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Now I have everything I need. Here are your ULTIMATE MBBS ECG Notes compiled from Harrison's 22e, Rosen's Emergency Medicine, The Washington Manual, Medical Physiology (Boron & Boulpaep), and Frameworks for Internal Medicine.

ULTIMATE MBBS ECG NOTES

How to Read Any ECG - Complete Guide from Medical Textbooks

PART 1: THE BASICS - What is an ECG?

An ECG provides a direct measurement of the rate, rhythm, and time-dependent electrical vector of the heart. It also reveals the origin and conduction of the cardiac action potential. Because different parts of the heart activate sequentially, changes in the electrical vector can be attributed to specific regions.

Medical Physiology (Boron & Boulpaep), BOX 21-2
Harrison's Principles of Internal Medicine 22E, Chapter 247

PART 2: THE ECG PAPER & CALIBRATION

Basic ECG waveforms and intervals: P wave (atrial depolarization), QRS complex (ventricular depolarization), ST segment (isoelectric plateau), T wave (ventricular repolarization), U wave. The J point is the junction between the end of QRS and start of ST. - Harrison's 22E, Fig. 247-2

Parameter	Value
Speed	25 mm/second
Small box (1 mm horizontal)	0.04 s (40 ms)
Large box (5 mm horizontal)	0.20 s (200 ms)
5 large boxes	1.0 second
Vertical: standard calibration	1 mV = 10 mm

PART 3: ECG WAVEFORMS - What Each Represents

Wave/Segment	Represents	Action Potential Phase
P wave	Atrial depolarization	-
PR interval	AV nodal delay	-
QRS complex	Ventricular depolarization	Phase 0 (rapid Na+ influx)
ST segment	Isoelectric plateau	Phase 2 (plateau)
T wave	Ventricular repolarization	Phase 3 (active repolarization)
U wave	Late ventricular repolarization (Purkinje)	-
J point	Junction of QRS end and ST start	-

Key Pharmacology: Drugs that decrease slope of Phase 0 by impairing Na+ influx (e.g., flecainide, hyperkalemia) increase QRS duration. Drugs that prolong Phase 2 or 3 (e.g., amiodarone, hypocalcemia) increase QT interval. Hypercalcemia and digoxin shorten QT. - Harrison's 22E

PART 4: NORMAL INTERVALS (MEMORIZE THESE)

Interval	Normal Range	What it Measures
PR interval	120-200 ms (3-5 small boxes)	Onset of atrial depolarization to onset of ventricular depolarization (includes AV nodal delay)
QRS duration	≤100-110 ms (<3 small boxes)	Duration of ventricular depolarization
QT interval	<460 ms women, <450 ms men	Ventricular depolarization + repolarization
QTc (corrected)	Bazett: QTc = QT/√RR	Rate-corrected QT

Framingham Formula: QT = QT + 0.154 (1000 - RR) in milliseconds - Harrison's 22E

PART 5: HEART RATE CALCULATION

Method 1 (Direct): Rate = 60 / R-R interval in seconds

Method 2 (Quick Rule - 300 Method): Count large boxes between R waves → Rate = 300 ÷ number of large boxes

Large boxes between R waves	Heart Rate
1	300 bpm
2	150 bpm
3	100 bpm
4	75 bpm
5	60 bpm
6	50 bpm

Mnemonic: 300-150-100-75-60-50

Medical Physiology, Table 21-6

PART 6: THE 12 LEADS - Placement & Territory

Limb Leads (Frontal Plane)

Lead	View	Looks at
I	0°	Lateral wall (LV lateral)
II	+60°	Inferior wall
III	+120°	Inferior wall
aVR	-150°	Right upper cavity (normally negative)
aVL	-30°	High lateral wall
aVF	+90°	Inferior wall

Precordial Leads (Horizontal Plane)

Lead	Position	Territory
V1	4th ICS, right sternal border	Septum / RV
V2	4th ICS, left sternal border	Septum
V3	Between V2 and V4	Anterior
V4	5th ICS, midclavicular line	Anterior / Apex
V5	Anterior axillary line	Lateral
V6	Mid-axillary line	Lateral

