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ECG (Electrocardiogram) - Comprehensive Guide

1. What is an ECG?

The ECG (or EKG) records tiny potential differences on the body surface that reflect the electrical activity of the heart. Because different parts of the myocardium depolarize and repolarize in a specific sequence (atria before ventricles; His-Purkinje system conducting ventricular activation rapidly), a pattern of voltage changes is detectable at the skin. - Costanzo Physiology 7th Ed.

2. The 12-Lead ECG

A standard 12-lead ECG uses 10 electrodes to produce 12 different views of cardiac electrical activity. - Roberts and Hedges' Clinical Procedures in Emergency Medicine

Limb leads (frontal plane)

Lead	Type	Positive Pole
I	Bipolar	Left arm
II	Bipolar	Left leg
III	Bipolar	Left leg (vs. LA)
aVR	Unipolar	Right arm
aVL	Unipolar	Left arm
aVF	Unipolar	Left leg

Precordial leads (horizontal/transverse plane)

V1-V2: Right side of heart / interventricular septum
V3-V4: Anterior wall
V5-V6: Lateral wall

ECG paper: At standard 25 mm/sec, each small box = 0.04 sec (40 ms), each large box = 0.20 sec (200 ms). Standard amplitude = 10 mm/mV.

Lead placement importance: Incorrect lead placement can mimic pathology and trigger unnecessary workup. The image below shows how LL position affects tracing morphology:

Limb lead placement effect on ECG morphology - leads I, II, III at two LL positions

3. Normal ECG Waveforms and Intervals

Normal ECG waveform with labeled P wave, QRS complex, T wave, PR interval, ST segment, and QT interval (Lead II)

Fig. Normal ECG measured from Lead II - Costanzo Physiology 7th Ed.

Waves

Component	Represents	Notes
P wave	Atrial depolarization	Duration reflects atrial conduction time. Atrial repolarization is buried in the QRS.
QRS complex	Ventricular depolarization	Q = initial septal, R = main ventricular, S = basal. Duration ~80-100 ms. Fast despite large mass due to His-Purkinje system.
T wave	Ventricular repolarization	Normally upright in most leads
U wave	(if present)	Slow repolarization of Purkinje fibers; prominent in hypokalemia

Intervals & Segments

Measurement	Normal	What it Reflects
PR interval	120-200 ms (≤160 ms typical)	Atrial depolarization + AV node conduction time
PR segment	Isoelectric	AV node delay alone
QRS duration	<120 ms	Ventricular conduction
ST segment	Isoelectric	Ventricular plateau phase - elevation or depression = pathology
QT interval	<440 ms (corrected for HR)	Total ventricular repolarization time; prolonged = arrhythmia risk

Key rule: Intervals include waves; segments do not.

4. Autonomic Effects on the ECG

Sympathetic stimulation (norepinephrine, beta-1): increases If (funny current) in SA node → faster phase 4 depolarization → shorter PR interval, faster heart rate
Parasympathetic stimulation (acetylcholine, M2 receptors): decreases If, opens K+-Ach channels, hyperpolarizes SA node → longer PR interval, slower heart rate

5. ECG in Specific Conditions

5a. Myocardial Infarction (STEMI)

Regional ST Elevation - leads affected indicate the culprit territory: - Rosen's Emergency Medicine

MI Location	Affected Leads	Artery
Anterior	V1-V4	LAD
Anterolateral	V2-V6, I, aVL	LAD/LCx
Lateral	I, aVL, V5, V6	LCx
Inferior	II, III, aVF	RCA
Right ventricular	V3R-V6R (V4R most sensitive)	RCA
Posterior	V8, V9 elevation; V1-V3 depression, tall R in V1-V2	RCA/LCx

Anterior STEMI (V1-V4):

Anterior STEMI - ST elevation in V1 to V4 with obliquely straight morphology

Fig. Anterior wall STEMI with ST elevation V1-V4. LAD stenosis confirmed on catheterization. - Rosen's Emergency Medicine

Anterolateral STEMI (V2-V6, I, aVL):

Anterolateral STEMI showing ST elevation in V2-V6, I and aVL in a 12-lead ECG

Fig. Anterolateral STEMI with in-stent thrombosis confirmed. - Rosen's Emergency Medicine

Posterior MI signs on standard leads: horizontal ST depression + upright T wave + tall wide R wave + R:S ratio >1 in V1-V3 (mirror image of posterior Q wave).

