ECG Interpretation

The normal 12-lead ECG records electrical activity from multiple angles of the heart over ~10 seconds. Key components: P wave (atrial depolarization, normally <120 ms wide, <2.5 mm tall), PR interval (atrial depolarization + AV node delay; normal 120-200 ms; prolongation suggests AV block), QRS complex (ventricular depolarization; normal <120 ms; wide QRS suggests bundle branch block or ventricular rhythm), ST segment (early repolarization; normally isoelectric at baseline), QT interval (ventricular repolarization; varies with heart rate; QTc corrected for rate should be <440 ms men, <460 ms women; prolongation increases risk of torsades de pointes), T wave (ventricular repolarization completion; normally upright in most leads), and U wave (late repolarization; visible in ~25% of normal ECGs). The baseline between QRS complexes is the isoelectric line; elevation or depression of ST segment or T waves signals pathology. Intervals and amplitudes vary slightly by age, sex, and body habitus, requiring interpretation in clinical context.

ST elevation is abnormal upward displacement of the ST segment (junction between QRS and T wave) above the isoelectric baseline. In acute myocardial infarction (MI), ST elevation indicates transmural ischemia (full thickness of myocardium is dying). The location of ST elevation corresponds to the coronary artery involved: inferior MI (ST elevation in leads II, III, aVF = right coronary artery occlusion), anterior MI (ST elevation in V1-V4 = left anterior descending LAD occlusion), lateral MI (ST elevation in I, aVL, V5-V6 = left circumflex occlusion), posterior MI (ST depression in V1-V3 = posterior descending artery). Acute ST elevation MI (STEMI) is a medical emergency requiring immediate reperfusion therapy (primary PCI or thrombolytics) within 12 hours of symptom onset; delays > 30 minutes significantly worsen outcomes. Not all ST elevation is MI: early repolarization (benign variant in young people, African descent), pericarditis (diffuse ST elevation), ventricular aneurysm (chronic ST elevation), and LBBB can mimic STEMI. Clinical correlation (chest pain, troponin rise, risk factors, prior ECG) is essential to differentiate true MI from benign mimics.

QTc (corrected QT interval) is the duration of ventricular depolarization and repolarization, adjusted for heart rate. Normal: <440 ms in men, <460 ms in women. Prolongation (>500 ms) indicates slow repolarization and increases risk of torsades de pointes, a dangerous polymorphic ventricular arrhythmia that can degenerate into ventricular fibrillation and sudden cardiac death. Causes of QT prolongation: (1) medications (antiarrhythmics like sotalol, antipsychotics like haloperidol, antibiotics like azithromycin, antiretrovirals), (2) electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), (3) structural heart disease (cardiomyopathy, myocarditis), (4) genetic: Long QT syndrome (congenital channelopathy increasing sudden death risk). Management: identify and remove offending drug/correct electrolytes, monitor ECG, consider magnesium supplementation, avoid strenuous exercise (genetic Long QT), and place on telemetry if high risk. Any ECG showing QTc > 500 ms should trigger review of medications and labs. Combining QT-prolonging drugs (e.g., antifungal + antiarrhythmic) is high-risk and should be avoided.

A bundle branch block occurs when conduction is delayed or blocked in one of the two main branches (left or right) that carry electrical signal to the ventricles. Right bundle branch block (RBBB): conduction delay down the right bundle → right ventricle depolarizes late, QRS widens (>120 ms), characteristic 'M' or 'rsR' pattern in V1-V2. Normal variant in ~0.5% of population; can occur acutely in PE, acute stroke. Left bundle branch block (LBBB): left ventricle depolarizes late, QRS widens, broad notched R wave in I, aVL, V5-V6 (sometimes called 'W' pattern). LBBB is more concerning: associated with LV dysfunction, cardiomyopathy, and increased mortality risk. LBBB can obscure MI diagnosis because ST elevation is expected and makes true MI hard to detect (Sgarbossa criteria help but are imperfect). Partial blocks (fascicular blocks) occur in branches of the left bundle (anterior or posterior fascicle) and cause axis deviation. New LBBB requires urgent evaluation for acute coronary syndrome or structural heart disease.

