ECG Waveform Components Chart

What it represents: Atrial depolarization — the electrical wave spreading from the SA node through both atria, causing atrial contraction.

Measurement: Begins at the initial deflection from baseline; ends at the return to baseline before the PR segment. Normal: < 0.12 sec duration and < 2.5 mm amplitude.

Normal morphology: Upright and rounded in lead II (positive P wave = SA node origin). Inverted in aVR (normal). Biphasic in V1 (normal variant).

Abnormalities:

• Absent P waves: Junctional rhythm, atrial fibrillation, ventricular rhythm, sinoatrial block
• Inverted P waves (lead II): Junctional rhythm, ectopic atrial focus, retrograde atrial activation
• Tall, peaked P waves (> 2.5 mm in II): “P pulmonale” — right atrial enlargement (COPD, pulmonary hypertension)
• Wide, notched P waves (> 0.12 sec): “P mitrale” — left atrial enlargement (mitral stenosis, hypertension)
• Multiple P wave morphologies: Multifocal atrial tachycardia (MAT) — at least 3 different P wave shapes

What it represents: Conduction time from the SA node through the atria, AV node, and bundle of His to the start of ventricular depolarization. Includes atrial depolarization (P wave) plus the AV node delay (PR segment).

Measurement: From the beginning of the P wave to the beginning of the QRS complex.

Abnormalities:

• Prolonged (> 0.20 sec): First-degree AV block, or higher-degree AV block
• Short (< 0.12 sec): Pre-excitation (WPW syndrome), junctional rhythm, accelerated conduction
• Progressive lengthening then dropped QRS: Mobitz I (Wenckebach)
• Constant PR with random dropped QRS: Mobitz II
• Variable — no consistent relationship to QRS: Third-degree AV block

What it represents: Ventricular depolarization — the electrical wave spreading through the ventricular myocardium via the His-Purkinje system, causing ventricular contraction (systole).

Components: Q wave (initial downward deflection before R wave), R wave (positive deflection), S wave (negative deflection after R wave). Not all three components must be present in every QRS complex.

Measurement: From the beginning of the Q wave (or R wave if no Q) to the end of the S wave. Normal: < 0.12 sec (3 small boxes).

Abnormalities:

• Wide QRS (≥ 0.12 sec): Bundle branch block, ventricular rhythm, hyperkalemia, antiarrhythmic toxicity, WPW syndrome (delta wave)
• Pathologic Q wave (≥ 1 small box wide and ≥ 25% of R wave height): Old MI — electrically silent necrotic tissue creates a “window” recording away from the infarct zone
• Low voltage: QRS amplitude < 5 mm in limb leads — consider pericardial effusion, cardiac tamponade, hypothyroidism, COPD
• Notched or bizarre morphology: Bundle branch block, WPW delta wave, ventricular paced rhythm

What it represents: The period between ventricular depolarization (end of QRS) and the beginning of repolarization (T wave). Corresponds to the plateau phase of the cardiac action potential.

Normal: Isoelectric — lies at the same baseline as the TP segment (typically within ±0.5 mm in limb leads and ±1 mm in precordial leads at the J point).

Abnormalities:

• ST elevation: Acute MI (STEMI), early repolarization (normal variant), pericarditis, vasospasm, ventricular aneurysm. STEMI criteria: ≥ 1 mm elevation in two contiguous limb leads or ≥ 2 mm in two contiguous precordial leads
• ST depression: Myocardial ischemia (demand ischemia), NSTEMI, digitalis effect, reciprocal changes, hypokalemia
• Saddle-shaped ST elevation: Pericarditis — diffuse ST elevation without reciprocal changes, concave upward morphology

What it represents: Ventricular repolarization — the return of ventricular cells to their resting electrical state after contraction. The T wave's vulnerable period (peak) corresponds to when a premature stimulus can trigger VF (R-on-T phenomenon).

Normal morphology: Asymmetric (gradual upslope, abrupt downslope), upright in leads I, II, V3–V6. Inverted normally in aVR. May be biphasic in V1–V2 (normal variant).

Abnormalities:

• Tall, peaked, symmetric T waves: Hyperkalemia (early), hyperacute MI (very early ischemia), left ventricular hypertrophy
• T wave inversion: Myocardial ischemia, non-STEMI, ventricular hypertrophy (strain pattern), bundle branch block, pulmonary embolism (right heart strain in V1–V4)
• Flattened T waves: Hypokalemia, hypomagnesemia, digoxin effect, nonspecific repolarization abnormality
• Biphasic T waves: Ischemia, Wellens' syndrome (critical LAD stenosis — biphasic or inverted T waves in V2–V3 without acute ST changes)

What it represents: The total duration of ventricular electrical activity — from the beginning of the QRS complex to the end of the T wave. Encompasses both ventricular depolarization and repolarization.

Rate correction: The QT shortens at faster heart rates, so the rate-corrected QTc is used. Bazett formula: QTc = QT ÷ √(RR interval in seconds). Normal QTc: ≤ 440 ms (men), ≤ 460 ms (women).

Abnormalities:

• Prolonged QTc (> 500 ms): High risk of Torsades de Pointes — a polymorphic ventricular tachycardia that can degenerate into VF. Causes: hypokalemia, hypomagnesemia, hypocalcemia, antiarrhythmic drugs (amiodarone, sotalol), antipsychotics, some antibiotics, congenital long QT syndrome
• Short QTc (< 350 ms): Hypercalcemia, digoxin toxicity, congenital short QT syndrome — associated with increased arrhythmia risk
• Nursing priority: Measure and document QTc before and after QT-prolonging medications. Report QTc > 500 ms to the provider immediately