STEMI mimics: LBBB, LVH, Brugada pattern, pericarditis, early repolarization - must be differentiated.

5b. Arrhythmias

Origin-based classification (from Robbins Basic Pathology):

Supraventricular - originate at or above AV node
Ventricular - originate in ventricular myocardium

Common arrhythmia types:

Arrhythmia	ECG Features	Notes
Sinus tachycardia	Normal P-QRS-T, HR >100	Most common supraventricular
Atrial fibrillation	No P waves, irregularly irregular R-R	From atrial dilation/irritability; stretch-sensitive ion channels
Atrial flutter	Sawtooth flutter waves ~300/min	Reentry in RA
SVT (AVNRT/AVRT)	Narrow complex, rapid, regular	May have retrograde P waves
Ventricular tachycardia	Wide complex (>120 ms), regular	Dangerous if sustained
Ventricular fibrillation	Chaotic, no recognizable complexes	Cardiac arrest
Asystole	Flat line	No electrical activity

5c. Heart Blocks (AV Blocks)

Degree	ECG Pattern	Clinical Meaning
1st degree	PR interval >200 ms, every P conducts	Asymptomatic AV node slowing
2nd degree - Mobitz I (Wenckebach)	Progressively lengthening PR until P drops	Usually benign; AV node disease
2nd degree - Mobitz II	Fixed PR, then sudden non-conducted P	More serious; infranodal disease
3rd degree (complete)	P waves and QRS completely dissociated	AV node or His-bundle failure

5d. Bundle Branch Blocks

RBBB: rSR' pattern ("M-shape") in V1; may be congenital or from organic heart disease. Wide QRS (>120 ms).
LBBB: Wide QRS, broad notched R in I, aVL, V5-V6; new LBBB in ischemic context = equivalent to STEMI changes.
Preexisting BBB causes false-positive stress test results due to baseline ST changes.

5e. Long QT Syndrome

Defined as QTc >440 ms; caused by mutations in cardiac ion channel genes (most commonly KCNQ1, encoding a K+ channel)
Risk: Torsades de Pointes (TdP) - polymorphic VT that can degenerate to VF
Acquired causes: drugs (antiarrhythmics, antibiotics, antipsychotics), electrolyte disturbances (hypokalemia, hypomagnesemia)
Congenital syndromes: Romano-Ward (autosomal dominant), Jervell-Lange-Nielsen (with congenital deafness)
TdP is characteristically preceded by a PVC after a long-short cycle sequence

5f. Preexcitation - Wolff-Parkinson-White (WPW)

ECG in sinus rhythm shows:

Shortened PR interval (<120 ms)
Delta wave (slurred upstroke of QRS)
Widened QRS

This results from conduction via an accessory pathway (Bundle of Kent) bypassing the AV node.

Preexcited AF in WPW is a medical emergency - can conduct rapidly to ventricles:

Preexcited atrial fibrillation in WPW showing chaotic wide-complex tachycardia across all 12 leads

Fig. Preexcited AF in WPW - rapid irregular wide-complex tachycardia. AV-nodal blockers (adenosine, verapamil, digoxin) are CONTRAINDICATED as they can accelerate conduction via the bypass tract. - Harrison's Principles of Internal Medicine 22E

5g. Pulmonary Embolism

Classic ECG signs (non-specific, seen in large PE):

HR >100
T-wave inversion V1-V4
Incomplete or complete RBBB
S1Q3T3 pattern: S wave in lead I, Q wave in lead III, T-wave inversion in lead III

6. Systematic ECG Reading Approach

A structured approach prevents errors:

Rate: Count R-R intervals. Large boxes: 300 ÷ number of large boxes between R waves
Rhythm: Regular or irregular? P before every QRS?
Axis: Normal axis -30° to +90°. Check leads I and aVF
P waves: Present? Morphology? One per QRS?
PR interval: Normal (120-200 ms)? Constant?
QRS duration: Narrow (<120 ms) or wide (>120 ms)?
ST segment: Elevation or depression? Which leads?
T waves: Upright? Inverted? Peaked?
QT interval: Prolonged?
Compare to prior ECGs whenever available

Sources: Costanzo Physiology 7th Ed., Rosen's Emergency Medicine, Roberts and Hedges' Clinical Procedures in Emergency Medicine, Harrison's Principles of Internal Medicine 22E, Robbins Basic Pathology, Braunwald's Heart Disease, Tintinalli's Emergency Medicine, Goldman-Cecil Medicine

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ECG - Complete Reference Guide

Sources: Costanzo Physiology 7th Ed., Roberts & Hedges' Clinical Procedures in Emergency Medicine, Rosen's Emergency Medicine, Braunwald's Heart Disease, Harrison's Principles of Internal Medicine 22E, Tintinalli's Emergency Medicine, Goldman-Cecil Medicine, Fuster & Hurst's The Heart 15th Ed., Robbins Basic Pathology, Katzung Pharmacology 16th Ed.

