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ECG (Electrocardiogram) - Complete Notes for 3rd Year Medical Students


1. INTRODUCTION

The ECG is a non-invasive recording of the electrical activity of the heart from the body surface. It was introduced by Einthoven in the early 1900s and remains one of the most important tools in clinical medicine. It provides direct measurement of:
  • Heart rate
  • Heart rhythm
  • Conduction pathways
  • Ischemia / infarction patterns
  • Hypertrophy and metabolic disturbances
"Electrocardiography allows simultaneous recording of myocardial activation from multiple vantage points on the body's surface, thereby permitting analysis of electrical activation in different myocardial regions." - Goldman-Cecil Medicine

2. THE CARDIAC CONDUCTION SYSTEM

Understanding the ECG starts with understanding how electrical impulses travel through the heart.
Cardiac conduction system showing SA node, AV node, Bundle of His, bundle branches, and Purkinje fibers
Cardiac conduction system - Goldman-Cecil Medicine
The sequence of normal electrical activation:
  1. SA node - located in the high lateral epicardial right atrium near the superior vena cava. Spontaneously depolarizes at the highest rate - it is the dominant pacemaker (60-100 bpm intrinsic rate).
  2. Atria - the wave front spreads through both atria. The Bachmann bundle speeds conduction to the left atrium. This produces the P wave.
  3. AV node - the only electrical connection between atria and ventricles (the AV rings are electrically insulated). Physiologic delay occurs here. This produces the PR interval.
  4. Bundle of His - exits the AV node; capable of rapid conduction.
  5. Bundle branches - the His bundle bifurcates into the right bundle branch and the left bundle branch. The left further divides into the left anterior fascicle and left posterior fascicle.
  6. Purkinje system - distal ramifications that rapidly deliver current to ventricular myocytes.
  7. Ventricular myocardium - depolarization produces the QRS complex; repolarization produces the T wave.

3. ECG PAPER AND TECHNICAL STANDARDS

Normal ECG waveform with labeled intervals, segments, and grid measurements
Normal ECG waveform with all intervals labeled - Goldman-Cecil Medicine
ParameterValue
Paper speed25 mm/sec
Small box (1 mm)0.04 sec horizontally; 0.1 mV vertically
Large box (5 mm)0.2 sec horizontally; 0.5 mV vertically
Standard calibration10 mm = 1 mV
Recording duration10 seconds (standard ECG)
A standard 12-lead ECG records 4 groups of leads simultaneously: (I, II, III), (aVR, aVL, aVF), (V1, V2, V3), (V4, V5, V6) - each for 2.5 seconds. A rhythm strip runs below for the full 10 seconds.

4. THE ECG LEADS

Limb Leads (Frontal Plane)

LeadPositive ElectrodeViews
Lead ILeft armLateral wall
Lead IILeft legInferior wall
Lead IIILeft legInferior wall
aVRRight armCavity (inverted)
aVLLeft armLateral wall
aVFLeft legInferior wall

Precordial Leads (Horizontal Plane)

LeadPositionViews
V14th ICS, right sternal borderSeptal / RV
V24th ICS, left sternal borderSeptal
V3Between V2 and V4Anterior
V45th ICS, midclavicular lineAnterior
V5Anterior axillary line (same level as V4)Lateral
V6Midaxillary line (same level as V4)Lateral
Key concept: Each lead looks at the heart from a different angle. A positive deflection means the electrical wavefront is traveling toward the positive electrode.

5. ECG WAVEFORMS - WHAT EACH REPRESENTS

Cardiac cycle diagram showing the relationship between ECG, ventricular pressure, aortic flow, and ventricular volume
Cardiac cycle correlated with the ECG - Miller's Anesthesia

P Wave

  • Represents: Atrial depolarization (both right and left atria)
  • Normal duration: < 0.12 sec (< 3 small boxes)
  • Normal amplitude: < 2.5 mm in limb leads; < 1.5 mm in precordial leads
  • Morphology: Upright in leads I, II, aVF, V4-V6; inverted in aVR
  • Abnormalities:
    • Broad/bifid P (P mitrale) → Left atrial enlargement
    • Tall/peaked P (P pulmonale, >2.5 mm) → Right atrial enlargement
    • Absent P waves → AF, junctional rhythm, SA block

