dDx Болей в грудной клетки

Etiology

Initial approach

• Focused history: quality & severity of pain; location & radiation; provoking & palliating factors; duration, frequency & pattern; setting in which it occurred; associated Sx

• Targeted exam: VS (including BP in both arms), cardiac gallops, murmurs, or rubs; signs of vascular disease (carotid or femoral bruits, ↓ pulses), signs of heart failure; lung & abdominal exam; chest wall exam for reproducibility of pain

• 12-lead ECG: obtain w/in 10 min; c/w priors & obtain serial ECGs; consider posterior leads (V7-V9) to reveal isolated posterior Ml if hx c/wACS but ECG unrevealing

• Cardiac biomarkers (Tn, CK-MB): serial testing at presentation, 6—12 h after sx onset troponin (I/T): most Se & Sp marker; level >99th %ile in approp. clinical setting is dx of Ml detectable 3—6 h after injury, peaks 24 h, may remain elevated for 7—10 d in STEMI high-sens. assays: 90—95% Se & Sp; 85% Se w/in 3 h of sx onset 'false C" (non-ACS myonecrosis): myocarditis/toxic CMP, severe CHF, HTN crisis, PE or severe resp. distress, cardiac trauma/cardioversion, sepsis, SAH, demand ischemia; ? renal failure (↓ clearance, skeletal myopathy vs. true microinfarctions) CK-MB: less Se & Sp (skel. muscle, tongue, diaphragm, intestine, uterus, prostate)

• CXR; other imaging (echo, PE CTA, etc.) as indicated based on H&P and initial testing

• Coronary CT angiography: 1/2 free of CAD → 0% w/ ACS; 1/2 w/ plaque →17% w/ ACS; even with signif stenosis, only 35% w/ ACS