Chest pain and approach to acs acc to harrison with defination

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Chest Pain & Approach to ACS — Harrison's Principles of Internal Medicine, 22nd Edition (2025)

1. DEFINITION — Ischemic Heart Disease & ACS

Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium; it typically occurs when there is an imbalance between myocardial oxygen supply and demand. The most common cause is atherosclerotic disease of an epicardial coronary artery sufficient to cause a regional reduction in myocardial blood flow.

Acute Coronary Syndrome (ACS) is an umbrella term encompassing the acute manifestations of IHD caused by abrupt reduction in coronary blood flow, most commonly from atherothrombotic plaque disruption (rupture or erosion). It spans three diagnoses:

Final Diagnosis	ECG	Biomarkers (hs-cTn)
Unstable Angina (UA)	No ST elevation	Non-elevated
NSTEMI	No ST elevation (± ST depression/T-wave changes)	Rise and fall (elevated)
STEMI	ST elevation	Rise and fall (elevated)

Harrison's, p. 2150 — FIGURE 285-1 (Spectrum of ACS)

Spectrum of ACS — clinical presentation, ECG findings, hs-cTn levels, and final diagnosis

2. CHEST PAIN — Characteristics of Angina Pectoris

The typical patient is a man >50 years or a woman >60 years:

Quality: Heaviness, pressure, squeezing, smothering, or choking — rarely frank pain
Location: Central, substernal — patient places a clenched fist over the sternum (Levine's sign)
Radiation: Either shoulder, both arms (especially ulnar aspects), back, interscapular region, root of neck, jaw, teeth, epigastrium
Duration: Typically 2–5 minutes; crescendo-decrescendo pattern
Triggers: Exertion (exercise, hurrying, sexual activity), emotion (stress, anger, fright)
Relief: Rest, nitroglycerin
Key negative: Does not radiate to the trapezius (that pattern suggests pericarditis)
Anginal equivalents (especially in women, elderly, diabetics): dyspnea, epigastric discomfort, nausea, weakness, diaphoresis

Harrison's, p. 2136

3. PATHOPHYSIOLOGY OF ACS

ACS follows plaque disruption — either rupture (thin fibrous cap, lipid-rich core) or erosion — leading to:

Platelet adhesion → activation → thromboxane A₂ release → vasoconstriction
GP IIb/IIIa receptor activation → fibrinogen cross-linking → platelet aggregation
Tissue factor exposure → coagulation cascade → thrombin → fibrin → thrombus

The final occlusion determines outcome:

Complete occlusion → STEMI
Partial/incomplete occlusion → NSTE-ACS (UA or NSTEMI)

ACS pathophysiology — plaque disruption, thrombus formation, and diagnostic classification

4. APPROACH TO ACS — NSTE-ACS (UA & NSTEMI)

Clinical Features (History & Physical)

Chest discomfort in NSTE-ACS has at least one of:

Occurrence at rest (or minimal exertion), lasting >10 min
Relatively recent onset (within prior 2 weeks)
Crescendo pattern — more severe, prolonged, or frequent than previous episodes

Physical examination may show: diaphoresis, pale cool skin, sinus tachycardia, S3/S4, basilar rales, hypotension, or cardiogenic shock in severe cases.

Always rule out life-threatening mimics: pulmonary embolism, aortic dissection, cardiac tamponade.

Risk Stratification

Key high-risk markers:

Age ≥65 years
Known CAD (≥50% stenosis)
ST deviation >0.5 mm on presenting ECG
Elevated cardiac biomarkers (hsTn)
≥2 ischemic episodes in prior 24 h
≥3 CAD risk factors

Investigations

ECG: Serial 12-lead; look for ST depression, T-wave inversions
hsTn: At presentation, 1 h, and if needed at 3 h — rise/fall pattern confirms NSTEMI
Stress testing or CT coronary angiography for intermediate-risk patients with diagnostic uncertainty
Continuous ECG monitoring for ST deviation and arrhythmias

5. TREATMENT — NSTE-ACS

Anti-Ischemic (Acute Phase)

Drug	Key Points	Avoid When
Nitrates	SL/buccal 0.3–0.6 mg q5 min × 3; then IV NTG 5–10 μg/min (titrate to relief or SBP <90)	PDE-5 inhibitor use (sildenafil/vardenafil within 24 h; tadalafil within 48 h); hypotension; RV infarction
Beta-blockers	Reduce MVO₂; IV for severe ischemia	Acute/severe HF, low output, severe bradycardia, high-degree AV block
Oxygen	Only if SpO₂ <90%, HF present	Routine use not indicated

Antithrombotic Therapy

Aspirin 325 mg loading → 75–100 mg maintenance
P2Y₁₂ inhibitor (ticagrelor preferred over clopidogrel in most)
Anticoagulation: UFH, enoxaparin, fondaparinux, or bivalirudin depending on strategy

Invasive vs. Conservative Strategy

Early invasive (angiography within 24 h): for high-risk features — elevated hsTn, dynamic ECG changes, TIMI/GRACE score elevation
Conservative/selective invasive: for low-risk, negative biomarkers, no ECG changes

6. STEMI — Key Additional Points

STEMI occurs when a completely occlusive thrombus forms rapidly at a disrupted plaque site. Management priorities:

Immediate reperfusion is the goal — primary PCI preferred (door-to-balloon ≤90 min at PCI-capable center)
Fibrinolysis if primary PCI unavailable within 120 min of first medical contact
Same antithrombotic backbone (aspirin + P2Y₁₂ + anticoagulation)

7. UNIVERSAL DEFINITION OF MI (Harrison's / Fourth Universal Definition 2018)

Myocardial Injury: Elevated cTn with at least one value above 99th percentile URL; acute if rise and/or fall pattern present.

Acute MI: Acute myocardial injury + clinical evidence of ischemia + at least one of:

Symptoms of ischemia
New ischemic ECG changes
Development of pathologic Q waves
Imaging evidence of new loss of viable myocardium/RWMA
Coronary thrombus on angiography or autopsy

MI Types

Type	Mechanism
Type 1	Atherothrombotic (plaque rupture/erosion)
Type 2	Supply-demand imbalance (non-thrombotic)
Type 3	Cardiac death before biomarkers available
Type 4a	PCI-related (cTn >5× 99th percentile URL)
Type 4b	Stent thrombosis
Type 5	CABG-related (cTn >10× 99th percentile URL)

Harrison's, p. 2161

Source: Harrison's Principles of Internal Medicine, 22nd Edition (2025), McGraw Hill Medical — Chapters 284 (Ischemic Heart Disease), 285 (Non-ST-Segment Elevation ACS), 286 (STEMI)

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