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324 mg chewable PO immediately (non-enteric coated)
Ticagrelor 180 mg PO OR Clopidogrel 600 mg PO loading dose
Heparin bolus 60 units/kg IV (max 4,000 U), then infusion 12 units/kg/h (max 1,000 U/h)
< 90 minutes for primary PCI (< 120 min if transferred); < 30 min for lytics
Avoid nitrates/diuretics; administer 500–1000 mL crystalloid bolus for hypotension
Ischemia at rest or with minimal exertion, accelerating pattern, without biochemical evidence of myocyte necrosis (negative troponin); risk-stratify with HEART score (score 0-3 candidate for early discharge).
Wellens syndrome (critical proximal LAD stenosis), de Winter T-waves (hyperacute symmetric T-waves with ST depression at J-point), Sgarbossa and Modified Sgarbossa criteria for LBBB/ventricular pacing, Posterior MI (tall R and ST depressions V1-V3), RV Infarction (ST elevation in V4R; preload dependent).
Bottom-Line Clinical Pearl
Time is myocardium. Do NOT wait for troponin results to activate the cardiac catheterization laboratory for STEMI or STEMI equivalents (Wellens syndrome, de Winter T-waves, Sgarbossa-positive LBBB/paced rhythm, posterior MI). In inferior wall myocardial infarctions (leads II, III, aVF), always obtain right-sided leads (V4R); if ST elevation is present in V4R, nitrates and morphine are ABSOLUTELY CONTRAINDICATED due to preload dependence.
Upon arrival of a patient with suspected acute coronary syndrome (retrosternal pressure, diaphoresis, dyspnea, nausea, radiation to jaw or arm), obtain and interpret a 12-lead electrocardiogram (ECG) within 10 minutes. Place continuous cardiac monitoring, establish bilateral intravenous access, and immediately assess hemodynamic stability.
Clinical Caution
Routine Supplemental Oxygen Caution: Withhold supplemental oxygen in normoxic patients (SpO2 >= 90%). The AVOID randomized trial demonstrated that routine hyperoxia in non-hypoxemic STEMI causes coronary artery vasoconstriction, increases myocardial infarct size, and worsens free-radical reperfusion injury.
| Phase | Immediate Action | Target Goal/Threshold | Clinical Rationale |
|---|---|---|---|
| 0–10 min | 12-Lead ECG Acquisition | < 10 min from door | Differentiates STEMI from NSTE-ACS; activates cath team immediately |
| Immediate | Aspirin Administration | 324 mg chewable PO | Irreversibly inhibits COX-1; reduces mortality by 23% in acute MI |
| Immediate | Vital Signs & SpO2 | Maintain SpO2 90–96% | Avoid hyperoxia; titrate O2 only if SpO2 < 90% or patient in respiratory distress |
| First 15 min | High-Sensitivity Troponin | Baseline (0h) level | Essential for baseline delta kinetics, but NEVER delay cath lab for troponin |
| First 15 min | Targeted Risk Stratification | HEART Score assessment | Identifies patients needing urgent vs routine observation/catheterization |
Classic STEMI is diagnosed by new ST-segment elevation at the J-point in >= 2 contiguous leads: >= 1 mm (0.1 mV) in all leads except V2–V3. In leads V2–V3, thresholds are sex- and age-specific: >= 2.5 mm in men < 40 years; >= 2.0 mm in men >= 40 years; and >= 1.5 mm in women of any age. New or presumed new Left Bundle Branch Block (LBBB) with hemodynamic instability is treated as STEMI equivalent.