PART 1: FUNDAMENTALS

What Is an ECG?

The electrocardiogram (ECG or EKG) records potential differences on the body surface caused by the sequential depolarization and repolarization of the myocardium. Because the atria depolarize before ventricles, and each chamber activates in a defined sequence via the His-Purkinje system, a predictable electrical pattern is detectable at skin electrodes. - Costanzo Physiology 7th Ed.

The Conduction System (Basis of the ECG)

Structure	Function	Rate if Pacemaker
SA node	Primary pacemaker; phase 4 spontaneous depolarization	60-100 bpm
AV node	Delays conduction to ventricles (PR segment)	40-60 bpm
Bundle of His	Rapid conduction to ventricles	40-60 bpm
Left/Right Bundle Branches	Distribute impulse to ventricular walls
Purkinje fibers	Final rapid activation of myocardium	20-40 bpm

Autonomic effects on SA node:

SA node action potentials showing normal firing (A), sympathetic stimulation causing faster phase 4 depolarization (B), and parasympathetic stimulation slowing it (C)

Sympathetic (beta-1, norepinephrine): increases If current → faster phase 4 depolarization, decreases threshold → faster HR, shorter PR
Parasympathetic (M2, acetylcholine): decreases If, opens K+-ACh channels, hyperpolarizes → slower HR, longer PR

PART 2: THE 12-LEAD ECG SYSTEM

ECG Paper and Calibration

Parameter	Standard Setting	Meaning
Paper speed	25 mm/sec	1 small box = 0.04 sec (40 ms); 1 large box = 0.20 sec (200 ms)
Amplitude	10 mm/mV	1 mm = 0.1 mV
Each lead recorded	2.5 seconds by default	Thick lines 5 mm apart, thin lines 1 mm apart

Electrodes and Lead Positions

Limb electrode color coding:

Location	Notation	Color
Right arm	RA	White
Left arm	LA	Black
Left leg	LL	Red
Right leg	RL	Green (ground)
V1	Precordial	Brown/red
V2-V6	Precordial	Brown/yellow, green, blue, orange, violet

Precordial Lead Placement

V1: Right sternal border, 4th intercostal space
V2: Left sternal border, 4th intercostal space
V3: Midway between V2 and V4
V4: Left midclavicular line, 5th intercostal space
V5: Left anterior axillary line, same horizontal level as V4
V6: Left midaxillary line, same horizontal level as V4 and V5

Caution: V4-V6 are placed at the same horizontal level, not following the curve of intercostal spaces. Landmark: palpate sternal angle (angle of Louis) = junction of manubrium and body of sternum = level of 2nd rib → count down to 4th ICS.

Posterior leads (V7, V8, V9): placed on the back at the same horizontal level as V6, used to detect posterior MI. Right-sided leads (V1R-V6R): mirror image on right chest, used to detect right ventricular MI.

The 12 Leads and Their Views

Lead Group	Leads	Plane	What They "See"
Limb (bipolar)	I, II, III	Frontal	Lateral, inferior, overall LV vectors
Augmented (unipolar)	aVR, aVL, aVF	Frontal	Right arm, left arm, left foot perspectives
Precordial (unipolar)	V1-V6	Horizontal/transverse	Anterior, septal, lateral walls

Key facts:

Lead I positive pole = left arm → records left-right vector
Lead II positive pole = left leg → most commonly used rhythm strip (best P-wave visibility)
aVR is the "opposite" lead - normally negative QRS/T; positive deflections in aVR = bad (global ischemia, misplaced electrodes)
V1-V2 = septal; V3-V4 = anterior; V5-V6 = lateral

Limb Lead Placement and Effect

Limb lead placement showing how LL position (A vs B) changes morphology in Leads I, II, III

PART 3: NORMAL WAVEFORMS AND INTERVALS

The Normal ECG Waveform

Normal ECG waveform (Lead II) with labeled P wave, Q, R, S complex, T wave, PR interval, ST segment, QT interval

