Explain in depth about ECG

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Electrocardiogram (ECG) - In-Depth Guide

1. What is an ECG?

An ECG (electrocardiogram, also written EKG from the German Elektrokardiogramm) is a graphical recording of the electrical potential differences generated by the heart, captured at the body surface. Because body fluids are good conductors (the body acts as a volume conductor), the algebraic sum of action potentials from millions of myocardial cells can be detected by surface electrodes. The result is a time-voltage tracing that reflects the sequence of electrical activation and recovery across the heart with each beat.

Ganong's Review of Medical Physiology, 26th Ed.

2. The Cardiac Conduction System (Basis of the ECG)

Before the ECG waveform makes sense, you must understand the electrical highway it reflects:

Normal spread of electrical activity in the heart - conduction system and corresponding ECG

Figure: Cardiac conduction system (A) and sequence of electrical activation with corresponding ECG waveforms (B). From Ganong's Review of Medical Physiology.

Structure	Function	Normal Conduction Velocity
SA node	Primary pacemaker; intrinsic rate 60-100/min	Slow (~0.05 m/s)
Internodal pathways	Spread depolarization through atria	Moderate
AV node	Gatekeeper; delays impulse ~0.1 s	Very slow (~0.05 m/s) - this delay is the PR interval
Bundle of His	Connects AV node to bundle branches	Fast
Left & right bundle branches	Transmit impulse rapidly to ventricles	Very fast (~2 m/s)
Purkinje fibers	Terminal network; depolarizes all ventricular myocytes in 0.08-0.1 s	Fastest (~4 m/s)

The AV nodal delay is modulated by the autonomic nervous system: sympathetic stimulation shortens it (speeds HR), vagal stimulation lengthens it (slows HR). Ventricular depolarization begins at the left side of the interventricular septum, sweeps across the mid-septum to the right, then down the septum to the apex, then back up the ventricular walls from endocardium to epicardium. The last regions to depolarize are the posterobasal left ventricle, pulmonary conus, and upper septum.

3. ECG Waveforms, Segments, and Intervals

Figure: Standard ECG waveform with all named components. From Ganong's Review of Medical Physiology, 26th Ed.

Waves

Wave	Represents	Normal Duration/Amplitude
P wave	Atrial depolarization (SA node → both atria)	Duration < 0.12 s; amplitude < 2.5 mm
Q wave	Initial septal depolarization (left→right)	Small, < 1/4 of R-wave height; < 0.04 s
R wave	Main ventricular depolarization (downward sweep)	Largest positive deflection
S wave	Terminal ventricular depolarization (base of heart)	Small negative deflection
T wave	Ventricular repolarization	Broad, upright; direction normally same as QRS
U wave	Inconstant; possibly ventricular myocytes with long action potentials	Small positive deflection after T wave

Why is there no "atrial repolarization wave"? Atrial repolarization is buried within the much larger QRS complex.

Intervals and Segments

Interval	Normal Value	Represents
PR interval	0.12-0.20 s (average 0.18 s)	AV conduction time (atria → ventricles through AV node)
QRS duration	< 0.10 s (average 0.08 s)	Ventricular depolarization
ST segment	Isoelectric (at baseline)	Period between ventricular depolarization and repolarization - all cells equally depolarized
QT interval	Up to 0.43 s (rate-corrected QTc < 0.44 s)	Duration of ventricular action potential (depol + repol)
PR segment	Isoelectric	Conduction through AV node + His-Purkinje

The isoelectric line (baseline) represents the period when no net electrical activity is detectable.

4. ECG and the Cardiac Cycle

Cardiac cycle diagram showing ventricular pressure, aortic pressure, ventricular volume, heart sounds, venous pulse, and ECG over time

Figure: Electrical and mechanical events during a single cardiac cycle correlated with the ECG. From Miller's Anesthesia, 10th Ed.