Coronary Territory - Which Leads to Infarct Vessel

Leads with Changes	Territory	Culprit Artery
V1-V4	Anterior	LAD (Left Anterior Descending)
V1-V2	Septal	Septal branches of LAD
V5-V6, I, aVL	Lateral	LCx (Left Circumflex)
II, III, aVF	Inferior	RCA (Right Coronary Artery, 80%) or LCx
V7-V9 (posterior leads) / reciprocal depression V1-V3	Posterior	RCA or LCx
V4R-V6R (right-sided leads)	Right Ventricle	RCA proximal

Harrison's 22E, Ch 247; Rosen's Emergency Medicine, Ch 64

PART 7: QRS AXIS DETERMINATION

Normal axis: -30° to +90°

Axis	Lead I	aVF	Cause
Normal	Positive	Positive	-
Left Axis Deviation (LAD)	Positive	Negative	LAFB, LVH, inferior MI, left bundle branch block
Right Axis Deviation (RAD)	Negative	Positive	RVH, RBBB, lateral MI, PE, dextrocardia
Extreme RAD ("No Man's Land")	Negative	Negative	Ventricular tachycardia, dextrocardia

Quick Axis Check:

If Lead I and aVF are BOTH positive → Normal axis
Lead I positive, aVF negative → Left axis (check if <-30° = LAD)
Lead I negative, aVF positive → Right axis deviation

Inspection method (quick): Find the most isoelectric limb lead → the axis is perpendicular to that lead. - Medical Physiology

PART 8: A SYSTEMATIC APPROACH - READ EVERY ECG IN ORDER

The RRIPPER Method (or your personal sequence - always be systematic):

R - Rate (300 ÷ large boxes)
R - Rhythm (regular or irregular? P before every QRS? QRS after every P?)
I - Intervals (PR, QRS, QT - normal vs prolonged)
A - Axis (Lead I + aVF rule)
P - P waves (present? normal morphology? one per QRS?)
Q - QRS morphology (width, Q waves, R wave progression, bundle branch blocks)
S - ST segment + T waves (elevation, depression, inversions, hyperacute T)
H - Hypertrophy (LVH/RVH criteria)
E - Extra findings (U waves, delta waves, pacemaker spikes)

PART 9: ISCHEMIA AND INFARCTION

Mechanism of ST Changes (Harrison's 22E)

Acute ischemia lowers resting membrane potential and shortens action potential duration. This creates a voltage gradient between normal and ischemic zones, generating currents of injury seen as ST deviation.

Transmural (epicardial) ischemia → ST vector shifts outward (epicardial) → ST ELEVATION in overlying leads
Subendocardial ischemia → ST vector shifts inward (toward cavity) → ST DEPRESSION in overlying leads

STEMI Diagnosis

Criteria for STEMI:

ST elevation ≥1 mm in ≥2 contiguous limb leads
ST elevation ≥2 mm in ≥2 contiguous precordial leads (V1-V4)
OR new LBBB with clinical picture of AMI

Earliest sign: Tall, peaked "hyperacute" T waves (before ST elevation) Evolution of STEMI:

Hyperacute T waves (minutes to 1 hour)
ST elevation (hours)
T wave inversion (hours to days)
Pathological Q waves (hours to days, often permanent)
ST returns to baseline (days to weeks)

ST Elevation Morphology

Morphology	ST Shape	Likely Cause
STEMI	Flat/convex (tombstone)	AMI
Benign early repolarization	Concave (smiley face), J-point notch	Normal variant, young males
Pericarditis	Concave, saddle-shaped, diffuse	Pericardial inflammation
LV aneurysm	Persistent ST elevation with deep Q waves, no reciprocal changes	Old MI with aneurysm