Waves

Wave	Represents	Normal Duration	Normal Amplitude
P wave	Atrial depolarization	<120 ms	<0.25 mV (2.5 mm) in II
Q wave	Initial septal depolarization (L→R)	<40 ms	<25% of R wave height
R wave	Main ventricular depolarization	-	Tallest deflection in QRS
S wave	Terminal depolarization (basal ventricles)	-	-
T wave	Ventricular repolarization	-	Upright most leads; inverted V1 normal
U wave	Purkinje repolarization (if visible)	-	Small, same direction as T; prominent in hypokalemia

Atrial repolarization is not visible on normal ECG - it is buried within the QRS complex.

Intervals and Segments

Measurement	Normal Range	What It Measures	Abnormal
PR interval	120-200 ms (3-5 small boxes)	Atrial depolarization + AV node conduction	>200 ms = heart block; <120 ms = preexcitation
PR segment	Isoelectric	AV node delay alone	Depression = pericarditis, atrial injury
QRS duration	<120 ms (<3 small boxes)	Ventricular conduction	>120 ms = BBB, ventricular rhythm, hyperkalemia
ST segment	Isoelectric (±0.5 mm)	Ventricular plateau (phase 2 action potential)	Elevation = STEMI, pericarditis; Depression = ischemia, NSTEMI
QT interval	<440 ms men; <460 ms women	Total ventricular repolarization	Prolonged = torsades risk
QTc (corrected)	QT ÷ √RR (Bazett formula)	QT corrected for heart rate	>440 ms = prolonged

Memory rule: Intervals include waves; segments do not.

Heart Rate Calculation

Method	Formula/Use
Regular rhythm (quick)	300 ÷ number of large boxes between R waves
Regular rhythm (precise)	1500 ÷ number of small boxes between R waves
Irregular rhythm	Count QRS complexes in 6 seconds × 10

PART 4: CARDIAC AXIS

The mean QRS axis represents the average direction of ventricular depolarization in the frontal plane.

Axis	Degrees	Leads to Check
Normal	-30° to +90°	I positive, aVF positive
Left axis deviation (LAD)	-30° to -90°	I positive, aVF negative
Right axis deviation (RAD)	+90° to +180°	I negative, aVF positive
Extreme axis	+180° to -90°	I negative, aVF negative

Quick method: Check Lead I and aVF

Both positive = normal axis
I positive, aVF negative = LAD
I negative, aVF positive = RAD
Both negative = extreme/northwest axis

Causes of LAD: LBBB, left anterior fascicular block, inferior MI, LVH, Wolff-Parkinson-White Causes of RAD: RVH, RBBB, lateral MI, pulmonary hypertension, PE, dextrocardia

PART 5: CHAMBER ENLARGEMENT AND HYPERTROPHY

Atrial Enlargement

Pattern	ECG Finding	Leads
Right atrial enlargement (RAE)	Peaked P wave (P pulmonale) >2.5 mm	II, III, aVF
Left atrial enlargement (LAE)	Biphasic P (wide negative terminal component) >40 ms & >1 mm deep	V1; broad notched P >120 ms in II (P mitrale)

Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH) - Sokolow-Lyon criteria:

S in V1 + R in V5 or V6 ≥35 mm
R in aVL ≥11 mm
R in Lead I + S in Lead III ≥25 mm
Associated: ST depression and T-wave inversion in lateral leads (strain pattern), LAE

Right Ventricular Hypertrophy (RVH):

RAD (>+90°)
R wave dominant in V1 (R > S in V1)
Deep S waves in V5-V6
Associated: RAE, ST depression/T inversion in V1-V3 (strain)

PART 6: ECG IN ISCHEMIA AND INFARCTION

Evolution of ECG Changes in STEMI

Stage	Time	ECG Changes
Hyperacute	Minutes	Tall, peaked (hyperacute) T waves; earliest change
Acute	Hours	ST elevation (convex upward / "tombstone"); Q waves begin to form
Subacute	Hours-days	ST elevation persisting; Q waves deepen; T wave inversion begins
Chronic/Established	Days-weeks	ST returns to baseline; T waves inverted; Q waves persist (scar)

Persistent ST elevation after weeks = suspect LV aneurysm.

