Clinical meaning
Advanced 12-lead ECG interpretation requires understanding of cardiac electrophysiology at the cellular level. The cardiac action potential progresses through five phases: Phase 0 (rapid depolarization via fast sodium channels), Phase 1 (early repolarization via transient outward potassium currents), Phase 2 (plateau phase maintained by L-type calcium channel influx balanced by delayed rectifier potassium efflux), Phase 3 (rapid repolarization via inward rectifier potassium channels), and Phase 4 (resting membrane potential maintained at approximately -90 mV by the inward rectifier potassium current IK1). The ECG represents the summation of all cardiac cellular electrical activity projected onto the body surface. P waves reflect atrial depolarization (SA node conduction through Bachmann's bundle to the left atrium and internodal pathways). The PR interval (120–200 ms) represents atrioventricular conduction including AV nodal delay. The QRS complex (< 120 ms normally) reflects ventricular depolarization through the His-Purkinje system. ST segment analysis is critical: ST elevation indicates transmural myocardial injury (current of injury from intracellular potassium leak in ischemic cells), while ST depression indicates subendocardial ischemia. Reciprocal changes in contiguous lead groups confirm acute MI localization. T wave morphology reflects ventricular repolarization — hyperacute T waves (peaked, symmetric, broad-based) are the earliest ECG finding in STEMI, preceding ST elevation. QT interval prolongation (corrected QTc > 470 ms in women, > 450 ms in men) increases risk of torsades de pointes, a polymorphic ventricular tachycardia. The NP must systematically evaluate rate, rhythm, axis, intervals, ST-T wave changes, and QRS morphology to identify acute coronary syndromes, conduction abnormalities, chamber enlargement, electrolyte disturbances, and drug effects.