ST segment morphology patterns from Rosen's Emergency Medicine

Fig. 64.2: ST segment-T wave morphology in STEMI, benign early repolarization (BER), and acute pericarditis. STEMI typically shows flat or convex ST; non-AMI causes (BER, pericarditis) show concavity. - Rosen's Emergency Medicine

Differential Diagnosis of ST Elevation (Rosen's, Table 64.3)

Acute MI
Acute pericarditis
Left ventricular hypertrophy
LV aneurysm
Ventricular paced rhythm
Benign early repolarization
Normal variant
Osborn wave of hypothermia
Hyperkalemia
Brugada syndrome
Pulmonary embolism
Acute cerebral hemorrhage
Prinzmetal (vasospastic) angina

NSTEMI / Unstable Angina - ECG Changes

ST depression (horizontal or downsloping is more concerning than upsloping)
T wave inversions (narrow, symmetrical)
No ST elevation, no Q waves

T Wave Inversions - Key Patterns

Pattern	Leads	Significance
Symmetrical deep T inversions	V1-V4	Anterior ischemia / Wellens syndrome
Wellens Syndrome Type I	V2-V3	Deep symmetrical T wave inversions - critical LAD lesion
Wellens Syndrome Type II	V2-V3	Biphasic T waves - critical LAD lesion
Diffuse T inversions	Multiple	PE, myocarditis, cardiomyopathy
Inferior T inversions	II, III, aVF	Inferior ischemia

Wellens syndrome = T wave changes in V2-V3 indicating critical LAD stenosis, may occur pain-free. Natural history: progression to anterior wall STEMI if not treated. - Rosen's Emergency Medicine

Posterior MI (often missed!)

No direct posterior leads on standard 12-lead
Look for: Tall R waves + ST depression in V1-V3 (reciprocal changes)
Do right-sided (V4R) and posterior leads (V7-V9) to confirm
Always check inferior leads for associated inferior MI

Q Waves - Pathological vs. Normal

Pathological Q waves:

Width ≥40 ms (1 small box)
Depth ≥25% of the R wave in the same lead
Present in leads other than III and aVR

Normal septal Q waves: Small (<40 ms), narrow, seen in I, aVL, V5-V6

PART 10: HEART BLOCKS (AV CONDUCTION DISTURBANCES)

AV Block Examples from Washington Manual - all degrees

A = First-degree AVB (PR >200ms, no dropped beats); B = Mobitz I second-degree (Wenckebach - group beating, progressively lengthening PR before dropped beat); C = Mobitz II second-degree (fixed PR, sudden dropped beat); D = 2:1 block; E = Third-degree (complete) block with AV dissociation - Washington Manual / Frameworks for Internal Medicine

First-Degree AV Block

PR interval >200 ms (>1 large box)
Every P wave is followed by a QRS - no dropped beats
Benign - only delayed, not actually "blocked"
Causes: AV nodal disease, digoxin, beta-blockers, inferior MI, enhanced vagal tone (athletes), electrolyte disturbances
AV node supplied by RCA in 80%, LCx in 10%, both in 10%
Frameworks for Internal Medicine

Second-Degree AV Block Type I (Mobitz I / Wenckebach)

Classic ECG features:

Progressive PR prolongation with successive beats
Each subsequent RR interval gets shorter
A dropped beat (P wave not followed by QRS)
"Group beating" pattern - regularly irregular
Block within the AV node (more proximal) → benign prognosis
Progression to complete heart block: uncommon

Second-Degree AV Block Type II (Mobitz II)

Classic ECG features:

PR interval remains constant before and after dropped beat
Sudden, unexpected dropped beat (P wave without QRS)
Often associated with bundle branch block
Block below the AV node (His-Purkinje) → serious!
High risk of progression to complete heart block → pacemaker usually needed

2:1 AV Block (special case)

Every other P wave is blocked (2P:1QRS)
Cannot differentiate Mobitz I from Mobitz II by definition
Clues for Mobitz I: associated first-degree block, improved conduction with faster heart rate
Clues for Mobitz II: associated bundle branch block, worsened conduction at faster rates