PR Interval

  • Represents: Time from start of atrial depolarization to start of ventricular depolarization (includes AV nodal delay)
  • Normal: 0.09 - 0.20 sec (90-200 msec)
  • Prolonged (>0.20 sec): 1st degree AV block (delay usually in AV node)
  • Short (<0.09 sec): Ventricular pre-excitation (WPW syndrome), junctional rhythm, or enhanced AV nodal conduction

QRS Complex

  • Represents: Ventricular depolarization
  • Normal duration: 0.075 - 0.11 sec (75-110 msec)
  • Nomenclature:
    • Capital letters (Q, R, S) = amplitude ≥ 5 mm (0.5 mV)
    • Lowercase letters (q, r, s) = amplitude < 5 mm
    • Q/q = initial negative deflection
    • R/r = positive deflection
    • S/s = negative deflection after a positive deflection
    • QS = entirely negative deflection
    • R' = second positive deflection (after S wave)
  • Prolonged QRS (>0.11 sec): Bundle branch block, ventricular rhythm, pre-excitation

ST Segment

  • Represents: Early ventricular repolarization (plateau phase of action potential)
  • Normal: Isoelectric (at baseline)
  • J point: Junction between the end of QRS and beginning of ST segment
  • Abnormalities:
    • ST elevation → Acute STEMI, pericarditis, Prinzmetal angina, LBBB, LVH
    • ST depression → NSTEMI/UA, subendocardial ischemia, digoxin effect, hypokalemia

T Wave

  • Represents: Ventricular repolarization
  • Normal: Upright in I, II, V3-V6; inverted in aVR (and often V1)
  • Amplitude: < 10 mm precordial; < 5 mm limb leads
  • Abnormalities:
    • Tall, peaked T waves → Hyperkalemia (early), STEMI (hyperacute T waves)
    • T wave inversion → Ischemia, ventricular hypertrophy strain pattern, RBBB, LBBB, CNS events

QT Interval

  • Represents: Total ventricular depolarization + repolarization
  • Measured: QRS onset to end of T wave; in leads II, V5, V6
  • Must be rate-corrected: Use Bazett's formula: QTc = QT / √RR (RR in seconds)
  • Normal QTc:
    • Males: 390-450 msec
    • Females: 390-460 msec
  • Prolonged QTc: Risk of Torsades de Pointes (TdP) and sudden cardiac death
    • Causes: Drugs (antiarrhythmics, antipsychotics, antibiotics), hypokalemia, hypomagnesemia, hypocalcemia, congenital long QT syndrome
  • Short QTc (<350 msec): Hypercalcemia, digoxin, congenital short QT syndrome

U Wave

  • Small deflection after the T wave; best seen in V2-V3
  • Represents: Repolarization of Purkinje fibers / interventricular septum (debated)
  • Prominent U waves: Hypokalemia, bradycardia, hypothermia
  • Note: Prominent U waves can complicate QTc measurement

J Wave (Osborn Wave)

  • Positive deflection at the J point (QRS downstroke)
  • Seen in: Hypothermia (most common), hypercalcemia, brain injury
  • May indicate risk of idiopathic ventricular fibrillation

6. HEART RATE CALCULATION

Method 1 (Precise) - R-R interval:
HR = 60 / R-R interval (in seconds) = 60,000 / R-R interval (in msec)
Method 2 (Quick) - Large box counting: Count large boxes between two consecutive R waves, then use:
300 - 150 - 100 - 75 - 60 - 50 (for 1, 2, 3, 4, 5, 6 large boxes) Formula: HR = 300 / (number of large boxes)
Method 3 (Irregular rhythm): Count number of QRS complexes in 10-second strip × 6
RateInterpretation
< 50 bpmBradycardia
50-100 bpmNormal
> 100 bpmTachycardia

7. NORMAL INTERVAL SUMMARY TABLE

Interval/WaveNormal ValueClinical Significance if Abnormal
HR50-100 bpmBrady/tachycardia
P wave duration< 120 msecAtrial enlargement if broad
PR interval90-200 msecAV block if long; WPW if short
QRS duration75-110 msecBBB if > 120 msec
QTc (male)390-450 msecTdP risk if prolonged
QTc (female)390-460 msecTdP risk if prolonged
QRS axis-30° to +90°LAD / RAD if deviated

8. QRS AXIS

The electrical axis is the overall direction of ventricular depolarization in the frontal plane.
Normal axis: -30° to +90°

Quick method using Leads I and aVF:

Lead ILead aVFAxis
PositivePositiveNormal (-30° to +90°)
PositiveNegativeLeft axis deviation (LAD)
NegativePositiveRight axis deviation (RAD)
NegativeNegativeExtreme RAD ("Northwest axis")
More precise: The axis points toward the lead where the QRS is most positive (or away from where it is most negative). The axis is perpendicular to the lead where the QRS is isoelectric (equal positive/negative deflection).

