Understanding the ECG Waveform

Introduction

The electrocardiogram (ECG or EKG) is one of the most essential diagnostic tools in modern medicine, providing a non-invasive, real-time window into the electrical activity of the heart. Since its invention by Willem Einthoven in the early 20th century, ECG has remained invaluable in diagnosing arrhythmias, conduction abnormalities, myocardial ischemia, electrolyte disturbances, and structural heart disease.

At its core, the ECG waveform represents the sum of electrical potentials generated by depolarization and repolarization of cardiac myocytes, recorded at the body surface. Understanding the morphology and timing of the waveform is crucial for accurate interpretation and clinical decision-making.

This article presents a detailed guide to the fundamental components of the ECG waveform—the P wave, QRS complex, and T wave—including their physiology, ionic mechanisms, morphology, clinical significance, and common abnormalities.

Section 1: Basics of Cardiac Electrophysiology

1.1 Cardiac Conduction System

The heart’s electrical system ensures coordinated contraction of atria and ventricles. Key components include:

Sinoatrial (SA) node: Primary pacemaker (~60–100 bpm). Initiates atrial depolarization.
Atrioventricular (AV) node: Delays conduction to allow atrial contraction.
Bundle of His and Purkinje fibers: Rapidly conduct impulses to ventricular myocardium.

1.2 Action Potential in Cardiac Myocytes

The ECG waveform reflects ion movements during the cardiac action potential:

Phase 0 (Depolarization): Rapid Na⁺ influx → steep upstroke.
Phase 1 (Initial repolarization): Transient K⁺ efflux.
Phase 2 (Plateau): Ca²⁺ influx balances K⁺ efflux.
Phase 3 (Repolarization): K⁺ efflux dominates.
Phase 4 (Resting potential): Na⁺/K⁺ ATPase maintains resting membrane potential.

ECG waves correspond to synchronized depolarization and repolarization of large myocardial masses, which are detectable at the body surface.

Section 2: The P Wave

2.1 Physiological Basis

The P wave represents atrial depolarization, originating from the SA node. It indicates the electrical activation of the right and left atria prior to atrial contraction.

2.2 Morphology

Usually smooth and rounded, positive in leads I, II, aVF.
Duration: 0.08–0.12 seconds.
Amplitude: <2.5 mm in limb leads.
Lead II is most commonly used to assess P wave morphology.

2.3 Ionic Mechanism

Depolarization involves rapid Na⁺ influx in atrial myocytes.
Conduction across atria is relatively slow compared to ventricles due to smaller fiber diameter and less gap junction density, which explains the relatively low amplitude.

2.4 Clinical Significance

Normal Variants

Slight variation in P wave size or shape is normal, reflecting heart position, age, and lead placement.

Abnormalities

P Mitrale
- Broad, notched P wave (>120 ms) in lead II.
- Indicates left atrial enlargement, commonly due to mitral stenosis or hypertension.
P Pulmonale
- Tall, peaked P waves (>2.5 mm) in lead II.
- Suggests right atrial enlargement, often from pulmonary hypertension or chronic lung disease.
Absent or abnormal P waves
- Seen in atrial fibrillation (AF) → chaotic atrial activity.
- Atrial flutter → sawtooth P waves.
- Sinoatrial arrest → absent P waves with junctional escape rhythms.

Section 3: The PR Interval

Although not a wave, the PR interval is intimately associated with the P wave.

3.1 Definition

Time from beginning of P wave to beginning of QRS complex.
Represents conduction through atria, AV node, and His-Purkinje system.

3.2 Normal Values

Duration: 0.12–0.20 seconds (3–5 small squares on ECG paper).

3.3 Clinical Significance

Short PR (<0.12s): Pre-excitation syndromes (e.g., Wolff-Parkinson-White).
Prolonged PR (>0.20s): First-degree AV block.
Variable PR: Second-degree AV block (Mobitz I and II).

