2.2 Acute Coronary Syndromes: Unstable Angina, NSTEMI & STEMI

The ACS Continuum

Acute coronary syndrome (ACS) describes a spectrum of conditions caused by sudden disruption of coronary blood flow: unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). In the large majority of cases, the trigger is rupture or erosion of an atherosclerotic plaque, which exposes thrombogenic material and triggers platelet aggregation and thrombus formation, partially or completely occluding the artery. The degree and duration of occlusion — not just the underlying plaque burden — determines where a patient falls on the ACS spectrum and drives the urgency of treatment.

Recognizing the Presentation

Classic ACS presents with substernal chest pressure, often radiating to the jaw, neck, or left arm, associated with diaphoresis, nausea, and dyspnea. Progressive care nurses must also recognize atypical presentations, which are common in women, older adults, and patients with diabetes: epigastric pain, unexplained fatigue, dyspnea without chest pain, or syncope. Missing an atypical presentation delays recognition and reperfusion, so any new, unexplained change in a progressive care patient — especially one with cardiac risk factors — warrants a 12-lead ECG.

Differentiating by ECG and Troponin

The 12-lead ECG and serial troponin values, taken together, separate the three ACS diagnoses:

• STEMI: New ST-segment elevation in two or more contiguous leads (or, in the appropriate clinical context, a new left bundle branch block, which is treated as a STEMI equivalent) indicates a fully occluded coronary artery causing transmural injury. STEMI is a time-critical emergency requiring immediate cath lab activation.
• NSTEMI: ST-segment depression and/or T-wave inversion, without ST elevation, in a patient with a positive troponin, indicates a partially occluded artery causing subendocardial (non-transmural) injury.
• Unstable angina: The same ischemic symptoms and similar (or normal/nonspecific) ECG changes as NSTEMI, but troponin remains negative on serial testing — myocardial cell death has not yet occurred.

The ECG leads that show changes localize the injury to a coronary territory: ST elevation in II, III, and aVF points to an inferior wall injury (right coronary artery); V1–V4 points to an anterior/septal injury (left anterior descending artery); I, aVL, V5–V6 points to a lateral injury (circumflex artery). Reciprocal ST depression in the opposite leads strengthens the diagnosis, and ST depression isolated to V1–V2 with tall R waves can represent a posterior STEMI, which is easy to miss without posterior leads.

Troponin is the preferred biomarker because of its cardiac specificity and sensitivity. It begins rising roughly 3–6 hours after myocardial injury, so a single negative troponin drawn at presentation does not rule out ACS. Guidelines call for serial troponin measurements to capture the rise and confirm or exclude infarction. A rising-and-falling troponin pattern, along with clinical context, confirms acute myocardial injury and helps distinguish it from chronically elevated troponin (seen in renal failure or chronic heart failure).

Reperfusion Strategy

For STEMI, "time is muscle": the goal is emergent reperfusion, preferably primary percutaneous coronary intervention (PCI) with a door-to-balloon time under 90 minutes. If PCI is not available within about 120 minutes of first medical contact, fibrinolytic therapy is used instead, provided there are no contraindications (active bleeding, recent hemorrhagic stroke, aortic dissection). For NSTEMI, management is guided by risk stratification; high-risk patients typically go to the cath lab within an early invasive window, often 24–48 hours, rather than as an emergency. Unstable angina is managed medically with close monitoring, since there is no established infarction to reperfuse emergently, though many patients still proceed to diagnostic catheterization.

MONA — Individualized, Not Automatic

The classic mnemonic MONA (Morphine, Oxygen, Nitrates, Aspirin) is a useful memory aid, but current evidence has changed how each component is applied — the PCCN exam tests the caveats, not blind administration of all four:

• Aspirin: 162–325 mg, chewed for rapid absorption, is given to essentially all ACS patients unless there is a true aspirin allergy, because it produces immediate antiplatelet effect.
• Oxygen: given only if the patient is hypoxic (SpO2 below approximately 90%). Routine supplemental oxygen in a patient with a normal SpO2 offers no benefit and may cause harm through vasoconstriction and increased oxidative stress.
• Nitrates: relieve ischemic pain and reduce preload, but must be avoided in hypotension and in right ventricular (RV) infarction (typically accompanying an inferior STEMI), because the RV-infarcted heart depends on preload to maintain cardiac output — nitrates, diuretics, and morphine can precipitate profound, refractory hypotension in this setting. Nitrates are also avoided within 24–48 hours of phosphodiesterase-5 inhibitor use due to severe hypotension risk.
• Morphine: reserved for pain refractory to nitrates, used cautiously — morphine can mask ongoing ischemic pain, and some observational data associate it with worse outcomes, so it is not first-line therapy.

Antiplatelet and Anticoagulant Therapy

Beyond aspirin, ACS management adds a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) as dual antiplatelet therapy, plus a parenteral anticoagulant — unfractionated heparin, low-molecular-weight heparin, or a direct thrombin inhibitor such as bivalirudin — to prevent thrombus propagation while the vessel is stabilized or opened. The progressive care nurse must monitor for bleeding complications from this combined antithrombotic regimen, watch coagulation studies where applicable, and hold or adjust therapy around any planned procedure.