Causes of Axis Deviation:

Left Axis Deviation (LAD, more negative than -30°):
  • Left anterior fascicular block (most common)
  • Left ventricular hypertrophy
  • Inferior STEMI
  • WPW (right-sided accessory pathway)
Right Axis Deviation (RAD, more positive than +90°):
  • Right ventricular hypertrophy
  • Left posterior fascicular block
  • Pulmonary embolism / cor pulmonale
  • WPW (left-sided accessory pathway)
  • Normal in children and tall thin adults

9. SYSTEMATIC APPROACH TO ECG INTERPRETATION

Use a consistent method every time. A reliable mnemonic is:
"Rate, Rhythm, Axis, Intervals, Hypertrophy, Ischemia/Infarction"

Step-by-Step:

  1. Rate - calculate using large-box method
  2. Rhythm - regular or irregular? Is there a P for every QRS? Is there a QRS for every P?
  3. P wave - present, morphology, axis (upright in I and II = sinus origin)
  4. PR interval - normal, prolonged, or short?
  5. QRS complex - duration, morphology, pathological Q waves?
  6. QRS axis - using leads I and aVF
  7. ST segment - elevation or depression?
  8. T waves - normal, inverted, tall/peaked?
  9. QT interval - calculate QTc
  10. Overall interpretation - put it all together

10. NORMAL SINUS RHYTHM (NSR) - Criteria

  • Regular rhythm
  • Rate 60-100 bpm
  • P wave upright in I, II, aVF; inverted in aVR
  • Every P followed by QRS; every QRS preceded by P
  • PR interval 120-200 msec
  • QRS < 120 msec
  • Normal axis

11. COMMON ARRHYTHMIAS

Sinus Arrhythmia

  • Subtle variation in heart rate with respiration
  • Inspiration → faster rate; expiration → slower rate
  • Normal variant - no treatment required

Sinus Tachycardia

  • Rate > 100 bpm; otherwise normal ECG
  • Causes: exercise, anxiety, fever, pain, anemia, hypovolemia, hyperthyroidism
  • Treat the underlying cause

Sinus Bradycardia

  • Rate < 60 bpm; otherwise normal ECG
  • Causes: athletes, sleep, hypothyroidism, sick sinus syndrome, medications (beta-blockers)

Atrial Fibrillation (AF)

  • Irregularly irregular rhythm
  • No distinct P waves - replaced by chaotic fibrillatory baseline
  • Narrow QRS (unless aberrant conduction)
  • Rate: variable (ventricular rate depends on AV node conduction)

Atrial Flutter

  • Regular sawtooth flutter waves at ~300 bpm (P waves)
  • Usually 2:1 AV block → ventricular rate ~150 bpm
  • Sawtooth most visible in leads II, III, aVF

Supraventricular Tachycardia (SVT)

  • Regular narrow-complex tachycardia, rate 150-250 bpm
  • P waves may be hidden in QRS or just after QRS
  • Includes AVNRT, AVRT

Ventricular Tachycardia (VT)

  • ≥3 consecutive wide QRS complexes at rate > 100 bpm
  • AV dissociation (independent P waves), fusion beats, capture beats
  • Emergency - risk of degeneration to VF

Ventricular Fibrillation (VF)

  • Chaotic, irregular wide complexes - no discernible QRS/T
  • No cardiac output - cardiac arrest
  • Treat with immediate defibrillation

12. AV BLOCKS

1st Degree AV Block

  • PR interval > 200 msec (one large box)
  • All P waves conduct to ventricles
  • Usually benign; no treatment needed

2nd Degree AV Block - Mobitz Type I (Wenckebach)

