Electrocardiogram (ECG) - A Detailed Guide

What Is an ECG?

• Goldman-Cecil Medicine, p. 420

1. The Cardiac Electrical Basis

The Conduction System

1. SA Node (Sinoatrial node) - Located in the high lateral epicardial right atrium near the superior vena cava. It spontaneously depolarizes at the highest rate (~60-100/min), making it the dominant pacemaker. Its depolarization is not visible on the surface ECG.
2. Atrial conduction - The depolarizing wavefront spreads through the right and left atria. The Bachmann bundle speeds conduction to the left atrium. Atrial depolarization triggers contraction, pushing blood through the mitral and tricuspid valves.
3. AV Node - The only normal electrical bridge between atria and ventricles (the AV valve rings are electrically insulated). The AV node intentionally slows conduction, providing the delay that allows atrial contraction to fill the ventricles before ventricular systole.
4. Bundle of His - Exits the AV node; specialized fast-conducting tissue.
5. Bundle Branches - The His bundle bifurcates into right bundle branch (RBB) and left bundle branch (LBB). The LBB further divides into left anterior fascicle (LAF) and left posterior fascicle (LPF).
6. Purkinje Fibers - The distal ramifications that deliver the impulse rapidly to ventricular myocardium.
7. Ventricular myocardium - Depolarizes from endocardium to epicardium, triggering ventricular contraction.

• Goldman-Cecil Medicine, p. 421; Guyton and Hall, p. 142

2. The ECG Waveforms

P Wave

• Represents atrial muscular depolarization
• Normally small, rounded, upright in most leads
• Normal amplitude: 0.1-0.3 mV; duration < 120 msec
• Absent in atrial fibrillation; abnormally tall in right atrial enlargement; wide/notched in left atrial enlargement

PR Interval

• Measured from the onset of the P wave to the onset of the QRS complex
• Represents: conduction time through atrial muscle + AV node delay + His-Purkinje system
• Normal: 0.09 to 0.20 second (90-200 msec)
• PR > 200 msec = first-degree AV block (delayed AV conduction)
• Short PR = ventricular preexcitation (Wolff-Parkinson-White syndrome) or junctional rhythm

QRS Complex

• Represents ventricular muscular depolarization
• Much larger than the P wave due to greater ventricular muscle mass
• Normal duration: 75-110 msec (< 3 small boxes); duration ≥ 120 msec = bundle branch block
• Wave naming convention:
  • Capital letters (Q, R, S) = large amplitude (≥ 5 mm / 0.5 mV)
  • Lowercase letters (q, r, s) = small amplitude (< 5 mm / 0.5 mV)
  • Q/q = initial negative deflection
  • R/r = positive deflection
  • S/s = negative deflection following an R wave
  • QS complex = entirely negative deflection
  • R' = second positive deflection after S wave

ST Segment

• The flat segment from the end of the QRS (J point) to the start of the T wave
• Normally isoelectric (on the baseline)
• ST elevation = myocardial injury/infarction, pericarditis, Brugada syndrome
• ST depression = ischemia, posterior MI, digitalis effect

T Wave

• Represents ventricular repolarization
• Ventricular repolarization begins ~0.20 seconds after QRS onset and extends for about 0.15 second
• Normally concordant with the QRS (same direction as main QRS deflection)
• Broader and lower amplitude than QRS because repolarization is more prolonged
• Inverted T waves suggest ischemia, ventricular hypertrophy, or bundle branch block

QT Interval

• Measured from QRS onset to end of T wave
• Represents the total ventricular depolarization + repolarization time
• Must be corrected for heart rate using Bazett's formula:

  QTc = QT / √RR (RR interval in seconds)

• Normal QTc: < 440 msec in men, < 460 msec in women
• Prolonged QTc increases risk of torsades de pointes (a life-threatening ventricular arrhythmia)
• Shortened by hypercalcemia, digitalis; prolonged by hypokalemia, hypomagnesemia, many drugs

U Wave

• A small, positive deflection after the T wave
• Likely represents late repolarization of Purkinje fibers or mid-myocardial (M) cells
• More prominent at slow heart rates and in hypokalemia
• Prominent U waves are a classic sign of hypokalemia