ST Elevation Criteria for STEMI

≥1 mm (0.1 mV) in 2 contiguous limb leads
≥2 mm (0.2 mV) in 2 contiguous precordial leads
New LBBB in the appropriate clinical context

Regional ECG Localization

MI Location	Leads with ST Elevation	Reciprocal ST Depression	Culprit Artery
Anterior	V1-V4	II, III, aVF	LAD (proximal)
Lateral	I, aVL, V5-V6	II, III, aVF	LCx or LAD diagonal
Anterolateral	V2-V6, I, aVL	II, III, aVF	LAD or LCx
Inferior	II, III, aVF	I, aVL	RCA (80%), LCx (20%)
Right ventricular	V3R-V6R (V4R most sensitive)	-	RCA
Posterior	V8-V9 elevation	ST depression + tall R + R:S >1 in V1-V3	RCA or LCx
aVR STE	aVR ≥1 mm + diffuse ST depression	Widespread ST depression	Left main or proximal LAD

Anterior STEMI (V1-V4 ST elevation):

Anterior wall STEMI with ST elevation V1-V4, obliquely straight morphology, 90% LAD stenosis confirmed

Anterolateral STEMI (V2-V6, I, aVL):

Anterolateral STEMI with STE in V2-V6, I and aVL; in-stent LAD thrombosis confirmed at catheterization

Pathological Q Waves

Q wave >40 ms (1 small box) wide OR >25% height of R wave in same lead = pathological
Represent electrically silent necrotic tissue
Persist as a permanent scar marker
Septal q waves (narrow, small) in I, aVL, V5-V6 are normal

NSTEMI / Unstable Angina

No ST elevation; instead: ST depression ≥0.5 mm in contiguous leads
Deep, symmetrical T-wave inversion (Wellens' syndrome variant: deep T inversion in V2-V3 = proximal LAD critical stenosis)
Non-specific ST/T changes
ECG may be completely normal in 5-10% of NSTEMI - troponin is the key distinguisher

STEMI Mimics (Differential Diagnosis of ST Elevation)

Condition	Key ECG Distinguisher
LBBB	Wide QRS, no true "ischemic" territory pattern
LVH with strain	Lateral ST depression, not territory-specific elevation
Pericarditis	Diffuse ST elevation + PR depression, no reciprocal changes
Brugada	RBBB + STE in V1-V3 only
Early repolarization	J-point elevation, notching, resolves with tachycardia
Prinzmetal angina	Transient STE during pain, resolves
Aortic dissection	STE (if coronary involved), but wide mediastinum on CXR
Ventricular aneurysm	Persistent STE with old Q waves

PART 7: ARRHYTHMIAS

Sinus Rhythms

Rhythm	Rate	Features
Normal sinus	60-100 bpm	Regular, P before every QRS, upright P in II
Sinus tachycardia	>100 bpm	Same; often secondary cause (fever, pain, anemia)
Sinus bradycardia	<60 bpm	Same; athletes, vagal tone, medications
Sinus arrhythmia	Variable	Varying R-R with respiration; normal in young

Supraventricular Arrhythmias

Arrhythmia	Rate	Rhythm	P Waves	QRS	Key Features
Atrial fibrillation (AF)	350-600 atrial; 60-170 ventricular	Irregularly irregular	No P waves; fibrillatory baseline (f waves)	Narrow (unless aberrant)	Most common sustained arrhythmia
Atrial flutter	250-350 atrial; ventricular varies by block	Regular sawtooth	Flutter (F) waves 300/min; sawtooth in II, III, aVF	Narrow	Classic 2:1 block = ventricular rate ~150
AVNRT	150-250	Regular	Retrograde P (hidden in QRS or just after)	Narrow	Most common paroxysmal SVT; "pseudo-R'" in V1
AVRT (WPW)	150-250	Regular	Retrograde P after QRS	Narrow (orthodromic); Wide (antidromic)	Delta wave in sinus rhythm
Ectopic atrial tachycardia	100-250	Regular	Different P morphology from sinus	Narrow	P-wave axis different from sinus
Multifocal atrial tachycardia (MAT)	>100	Irregular	≥3 different P morphologies	Narrow	COPD commonest cause
Junctional rhythm	40-60	Regular	No P, or retrograde P	Narrow	AV nodal escape