Atrial fibrillation (AF) is an arrhythmia in which the atria beat irregularly and rapidly (400-600 bpm) instead of in organized contractions. ECG findings: (1) no clear P waves (replaced by irregular baseline oscillations or fibrillatory waves), (2) irregularly irregular QRS rhythm (intervals vary beat-to-beat in no pattern, unlike the regular irregularity of PVCs or PACs), (3) variable ventricular rate (commonly 80-150 bpm if untreated). AF can be paroxysmal (comes and goes), persistent (lasts >7 days), or permanent. Causes: hypertension, heart disease (MI, cardiomyopathy), thyroidism, pulmonary disease, alcohol, sepsis. AF is dangerous because (1) loss of atrial contraction reduces cardiac output (LV loses ~20% of filling), (2) blood stasis in the atria increases stroke risk 5-fold, requiring anticoagulation. Management: rate control (beta-blockers, calcium-channel blockers, digoxin), rhythm control (antiarrhythmics, cardioversion, ablation), and anticoagulation (warfarin or DOACs if stroke risk is elevated per CHA2DS2-VASc score). Acute AF with rapid ventricular rate and hypotension requires urgent rate control or cardioversion.

Left ventricular hypertrophy (LVH) is thickening of the LV wall, usually due to chronic hypertension, aortic stenosis, or cardiomyopathy. The hypertrophied muscle produces more electrical activity, increasing voltage. ECG criteria for LVH: (1) increased QRS voltage (Sokolow-Lyon: S in V1 + R in V5/V6 > 35 mm; Cornell: R in aVL + S in V3 > 20 mm women or > 28 mm men), (2) left axis deviation, (3) ST-T wave changes (ST depression and T wave inversion in V5-V6, called strain pattern). LVH indicates the heart is working too hard against resistance. Long-standing LVH increases risk of heart failure, arrhythmias, and sudden death. The ECG criteria have poor sensitivity (only ~50% of LVH cases meet voltage criteria), so echocardiography is more accurate. Management: treat underlying cause (blood pressure control, valve replacement), monitor for decompensation, and use ACE inhibitors or ARBs to promote LV remodeling and reduce hypertrophy over time.

Hyperkalemia (serum potassium > 5.5 mEq/L) is dangerous because potassium controls electrical conduction; excess raises resting membrane potential and slows conduction. ECG changes follow a predictable sequence with increasing K: (1) peaked T waves (tall, narrow, symmetric T waves, best seen in precordial leads V2-V4; occurs at K 5.5-6.5 mEq/L), (2) prolonged PR interval and widened QRS complex (K 6.5-7.5), (3) diminished P wave amplitude or disappearance of P wave (K > 7.5), (4) sine wave pattern (marked QRS widening and T-wave enlargement merge into a sinusoidal pattern; imminent cardiac arrest, K > 8). Hyperkalemia is a medical emergency: even mild hyperkalemia increases arrhythmia risk, especially in settings of digitalis or ischemia. Treatment: calcium gluconate (stabilizes membrane), insulin + glucose (shifts K into cells), beta-2 agonists (albuterol), diuretics, or dialysis (definitive). Any patient with peaked T waves should have potassium checked immediately. Common causes: renal failure, ACE inhibitors, NSAIDs, rhabdomyolysis, tumor lysis.

A 12-lead ECG is performed by placing 10 electrodes: 4 limb electrodes (right arm, left arm, right leg ground, left leg), and 6 precordial electrodes (V1-V6 along the left chest). Patient is supine, relaxed, limbs supported. The machine records electrical activity at 25 mm/sec paper speed for 10 seconds, producing a standard 12-lead tracing. Quality checks: (1) proper electrode placement (off-placement causes artifact and false findings), (2) no patient movement (wiggling creates baseline drift), (3) no muscle tension (patient relaxation reduces noise), (4) proper gain (amplitude should be 10 mm = 1 mV), (5) clean leads (dirty electrodes increase artifact), (6) patient identification (label with name, DOB, date/time, indication). Common artifacts: 60 Hz electrical interference (look for fine-line noise), loose electrode (intermittent signal loss), patient movement (baseline wanders), muscle tension (coarse baseline), or wandering baseline (loose electrode or patient breathing irregularly). A poor-quality ECG should be repeated before clinical interpretation; never interpret a noisy tracing as normal.