Electrocardiogram (ECG) - A Detailed Explanation

What Is an ECG?

• Guyton and Hall Textbook of Medical Physiology, p. 142

The Cardiac Conduction System - The Origin of the ECG Signal

1. SA node (right atrium, near SVC junction) - the natural pacemaker, fires spontaneously at 60-100 bpm
2. Depolarization spreads across both atria → atrial contraction → produces the P wave
3. Impulse reaches the AV node - conduction deliberately slows here (physiologic delay ~100-200 ms), allowing ventricles to fill before contracting → produces the PR interval
4. Impulse passes through the Bundle of His → splits into right and left bundle branches
5. Left bundle branch fans into left anterior and left posterior fascicles
6. Signal reaches Purkinje fibers → rapidly activates ventricular myocardium endocardium-to-epicardium → produces the QRS complex
7. Ventricular muscle then repolarizes → produces the T wave

• Harrison's Principles of Internal Medicine 22E, p. 1911

The Normal ECG Waveform - All Waves and Intervals

The Complete ECG Diagram with Labeled Intervals:

Relationship of ECG to the Action Potential:

Each Wave Explained in Detail

1. P Wave

• Represents: Atrial depolarization
• Duration: 80-100 ms (0.08-0.10 s)
• Amplitude: Up to 2.5 mm in height; up to 120 ms in width
• Morphology: Small, rounded, positive in leads I, II, aVF, V4-V6
• Physiology: SA node fires → depolarization spreads across right then left atrium → atrial contraction begins at the onset of P wave
• Note: Atrial repolarization (atrial T wave) also occurs, but it is buried under the large QRS complex and is not normally visible

2. PR Interval

• Measured: From start of P wave to start of QRS complex
• Normal: 120-200 ms (3-5 small squares on ECG paper)
• Represents: Time from start of atrial depolarization to start of ventricular depolarization - essentially the AV nodal delay
• Clinical significance:
  • Short PR (<120 ms) → Pre-excitation (e.g., WPW syndrome) or junctional rhythm
  • Long PR (>200 ms) → First-degree AV block

3. PR Segment

• The flat (isoelectric) line between the end of the P wave and the start of QRS
• Represents electrical silence while the impulse creeps through the AV node and His bundle
• Used as the baseline reference for measuring ST deviation

4. QRS Complex

• Represents: Ventricular depolarization
• Normal duration: 80-100 ms (up to 110 ms is acceptable); if >120 ms → bundle branch block
• Components:
  • Q wave - first negative deflection; represents initial septal depolarization (left to right)
  • R wave - first positive deflection after Q; tall R in lateral leads means good left ventricular function
  • S wave - negative deflection after R; represents basal depolarization
• Physiology: Rapid phase 0 upstroke of the ventricular action potential corresponds to QRS onset; impulse travels endocardium → epicardium via Purkinje system
• Clinical significance: Wide QRS (>120 ms) = LBBB, RBBB, hyperkalemia, ventricular tachycardia, or sodium channel blockers

5. ST Segment

• From: J point (junction of QRS end and ST start) to start of T wave
• Normal: Isoelectric (on the baseline); corresponds to phase 2 (plateau) of action potential when all ventricular cells are equally depolarized so no net current flows
• J point - the junction between QRS and ST segment
• Clinical significance:
  • ST elevation → STEMI (transmural ischemia), pericarditis, Brugada syndrome
  • ST depression → NSTEMI, subendocardial ischemia, digoxin effect

6. T Wave

• Represents: Ventricular repolarization
• Duration: 0.10-0.25 s (prolonged because repolarization is not simultaneous - different fibers repolarize at different times, from epicardium to endocardium, opposite to depolarization)
• Normal morphology: Upright and asymmetric; ascending limb is gradual, descending limb is steeper; positive in I, II, V3-V6
• Clinical significance:
  • Peaked T waves → Hyperkalemia (earliest change), hyperacute STEMI
  • Flat/inverted T waves → Ischemia, LVH, bundle branch block, electrolyte disturbance

7. QT Interval

• Measured: From start of QRS to end of T wave
• Represents: Total ventricular depolarization + repolarization time
• Normal: Rate-dependent; corrected QT (QTc) should be <450 ms in men, <460 ms in women (Framingham formula: QTc = QT + 0.154 × (1000 - RR) in ms)
• Physiology: Corresponds to phases 0, 1, 2, and 3 of ventricular action potential
• Clinical significance: Prolonged QTc → risk of Torsades de Pointes and sudden death; caused by drugs (amiodarone, antipsychotics, macrolides), hypocalcemia, hypokalemia, hypomagnesemia, congenital long QT syndromes

8. U Wave

• Small, positive deflection after T wave (not always visible)
• Origin: Likely late repolarization of Purkinje fibers or mid-myocardial M cells
• More prominent in: Hypokalemia, bradycardia, hypothermia
• Inverted U wave → may indicate ischemia or LVH
• Guyton and Hall Textbook of Medical Physiology, p. 143-144
• Harrison's Principles of Internal Medicine 22E, pp. 1911-1912

ECG Grid Paper - How to Read the Paper

• Count RR interval in large squares → Rate = 300 ÷ (number of large squares between R waves)
• Or: Rate = 1500 ÷ (number of small squares between R waves)

The 12-Lead ECG - Viewing the Heart from Multiple Angles

Limb Leads (Frontal Plane):

Precordial (Chest) Leads (Horizontal Plane):

• Harrison's Principles of Internal Medicine 22E, p. 1912

ECG in Context of the Cardiac Cycle

• P wave → Atrial systole ("atrial kick")
• End of R wave → Mitral/tricuspid valve closure (S1 heart sound); beginning of isovolumic contraction
• QRS complex → Start of ventricular systole; ventricular pressure rises rapidly
• ST segment → Isovolumic contraction → then rapid ejection → aortic valve opens
• T wave → Ventricular repolarization; corresponds to end of systole and start of isovolumic relaxation
• After T wave → AV valves open; ventricular filling begins (diastole)

Quick Summary Table of Normal Intervals

Clinical Uses of the ECG

1. Myocardial infarction - ST elevation, Q waves, T wave changes
2. Arrhythmias - Rate, rhythm, P wave morphology, RR regularity
3. Bundle branch blocks - Wide QRS (>120 ms), characteristic morphology
4. Electrolyte disturbances - Hyperkalemia (tall peaked T → wide QRS → sine wave), hypokalemia (U waves, flat T), hypercalcemia (short QT)
5. Drug toxicity - Digoxin (downsloping ST, short QT), quinidine/amiodarone (long QT)
6. Chamber hypertrophy - Voltage criteria for LVH, RVH, atrial enlargement
7. Pericarditis - Diffuse saddle-shaped ST elevation, PR depression

• Harrison's Principles of Internal Medicine 22E, pp. 1911-1916
• Guyton and Hall Textbook of Medical Physiology, p. 142-145
• Miller's Anesthesia, 10e, pp. 1364-1368