ECG

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What is an ECG?

The electrocardiogram (ECG or EKG) is a recording of tiny potential differences on the body surface that reflect the electrical activity of the heart. Because cardiac depolarization and repolarization wavefronts have both direction and magnitude, they can be represented as vectors and recorded from multiple spatial angles simultaneously. - Costanzo Physiology 7th Edition

Cardiac Conduction System (The Basis of the ECG)

Cardiac conduction system showing SA node, AV node, His bundle, bundle branches, and Purkinje fibers

The normal sequence of electrical activation:

SA node (high lateral right atrium) - dominant pacemaker due to fastest spontaneous depolarization rate
Impulse spreads through right and left atria (Bachmann bundle speeds conduction to left atrium)
AV node - physiologic conduction delay (the only normal electrical bridge between atria and ventricles)
Bundle of His → bifurcates into right bundle branch and left bundle branch (which further divides into left anterior and left posterior fascicles)
Purkinje fibers → rapid spread to ventricular myocardium (endocardium to epicardium)

The Purkinje system conducts far faster than atrial tissue, which is why the QRS complex (large ventricles) has a similar duration to the P wave (smaller atria). - Harrison's Principles of Internal Medicine 22E

The Basic ECG Waveforms and Intervals

Normal ECG waveform from lead II showing P wave, QRS complex, ST segment, T wave, PR interval, and QT interval

Fig. 4.17 - ECG measured from lead II. (Costanzo Physiology 7th Ed.)

Waves

Wave	Represents	Notes
P wave	Atrial depolarization	Duration reflects atrial conduction time. Atrial repolarization is buried under QRS and not seen.
Q wave	Initial septal depolarization	Pathologic if >40 ms wide or >25% of R wave height
R wave	Main ventricular depolarization	Positive (upward) deflection
S wave	Terminal ventricular depolarization	Negative deflection after R
T wave	Ventricular repolarization	Normally upright in most leads
U wave	Slow repolarization (Purkinje?)	Small, after T wave; prominent in hypokalemia
J wave (Osborn wave)	Altered transmural action potential	Seen in hypothermia; convex "hump" at J point

Intervals and Segments

Measurement	Normal Values	What It Reflects
PR interval	120-200 ms (0.12-0.20 s)	Atrial depolarization + AV node conduction delay
QRS duration	≤100-110 ms	Ventricular depolarization
ST segment	Isoelectric (flat)	Corresponds to action potential plateau (phase 2); no net voltage change
QT interval	<450 ms (men), <460 ms (women)	Total ventricular depolarization + repolarization
RR interval	600-1000 ms (HR 60-100)	One complete cardiac cycle

Key physiology link: The QRS upstroke corresponds to action potential phase 0 (rapid Na+ influx). The flat ST segment corresponds to phase 2 (plateau). The T wave corresponds to phase 3 (active repolarization). This is why drugs blocking Na+ channels (e.g., flecainide) widen the QRS, while drugs prolonging phase 3 (e.g., amiodarone, hypocalcemia) lengthen the QT interval. - Harrison's 22E

Paper Speed and Calibration

Standard speed: 25 mm/s → 1 small box = 40 ms, 1 large box = 200 ms
Standard calibration: 1 mV = 10 mm (amplitude)
Heart rate formula: 300 ÷ number of large boxes between R waves (or 1500 ÷ small boxes)

The 12 Leads

The 12 leads each "look" at the heart from a different spatial angle - like 12 different camera positions recording the same electrical events.

6 Limb leads (frontal plane):

Standard bipolar: I (left arm - right arm), II (left leg - right arm), III (left leg - left arm)
Augmented unipolar: aVR (right arm), aVL (left arm), aVF (left foot)

6 Precordial (chest) leads (horizontal plane):

V1-V2: Right ventricle
V3-V4: Interventricular septum / anterior wall
V5-V6: Lateral left ventricle

Mean QRS axis (normal: -30° to +90°): Assessed using the frontal limb leads. Left axis deviation (<-30°) is seen with left anterior fascicular block, inferior MI, LVH. Right axis deviation (>+90°) occurs with right ventricular hypertrophy, left posterior fascicular block, lateral MI. - Harrison's 22E, Goldman-Cecil Medicine

Systematic ECG Interpretation (14-Parameter Approach)

According to Harrison's 22E, a systematic approach is essential to avoid errors of omission. Always check:

Standardization/calibration - confirm 1 mV = 10 mm
Heart rate (atrial and ventricular)
Rhythm (regular vs. irregular)
PR interval (AV conduction)
QRS duration (intraventricular conduction)
QT/QTc interval
Mean QRS axis (frontal plane)
P wave morphology (atrial enlargement?)
QRS amplitude (hypertrophy, low voltage)
Precordial R wave progression (normal V1 to V6 increase)
Pathologic Q waves (infarction?)
ST segment (elevation or depression?)
T wave morphology (inversion, peaked, flat?)
U waves (prominent?)

