The electrocardiogram (ECG) is the graphic representation of electrical activity in the heart. Each wave and interval corresponds to specific events in the cardiac conduction system and the working myocardium.
ECG Waves and Their Anatomic Correlates
P Wave: Atrial Depolarization
Origin: SA node activation spreads through the right and left atria
Duration: < 120 ms (3 small squares)
Normal amplitude: < 2.5 mm (0.25 mV) in II, < 1.5 mm in V1
Components:
- Initial portion (first third): Right atrial depolarization
- Terminal portion (last third): Left atrial depolarization
- Mid portion: Combined right and left atrial depolarization
Anatomic correlates:
- P wave begins: SA node fires (crista terminalis area)
- Right atrial activation: Via crista terminalis and Bachmann bundle
- Left atrial activation: Via Bachmann bundle (interatrial pathway)
- P wave ends: Last atrial tissue depolarized (left atrial appendage)
Abnormal P waves:
| Finding | Anatomic Correlate | Etiology |
|---|---|---|
| Right atrial enlargement (P pulmonale) | Tall, peaked P in II, III, aVF | RVH, pulmonary hypertension, COPD |
| Left atrial enlargement (P mitrale) | Bifid P in II, prolonged negative P in V1 | Mitral stenosis, LVH, cardiomyopathy |
| Biatrial enlargement | Tall + bifid P | Mixed pathology |
| Flutter waves (sawtooth) | Rapid atrial activity without P waves | Atrial flutter (right atrial reentry) |
PR Interval: AV Conduction
Origin: Impulse travels from SA node through atria, AV node, Bundle of His, and bundle branches
Duration: 120-200 ms (3-5 small squares)
Components:
- Atrial conduction: 60-80 ms (through atrial myocardium)
- AV node delay: 80-120 ms (the major component)
- His-Purkinje conduction: 30-50 ms
Anatomic correlates:
- PR segment begins: Atrial depolarization complete
- AV node: Impulse slows in the compact node
- Bundle of His: Fast conduction through the penetrating bundle
- Purkinje system: Rapid distribution to ventricular myocardium
Abnormal PR intervals:
| Finding | Anatomic Correlate | Etiology |
|---|---|---|
| Prolonged PR (> 200 ms) | First-degree AV block | AV node delay (most common) |
| Short PR (< 120 ms) | Pre-excitation | Accessory pathway (WPW), accelerated AV conduction |
| Variable PR | Wenckebach block | AV nodal ischemia, drug effect |
| Fixed PR with dropped QRS | Mobitz II block | Infranodal disease (His-Purkinje) |
QRS Complex: Ventricular Depolarization
Origin: Activation of the ventricular myocardium via the His-Purkinje system
Duration: 80-110 ms (2-3 small squares)
Normal amplitude: Highly variable by lead
Components:
- Septal Q wave: Initial septal activation (left-to-right)
- R wave progression: Anterior-to-posterior activation
- Terminal S wave: Late basal activation
Anatomic correlates:
- Initial 10-20 ms: Septal depolarization (left to right)
- 20-40 ms: Apical depolarization (free walls)
- 40-60 ms: Lateral wall depolarization
- 60-100 ms: Basal and posterolateral depolarization
Q wave significance:
- Small septal Q: Normal, < 40 ms, < 1/3 R wave amplitude
- Pathologic Q: > 40 ms, > 1/3 R wave amplitude, indicates infarction
ST Segment: Early Ventricular Repolarization
Origin: Phase 2 of the ventricular action potential (plateau phase)
Duration: 80-120 ms
Normal: Isoelectric (same level as TP segment)
Anatomic correlates:
- All ventricular cells are depolarized (no voltage difference)
- Small currents at the border of ischemic tissue cause elevation or depression
T Wave: Ventricular Repolarization
Origin: Phase 3 of the ventricular action potential
Duration: 120-200 ms
Normal: Upright in most leads (except aVR, V1 may be inverted)
Anatomic correlates:
- Ventricular repolarization
- Opposite direction to QRS (discordance is normal in precordial leads)
- Longer than QRS due to slower repolarization
T wave morphology and anatomy:
- Dispersion of repolarization: Endocardium to epicardium gradient
- M cells: Mid-myocardial cells have longest APD, create the T wave peak
- Purkinje fibers: Longest APD in the heart, contribute to terminal T wave