Third-Degree (Complete) Heart Block

ALL atrial impulses fail to reach the ventricles
Complete AV dissociation: P waves and QRS complexes independent, "A rate > V rate"
P waves march through independently (often faster)
QRS from junctional escape (narrow, 40-60 bpm) or ventricular escape (wide, 20-40 bpm)
Medical emergency - may require pacemaker

High-Degree (Advanced) AV Block

More than one consecutive P wave blocked (3:1, 4:1, etc.)
Some P waves DO conduct (distinguishes from third-degree)
Washington Manual of Medical Therapeutics; Frameworks for Internal Medicine

PART 11: BUNDLE BRANCH BLOCKS

Right Bundle Branch Block (RBBB)

ECG Criteria:

QRS duration ≥120 ms (≥3 small boxes) - wide QRS
rSR' pattern ("rabbit ears") in V1/V2 - the hallmark
Wide, slurred S wave in I, aVL, V5, V6
T wave inversion in V1-V2 (secondary repolarization change - normal with RBBB)

Causes: RV strain (PE, cor pulmonale), ischemic heart disease, cardiomyopathy, normal variant (isolated RBBB)

Left Bundle Branch Block (LBBB)

ECG Criteria:

QRS duration ≥120 ms - wide QRS
Broad monophasic R wave in I, aVL, V5, V6 (no septal Q waves)
No Q waves in V5/V6, I, aVL
Predominantly negative QRS in V1 (QS or rS)
ST elevation in V1-V3 and ST depression in V5-V6 (discordant - secondary changes, NORMAL for LBBB)
T wave opposite polarity to last QRS deflection (T wave discordance)

LBBB and AMI - Sgarbossa Criteria (look for AMI in presence of LBBB or ventricular paced rhythm):

ST elevation ≥1 mm concordant with QRS (same direction) → Score 5 (most specific)
ST depression ≥1 mm in V1, V2, or V3 → Score 3
ST elevation ≥5 mm discordant with QRS (opposite direction) → Score 2

Total score ≥3 = AMI likely - Rosen's Emergency Medicine

Fascicular Blocks (Hemiblocks)

Block	QRS Duration	Axis	ECG Pattern
Left Anterior Fascicular Block (LAFB)	Normal (<120 ms)	Left axis deviation (more negative than -45°)	Small Q in I, aVL; Small R in II, III, aVF
Left Posterior Fascicular Block (LPFB)	Normal (<120 ms)	Right axis deviation (>+110-120°)	Requires exclusion of other causes of RAD (very rare in isolation)
Bifascicular block	Wide	RAD	RBBB + LAFB

PART 12: ARRHYTHMIAS

Sinus Rhythms

Rhythm	Rate	P wave	QRS	Notes
Normal Sinus Rhythm	60-100 bpm	Normal, before each QRS	Narrow (<120 ms)
Sinus Tachycardia	>100 bpm	Normal	Normal	Anxiety, exercise, hyperthyroidism, sepsis
Sinus Bradycardia	<60 bpm	Normal	Normal	Athletes, hypothyroidism, sleep, drugs (beta-blockers)
Sinus Arrhythmia	Variable	Normal	Normal	HR varies with respiration - normal variant

Supraventricular Tachycardias (SVT) - Narrow Complex

Atrial Fibrillation (AF):

Irregularly irregular rhythm (no two RR intervals the same)
No distinct P waves - replaced by fibrillatory baseline (f waves, >350 deflections/min)
Narrow QRS (unless aberrant conduction)
Ventricular rate variable (100-160 bpm if uncontrolled)
No "a wave" on JVP

Atrial Flutter:

Regular "sawtooth" flutter waves at ~300 bpm (2.5-3 mm/cycle)
Usually 2:1 block → ventricular rate ~150 bpm (classic)
Can have 3:1, 4:1, variable block
Best seen in inferior leads (II, III, aVF) and V1

AVNRT (AV Nodal Re-entry Tachycardia):