Major ECG Patterns and Their Causes

1. Chamber Enlargement / Hypertrophy

Finding	Cause	ECG Features
Left atrial enlargement	Mitral stenosis, HTN, LV dysfunction	Broad, notched P ("P mitrale"); P >120 ms in II; deep negative terminal P in V1
Right atrial enlargement	Pulmonary HTN, COPD	Tall, peaked P ("P pulmonale") >2.5 mm in II
LVH	HTN, aortic stenosis	Sokolow-Lyon: S in V1 + R in V5/V6 ≥35 mm; ST-T "strain" pattern
RVH	Pulmonary HTN, pulmonic stenosis	Right axis deviation; R > S in V1; S persists in V5-V6

2. Bundle Branch Blocks

Block	QRS	V1 Pattern	V6 Pattern
RBBB	≥120 ms	RSR' ("rabbit ears")	Wide, slurred S
LBBB	≥120 ms	Broad QS or rS	Broad monophasic R, no septal Q
LAFB	100-120 ms (normal)	Normal	Left axis deviation (-45° to -90°)
LPFB	Normal	Normal	Right axis deviation (+90° to +120°)

3. Myocardial Ischemia and Infarction

Anterior MI sequence showing ST elevation acutely and evolving Q waves

FIGURE 247-13 - Anterior (top) and inferior (bottom) STEMI sequences showing acute ST elevation evolving to Q-wave infarction. (Harrison's 22E)

Evolution of STEMI:

Hyperacute (minutes): Peaked, tall T waves ("hyperacute T waves")
Acute (hours): ST elevation (convex/tombstone) in territory leads + reciprocal ST depression opposite
Evolving (days): Pathologic Q waves develop; ST begins to normalize; T wave inversion
Old/chronic: Persistent Q waves, T wave may normalize

Territory localization:

Territory	Leads with Changes	Artery
Anterior	V1-V4	LAD
Lateral	I, aVL, V5-V6	LCx
Inferior	II, III, aVF	RCA (or LCx)
Posterior	Tall R + ST depression in V1-V2 (reciprocal)	RCA or LCx
RV	V3R-V4R ST elevation	Proximal RCA

Reciprocal changes are key: anterior STEMI causes ST depression in II, III, aVF; inferior STEMI causes ST depression in V1-V3.

4. Arrhythmia Patterns

Rhythm	Rate	Regularity	P waves	PR	QRS
Normal sinus	60-100	Regular	Upright II, inverted aVR	Normal	Normal
Sinus tachycardia	>100	Regular	Normal	Normal	Normal
Sinus bradycardia	<60	Regular	Normal	Normal	Normal
Atrial fibrillation	Variable	Irregularly irregular	Absent (fibrillatory baseline)	None	Narrow (unless aberrant)
Atrial flutter	250-350 atrial; 2:1/4:1 ventricular	Regular	Sawtooth pattern (II, III, aVF)	Variable	Narrow
SVT (AVNRT)	150-250	Regular	Hidden in QRS or just after	Short/retrograde	Narrow
VT	>100	Regular	Dissociated (AV dissociation)	-	Wide (>120 ms)
VF	Chaotic	Absent	Absent	-	Chaotic
1° AV block	Normal	Regular	Normal	>200 ms	Normal
2° AV block Mobitz I	Normal	Irregular	Normal	Progressive lengthening → dropped QRS	Normal
2° AV block Mobitz II	Normal	Irregular	Normal	Constant until sudden drop	Normal
3° AV block (complete)	Variable	Regular (atria and ventricles independently)	Normal, no relationship to QRS	Variable	Wide (junctional or ventricular escape)

5. ST-Segment Changes (Non-Ischemic)

Cause	ECG Pattern
Acute pericarditis	Diffuse (saddle-shaped) ST elevation + PR depression in most leads; no reciprocal changes (except aVR)
Early repolarization	Benign concave ST elevation, most prominent V2-V5; "fish-hook" J-point notching
Cardiac tamponade	Sinus tachycardia + low QRS voltages + electrical alternans (alternating QRS height)
Brugada syndrome	Type 1: coved ST elevation ≥2 mm in V1-V2; associated with risk of sudden death
LV aneurysm	Persistent ST elevation weeks after MI

6. QT Prolongation

The QT interval represents total ventricular repolarization. Prolongation (>450 ms men, >460 ms women) increases risk of torsades de pointes (a polymorphic VT).