The ECG correlates precisely with the mechanical cardiac cycle:

P wave → onset of atrial systole (atrial "kick")
End of R wave (QRS) → mitral/tricuspid valves close; ventricular systole begins
QRS complex → isovolumetric contraction → ventricular ejection (aortic/pulmonic valves open)
T wave → isovolumetric relaxation; ventricular repolarization
After T wave → rapid ventricular filling begins
Miller's Anesthesia, 10th Ed.

5. ECG Leads: How the 12-Lead ECG is Built

The standard 12-lead ECG uses 10 electrodes to generate 12 views of cardiac electrical activity.

Lead placement diagram showing V1-V6 chest positions and aVR, aVL, aVF on the torso

Figure: Electrode placement for unipolar leads (precordial V1-V6 and augmented limb leads aVR, aVL, aVF). From Ganong's Review of Medical Physiology, 26th Ed.

Bipolar Limb Leads (Einthoven's Triangle)

These record the potential difference between two limb electrodes:

Lead	Positive electrode	Negative electrode	View
I	Left arm (LA)	Right arm (RA)	Lateral
II	Left leg (LL)	Right arm (RA)	Inferior
III	Left leg (LL)	Left arm (LA)	Inferior

Einthoven's law: Lead II = Lead I + Lead III at any instant.

Augmented Unipolar Limb Leads

These record potential at a single limb against the average of the other two:

Lead	Electrode	View
aVR	Right arm	Looks into the cavities of ventricles; all major deflections normally negative
aVL	Left arm	High lateral wall
aVF	Left foot	Inferior wall

Precordial (Chest) Leads V1-V6

Six electrodes placed on the anterior chest wall:

Lead	Position	Anatomic Region
V1	4th intercostal space, right sternal border	Septal/RV
V2	4th intercostal space, left sternal border	Septal/RV
V3	Between V2 and V4	Anterior
V4	5th intercostal space, midclavicular line	Anterior/apex
V5	Anterior axillary line	Lateral
V6	Midaxillary line	Lateral

R-wave progression: In normal hearts, the R wave grows progressively from V1 (small or absent) to V5/V6 (large), reflecting the transition from right-sided to left-sided dominance.

Ganong's Review of Medical Physiology, 26th Ed.

6. The Electrical Axis

The mean QRS axis is the average direction of ventricular depolarization in the frontal plane, estimated from the limb leads using the Einthoven triangle.

Normal axis: -30° to +110°
Left axis deviation (LAD): < -30° → suggests left ventricular hypertrophy, left anterior fascicular block
Right axis deviation (RAD): > +110° → suggests right ventricular hypertrophy, left posterior fascicular block, pulmonary embolism

A quick clinical trick: if the QRS is positive in Lead I and positive in aVF, the axis is normal.

7. Systematic ECG Interpretation - Step-by-Step Approach

A structured approach prevents missing findings:

Rate - Count R-R intervals. At 25 mm/s paper speed: Rate = 300 ÷ number of large boxes between R waves
- Normal: 60-100/min
- Bradycardia: < 60/min
- Tachycardia: > 100/min
Rhythm - Is it regular? Is there a P wave before every QRS? Is every P followed by a QRS?
Axis - Normal, LAD, or RAD?
P wave - Morphology, duration, axis (should be upright in I and II)
PR interval - Normal 0.12-0.20 s
QRS complex - Width (< 0.10 s = narrow = supraventricular origin; > 0.12 s = wide = bundle branch block or ventricular origin), morphology
ST segment - Elevation or depression from baseline?
T wave - Upright, inverted, peaked?
QT interval - Corrected QTc = QT ÷ √(RR interval in seconds) [Bazett formula]

8. Key Pathological Patterns

Myocardial Infarction

The ECG evolves through stages in STEMI:

Stage	ECG Finding
Hyperacute (minutes)	Tall, peaked T waves (hyperacute T waves)
Acute (hours)	ST-segment elevation (tombstone pattern in severe cases)
Hours-days	Q waves develop; T waves invert
Weeks-months	Q waves persist; ST returns to baseline

Localizing the infarct by leads:

Territory	Leads with changes	Artery
Anterior	V1-V4	LAD
Inferior	II, III, aVF	RCA (or LCx)
Lateral	I, aVL, V5-V6	LCx
Posterior	Tall R in V1, ST depression V1-V2	RCA/LCx
Right ventricular	ST elevation in V1, V4R	RCA

NSTEMI/UA: ST depression and/or T-wave inversions without ST elevation.