Most common SVT
Rate 150-250 bpm, regular
P waves buried in or just after QRS (retrograde P = "pseudo R' in V1", "pseudo S in inferior leads")
Narrow QRS

WPW (Wolff-Parkinson-White):

Delta wave (slurred QRS upstroke) - pre-excitation
Short PR interval (<120 ms)
Wide QRS (>120 ms)
Pseudo ST/T changes
Can degenerate into AF with very rapid conduction

Ventricular Arrhythmias - Wide Complex

Anterior wall ischemia precordial leads V1-V6

Severe anterior wall ischemia showing prominent T-wave inversions V1-V6 - Harrison's 22E, Fig. 247-12

Premature Ventricular Contraction (PVC):

Wide QRS (>120 ms), bizarre morphology
No preceding P wave
Compensatory pause after PVC
T wave in opposite direction to QRS (discordant)

Ventricular Tachycardia (VT):

Rate >100 bpm, wide QRS (>120 ms), regular
AV dissociation (P waves independent of QRS)
Fusion beats and capture beats (pathognomonic of VT)
Cannon a waves on JVP
RBBB or LBBB morphology
Axis in "no man's land" (both I and aVF negative)

Distinguishing VT from SVT with aberrancy:

If in doubt, treat as VT
AV dissociation = VT
Concordance (all V1-V6 positive or all negative) = VT
QRS width >160 ms = VT more likely
History of structural heart disease = VT more likely

Ventricular Fibrillation (VF):

Chaotic, irregular waveforms - no recognizable QRS
No cardiac output - cardiac arrest
Immediate defibrillation required

Torsades de Pointes:

Polymorphic VT with QRS complexes that appear to rotate around baseline
Associated with prolonged QT interval
Causes: hypokalemia, hypomagnesemia, drugs (antiarrhythmics, antipsychotics, antibiotics), congenital long QT

PART 13: VENTRICULAR HYPERTROPHY

Left Ventricular Hypertrophy (LVH)

Voltage criteria (any one sufficient):

Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35 mm
Cornell: R in aVL + S in V3 ≥28 mm (men) or ≥20 mm (women)
R in aVL ≥11 mm
R in V5 or V6 ≥26 mm

Associated findings (increase specificity):

Left axis deviation
ST depression + T inversion in I, aVL, V5-V6 ("LV strain" pattern)
Prolonged QRS (90-110 ms)
P mitrale (broad, bifid P wave in I, V5 - left atrial enlargement)

Causes: Hypertension (most common), aortic stenosis, aortic regurgitation, hypertrophic cardiomyopathy

Right Ventricular Hypertrophy (RVH)

ECG criteria:

Right axis deviation (>+110°)
R:S ratio in V1 >1 (tall R in V1)
R wave in V1 ≥7 mm
Persistence of S in V5/V6 (S>R in V5-V6)
ST depression + T inversion in V1-V3 (RV strain)

Causes: Pulmonary hypertension, cor pulmonale, pulmonic stenosis, ASD, chronic lung disease

PART 14: ELECTROLYTE CHANGES ON ECG

Hyperkalemia (K+ elevated)

Progressive changes with increasing K+:

Mild (5.5-6.5 mEq/L): Tall, peaked (tented) T waves, narrow base - V2-V4 most prominent
Moderate (6.5-7.5 mEq/L): PR prolongation, P wave flattening/disappearance, QRS widening
Severe (>7.5 mEq/L): Very wide QRS (sine wave pattern), AV dissociation
Critical: VF or asystole

Mnemonic: T-Peak-P-QRS-Sine-VF (tall T → peak T → P loss → QRS widens → sine wave → fatal arrhythmia)

Hypokalemia (K+ low)

Flat/inverted T waves
Prominent U waves (may fuse with T wave - "TU fusion")
ST depression
Prolonged QU interval (looks like prolonged QT)
Increased risk of torsades de pointes

Hypercalcemia

Short QT interval (QTc <350 ms)
Short ST segment (or absent ST)
J-wave/Osborn waves in severe cases

