Perioperative myocardial ischemia and infarction

Why examiners ask this

Ischemia is the examiner's favorite way to test whether you understand supply and demand rather than recite it. The stem gives a 68-year-old with hypertension and a remote stent having a colectomy; the ST segments sag at the moment of a hypotensive episode, and the examiner wants to see you treat the physiology, communicate, and decide whether the operation continues. It stresses application of knowledge and judgment, and the postoperative chest pain inject tests adaptability.

The 60-second answer

Decision points and the "why"

• Which leads I monitor — V5 catches about 75% of ischemic events and II adds the inferior wall and the rhythm; together they detect roughly 80–90%. I set the ST analysis to the diagnostic filter mode, because the monitor mode filters out the ST segment I need.
• Treat the cause before the ST segment — most intraoperative ischemia is demand-driven (type 2 infarction: supply-demand mismatch from tachycardia, hypotension, anemia, hypoxemia), rather than type 1 plaque rupture.¹ Fixing the number without fixing the cause invites the next episode. I change my approach if the ST segments elevate with a stable heart rate and pressure, because that suggests plaque rupture or spasm and needs cardiology.
• Beta-blockade with esmolol — heart rate is the dominant determinant of oxygen demand and the only variable that also shortens diastolic filling time. I titrate 10–20 mg boluses to a rate in the 60s and stop if the pressure falls below the patient's baseline minus 20%.
• Nitroglycerin after pressure is restored — it reduces preload and wall tension and dilates epicardial vessels, but it drops the diastolic pressure that perfuses the subendocardium. I start at 0.5 mcg/kg/min only with a systolic above 100 mmHg.
• Transfusion threshold of 8 g/dL — in a patient with active ischemia I transfuse earlier than the 7 g/dL I use for everyone else, because oxygen delivery is the problem; in acute infarction I do not let it drift lower and I individualize upward.
• Whether to continue — I weigh the surgical stage against the ischemic burden. A colectomy can be closed; an open aneurysm cannot be abandoned. I state the plan to the surgeon rather than asking for permission.
• TEE if I have it — a new regional wall-motion abnormality appears before the ECG changes; it also separates hypovolemia from pump failure in a hypotensive patient.

The complication they will inject

In the PACU the patient reports chest pressure, the pressure is 85/50, and the ECG shows 3 mm ST elevation in II, III and aVF. This is an inferior ST-elevation infarction with likely right ventricular involvement. I recognize it as an occlusion, not a demand problem, so beta-blockers and nitroglycerin are the wrong drugs. Inferior ST elevation with hypotension, distended neck veins and clear lungs points to right ventricular infarction.¹ I give oxygen, aspirin 162–325 mg chewed,¹ a careful fluid bolus for the right ventricle, and norepinephrine for the pressure. I call cardiology for primary percutaneous intervention, which is preferred for STEMI when timely,¹ because this patient is hours out of bowel surgery and major surgery within 3 weeks is a contraindication to fibrinolysis that the bleeding risk makes effectively absolute here.² I discuss heparin and a P2Y12 inhibitor with the surgeon and cardiologist together, accepting bleeding risk because the alternative is a dead myocardium. I send troponin, place an arterial line, and move him to a monitored bed with defibrillator pads on, because inferior infarcts cause bradycardia and block.

Pitfalls that cost points

• Reaching for nitroglycerin while the patient is hypotensive.
• Saying "I would give a beta-blocker" without a drug, a dose and an endpoint.
• Treating a 1 mm ST change as noise because the surgeon is busy; the examiner wants you to act and communicate.
• Listing lead V5 without saying why it matters.
• Giving fibrinolytics to a fresh surgical patient; the answer is the catheterization lab.

Rapid-why

Q: Why is the subendocardium the first to become ischemic? A: It is perfused only in diastole and sits under the highest wall tension, so tachycardia and high end-diastolic pressure hit it first.

Q: Why does ST depression suggest demand ischemia and ST elevation suggest occlusion? A: Depression reflects subendocardial ischemia from supply-demand mismatch; elevation reflects transmural ischemia from an occluded vessel.

Q: Why not just transfuse to a hemoglobin of 10 g/dL? A: Liberal transfusion adds volume load and transfusion-related morbidity; in acute infarction the large MINT trial did not show a clear reduction in death or reinfarction with a 10 g/dL threshold, though the trend favored it, so I avoid falling below 8 and decide case by case.

Q: What is myocardial injury after non-cardiac surgery, and why does it matter? A: A postoperative troponin rise above the 99th percentile from ischemia, usually without symptoms; it is linked to higher 30-day mortality,³ so postoperative troponins are reasonable in high-risk patients,⁴ and those with MINS get outpatient cardiology follow-up.³ In the VISION cohort roughly one in ten died within 30 days.

Numbers to know

Links

• Preoperative cardiac evaluation for non-cardiac surgery, Recent MI, coronary stents and antiplatelet therapy, Intraoperative hypotension: differential and management, Perioperative hypertension, Intraoperative cardiac arrest
• Atlas: Monitor atlas: perioperative cardiac events; Ventricular function and wall motion
• ACC/AHA guideline on perioperative cardiovascular management for non-cardiac surgery; ACC/AHA guideline on acute coronary syndromes