Causes of QT prolongation:

Drugs: Class IA antiarrhythmics (quinidine, procainamide), class III (sotalol, amiodarone), antipsychotics (haloperidol, ziprasidone), macrolides, fluoroquinolones
Electrolytes: Hypokalemia, hypomagnesemia, hypocalcemia
Congenital: Long QT syndrome (LQTS 1, 2, 3 - channelopathies)
Other: Hypothermia, hypothyroidism, subarachnoid hemorrhage

Causes of QT shortening: Hypercalcemia, digoxin, hereditary short QT syndrome

7. Metabolic / Drug Effects

Condition	Key ECG Change
Hyperkalemia	Peaked T → wide QRS → loss of P waves → sine wave → VF
Hypokalemia	Flat T waves + prominent U waves; QT prolongation
Hypercalcemia	Short QT (short ST segment)
Hypocalcemia	Long QT (prolonged ST segment)
Digoxin toxicity	"Scooped" ST depression; bradycardia; AV block; bidirectional VT
Tricyclic overdose	Wide QRS + prolonged QT + sinus tachycardia + right axis deviation
Hypothermia	Osborn (J) waves; sinus bradycardia; prolonged intervals

Quick Reference: Normal ECG Values

Parameter	Normal Range
Heart rate	60-100 bpm
PR interval	120-200 ms
QRS duration	≤110 ms
QT (men)	<450 ms
QT (women)	<460 ms
QRS axis	-30° to +90°
P wave duration	<120 ms
P wave amplitude	<2.5 mm
R-wave progression	V1 (small r) → V5-V6 (dominant R)

Sources: Harrison's Principles of Internal Medicine 22E (2025); Goldman-Cecil Medicine International Edition; Costanzo Physiology 7th Edition; Harrison's 22E Chapter 247 (ECG)

Leads of ecg

The 12-lead ECG uses 10 electrodes placed on limbs and chest to record electrical activity from 12 different angles. Limb leads look at the frontal plane; chest leads look at the horizontal plane.

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ECG Leads - Complete Overview

The 12-lead ECG uses 10 electrodes to generate 12 views of the heart's electrical activity. Each lead is like a different camera angle - recording the same electrical events from a different spatial direction. A positive (upward) deflection occurs when depolarization moves toward that lead's positive pole; a negative deflection when it moves away. - Harrison's Principles of Internal Medicine 22E

The Two Groups of Leads

The 12 leads split into two groups based on the plane they record:

Group	Leads	Plane Recorded
Limb leads (6)	I, II, III, aVR, aVL, aVF	Frontal plane (up/down, left/right)
Precordial leads (6)	V1, V2, V3, V4, V5, V6	Horizontal plane (front/back, left/right)

Group 1: Limb Leads (Frontal Plane)

Einthoven's Triangle - Standard Bipolar Leads (I, II, III)

These measure the voltage difference between two limb electrodes:

Lead	Positive Pole	Negative Pole	Einthoven's equation
I	Left arm (LA)	Right arm (RA)	LA - RA
II	Left leg (LL)	Right arm (RA)	LL - RA
III	Left leg (LL)	Left arm (LA)	LL - LA

Einthoven's Law: Lead I + Lead III = Lead II (at any instant)

Augmented Unipolar Limb Leads (aVR, aVL, aVF)

These measure potential at one limb electrode relative to the combined average of the other two (Wilson's central terminal):

Lead	Positive Pole	Looks At
aVR	Right arm	Base of heart (cavity); normally negative - all normal deflections point away from it
aVL	Left arm	High lateral wall of LV
aVF	Left foot	Inferior wall of LV (diaphragmatic surface)

The "a" = augmented (signal is boosted ~50% because one electrode is disconnected, increasing amplitude)

Hexaxial Reference System (Frontal Plane Axis)

Hexaxial diagram showing all 6 limb leads with angular positions and axis deviation zones

FIGURE 247-4 - Hexaxial diagram showing each limb lead's angular orientation. Normal QRS axis = -30° to +90° (yellow zone). - Harrison's 22E

Each limb lead sits at a specific angle around the heart:

Lead	Angle
I	0°
II	+60°
III	+120°
aVF	+90°
aVL	-30°
aVR	-150°

Axis deviation:

Normal: -30° to +90°
Left axis deviation (LAD): -30° to -90° → causes: LAFB, inferior MI, LVH, LBBB
Right axis deviation (RAD): +90° to +180° → causes: RVH, LPFB, lateral MI, RBBB, cor pulmonale
Extreme axis: -90° to ±180° → causes: severe RVH, VT, dextrocardia

Quick axis check: If QRS is positive in both I and aVF → normal axis. If positive in I, negative in aVF → LAD. If negative in I, positive in aVF → RAD.