Hypocalcemia

Long QT interval (prolonged QTc)
Normal T wave amplitude
Long ST segment

Hypomagnesemia

Similar to hypokalemia
Prolonged QT
Increased risk of torsades de pointes (often coexists with hypokalemia)

PART 15: PERICARDITIS VS. STEMI

Feature	Pericarditis	STEMI
ST elevation	Diffuse, concave (saddle-shaped)	Focal (territory-based), convex
Lead distribution	All leads EXCEPT aVR (depressed)	Contiguous leads in territory
Reciprocal changes	Absent (or only aVR)	Present (hallmark of STEMI)
PR depression	Yes (characteristic)	No
Q waves	No	Yes (develop over hours-days)
Evolution	Slow, resolves over weeks	Hours-days (evolving pattern)
Symptoms	Pleuritic chest pain, worse lying flat, better sitting forward	Pressure, radiation to arm/jaw

4 Stages of Pericarditis ECG:

Diffuse ST elevation, PR depression (acute phase)
ST normalizes, T waves flatten
T wave inversions
ECG returns to normal

PART 16: PULMONARY EMBOLISM (PE) on ECG

Most common findings:

Sinus tachycardia (most common, >40% of cases)
S1Q3T3 pattern (classic but only ~20% sensitive): S wave in lead I, Q wave in lead III, T inversion in lead III
Right axis deviation
RBBB (new)
T wave inversions in V1-V4 (right heart strain)
P pulmonale (tall P waves in II >2.5 mm)

Note: The ECG in PE is often non-specific. The main value is excluding other diagnoses (STEMI, arrhythmia) and showing right heart strain pattern.

PART 17: SPECIAL PATTERNS TO KNOW

Brugada Syndrome

RBBB pattern with ST elevation in V1-V3 (coved or saddle-back morphology)
Associated with sudden cardiac death in structurally normal heart
Type 1 (coved): descending ST elevation ≥2 mm followed by T inversion - diagnostic
Type 2 (saddle-back): ST elevation ≥2 mm, upright T - suspect pattern

Long QT Syndrome

QTc >460 ms (women) or >450 ms (men)
Risk of torsades de pointes
Congenital (LQTS1 - Romano-Ward) or acquired (drugs, electrolytes)

Wolff-Parkinson-White (WPW)

Short PR (<120 ms)
Delta wave (slurred QRS onset)
Wide QRS
Secondary ST/T changes
Risk: AF with rapid conduction via accessory pathway (can be fatal)

Digoxin Effect vs. Digoxin Toxicity

Effect (therapeutic): Scooped ST depression ("Salvador Dali moustache"), shortened QT, mild PR prolongation
Toxicity: Any arrhythmia (PAT with block is classic), AV blocks, bidirectional VT

Hypothermia

Osborn wave (J wave): Positive deflection at J point, best seen in inferior and lateral leads
Sinus bradycardia
AF, VF possible

PART 18: LOCALIZATION OF INFARCTION - QUICK REFERENCE

ST Elevation in	Territory	Artery
V1-V2	Septal	Septal perforators of LAD
V3-V4	Anterior	LAD
V1-V4	Anteroseptal	LAD (proximal)
V5-V6, I, aVL	Lateral	LCx
V1-V6 + I + aVL	Extensive anterior	LAD (proximal to major diagonal)
II, III, aVF	Inferior	RCA (80%), LCx (20%)
II, III, aVF + V1-V2 (ST elev V4R)	Inferior + RV	Proximal RCA
Tall R + ST depression V1-V3	Posterior	RCA or LCx

Right ventricular MI:

Occurs with inferior STEMI (proximal RCA occlusion)
ST elevation in V4R (right-sided lead)
Clinical: Hypotension + raised JVP + clear lungs (Kussmaul's sign)
Avoid nitrates and diuretics (preload-dependent)