| Infarct Territory | Leads with ST Elevation | Reciprocal Depression | Culprit Coronary Artery |
|---|---|---|---|
| Anteroseptal | V1, V2, V3, V4 | II, III, aVF (variable) | Left Anterior Descending (LAD) artery |
| High Lateral/Lateral | I, aVL, V5, V6 | II, III, aVF | Left Circumflex (LCx) or Diagonal branch of LAD |
| Inferior | II, III, aVF | I, aVL | Right Coronary Artery (RCA) 85% > LCx 15% |
| Right Ventricle | V4R (right-sided lead) | I, aVL | Proximal RCA (Preload dependent; avoid nitrates!) |
| Posterior | V7, V8, V9 (or tall R + STD V1–V3) | None (primary STD in V1–V3) | Posterior Descending Artery (PDA from RCA or LCx) |
| Apical/Extensive Anterior | V1–V6, I, aVL | II, III, aVF | Proximal LAD ('Widow Maker') occlusion |
Up to 25–30% of acute coronary occlusions present without meeting conventional STEMI millimeter criteria. These 'Occlusion Myocardial Infarction' (OMI) equivalents carry identical mortality to classic STEMI and mandate immediate catheterization laboratory activation.
- Wellens Syndrome: Deeply inverted symmetric T-waves (Type B, 75%) or biphasic T-waves (Type A, 25%) in leads V2–V3 in a pain-free patient with prior chest pain. Represents critical proximal LAD stenosis (89–100%). Cardiac biomarkers are often normal or minimally elevated. Cardiac stress testing is STRICTLY CONTRAINDICATED as it precipitates massive anterior wall infarction. See the dedicated Wellens Syndrome Clinical Protocol for full criteria, mimics, and cath lab timing.
- de Winter T-Waves: 1–3 mm upsloping ST depression at the J-point in leads V1–V6 that transitions into tall, prominent, symmetric T-waves, accompanied by 1–2 mm ST elevation in lead aVR. Represents acute proximal LAD occlusion seen in 2% of anterior infarctions without classic ST elevation.
- Modified Sgarbossa Criteria (Smith Modification for LBBB and Ventricular Pacing): Evaluates acute ischemia in bundle branch blocks or paced rhythms. 1) Concordant ST elevation >= 1 mm in any lead with a positive QRS (5 points, spec 98%); 2) Concordant ST depression >= 1 mm in leads V1, V2, or V3 (3 points, spec 95%); 3) Excessively discordant ST elevation relative to the preceding S-wave (ST elevation/S-wave amplitude ratio <= -0.25) (Smith rule, sensitivity 91%, specificity 99%). Any positive criterion warrants emergency catheterization.
- Lead aVR Elevation with Multi-Lead ST Depression: ST elevation >= 1 mm in aVR (often aVR > V1) with diffuse, prominent ST depression across 6 or more leads (leads I, II, aVF, and V4–V6). Indicates acute left main coronary artery (LMCA) occlusion or severe triple-vessel coronary disease with critical subendocardial ischemia.
- Isolated Posterior MI: Horizontal ST depression, prominent tall R-waves (R/S ratio > 1.0), and upright T-waves in leads V1–V3. Placing posterior leads V7–V9 demonstrates ST elevation >= 0.5 mm, confirming transmural occlusion of the LCx or distal RCA.
- Aslanger Pattern: In patients with inferior ischemia and preexisting multivessel disease: ST elevation isolated to lead III (without II or aVF elevation), ST depression in leads V4–V6 with upright T-waves, and ST elevation in lead aVR greater than V1. Represents acute inferior occlusion masked by reciprocal anterior subendocardial ischemia.
- Hyperacute T-Waves: Earliest ECG manifestation of transmural ischemia, preceding ST elevation by minutes to hours. Symmetrical, broad-based, towering T-waves that merge smoothly with the ST segment without an intervening isoelectric baseline.
