + repeated at 3 + 6 hr establishes the diagnosis post-hoc.
Type 2 typically has lower peak troponin than Type 1.
Immediate intraop response
100% O₂.
Restore MAP to 80-100 mmHg with vasopressor (norepinephrine 1st line) + fluid + blood as indicated.
Control heart rate to <70 with esmolol 10-30 mg boluses or infusion, or labetalol 5-10 mg, unless hypotensive.
Correct anemia — transfuse to Hgb >8-9 g/dL with active ischemia.
Nitroglycerin 25-50 mcg boluses or infusion 0.25-1 mcg/kg/min reduces preload + dilates coronaries if MAP supports it.
Heparin bolus + infusion for confirmed Type 1 — but only after the surgeon agrees the bleeding risk is acceptable.
Intra-aortic balloon pump or Impella for cardiogenic shock from confirmed Type 1.
Anti-thrombotic decision-making intraop
Type 1 needs dual antiplatelet (aspirin + P2Y12 inhibitor) + anticoagulation + cath lab.
The surgical wound usually prohibits all three.
The decision tree: (1) Is the surgery near completion?
Finish + transfer to cath lab.
Then expedite closure + revascularize.
Continue + treat as Type 2 + revascularize after.
ASA 162-325 mg can usually be given even with surgical bleeding.
P2Y12 + heparin require explicit surgical sign-off.
Coordinate with cardiology + cardiothoracic surgery early — don't wait for cath lab handoff to start the conversation.
Post-op cath + the periop mortality picture
Door-to-balloon time targets apply when feasible.
Bare-metal stents historically preferred over drug-eluting for periop indication because dual antiplatelet duration is shorter (~1 month vs 6-12 months) — though modern second-generation DES with abbreviated DAPT protocols have narrowed the gap.
Periop MI 30-day mortality is 15-25%, vs 5-10% for community-onset MI.
- delayed recognition
- bleeding constraints limiting standard therapy
- comorbid surgical illness
ICU admission, serial troponins, telemetry, echo to assess LV function + structural complications.
Prevention + risk stratification
2 mg/dL — ≥2 factors = elevated risk.Continue chronic beta-blockers; do NOT acutely initiate (POISE 2008 — acute high-dose metoprolol increased stroke + mortality despite reducing MI).
Statins continued (or initiated in vascular surgery).
Aspirin continuation is individualized per POISE-2; usually continued for high-risk patients undergoing non-neuraxial surgery.
Avoid hypotension <65 MAP — every 10-min episode below 65 increases MI + AKI risk in observational data.
Maintain normothermia + Hgb >8 in CAD patients.
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