Group 2: Precordial (Chest) Leads - Horizontal Plane

Horizontal plane diagram showing V1-V6 positions encircling the heart from right to left lateral

FIGURE 247-3B - Horizontal plane leads V1-V6 encircling the heart. - Harrison's 22E

Electrode Placement

FIG. 32.4 - Proper anatomic location of all 10 electrodes. - Miller's Anesthesia 10e

Lead	Position	Region of Heart Viewed
V1	4th intercostal space, right sternal border	Right ventricle / septum
V2	4th intercostal space, left sternal border	Right ventricle / septum
V3	Between V2 and V4 (diagonal)	Anterior septum / anterior wall
V4	5th intercostal space, midclavicular line	Anterior LV apex
V5	Same level as V4, anterior axillary line	Lateral LV
V6	Same level as V4, midaxillary line	Lateral LV

How to find the positions: Locate the sternal angle of Louis (manubriosternal junction) → the rib immediately below is the 2nd rib → count down to the 4th and 5th intercostal spaces. V4 sits at the 5th ICS midclavicular line. V5 and V6 move horizontally lateral from V4. - Miller's Anesthesia 10e

What Each Lead "Sees" - Coronary Territory Correlation

Cardiac Region	Leads	Artery
Inferior wall	II, III, aVF	RCA (right coronary artery)
Lateral wall	I, aVL, V5, V6	LCx (left circumflex)
Anterior wall	V1-V4	LAD (left anterior descending)
Septal	V1-V2	Septal perforators of LAD
High lateral	I, aVL	Diagonal branch of LAD or LCx
Posterior wall	V1-V2 (reciprocal - tall R + ST depression)	RCA or LCx

Normal R-Wave Progression Across Precordial Leads

As you move from V1 → V6, the R wave should progressively increase in height (R-wave progression):

Lead	Normal QRS	Reason
V1	Small r, deep S (rS pattern)	Right ventricle faces this lead; LV depolarization moves away
V2	r grows slightly	Transitional
V3	Transitional (r ≈ S)
V4	R > S (transition zone)	LV now dominates
V5	Tall R, small S	LV lateral wall
V6	Tall R, small or no S	LV lateral wall

Transition zone (where R = S, i.e., equiphasic) normally occurs at V3 or V4. Poor R-wave progression (rS in V1-V4) suggests anterior MI, LVH, or LBBB.

Additional / Supplemental Leads

Lead	Position	Use
V4R	Mirror of V4 on right side (4th ICS, right MCL)	Best for right ventricular MI (inferior STEMI with RV involvement)
V7	Posterior axillary line	Posterior MI diagnosis
V8	Tip of left scapula	Posterior MI
V9	Left paravertebral	Posterior MI
Right-sided leads V3R-V6R	Mirror image positions on right chest	RV ischemia/infarction

AHA Color Coding for Electrode Wires

Electrode	Color (AHA/US)
Right arm (RA)	White
Left arm (LA)	Black
Right leg (RL)	Green (ground)
Left leg (LL)	Red
Precordial (V)	Brown/red

Note: The international IEC color code differs from the AHA system. - Miller's Anesthesia 10e

Key Points to Remember

10 electrodes → 12 leads (6 limb + 6 chest). No new electrodes are needed for the augmented leads - they are calculated from the same 4 limb electrodes.
aVR is the "reciprocal" lead - it looks at the cavity of the heart from the right shoulder. ST elevation in aVR with diffuse ST depression suggests left main or proximal LAD occlusion.
V5 is the most sensitive single lead for ischemia during monitoring; mid-precordial leads (V3-V5) are best for detecting LAD ischemia.
Lead II is the best for rhythm analysis (P waves are most clearly visible; it runs parallel to the normal P-wave vector).
Right leg (RL/green) electrode is purely a ground - its placement does not affect any lead recording.

Sources: Harrison's Principles of Internal Medicine 22E (2025), Miller's Anesthesia 10e, Goldman-Cecil Medicine International Edition

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