| Drug Class | Specific Agent & Dose | Route & Frequency | Clinical Pearls & Strict Contraindications |
|---|---|---|---|
| Antiplatelet (First-line) | Aspirin 324 mg | PO chewable x 1 dose | Non-enteric coated; administer immediately to all patients without true anaphylaxis. |
| P2Y12 Inhibitor (Preferred) | Ticagrelor 180 mg loading | PO x 1, then 90 mg BID | Preferred over clopidogrel; faster onset and greater mortality reduction in ACS. Reversible binding. |
| P2Y12 Inhibitor (Alternative) | Clopidogrel 600 mg loading | PO x 1, then 75 mg daily | Used if ticagrelor contraindicated, patient receiving fibrinolytics, or on oral anticoagulation. |
| P2Y12 Inhibitor (PCI Only) | Prasugrel 60 mg loading | PO x 1, then 10 mg daily | Contraindicated if prior stroke/TIA, age >= 75 yr, or weight < 60 kg due to lethal bleeding risk. |
| Anticoagulant (UFH) | Heparin 60 units/kg bolus | IV (max 4,000 U), 12 U/kg/h | Target aPTT 50–70 seconds. Easily reversible with protamine; preferred if CABG possible. |
| Anticoagulant (LMWH) | Enoxaparin 1 mg/kg | SubQ q12h (or 30 mg IV bolus in STEMI) | Dose adjust in renal failure (1 mg/kg q24h if CrCl < 30 mL/min). Avoid if emergent CABG anticipated. |
| Nitrate Vasodilator | Nitroglycerin 0.4 mg SL/10–200 mcg/min IV | SL q5min x 3 doses, then IV titration | Reduces preload/afterload. Contraindicated if SBP < 90, RV infarct, or PDE-5 inhibitor in last 24–48h. |
| Beta-Blocker | Metoprolol tartrate 25–50 mg | PO q6h (titrate to HR 55–60) | AVOID routine IV beta-blockers in acute ED setting (COMMIT trial: increased cardiogenic shock). |
| Statin (High-intensity) | Atorvastatin 80 mg | PO x 1 dose immediately | Plaque stabilization, anti-inflammatory effect, and improved long-term vascular endothelial function. |
Critical Pitfall / Contraindication
Right Ventricular Infarction Hemodynamic Hazard: In patients with inferior STEMI, 30–50% have concomitant right ventricular (RV) involvement. The ischemic RV cannot pump blood across the pulmonary bed without high preload. Administration of nitroglycerin, morphine, or loop diuretics causes catastrophic precipitous hypotension and cardiovascular collapse. Diagnostic step: Obtain right-sided lead V4R immediately (ST elevation >= 1 mm in V4R confirms RV infarct). Treatment: Aggressive isotonic crystalloid boluses (500–1000 mL) to maintain preload; start Norepinephrine if MAP remains < 65 mmHg.
Reperfusion is indicated for all STEMI patients presenting within 12 hours of symptom onset (or ongoing ischemic symptoms up to 24 hours). Primary Percutaneous Coronary Intervention (PCI) is the gold standard when door-to-balloon time is under 90 minutes (or under 120 minutes if transferred from a non-PCI center). If transfer to a PCI facility will exceed 120 minutes, emergency intravenous fibrinolytic therapy must be administered within 30 minutes of door time ('door-to-needle').
| Reperfusion Pathway | Time Benchmark | Regimen & Dosing | Key Contraindications & Clinical Cautions |
|---|---|---|---|
| Primary PCI | Door-to-balloon < 90 min (transfer < 120 min) | Direct stent deployment via radial/femoral artery | Preferred modality across all age groups and cardiogenic shock presentations. |
| Fibrinolysis (Tenecteplase: TNK) | Door-to-needle < 30 min | Weight-based IV bolus over 5 sec: <60kg=30mg, 60-69kg=35mg, 70-79kg=40mg, 80-89kg=45mg, >=90kg=50mg | Single bolus; weight-adjusted; 50% dose reduction if age >= 75 years. |
| Fibrinolysis (Alteplase: tPA) | Door-to-needle < 30 min | Accelerated 90-min infusion: 15 mg IV bolus, then 0.75 mg/kg (max 50 mg) over 30 min, then 0.5 mg/kg (max 35 mg) over 60 min | Total max dose 100 mg. Requires concomitant unfractionated heparin infusion for 48 hours. |
Critical Pitfall / Contraindication
Absolute Contraindications to Fibrinolytic Therapy: 1) Any prior intracranial hemorrhage; 2) Known structural cerebral vascular lesion (e.g., AVM, aneurysm); 3) Known malignant intracranial neoplasm; 4) Ischemic stroke within 3 months (except acute ischemic stroke < 4.5 hours); 5) Suspected aortic dissection; 6) Active internal bleeding (excluding menses); 7) Significant closed head injury or facial trauma within 3 months.