PART 19: HIGH-YIELD MBBS EXAM SUMMARY

Must-Know Numbers

Finding	Value
Normal PR	120-200 ms
Normal QRS	<100-110 ms
Normal QTc	<450 ms men, <460 ms women
STEMI: limb leads	ST elevation ≥1 mm in ≥2 contiguous leads
STEMI: precordial	ST elevation ≥2 mm in ≥2 contiguous leads
Pathological Q wave	≥40 ms wide, depth ≥25% of R wave
LBBB/RBBB	QRS ≥120 ms
First-degree block	PR >200 ms
LVH (Sokolow)	SV1 + RV5/V6 ≥35 mm
Tall T wave hyperkalemia	Peaked, narrow base
WPW	Short PR + delta wave

Classic Exam Scenarios

Scenario	Key ECG Finding
Chest pain + ST elevation inferior leads	RCA occlusion (Inferior STEMI)
Chest pain + tall R in V1 + ST depression V1-V3	Posterior MI
Shock + inferior MI + high JVP	RV MI (check V4R)
Palpitations + regular narrow tachycardia ~150	Atrial flutter with 2:1 block
Irregularly irregular + absent P waves	Atrial fibrillation
Wide complex tachycardia + AV dissociation	Ventricular tachycardia
Short PR + delta wave + SVT	WPW
Progressive PR then dropped beat	Mobitz I (Wenckebach)
Fixed PR + sudden dropped beat	Mobitz II
Complete AV dissociation	Third-degree (complete) heart block
Prolonged QT + polymorphic VT	Torsades de pointes
Diffuse ST elevation + PR depression	Pericarditis
Peaked T waves + widening QRS	Hyperkalemia
Prominent U waves + flat T	Hypokalemia
Tall R wave V1-V3 + ST elevation	Brugada syndrome
S1Q3T3 + sinus tachycardia	Pulmonary embolism
J-wave (Osborn wave) + bradycardia	Hypothermia
V2-V3 deep T inversions	Wellens syndrome (critical LAD stenosis)
LV aneurysm	Persistent ST elevation + mature Q waves, no reciprocal changes

SOURCES

Harrison's Principles of Internal Medicine, 22nd Edition (2025) - Chapters 247, 248 (Electrocardiography, Arrhythmias)
Rosen's Emergency Medicine: Concepts and Clinical Practice - Chapter 64 (Acute Coronary Syndromes ECG)
The Washington Manual of Medical Therapeutics - Chapter 7 (Arrhythmias)
Medical Physiology (Boron & Boulpaep) - Chapter 21, Box 21-2 (ECG interpretation)
Frameworks for Internal Medicine - Chapter 3 (AV Blocks)

---There you go - your complete MBBS ECG notes compiled directly from 5 major medical textbooks (Harrison's 22E, Rosen's Emergency Medicine, Washington Manual, Medical Physiology, and Frameworks for Internal Medicine). Here's what's covered:

19 sections total:

What is an ECG - basic concept
Paper & calibration - grid values, speeds
Waveforms - what P, QRS, ST, T, U mean physiologically
Normal intervals - PR, QRS, QT with exact values
Heart rate calculation - the 300-method trick
12 leads - placement + coronary territory table
QRS axis - quick Lead I + aVF method
Systematic approach - RRIPPER method
Ischemia & infarction - STEMI, NSTEMI, Wellens, posterior MI, Q waves
Heart blocks - 1st, 2nd (Mobitz I/II), 3rd degree with images
Bundle branch blocks - RBBB, LBBB, Sgarbossa criteria, fascicular blocks
Arrhythmias - AF, flutter, AVNRT, WPW, VT, VF, torsades
Hypertrophy - LVH (Sokolow-Lyon, Cornell), RVH criteria
Electrolytes - hyperkalemia, hypokalemia, Ca²⁺, Mg²⁺
Pericarditis vs STEMI - comparison table
Pulmonary embolism - S1Q3T3, RV strain
Special patterns - Brugada, Long QT, WPW, digoxin, hypothermia
Infarct localization - territory-artery table
High-yield exam summary - all key numbers + 25 classic exam scenarios

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