3.1 Acute Coronary Syndrome & Myocardial Infarction

Acute Coronary Syndrome: The Ischemic Spectrum

Acute coronary syndrome (ACS) describes a continuum of myocardial ischemia caused by acute atherosclerotic plaque rupture with thrombus formation in a coronary artery. The CCRN tests ACS as three overlapping diagnoses distinguished by the electrocardiogram (ECG) and cardiac troponin: unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).

• Unstable angina (UA) — ischemic chest pain at rest or in a crescendo pattern; the ECG may show ST depression or T-wave inversion, but troponin is negative. There is ischemia without measurable myocardial cell death.
• NSTEMI — a partial (subtotal) occlusion that produces necrosis. Troponin is positive; the ECG shows ST depression and/or T-wave inversion but no persistent ST elevation.
• STEMI — a complete, transmural occlusion. Troponin is positive and the ECG shows new ST elevation or a new left bundle branch block. STEMI is a time-critical emergency requiring immediate reperfusion.

ST-Elevation Criteria and ECG Localization

STEMI is defined as ST elevation greater than or equal to 1 mm in two contiguous leads, except in V2-V3, where the thresholds are greater than or equal to 2 mm in men 40 and older, 2.5 mm in men under 40, and 1.5 mm in women (Fourth Universal Definition of MI). The lead pattern localizes the infarct and predicts the culprit vessel — a classic CCRN mapping item.

The inferior clue is tested repeatedly: ST elevation in II, III, and aVF points to the RCA. Because the RCA also supplies the SA and AV nodes and the right ventricle, inferior STEMI carries a high risk of RV infarction and bradydysrhythmias/heart block. Obtain right-sided leads (V4R) with every inferior MI; ST elevation in V4R confirms RV involvement.

Biomarkers

Cardiac troponin (I or T) is the most sensitive and specific marker of myocardial injury. High-sensitivity troponin begins to rise within 1-3 hours, peaks at 12-24 hours, and may remain elevated 7-14 days. Serial sampling with a 0/1-hour or 0/3-hour protocol improves early rule-in/rule-out. A single value is never diagnostic alone; a rise and/or fall in the appropriate clinical context is required. CK-MB has been largely supplanted by troponin but normalizes faster, which makes it useful for detecting re-infarction.

Clinical Presentation and Risk Stratification

Classic ACS presents with substernal chest pressure radiating to the left arm or jaw, accompanied by diaphoresis, nausea, and dyspnea. Atypical presentations are common and must never be dismissed in women, older adults, and patients with diabetes, who may report only fatigue, epigastric discomfort, or isolated dyspnea (a silent MI). For NSTEMI and unstable angina, validated risk scores such as TIMI and GRACE stratify short-term risk of death and re-infarction; higher scores favor an early invasive strategy with angiography within 24 hours. A rising troponin, dynamic ECG changes, hemodynamic instability, or refractory ischemia all push toward urgent catheterization rather than a conservative ischemia-guided approach.

Pharmacologic Therapy: Beyond MONA

The classic mnemonic MONA (Morphine, Oxygen, Nitroglycerin, Aspirin) is outdated in its priority order. Current early management is:

• Aspirin 162-325 mg chewed immediately — the single most important early drug.
• P2Y12 inhibitor — ticagrelor, prasugrel, or clopidogrel (dual antiplatelet therapy).
• Anticoagulation — unfractionated heparin or a low-molecular-weight heparin.
• Nitroglycerin for ischemic pain/hypertension — contraindicated in RV infarction, hypotension (SBP under 90), or recent phosphodiesterase-5 inhibitor (sildenafil) use.
• High-intensity statin started early.
• Beta-blocker within 24 hours only if there is no heart failure, shock, bradycardia, or high-degree block.
• Oxygen only when SpO2 is below 90% — routine oxygen provides no benefit and may harm.
• Morphine is now reserved for refractory pain because it can blunt and delay P2Y12 absorption.

Reperfusion — The Clock That Matters

For STEMI, reperfusion is time-driven:

• Primary PCI (percutaneous coronary intervention) is preferred, with a door-to-balloon goal of 90 minutes or less (120 minutes or less if the patient must be transferred to a PCI-capable center).
• Fibrinolysis is used when PCI cannot be achieved within 120 minutes, with a door-to-needle goal of 30 minutes or less. Absolute contraindications include prior intracranial hemorrhage, ischemic stroke within 3 months, active internal bleeding, and suspected aortic dissection.

NSTEMI and UA are managed with an early invasive or ischemia-guided strategy; fibrinolytics are never given for NSTEMI.

Complications

Mechanical and electrical complications the CCRN emphasizes: cardiogenic shock (the leading cause of in-hospital MI death), papillary muscle rupture causing acute mitral regurgitation and flash pulmonary edema, ventricular septal rupture (new harsh holosystolic murmur and step-up in oxygen saturation), free-wall rupture with tamponade, LV aneurysm, pericarditis (including late Dressler syndrome), and reperfusion or ischemic dysrhythmias. RV infarction presents with the triad of hypotension, clear lungs, and elevated jugular venous pressure; because the failing RV is preload-dependent, treat with fluid loading and avoid nitrates, diuretics, and morphine. A frequent trap: giving nitroglycerin for chest pain in an inferior/RV STEMI, which collapses preload and precipitates profound hypotension.