For patients with suspected acute coronary syndrome without diagnostic ST elevation, the HEART Score is the most validated bedside risk-stratification instrument in emergency medicine. It predicts the 6-week risk of Major Adverse Cardiac Events (MACE: all-cause mortality, MI, or coronary revascularization).
| HEART Component | 0 Points | 1 Point | 2 Points |
|---|---|---|---|
| History (H) | Slightly/non-suspicious | Moderately suspicious | Highly suspicious (retrosternal pressure, diaphoresis, radiation) |
| ECG (E) | Normal baseline | Non-specific repolarization/LBBB/pacing | Significant ST depression or T-wave inversion not due to LBBB |
| Age (A) | < 45 years | 45–64 years | >= 65 years |
| Risk Factors (R) | 0 known risk factors | 1–2 risk factors (HTN, DM, lipids, smoking, fam hx) | >= 3 risk factors OR history of CAD, PCI, CABG, stroke, PVD |
| Troponin (T) | <= Normal limit | 1–3x Normal limit | > 3x Normal limit |
| Score Range | Risk Category | 6-Week MACE Rate | Recommended Emergency Department Disposition |
|---|---|---|---|
| 0–3 Points | Low Risk | 0.8–1.7% | Eligible for early discharge from ED with outpatient follow-up within 72 hours. |
| 4–6 Points | Moderate Risk | 12–16% | Admission to ED observation unit or telemetry; serial delta-troponins, provocative testing. |
| 7–10 Points | High Risk | 50–65% | Immediate inpatient cardiology admission; early invasive angiography within 24 hours. |
Mechanical complications typically manifest 2 to 7 days post-infarct due to coagulative necrosis, neutrophilic infiltration, and enzymatic myocardial softening. They present with sudden catastrophic hemodynamic collapse, pulmonary edema, or electromechanical dissociation.
| Complication | Culprit Territory | Clinical Presentation & Murmur | Bedside POCUS/Echo Findings | Emergency Management |
|---|---|---|---|---|
| Papillary Muscle Rupture | Inferior MI (posteromedial papillary muscle supplied solely by PDA) | Acute pulmonary edema, flash pulmonary congestion, cardiogenic shock. New harsh apical holosystolic murmur radiating to axilla. | Severe eccentric mitral regurgitation jet on color Doppler; flail mitral valve leaflet into left atrium. | Intra-aortic balloon pump (IABP)/Impella, emergent cardiac surgery for valve repair/replacement. |
| Ventricular Septal Rupture (VSR) | Anterior (LAD) or Inferior (RCA) MI | Biventricular failure, hypotension. Loud, harsh holosystolic murmur with palpable thrill at left lower sternal border. | Left-to-right color Doppler flow across the interventricular septum; dilated right heart. | Afterload reduction (nitroprusside), IABP, emergent surgical closure (high operative mortality). |
| Free Wall Rupture | Anterior or Lateral wall (LAD or LCx) | Sudden cardiac tamponade, Beck's triad (hypotension, JVD, muffled sounds), rapid progression to PEA arrest. | Large pericardial effusion with right ventricular diastolic collapse; internal echoes (hemopericardium). | Emergency bedside pericardiocentesis, immediate surgical thoracotomy/pericardial patch. |
| Left Ventricular Pseudoaneurysm | Inferoposterior wall | Contained myocardial rupture held only by pericardium; high risk of catastrophic rupture. Systolic murmur. | Saccular outpouching with narrow neck (orifice < 50% of max diameter) and turbulent color flow. | Immediate surgical repair; anticoagulation is strictly contraindicated. |
| Cardiogenic Shock | Extensive anterior MI (> 40% LV loss) | Cool clammy extremities, oliguria, altered mental status, severe hypotension (SBP < 90 mmHg, CI < 2.2). | Severely depressed LV ejection fraction, elevated filling pressures, hyperdynamic RV. | Norepinephrine first-line, Dobutamine inotropic support, mechanical circulatory support (Impella/IABP). |
Patients with Non-ST-Elevation ACS (NSTE-ACS) who exhibit any of the following high-risk features have ongoing transmural ischemia or imminent circulatory collapse and mandate emergent invasive coronary angiography within 2 hours, bypassing standard observation protocols:
- Hemodynamic instability or cardiogenic shock refractory to initial fluid resuscitation.
