Analyzes 12-lead ECGs for acute findings requiring emergent intervention. Use when reading emergency ECGs, identifying STEMI patterns, or flagging critical arrhythmias.
Analyzes 12-lead ECGs for acute findings requiring emergent intervention, using a systematic approach to identify STEMI patterns, life-threatening arrhythmias, and high-risk ECG signatures.
The 12-lead ECG is the single most important initial diagnostic test in acute chest pain evaluation and is required within 10 minutes of ED arrival per ACC/AHA guidelines. STEMI misdiagnosis or delayed cath lab activation carries catastrophic consequences — door-to-balloon time >90 minutes is associated with a 7.5% increase in in-hospital mortality per 30-minute delay. Conversely, false-positive cath lab activations waste resources and expose patients to unnecessary invasive procedures (false activation rates range 10-30% across institutions).
Beyond ACS, the emergency ECG must be screened for lethal arrhythmias (complete heart block, wide-complex tachycardia), metabolic emergencies (severe hyperkalemia), drug toxicity (sodium channel blockade, QT prolongation), and structural pathology (PE, pericarditis, Brugada). Emergency physicians must interpret ECGs with higher sensitivity than specificity — the cost of a miss far exceeds the cost of a false alarm. This skill provides a systematic, reproducible framework for emergency ECG interpretation.
Follow this exact sequence on every ECG before pattern recognition:
| Interval | Normal | Abnormal | Emergency Significance |
|---|---|---|---|
| PR | 120-200 ms | >200 ms = 1st degree AV block; progressively lengthening = 2nd degree Type I; dropped beats without lengthening = 2nd degree Type II; complete dissociation = 3rd degree | 2nd degree Type II and 3rd degree = emergent pacing |
| QRS | <120 ms | 120-200 ms = BBB or aberrancy; >200 ms = ventricular origin or severe toxicity | New BBB in ACS context = consider STEMI equivalent |
| QTc | <440 ms (M), <460 ms (F) | >500 ms = high risk for Torsades de Pointes | Discontinue offending agents, replete Mg2+ and K+ |
RBBB (V1 = rSR', V6 = qRS, wide S in I and V6):
LBBB (V1 = rS or QS, V6 = tall R without Q, I = monomorphic R):
| Territory | Leads with ST Elevation | Culprit Artery |
|---|---|---|
| Anterior | V1-V4 | LAD |
| Lateral | I, aVL, V5-V6 | LCx or diagonal |
| Inferior | II, III, aVF | RCA (85%) or LCx (15%) |
| Right ventricular | V4R (obtain if inferior STEMI) | Proximal RCA |
| Posterior | V7-V9 (obtain if tall R in V1-V2 with ST depression) | PDA or LCx |
STEMI criteria (in ≥2 contiguous leads):
| Pattern | ECG Findings | Emergency Action |
|---|---|---|
| Hyperkalemia | Peaked T waves → widened QRS → sine wave → asystole | Calcium gluconate 10 mL of 10% IV over 2-3 min |
| Severe hypokalemia | Prominent U waves, flattened T waves, ST depression | Replete K+ aggressively, cardiac monitoring |
| PE (right heart strain) | S1Q3T3, RBBB, TWI V1-V4, sinus tachycardia, RAD | CTA pulmonary angiography, anticoagulation |
| Pericarditis | Diffuse ST elevation (concave up), PR depression, Spodick sign | NSAIDs + colchicine, rule out myocarditis |
| Brugada Type 1 | Coved ST elevation ≥2 mm in V1-V2 with T-wave inversion | Cardiology consult, avoid triggering drugs, consider ICD |
| Digitalis toxicity | Scooped ST ("Salvador Dali"), PAT with block, bidirectional VT | Digibind (digoxin-specific Fab fragments) |
| Sodium channel blockade (TCA, cocaine) | Wide QRS >100 ms, tall R in aVR >3 mm | Sodium bicarb boluses 1-2 mEq/kg IV |
| WPW | Short PR, delta wave, wide QRS | If AFib with WPW: procainamide or cardioversion; AVOID AV nodal blockers |
ECG Time: [HH:MM] | Clinical Context: [chief complaint, age, sex]
Rate: [ ] bpm | Rhythm: [regular/irregular, sinus/non-sinus]
Axis: [normal/LAD/RAD] | PR: [ ] ms | QRS: [ ] ms | QTc: [ ] ms
ST Changes: [describe by lead group]
T-Wave Changes: [describe]
Comparison to Prior: [new/unchanged/improved]
Interpretation: [final impression]
Action Taken: [cath lab activation / serial ECG ordered / cardiology consulted / none needed]