Ventricular Arrhythmias

Arrhythmia	Rate	QRS	Key Features
PVC	Normal background rate	Wide (>120 ms), bizarre, compensatory pause	May be benign or indicate structural disease
Ventricular tachycardia (VT)	100-250	Wide (>120 ms), regular	AV dissociation; fusion beats; capture beats; Brugada criteria
Ventricular fibrillation (VF)	Chaotic	No recognizable complexes	Cardiac arrest; defibrillate immediately
Torsades de Pointes	150-250	Wide; "twisting" around baseline	Long QT precondition; polymorphic VT; often self-terminates
Accelerated idioventricular	40-100	Wide	Reperfusion arrhythmia; usually benign

VT vs SVT with aberrancy - features favoring VT:

AV dissociation (independent P waves and QRS) = pathognomonic
QRS >160 ms
Fusion beats or capture beats
Extreme axis deviation (northwest)
Concordance (all V leads positive or all negative)
No RS complex in any precordial lead

Heart Blocks (AV Blocks)

Block	ECG	Symptoms	Treatment
1st degree	PR >200 ms; every P conducts	None	None needed
2nd degree Mobitz I (Wenckebach)	PR progressively lengthens until P dropped; group beating	Usually none	Monitor; atropine if symptomatic
2nd degree Mobitz II	Fixed PR, then sudden non-conducted P; QRS often wide	May cause syncope	Pacing often required
3rd degree (complete)	P waves and QRS completely dissociated; ventricular escape rhythm	Syncope, heart failure, shock	Temporary then permanent pacing
2:1 AV block	Every other P dropped	Variable	Distinguish Mobitz I vs II by clinical context

SA node damage (sick sinus syndrome) → other pacemakers take over at slower rates (bradycardia).

Bundle Branch Blocks

Block	QRS	Specific Features	Causes
RBBB	≥120 ms	rSR' ("rabbit ears / M-shape") in V1-V2; wide slurred S in I, aVL, V5-V6	PE, RVH, congenital, ischemia
LBBB	≥120 ms	Broad, notched R in I, aVL, V5-V6; QS or rS in V1; no septal q in V6	CAD, cardiomyopathy, hypertension
Left anterior fascicular block (LAFB)	<120 ms	LAD (-45° to -90°); small q in I, aVL; small r in II, III, aVF	Common; benign or structural
Left posterior fascicular block (LPFB)	<120 ms	RAD (+90° to +180°); diagnosis of exclusion	Less common; structural

New LBBB in acute chest pain = treat as STEMI equivalent (Sgarbossa criteria may help).

Fascicular/Bifascicular/Trifascicular Blocks

Bifascicular block: RBBB + LAFB (most common) or RBBB + LPFB
Trifascicular block: Bifascicular + 1st degree AV block - high risk for complete heart block

PART 8: SPECIAL ECG PATTERNS

Wolff-Parkinson-White (WPW) Syndrome

ECG in sinus rhythm:

Short PR (<120 ms) - bypass of AV node delay
Delta wave (slurred initial upstroke of QRS) - ventricular pre-excitation
Wide QRS (>120 ms)
Secondary ST-T changes

Preexcited AF in WPW (medical emergency):

Preexcited AF in WPW showing rapid, irregular, wide-complex tachycardia with varying QRS morphology across all leads

DANGER: In WPW with AF, AV-nodal blockers (adenosine, verapamil, digoxin, beta-blockers) are CONTRAINDICATED - they can accelerate accessory pathway conduction and cause VF. Treat with procainamide or cardioversion. - Harrison's Principles 22E

Long QT Syndrome (LQTS)

Congenital: Mutations in K+ channel genes (KCNQ1 most common), also SCN5A (Na+ channel)
Acquired causes: Drugs (class IA/III antiarrhythmics, macrolides, fluoroquinolones, antipsychotics), hypokalemia, hypomagnesemia, hypothyroidism, bradycardia
QTc >440 ms (men) / >460 ms (women) = abnormal
Risk: Torsades de Pointes → can degenerate to VF → sudden cardiac death
Characteristic trigger: TdP preceded by a PVC after a long pause (long-short sequence)
Romano-Ward syndrome: autosomal dominant; no deafness
Jervell-Lange-Nielsen syndrome: autosomal recessive; associated with congenital deafness

Brugada Syndrome

Autosomal dominant channelopathy (SCN5A mutation in ~25%)
ECG: RBBB morphology + ST elevation in V1-V3 (coved or saddle-back pattern)
Type 1 (diagnostic): Coved-type STE ≥2 mm in V1-V2 with downsloping ST
Risk: VF, sudden cardiac death, often at night/rest
ECG may be concealed at rest; provocation with Na-channel blockers (ajmaline, flecainide) unmasks it
Management: ICD for symptomatic patients - Fuster & Hurst's The Heart 15th Ed.