- Recurrent or ongoing refractory anginal chest pain despite optimal medical therapy (nitrates and beta-blockers).
- Life-threatening cardiac arrhythmias (sustained Ventricular Tachycardia or Ventricular Fibrillation).
- Mechanical complications of myocardial infarction (new severe mitral regurgitation or ventricular septal defect).
- Acute heart failure directly related to ongoing myocardial ischemia (pulmonary rales, S3 gallop, flash pulmonary edema).
- Dynamic or recurrent ST-segment and T-wave changes on serial ECGs (especially dynamic ST depression > 1 mm).
Critical Pitfall / Contraindication
Top 5 Emergency Medicine ACS Traps: 1) Missing an acute ascending aortic dissection presenting as inferior STEMI (dissection flap occludes the RCA ostium; giving thrombolytics or heparin is uniformly fatal—always check bilateral arm BPs and pulse deficits); 2) Routine administration of morphine (CRUSADE registry showed morphine delays P2Y12 absorption by 2–4 hours and correlates with increased mortality); 3) Misinterpreting isolated ST depression in V1–V3 as 'anterior subendocardial ischemia' rather than a true transmural posterior STEMI; 4) Administering nitrates to an inferior STEMI patient who recently ingested Sildenafil (within 24h) or Tadalafil (within 48h), leading to refractory cyclic GMP-mediated vasoplegic shock; 5) Discharging a patient with high-risk anginal features based on a single negative baseline troponin taken within 2 hours of symptom onset.
Test Your Acute Coronary Syndromes & STEMI Equivalents Clinical Acumen
Directly launch an active-recall practice block from our validated question bank with comprehensive explanations and distractor analyses.
Distinguish primary life-threats from mimics. On board exams (COMLEX Level 1, 2-CE, 3 & USMLE), initial stabilizing interventions (airway, IV access, non-invasive ventilation, empiric reversal) always take precedence over diagnostic imaging.
Evaluate autonomic tone: Sympathetic viscerosomatics (T1–L2) cause acute paraspinal tissue texture changes (erythema, bogginess, hypertonicity). Suboccipital release (CN X Vagus) and rib raising normalize autonomic outflow and thoracic cage mechanics.
Related Emergency Protocols & Differentials
Wellens Syndrome & Critical Proximal LAD Stenosis
High-risk precordial T-wave pattern, stress test contraindication, and urgent revascularization.
Open Protocol Related EM ProtocolAcute Pulmonary Embolism
Differential diagnosis for acute chest pain and right ventricular strain.
Open Protocol Related EM ProtocolCardiac Arrest & Resuscitation
Post-ROSC catheterization criteria and refractory VF arrest.
Open Protocol Related EM ProtocolShock & Undifferentiated Hypotension
Cardiogenic shock hemodynamics and inotropic support.
Open Protocol