12-lead shows ST elevation in leads II, III, aVF. What artery is likely occluded?
Choose an answer, then check it.
Pathophysiology · ELI Explains: Cardiovascular Pathophysiology (book 2)
Angina and Acute Coronary Syndrome
On this page 6 sections
The college version
Clinical Orientation
A 62-year-old woman calls 911 at 3 AM. "I woke up with this heavy pressure in my chest. It goes to my jaw. I feel sick to my stomach and I can't catch my breath." In the ED, her ECG shows ST depression in leads V3-V6. Her troponin is elevated. She has NSTEMI. This chapter answers: What mechanism links angina and ACS to bedside findings, tests, red flags, and nursing priorities?
What Is Normal?
Myocardial oxygen supply and demand: The heart continuously requires oxygen. Supply depends on coronary blood flow (determined by coronary artery patency, diastolic time, and oxygen content). Demand depends on heart rate, contractility, and wall tension (afterload × chamber radius / wall thickness). When demand exceeds supply → ischemia.
Coronary reserve: The ability to increase coronary flow 3-5× above baseline through vasodilation. Reduced by fixed stenosis, microvascular disease, and elevated resting flow (tachycardia, LVH).
Stable angina: Predictable, exertional chest discomfort from fixed coronary stenosis. Demand (exercise, stress) exceeds the limited supply. Resolves with rest (reduced demand) or nitroglycerin (vasodilation → increased supply + decreased demand).
What Goes Wrong?
Acute Coronary Syndrome (ACS): A spectrum from unstable angina → NSTEMI → STEMI. The common mechanism: atherosclerotic plaque disruption → thrombus formation → sudden reduction in coronary blood flow.
- Unstable angina: Plaque disruption with partial thrombosis. Myocardial ischemia without necrosis. Troponin normal. ECG may show ST depression or T-wave inversion (or be normal).
- NSTEMI: Plaque disruption with partial thrombosis causing subendocardial necrosis. Troponin elevated. ECG: ST depression or T-wave inversion.
- STEMI: Complete thrombotic occlusion of a coronary artery → transmural necrosis. Troponin elevated. ECG: ST segment elevation in leads facing the infarct.
Why unstable angina and NSTEMI are managed differently from STEMI: STEMI demands immediate reperfusion (PCI within 90 minutes or fibrinolysis within 30 minutes). NSTEMI/UA management is risk-stratified — high-risk patients need early invasive strategy (angiography within 24 hours); low-risk may be managed medically.
ACS Types Comparison
| Unstable Angina | NSTEMI | STEMI | |
|---|---|---|---|
| Pathology | Plaque disruption, partial thrombus | Plaque disruption, partial thrombus, subendocardial necrosis | Complete thrombotic occlusion, transmural necrosis |
| ECG | ST depression, T inversion, or normal | ST depression, T inversion | ST elevation (or new LBBB) |
| Troponin | Normal | Elevated | Elevated |
| Reperfusion urgency | Early invasive (within 24h if high-risk) | Early invasive (within 24h if high-risk) | EMERGENT — PCI within 90 min or lytics within 30 min |
What the Nurse May See
Chest pain characteristics:
- Quality: Pressure, squeezing, heaviness, tightness, burning. NOT typically sharp or stabbing.
- Location: Substernal, may radiate to left arm, jaw, neck, back, epigastrium.
- Associated: Dyspnea, diaphoresis, nausea/vomiting, lightheadedness, sense of impending doom.
- Atypical presentations: Women more likely to have dyspnea, fatigue, nausea, jaw/back pain without classic chest pressure. Elderly may present with confusion, syncope, weakness. Diabetics may have silent ischemia.
Assessment: Obtain full set of vitals. Auscultate heart (new murmur = papillary muscle dysfunction or rupture; S3 = pump failure). Auscultate lungs (crackles = pulmonary edema from pump failure). Check for JVD (right ventricular involvement).
Tests and Monitoring
- 12-lead ECG within 10 minutes of arrival: The single most important test. Look for ST elevation (≥1 mm in two contiguous limb leads or ≥2 mm in two contiguous precordial leads), ST depression, T-wave inversion, new LBBB.
- Serial troponin: Rises 2-4 hours after injury, peaks at 24-48 hours. High-sensitivity troponin assays can detect injury earlier. A rising/falling pattern confirms acute injury.
- Continuous cardiac monitoring: Arrhythmias are common in ACS — VT/VF is the leading cause of prehospital death.
Nursing Priorities
- MONA is outdated. Current priorities: 12-lead ECG (10 min), aspirin (162-325 mg chewed), oxygen ONLY if hypoxemic (SpO2 <90%), nitroglycerin for ongoing pain, morphine for pain unrelieved by NTG.
- For STEMI: Activate cath lab immediately. Door-to-balloon time ≤90 minutes. If PCI unavailable within 120 minutes, consider fibrinolysis if no contraindications.
- Serial ECGs: ST changes can evolve. Repeat with any symptom change.
- Monitor for complications: Arrhythmias (VT/VF — have defibrillator ready), heart failure (crackles, S3, hypoxia), cardiogenic shock (hypotension, oliguria, altered mentation), mechanical complications (new murmur = papillary muscle rupture or VSD).
Red Flags
| Red Flag | Why Dangerous |
|---|---|
| New ST elevation | Ongoing transmural infarction — every minute of delay kills myocardium. |
| Ventricular tachycardia/fibrillation | Cardiac arrest — most common cause of death in first hours of MI. |
| New holosystolic murmur + pulmonary edema | Papillary muscle rupture → acute severe mitral regurgitation → rapidly fatal without emergency surgery. |
| Hypotension with clear lungs + JVD | Right ventricular infarction — nitrates can cause dangerous hypotension. |
Eli explains
The same idea, in plain words
Explain it like I’m 10
The heart muscle is like a car engine that cannot be turned off.
- The engine needs a constant fuel supply (oxygenated blood through coronary arteries).
- Normally, when the engine works harder (exercise), the fuel line opens wider (vasodilation) to deliver more fuel.
- A partial blockage in the fuel line means there's enough fuel at idle (rest) but not enough when accelerating (exertion) — this is stable angina.
- A sudden crack in the fuel line plaque causes a clot that suddenly restricts fuel flow — this is ACS. If flow is reduced but not stopped: NSTEMI/UA. If flow stops completely: STEMI — the engine is seizing.
| Analogy | Real Physiology |
|---|---|
| Car engine = heart | Myocardium requiring constant oxygen |
| Fuel line = coronary artery | Coronary blood flow |
| Partial blockage = fixed stenosis | Stable angina |
| Crack in fuel line + clot = ACS | Plaque rupture → thrombus |
| Engine seizing = STEMI | Complete occlusion → transmural infarction |
Key takeaways
- ACS = plaque rupture + thrombus. Spectrum: UA → NSTEMI → STEMI.
- STEMI = ST elevation = complete occlusion = emergency reperfusion.
- ECG within 10 minutes.
- Troponin differentiates NSTEMI (elevated) from UA (normal).
- ---
Check yourself
1 review question from the chapter. Try each one, then open the answer.
Q1 (Priority): 12-lead shows ST elevation in leads II, III, aVF. What artery is likely occluded? A. Left anterior descending B. Right coronary artery C. Left circumflex D. Left main
Show answer
B. Inferior leads (II, III, aVF) reflect the inferior wall, supplied by the RCA (most commonly) or LCX. Anterior leads (V1-V4) = LAD. Lateral leads (I, aVL, V5-V6) = LCX.
Quick check
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Why is aspirin given immediately in ACS?
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