Heart Block (AV Conduction Disorders)

Type	ECG Feature
1st degree	PR interval > 0.20 s; all P waves conduct
2nd degree Mobitz I (Wenckebach)	Progressive PR lengthening until a P wave is not conducted; pattern repeats
2nd degree Mobitz II	Fixed PR interval with sudden non-conducted P waves; high risk of progression
3rd degree (complete)	P waves and QRS complexes are completely dissociated; ventricular rate 35-45/min (Stokes-Adams syndrome with syncope)

Bundle Branch Blocks

RBBB: Wide QRS > 0.12 s, RSR' ("rabbit ears") in V1, slurred S in I, V5, V6
LBBB: Wide QRS > 0.12 s, broad R in I, V5, V6 with no septal Q; discordant ST/T changes

Atrial Fibrillation

Absent P waves; replaced by chaotic fibrillatory baseline
Irregularly irregular RR intervals
Narrow QRS (unless aberrant conduction)

Atrial Flutter

Sawtooth flutter waves at 250-350/min in inferior leads (II, III, aVF)
Regular ventricular response at 2:1, 3:1, or 4:1 block

Ventricular Tachycardia

Wide QRS (> 0.12 s), rate 100-250/min, AV dissociation
Capture beats and fusion beats are pathognomonic

Long QT Syndrome

QTc > 0.44 s (men) / 0.46 s (women)
Risk of Torsades de Pointes
Causes: congenital (LQT1-LQT8), drugs (antiarrhythmics, macrolides, antipsychotics), hypokalemia, hypomagnesemia

9. His Bundle Electrogram (HBE)

In complex conduction disorders, an invasive catheter-mounted electrode near the tricuspid valve records the His bundle electrogram, showing:

A deflection: AV nodal activation
H spike: His bundle conduction
V deflection: Ventricular depolarization

Normal intervals: PA ~27 ms, AH ~92 ms, HV ~43 ms. The AH interval reflects AV nodal conduction time; prolongation indicates AV nodal disease.

10. ECG Monitoring Modalities

Type	Use
Standard 12-lead ECG	Snapshot diagnosis - arrhythmia, ischemia, blocks
Holter monitor (24-48 h)	Ambulatory continuous recording; detects paroxysmal arrhythmias, sick sinus syndrome
Event monitor / loop recorder	Patient-activated; weeks to months; for infrequent palpitations/syncope
Exercise stress ECG	Provokes ischemia (ST changes) under controlled exertion; sensitivity ~70%, specificity ~75% for CAD
ICU/telemetry monitoring	Continuous rhythm monitoring with alarm systems
Implantable loop recorder	Subcutaneous device; up to 3 years; for unexplained syncope

11. Clinical Applications Summary

Indication	What the ECG Shows
Chest pain	ST elevation/depression, T-wave changes - rule in/out ACS
Palpitations	Arrhythmia type, rate, regularity
Syncope	Arrhythmia, block, long QT, Brugada pattern
Shortness of breath	RV strain (PE), LVH, atrial fibrillation
Electrolyte disturbances	Hyperkalemia (peaked T, wide QRS, sine wave), hypokalemia (flat T, U waves, ST depression)
Drug toxicity	QT prolongation, digoxin toxicity (scooped ST, bidirectional VT)
Pre-operative assessment	Baseline rhythm, LVH, old infarcts, conduction disease

Key references:

Ganong's Review of Medical Physiology, 26th Ed. - Chapter 29, "The Electrocardiogram"
Miller's Anesthesia, 10th Ed. - Chapter 13, "Electrical Events and the ECG"
Tintinalli's Emergency Medicine - ECG in ACS
Goldman-Cecil Medicine - Coronary artery disease and ECG patterns

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