Acute Pericarditis

ECG Stages: - Braunwald's Heart Disease

Stage	ECG Changes	Timing
Stage 1	Diffuse ST elevation (concave up/"saddle-shaped") + PR depression in all leads except aVR; PR elevation in aVR	Hours to days
Stage 2	ST normalization	Days
Stage 3	T-wave inversion	Weeks
Stage 4	ECG normalization	Weeks-months

Key distinguishing features from STEMI:

ST elevation is diffuse (not territory-specific)
ST morphology is concave upward (vs. convex in STEMI)
PR depression (pathognomonic) - pericardium itself is electrically silent; changes reflect epicardial myocardial injury
No reciprocal ST depression (except aVR, V1)
No Q waves (no necrosis)
PR depression can be the only ECG sign in some cases

Pulmonary Embolism (PE)

Classic ECG findings (seen in massive/submassive PE - non-specific individually):

Sinus tachycardia (most common)
S1Q3T3: S wave in Lead I + Q wave in Lead III + T-wave inversion in Lead III
T-wave inversion V1-V4 (RV strain pattern)
New incomplete or complete RBBB
RAD
P pulmonale (peaked P waves in II)

Hyperkalemia

K+ Level	ECG Changes
5.5-6.5 mEq/L	Peaked, narrow, tall T waves ("tent-shaped")
6.5-7.5 mEq/L	Widened QRS, prolonged PR, flattened P
>7.5 mEq/L	P waves disappear; wide bizarre QRS; sine-wave pattern
>8.0 mEq/L	VF or asystole

Hypokalemia

Flattening/inversion of T waves
U waves become prominent (U > T in same lead = significant)
Pseudo-prolonged QT (actually QU interval)
Increased arrhythmia risk

Hypothermia

Osborn (J) wave: positive deflection at J-point (QRS-ST junction), most prominent in V5-V6 and II
Sinus bradycardia → AF → VF as core temperature drops
Prolongation of all intervals

PART 9: SYSTEMATIC ECG INTERPRETATION (10-STEP METHOD)

Always interpret ECGs systematically to avoid missing findings:

Step	What to Assess	Key Normal Values
1. Rate	300 ÷ large boxes (or count 6 sec × 10)	60-100 bpm
2. Rhythm	Regular or irregular? P before every QRS?	Regular
3. P waves	Present? Morphology? One before each QRS?	Upright in II, inverted in aVR
4. PR interval	Constant? Short? Long?	120-200 ms
5. QRS duration	Narrow or wide?	<120 ms
6. QRS morphology	Bundle branch block? Q waves?	Normal
7. Axis	Normal? LAD? RAD?	-30° to +90°
8. ST segment	Elevation? Depression? Which leads?	Isoelectric ±0.5 mm
9. T waves	Upright? Inverted? Peaked?	Upright I, II, V3-V6
10. QT interval	Prolonged?	QTc <440 ms

Always compare to prior ECG when available - "new changes" vs "old" changes is often the most important determination.

Lead Groups as Territories (Quick Reference)

Septal:    V1, V2
Anterior:  V3, V4
Lateral:   I, aVL, V5, V6
Inferior:  II, III, aVF
Right:     aVR (cavity), V4R (RV)

Reciprocal changes = ST depression in the lead directly opposite the infarct zone. They support the diagnosis of STEMI.

ECG Limitations

A normal ECG does not exclude ACS (5-10% of MIs have normal initial ECG)
Serial ECGs (every 15-30 min in chest pain) and troponin are always needed
Prehospital ECG transmission reduces door-to-balloon time in STEMI significantly
Electrode misplacement can mimic pathology (e.g., LA-RA swap = inverted P in I, negative QRS in I mimicking dextrocardia)
80-lead body surface mapping improves STEMI detection in "electrically silent" zones (far inferior wall, posterior wall, RV)

This guide covers: ECG basics, 12-lead system, waveforms and intervals, cardiac axis, chamber enlargement, ischemia/infarction patterns, arrhythmias (supraventricular, ventricular, heart blocks, bundle branch blocks), and special patterns (WPW, LQTS, Brugada, pericarditis, PE, electrolytes, hypothermia).

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