Section 4: The QRS Complex

4.1 Physiological Basis

The QRS complex represents ventricular depolarization, which precedes ventricular contraction. The magnitude of the QRS reflects mass and synchrony of ventricular activation.

4.2 Morphology

Duration: 0.08–0.10 seconds (up to 0.12 s).
Components:
- Q wave: Initial negative deflection (septal depolarization left to right).
- R wave: First positive deflection (main ventricular depolarization).
- S wave: Downward deflection following R wave (late ventricular depolarization).

4.3 Ionic Mechanism

Rapid phase 0 Na⁺ influx in ventricular myocytes.
Purkinje fibers ensure synchronous ventricular activation → narrow QRS.
Abnormal conduction (bundle branch blocks) widens QRS.

4.4 Clinical Significance

Q Wave Abnormalities
- Pathological Q waves: >0.04 s and >25% of R wave amplitude.
- Indicates previous myocardial infarction (MI).
R Wave Progression
- Normal: R wave increases from V1 to V5.
- Poor R wave progression: anterior MI, LVH, conduction abnormalities.
QRS Duration Abnormalities
- Wide QRS (>0.12 s): Bundle branch blocks, ventricular pacing, hyperkalemia.
- Narrow QRS: Normal or supraventricular arrhythmias.
Amplitude Variations
- Low voltage QRS (<5 mm limb leads, <10 mm precordial): pericardial effusion, obesity, hypothyroidism.
- High voltage: LVH, RVH, athletic heart.

Section 5: The ST Segment and J Point

Though not a wave, the ST segment connects the QRS and T wave.

Represents early ventricular repolarization (Phase 2 plateau).
Usually isoelectric.
Elevation: Acute MI, pericarditis, early repolarization.
Depression: Myocardial ischemia, digitalis effect, LVH strain pattern.

Section 6: The T Wave

6.1 Physiological Basis

The T wave represents ventricular repolarization.
Reflects Phase 3 K⁺ efflux returning ventricular myocytes to resting potential.
Direction generally same as QRS due to coordinated repolarization.

6.2 Morphology

Upright in most leads (I, II, V3–V6).
Amplitude: 0.5–10 mm in limb leads, 10–15 mm in precordial leads.
Duration: 0.10–0.25 s.

6.3 Clinical Significance

T Wave Inversions
- Myocardial ischemia, ventricular hypertrophy, bundle branch block.
Peaked T Waves
- Hyperkalemia → tented, symmetrical T waves.
Flattened T Waves
- Hypokalemia, hypomagnesemia, digitalis effect.
Biphasic T Waves
- Can indicate ischemia, particularly Wellens’ syndrome (critical LAD stenosis).

Section 7: QT Interval

Measured from start of QRS to end of T wave.
Represents total ventricular depolarization and repolarization.
Normal: <440 ms (men), <460 ms (women).

Clinical Significance

Prolonged QT: Risk of torsades de pointes, congenital long QT syndromes, electrolyte disturbances, drugs (antiarrhythmics, antibiotics).
Shortened QT: Hypercalcemia, digoxin effect.

Section 8: ECG Lead Systems and Wave Orientation

Limb leads (I, II, III, aVR, aVL, aVF): Frontal plane.
Precordial leads (V1–V6): Horizontal plane.
Wave morphology can differ by lead due to vector orientation of depolarization/repolarization.

Section 9: Common Abnormal ECG Patterns

9.1 Atrial Abnormalities

P mitrale, P pulmonale, absent P waves (AF).

9.2 Ventricular Hypertrophy

LVH: High-amplitude R waves in left precordial leads, deep S in right leads.
RVH: Tall R in V1, right axis deviation.

9.3 Myocardial Infarction

ST elevation, pathological Q waves, T wave inversion depending on MI stage and territory.

9.4 Conduction Blocks

Bundle branch blocks: Wide QRS with characteristic morph