J Point and J Wave

• J point = junction between end of QRS and beginning of ST segment
• J wave (Osborn wave) = positive deflection at the J point; classically seen in hypothermia; also in hypercalcemia and brain injury; may indicate risk of idiopathic ventricular fibrillation
• Goldman-Cecil Medicine, pp. 421-423; Guyton and Hall, pp. 142-144

3. ECG Paper and Calibration

4. The 12 ECG Leads

Limb Leads (Bipolar) - Leads I, II, III

• Lead I: Left arm (+) vs Right arm (-) - views left lateral wall
• Lead II: Left leg (+) vs Right arm (-) - views inferior wall
• Lead III: Left leg (+) vs Left arm (-) - views inferior wall

Augmented Limb Leads (Unipolar) - aVR, aVL, aVF

• aVR (augmented Vector Right): looks at the heart from the right shoulder
• aVL (augmented Vector Left): looks from the left shoulder
• aVF (augmented Vector Foot): looks from below (inferior view)

Precordial (Chest) Leads - V1 through V6

5. Calculating Heart Rate

• Regular rhythm: Rate = 300 ÷ (number of large boxes between R waves)
• Or: Rate = 1500 ÷ (number of small boxes between R waves)
• Irregular rhythm: Count QRS complexes in a 10-second strip × 6

6. Cardiac Axis

7. Common Abnormal Patterns

Bundle Branch Blocks

• LBBB (Left Bundle Branch Block): QRS ≥ 120 msec; broad notched R in V5/V6 (M-shaped), deep S in V1; no septal q waves in lateral leads; discordant ST-T changes. Isolated LBBB doubles cardiovascular risk.
• RBBB (Right Bundle Branch Block): QRS ≥ 120 msec; RSR' ("rabbit ears") in V1, broad S wave in I, V5, V6.

AV Blocks

• 1st degree: PR > 200 msec; every P wave conducts
• 2nd degree - Mobitz I (Wenckebach): Progressive PR lengthening until a P wave is blocked (non-conducted)
• 2nd degree - Mobitz II: Constant PR, then sudden non-conducted P wave; higher risk of complete block
• 3rd degree (complete): No relationship between P waves and QRS; complete AV dissociation

ST Changes

• ST elevation: STEMI (localized to territory), pericarditis (diffuse, saddle-shaped), Brugada (V1-V2 coved pattern)
• ST depression: NSTEMI/unstable angina, subendocardial ischemia, posterior STEMI (reciprocal)

Hypertrophy

• LVH: Increased QRS voltages (e.g., S in V1 + R in V5 or V6 ≥ 35 mm = Sokolov-Lyon criterion); lateral ST-T changes
• RVH: Dominant R in V1, right axis deviation, deep S in lateral leads

8. Clinical Uses of the ECG

• Arrhythmias (AF, flutter, SVT, VT, VF, bradycardias)
• Acute myocardial infarction (STEMI, NSTEMI)
• Conduction defects (bundle branch blocks, fascicular blocks, AV blocks)
• Electrolyte abnormalities (hyperkalemia peaked T waves and sine wave; hypokalemia U waves; hypercalcemia short QT)
• Drug effects (digoxin "reverse tick" ST depression; QT-prolonging drugs)
• Structural disease (hypertrophy, pre-excitation syndromes)
• Pericarditis and myocarditis

9. Limitations

• A normal ECG does not exclude cardiac disease (e.g., significant CAD between events)
• Single time-point recordings miss intermittent arrhythmias - ambulatory (Holter) monitoring records over 24-48 hours for infrequent events
• Computerized interpretation algorithms improve accuracy but require physician review
• Obesity, emphysema, and poor electrode contact reduce signal quality

Summary Table: Normal ECG Intervals

• Goldman-Cecil Medicine International Edition, Chapter 42: Electrocardiography, pp. 420-423
• Guyton and Hall Textbook of Medical Physiology, Chapter 11: Fundamentals of Electrocardiography, pp. 142-148

What's inside (13 slides, deep navy + crimson theme):