U Wave
Origin: Controversial, likely Purkinje fiber repolarization or late repolarization of M cells
Duration: Appears after T wave, best seen in V2-V3
Normal: Small, same direction as T wave
Abnormal U waves:
- Prominent U: Hypokalemia, bradycardia, drug effect (amiodarone)
- Inverted U: Ischemia, left ventricular hypertrophy
ECG Intervals and Their Anatomic Significance
RR Interval
Distance between consecutive R waves
Significance:
- Represents the cardiac cycle length
- Determines heart rate
- Variation indicates sinus arrhythmia or atrial fibrillation
QT Interval
Anatomic correlates:
- Total duration of ventricular action potential
- Includes depolarization + repolarization
- Prolonged QT: Increased risk of torsades de pointes
QT prolongation mechanisms:
- Congenital: Ion channel mutations (KCNQ1, KCNH2, SCN5A)
- Acquired: Drugs, electrolyte abnormalities, ischemia
Lead Systems and Cardiac Anatomy
Limb Leads (Bipolar: I, II, III)
| Lead | Positive Electrode | Negative Electrode | Cardiac View |
|---|---|---|---|
| I | Left arm | Right arm | Lateral wall (high) |
| II | Left leg | Right arm | Inferior wall |
| III | Left leg | Left arm | Inferior wall (right) |
Augmented Limb Leads (Unipolar: aVR, aVL, aVF)
| Lead | Positive Electrode | Cardiac View |
|---|---|---|
| aVR | Right arm | Right atrium, LV base (internal) |
| aVL | Left arm | High lateral wall |
| aVF | Left foot | Inferior wall |
Precordial Leads (V1-V6)
| Lead | Position | Cardiac View |
|---|---|---|
| V1 | Right 4th intercostal space, sternal edge | Septum, RV |
| V2 | Left 4th intercostal space, sternal edge | Septum, anterior |
| V3 | Between V2 and V4 | Anterior wall |
| V4 | Left 5th intercostal space, midclavicular | Anterior wall, apex |
| V5 | Left 5th intercostal space, anterior axillary | Lateral wall |
| V6 | Left 5th intercostal space, midaxillary | Lateral wall |
ECG Patterns in Conduction Abnormalities
SA Node Dysfunction
| Pattern | Finding | Mechanism |
|---|---|---|
| Sinus bradycardia | HR < 60, normal P waves | Reduced SA node automaticity |
| Sinus arrest | Absent P wave, pause > 3s | SA node fails to fire |
| SA exit block | Pause is multiple of PP interval | Block between SA node and atria |
| Tachy-brady syndrome | Alternating fast and slow rates | SA node disease with atrial fibrillation |
AV Node Dysfunction
| Pattern | Finding | Location of Block |
|---|---|---|
| First-degree AVB | PR > 200 ms, all conducted | AV node (usually) |
| Mobitz I (Wenckebach) | Progressive PR, dropped QRS | AV node |
| Mobitz II | Fixed PR, dropped QRS | Infranodal |
| Complete heart block | AV dissociation | Varies |
Bundle Branch Block
RBBB:
- QRS > 120 ms
- rSR in V1-V2 (rabbit ears)
- Wide S in I, V6
- Causes: RVH, PE, CAD, normal variant
LBBB:
- QRS > 120 ms
- Broad, notched R in I, V5, V6
- No Q in I, V5, V6
- Causes: HTN, AS, CAD, cardiomyopathy
Fascicular Block
LAFB:
- Left axis deviation (-45 to -90)
- Normal QRS duration
- qR in I, rS in II, III, aVF
LPFB:
- Right axis deviation (+90 to +180)
- Normal QRS duration
- rS in I, qR in II, III, aVF
Clinical Approach to ECG-Anatomy Correlation
Step-by-step Analysis
- Rate: Determine if sinus rhythm or not (P wave analysis)
- P wave: Look for atrial abnormality
- PR interval: Assess AV conduction
- QRS width: Assess ventricular conduction
- QRS axis: Determine fascicular block or ventricular hypertrophy
- ST segment: Look for ischemia or injury
- T wave: Assess repolarization abnormalities
- QT interval: Assess for long QT syndrome
Localization of Myocardial Infarction
| Territory | ECG Leads | Coronary Artery |
|---|---|---|
| Anterior | V3-V4 | LAD (mid) |
| Anteroseptal | V1-V2 | LAD (proximal, septal) |
| Anterolateral | V5-V6, I, aVL | LAD (diagonal) or LCx |
| Extensive anterior | V1-V6, I, aVL | LAD (proximal) |
| Inferior | II, III, aVF | RCA or LCx |
| Lateral | I, aVL, V5-V6 | LCx |
| Posterior | ST depression V1-V3 | RCA (PDA) or LCx |
| Right ventricle | V4R | RCA (proximal) |