What is the management of an intraoperative myocardial infarction (MI)?

Management of Intraoperative Myocardial Infarction

When MI occurs during surgery, immediately optimize coronary perfusion by managing heart rate, blood pressure, and ventricular filling pressures, while simultaneously determining if this represents acute coronary occlusion (Type 1 MI) requiring emergency revascularization versus supply-demand mismatch (Type 2 MI) requiring correction of precipitating factors. 1, 2

Immediate Recognition and Hemodynamic Stabilization

Optimize determinants of coronary arterial perfusion immediately: target heart rate control (ideally 60-70 bpm), maintain diastolic/mean arterial pressure, and optimize right ventricular and left ventricular end-diastolic pressures to reduce perioperative myocardial ischemia and infarction. 1

• Obtain 12-lead ECG immediately to identify ST-segment elevation (≥1 mV in contiguous leads) or new Q waves, which indicate acute coronary occlusion. 2
• Measure troponin immediately, as troponin elevation with appropriate clinical context is more diagnostic than isolated ECG changes. 2, 3
• Perform intraoperative transesophageal echocardiography for acute, persistent, and life-threatening hemodynamic disturbances that have not responded to treatment. 1

Critical Decision Point: Distinguish MI Type

The management strategy hinges entirely on distinguishing Type 1 MI (acute plaque rupture with thrombotic occlusion) from Type 2 MI (supply-demand mismatch). 2, 4

Type 1 MI (Acute Coronary Occlusion)

• Presents with ST-segment elevation, new Q waves, or regional wall motion abnormalities on echocardiography. 2
• Requires consideration for emergency cardiac catheterization and PCI if feasible within 12 hours of symptom onset. 2, 4
• Fibrinolytic therapy is contraindicated in the immediate postoperative period due to substantial bleeding risk at the surgical site. 1

Type 2 MI (Supply-Demand Mismatch)

• More common in the perioperative setting, caused by tachycardia, hypertension, hypotension, anemia, or hypoxemia. 2, 4
• Focus on correcting the underlying precipitating cause rather than invasive intervention. 2, 4

Immediate Medical Therapy

Initiate standard medical therapy immediately regardless of MI type: 2, 4

• Aspirin: Loading dose immediately, continue indefinitely unless bleeding risk is prohibitive. 2, 4
• Beta-blockers: Start immediately to reduce myocardial oxygen demand through heart rate and blood pressure control, targeting heart rate 60-70 bpm and systolic BP >100 mmHg. 2, 4, 5
  • For hemodynamically stable patients with definite or suspected acute MI, administer metoprolol tartrate 5 mg IV bolus at 2-minute intervals for three doses (total 15 mg), monitoring blood pressure, heart rate, and ECG continuously. 5
  • Fifteen minutes after the last IV dose, initiate oral metoprolol 50 mg every 6 hours if full IV dose tolerated. 5
• Intravenous anticoagulation with heparin: Initiate to prevent further thrombosis. 2
• ACE inhibitors: Especially beneficial in patients with low ejection fractions or anterior infarctions. 2, 4
• Nitrates: For ongoing chest pain and to reduce preload. 3

Revascularization Decision Algorithm

For ST-Elevation MI or Hemodynamic Instability

Perform coronary angiography and PCI within 60 minutes from onset of symptoms if bleeding risk permits. 2, 4

• Emergency CABG is recommended when: 1
  • Primary PCI has failed or cannot be performed
  • Coronary anatomy is suitable for CABG
  • Persistent ischemia of a significant myocardial area at rest and/or hemodynamic instability refractory to nonsurgical therapy is present
• Emergency CABG is recommended for cardiogenic shock patients suitable for CABG irrespective of time interval from MI to onset of shock. 1

For Non-ST-Elevation MI

Optimize medical therapy first; reserve catheterization for patients with recurrent instability, ongoing ischemia, or heart failure. 2

Management of Mechanical Complications

Sudden hemodynamic deterioration with low cardiac output or pulmonary edema requires immediate consideration of mechanical defects. 2, 3

• Perform urgent transesophageal echocardiography to diagnose ventricular septal defect, acute mitral regurgitation, or free wall rupture. 2
• The presence of a new systolic murmur indicates possible ventricular septal rupture or mitral regurgitation. 1
• Emergency surgical repair (with or without CABG) is indicated in most cases of mechanical complications: 1
  • Ventricular septal rupture
  • Mitral valve insufficiency due to papillary muscle infarction/rupture
  • Free wall rupture
• Intra-aortic balloon pump can provide temporary circulatory support while preparing for surgery. 1

Surgical Procedure Considerations

If the surgical procedure is not immediately life-threatening, strongly consider aborting or abbreviating the operation to facilitate cardiac management. 2

• If bare metal stents are placed and further surgical revascularization is predictable, use bare metal stents instead of drug-eluting stents to avoid acute perioperative stent thrombosis. 1
• For patients requiring CABG with multivessel disease, treat the infarct-related lesion by PCI and perform CABG later in more stable conditions. 1

Common Pitfalls to Avoid

• Do not routinely use fibrinolytic therapy in the immediate postoperative period due to high bleeding risk at surgical sites; direct angioplasty is preferred if revascularization is needed. 1
• Do not perform emergency CABG after failed PCI in the absence of ischemia or threatened occlusion. 1
• Do not delay beta-blocker therapy in hemodynamically stable patients, as early administration reduces myocardial oxygen demand and improves outcomes. 5
• Do not assume all troponin elevations require invasive management; Type 2 MI from supply-demand mismatch is more common perioperatively and requires correction of precipitating factors. 2, 4

Post-Event Management Requirements

Before hospital discharge, all patients must have: 2, 3, 4

• Left ventricular function evaluated with echocardiography
• Standard post-infarction medical therapy prescribed: aspirin, beta-blockers, ACE inhibitors, and high-intensity statin therapy
• Risk stratification with exercise testing or pharmacological stress testing
• Aggressive cardiovascular risk factor modification including blood pressure control, smoking cessation, and management of diabetes and hyperlipidemia

Prognostic Context

Intraoperative nonfatal MI carries extremely high mortality risk (40-70% for symptomatic MI) and substantially increases risk of future cardiac events. 1, 2, 4 Patients presenting with perioperative MI have nearly one-third mortality or readmission rate at 30 days, highlighting the critical importance of aggressive acute management and close follow-up. 2, 4