Chest discomfort is the most common symptom of myocardial ischemia, and the initial evaluation of chest pain or classic cardiac symptoms (eg, radiation to neck, jaw, or arm; diaphoresis; nausea) should differentiate angina, acute coronary syndrome (ACS), or noncardiac chest pain. Electrocardiographic (ECG) changes can help differentiate cardiac from noncardiac origins. ECG changes without typical anginal symptoms (“silent” ischemia) are common, especially in patients with diabetes, are older adults, or postoperative. Typical angina may be blunted by postoperative pain medications including epidural analgesia or postoperative sedation.

1. Angina Pectoris is retrosternal tightness, pressure, or pain that occurs at rest or with physical or emotional stress, lasting up to 10 minutes. It can radiate to the back, jaw, arm, or shoulder, usually on the left. Angina usually reflects compromise of at least one epicardial artery and implies ischemia but not necessarily myocardial necrosis. Symptoms also include nausea, vomiting, diaphoresis, and shortness of breath. Angina may present in valvular heart disease, hypertrophic cardiomyopathy, or uncontrolled HTN. The Canadian Cardiovascular Society Classification System grades angina severity from Class I (ordinary physical exertion does not cause angina) to Class IV (angina with minimal exertion or at rest).
1. Stable angina demonstrates a pattern that has not changed in frequency, duration, or ease of relief for several months. Predictable symptoms present with exertion and abate with rest. A fixed coronary atheroma with a fibrous cap is generally to blame.
2. Variant (Prinzmetal) angina occurs at rest, is often worse in the morning, lasts several minutes, and is accompanied by transient ST-segment elevation and/or ventricular dysrhythmias. It can be induced by exercise, stemming from vasospasm in a coronary artery that may not have significant atheromatous disease. Smoking is a major risk factor. Hyperventilation, hypocalcemia, cocaine, pseudoephedrine, and ephedrine have also been implicated.
2. Acute Coronary Syndromes (ACSs) are three conditions associated with acute myocardial ischemia secondary to poor myocardial blood supply: unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).
1. UA has a recent onset (2 months) with increasing frequency and intensity, and recurs at progressively lower levels of stress, or even at rest. Ten percent of patients have significant disease of the left main coronary artery, and approximately 20% of patients will suffer an acute MI within 3 months. Plaque rupture, platelet aggregation, thrombosis, and vasospasm are the underlying causes.
2. NSTEMI presents with ST-segment depressions or prominent T waves and may be associated with a rise in cardiac biomarkers. The management of NSTEMI focuses on improving oxygen (O₂) supply and reducing demand in at-risk myocardium, thus preventing progression of damage. It must always be borne in mind that a nondiagnostic ECG does not rule out MI.
3. STEMI reflects severe, possibly irreversible, damage to the myocardium. The joint 2018 European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation (ESC/ACCF/AHA/WHF) ECG criteria for diagnosis of STEMI are as follows:
1. New horizontal or downsloping ST depression greater than 0.5 mm in two contiguous leads, and/or:
2. T inversion greater than 1 mm in two contiguous leads with prominent R wave or R/S ratio greater than 1
3. The appearance of a new ST-segment elevation at the J point in two contiguous leads greater than 0.1 mV in all leads other than leads V₂ to V₃
4. For leads V₂ to V₃: greater than or equal to 2 mm in men 40 years or older, or greater than or equal to 1.5 mm in women regardless of age
5. Left bundle branch block (BBB), left ventricular (LV) hypertrophy, hyperkalemia, pericarditis, early repolarization, or paced rhythms complicate the diagnosis. Treatment focuses on timely reperfusion.
4. Noncardiac chest pain is not related to coronary ischemia, but life-threatening causes such as aortic dissection, pulmonary embolism, and pneumothorax should be ruled out immediately.
5. Perioperative MI is one of the major adverse cardiac events in major noncardiac surgery. Patients that suffer MI after surgery have a 15% to 25% risk of in-hospital death and a significant increase in 6-month morbidity and mortality. Although there is controversy over accepted definitions of perioperative MI, its incidence may be up to 6% in patients with CAD. Although MI is normally diagnosed on the basis of three criteria (chest pain, biomarker levels, and ECG changes), a perioperative MI may be obscured by pain or pain control techniques to the point of being “silent.” A high index of suspicion is critical and increased consideration should be given to the ECG and cardiac enzymes.
6. Acute MI is the term used when there is an acute myocardial injury with clinical evidence of acute myocardial ischemia and detection of a rise and/or fall of cardiac troponin (cTn) values, with at least one value greater than the 99th percentile and at least one of the following:
1. Symptoms of myocardial ischemia
2. New ischemic ECG changes
3. Development of pathologic Q waves
4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with ischemic etiology
5. Identification of a coronary thrombus by angiography or autopsy
3. Pathophysiology
1. Myocardial O₂supply-demand balance: Even at rest, the myocardium extracts O₂ maximally. During exertion, O₂ delivery must increase to meet demand. Myocardial ischemia and infarction occur when O₂ demand exceeds delivery.
1. Myocardial O₂supply is determined by the following:
1. Coronary blood flow is determined by the difference between transmural pressure and the aortic root pressure at the beginning of diastole. Because transmural resistance is low in diastole, myocardial blood flow is higher during this period. Tachycardia, which minimizes diastolic time, can thus induce ischemia. Normal coronaries compensate by dilating to increase blood flow 4- to 5-fold during exercise or stress. However, stenoses can reduce the coronaries’ ability to dilate and thus limit O₂ supply downstream. Polycythemia, hyperviscosity, and sickle cell disease may further compromise coronary flow.
2. O₂content is dependent on hemoglobin (Hgb) concentration and its saturation with O₂ (Sao₂), and to a lesser extent on dissolved O₂ concentration (see Chapter 2). An ideal Hgb level is not known but compensation through increased cardiac output (CO) occurs with anemia.
2. Myocardial O₂demand is influenced by the following:
1. Ventricular wall tension (T), which according to LaPlace’s Law is

   

where P is transmural pressure, R is ventricular radius, and h is wall thickness. Increase in pressure or radius will increase O₂ demand.

2. Heart rate (HR), which increases O₂ demand by increasing contractility. Tachycardia shortens diastole and maximal coronary perfusion in atherosclerotic vessels, also limiting O₂ supply. Hyperthyroidism, sympathomimetics (eg, cocaine), or anxiety can increase HR and O₂ demand.
3. Contractility, which is the intrinsic property of the myocyte to contract against a load, is proportional to O₂ demand. Positive inotropes (eg, digoxin, norepinephrine) increase O₂ demands of myocardium that might already be at risk.
4. Etiologies of myocardial O₂demand imbalance: Over 90% of myocardial ischemia and infarction result from atherosclerosis. Most perioperative MIs stem from abrupt, unpredictable partial or complete occlusion secondary to acute atherosclerotic plaque rupture. Other causes include coronary vasospasm or thromboembolism, vasculitis, trauma, valvular heart disease (eg, aortic stenosis), hypertrophic or dilated cardiomyopathies, and thyrotoxicosis.