Approach
• See Approach above
Definitions
• ACS: Represents a clinical spectrum ranging from UA through NSTEMI & STEMI
ACS develops when a vulnerable or high-risk plaque undergoes disruption of the fibrous cap which is a stimulus for thrombogenesis w/ ultimate imbalance b/w myocardial O2 supply & demand
• UA (subtotal coronary thrombosis, angina that is new onset, crescendo, OR at rest, usually <30 min, ±ST depression &/or TWI)
• Rest angina: Angina occurring at rest & prolonged, usually >20 min
• New-onset angina: New-onset angina of at least CCS class III severity
• Increasing angina: Previously diagnosed angina that has become distinctly more frequent longer in duration, or lower in threshold (ie, increase by 1 or more CCS class)
• NSTEMI (same as UA but w/ +troponin)
• STEMI (total coronary thrombosis, angina usually at rest >30 min, ST elevations, +troponin)
• Note: Most troponin elevations in ED are not due to primary ACS, but demand ischemia
History (NEJM 2005;294:2623)
• Typical sxs
• Angina (substernal pressure/pain/tightness, radiation to neck/jaw/arms, precipitated by exertion/relieved w/ rest or NTG); w/ ACS, new onset, crescendo, or at rest
• Associated sxs: Dyspnea diaphoresis, N/V, palpitations, LH; ∼23% MIs lack typical sxs (AJC 1973;32:1)
Physical Exam
• Usually unremarkable exam
Evaluation
• ECG: ST change (up or down), TWI, LBBB that is new. Q wave or PRWP suggests prior MI → CAD. Always check ECG w/i 10 min, w/ changes in sxs, at 6–12 h & c/w baseline. If pain persists, repeat q15–30min.
• It is reasonable to obtain supplemental ECG leads V7–V9 in pts whose initial
ECG is nondiagnostic to r/o MI due to L circumflex occlusion
• Sgarbossa’s criteria: In setting of old LBBB, STEMI Dx requires ≥1 mm STE concordant w/ QRS (sens 73%, spec 92%) or ≥5 mm discordant (sens 31%, spec 92%) any lead (NEJM 1996;334:481).
Cardiac Biomarkers
• Requires serial testing at 6 & 12 h after sx onset. It is reasonable to remeasure positive biomarkers at 6- to 8-h intervals 2–3 times or until levels have peaked, as an index of infarct size & dynamics of necrosis.
• Troponin (I or T) is most sens & spec. Also seen in myocarditis, CMP, severe CHF, cardiac trauma, cardioversion, sepsis, ICH, renal failure.
• Cardiac index, CI = (CK – MB/CK) × 100. CI <3 suggests skeletal source, CI 3–5 → indeterminate, CI >5 suggests cardiac source
Figure 1.1
• Other labs: Chem 7, CBC, coags, T/S (if intervention planned), tox (if cocaine suspected)
• CXR: Check for cardiomegaly, pulmonary edema
• Echo: If ECG is not interpretable (prior LBBB, paced) & suspicion for ACS is high, can obtain echo to evaluate for regional wall abnlty.
• CTCA: May be useful for evaluating pts w/ intermed & low PreTP for CAD w/ nl serial ECGs/biomarkers (Circulation 2006;114:1761; JACC 2006;48:1475; NEJM 2012;366(15):393; NEJM2012;367(4):299)
Treatment
• See STEMI & UA/STEMI for details
Disposition
• If hx & initial ECG/biomarkers are non-Dx: Repeat ECG/biomarkers at 3 & 6 h from 1st set & if suspicion for ACS is low, may monitor for recurrent sx. If no ACS, can evaluate for inducible ischemia via stress test.
• Stress testing may be done as an outpt if low risk (age <70, no prior CAD, CVD, PAD; no rest angina) at 72 h (0% mortality, <0.5% MI, [Ann Emerg Med 2006;47:427])
• If STEMI or UA/NSTEMI: Admit (see below)
Pearls
• Give ASA if you suspect ACS & there are no CIs. It provides the greatest morbidity/mortality benefit of any tx in the ED for ACS (50–70% drop D/MI for UA/NSTEMI, NEJM 1988;319:1105; 23% drop death in STEMI, ISIS-2, Lancet 1988;ii:349).
• Women, diabetics, & elderly pts often present w/o CP; anginal equivalents: SOB, fatigue, weakness