  • Progressive PR prolongation until a P wave is not conducted (dropped QRS)
  • Then cycle repeats
  • Site of block: usually AV node
  • Usually benign

2nd Degree AV Block - Mobitz Type II

  • Fixed PR interval with sudden dropped QRS (no progressive lengthening)
  • Site of block: His-Purkinje system (below the AV node)
  • More serious - can progress to complete heart block
  • May need pacemaker

3rd Degree (Complete) AV Block

  • Complete dissociation between P waves and QRS complexes
  • P waves and QRS have independent regular rates
  • Ventricular escape rhythm: rate 20-40 bpm, wide QRS (if ventricular) or narrow QRS (if junctional)
  • Emergency - needs pacemaker

13. BUNDLE BRANCH BLOCKS

Right Bundle Branch Block (RBBB)

Criteria:
  • QRS ≥ 0.12 sec (≥ 120 msec)
  • RSR' pattern ("rabbit ears") in V1
  • Wide, slurred S wave in leads I, V5, V6
  • Secondary T wave changes (T wave inversion in V1-V3)
Mnemonic: "WiRRoW" - W shape in V1 (actually RSR'), M in V6 ... use "RsR' in Right V1"
Causes: Right heart strain (PE, cor pulmonale), congenital heart disease, ischemia, normal variant

Left Bundle Branch Block (LBBB)

Criteria:
  • QRS ≥ 0.12 sec
  • Broad, notched R wave in I, aVL, V5, V6 (no Q wave in V5-V6)
  • QS or rS in V1
  • ST and T wave changes opposite to QRS direction (discordant)
Clinical significance: LBBB almost always indicates significant underlying heart disease (CAD, cardiomyopathy, hypertension). New LBBB in chest pain context = treat as STEMI equivalent (Sgarbossa criteria apply).
Mnemonic: "WiLLiaM MoRRoW" - W in V1 and M in V6 for LBBB; M in V1 and W in V6 for RBBB

14. VENTRICULAR HYPERTROPHY

Left Ventricular Hypertrophy (LVH)

Sokolow-Lyon Criteria (most commonly used):
  • S in V1 + R in V5 or V6 > 35 mm
  • Or: R in aVL > 11 mm
Other features:
  • Strain pattern: ST depression + T wave inversion in lateral leads (I, aVL, V5, V6)
  • Left axis deviation
  • Wide QRS (though < 120 msec)
Causes: Hypertension (most common), aortic stenosis, hypertrophic cardiomyopathy

Right Ventricular Hypertrophy (RVH)

Criteria:
  • R > S in V1 (tall R wave in V1, R ≥ 7 mm)
  • Right axis deviation (> +90°)
  • Strain pattern: ST depression/T inversion in V1-V3, II, III, aVF
Causes: Pulmonary hypertension, pulmonary stenosis, cor pulmonale, congenital heart disease (ASD, VSD)

15. ISCHEMIA AND INFARCTION

Sequence of ECG Changes in STEMI:

TimeECG Change
MinutesHyperacute (tall, peaked) T waves
HoursST elevation
Hours-daysT wave inversion
Days-weeksPathological Q waves form
Weeks-monthsST returns to baseline
PermanentQ waves may persist

Pathological Q Waves

  • Width ≥ 0.04 sec (1 small box) or duration ≥ 40 msec
  • Depth ≥ 25% of R wave amplitude in the same complex
  • Represent dead/electrically silent myocardium (transmural infarction)
  • Note: Septal Q waves in I, aVL, V5, V6 are normal (small, narrow)

Localizing the Infarct by Territory:

TerritoryLeads with changesCoronary Artery
InferiorII, III, aVFRCA (80%), LCx (20%)
LateralI, aVL, V5, V6LCx or diagonal
AnteriorV1-V4LAD
SeptalV1-V2Septal perforators of LAD
PosteriorTall R and ST depression in V1-V2 (reciprocal)RCA or LCx
Right ventricularV1, ST elevation in V4RRCA

STEMI vs. Pericarditis ST Elevation:

FeatureSTEMIPericarditis
DistributionRegional (one territory)Diffuse (all leads except aVR/V1)
MorphologyConvex ("tombstone")Concave (saddle-shaped)
PR depressionAbsentPresent (pathognomonic)
Reciprocal changesPresentAbsent
Q wavesDevelopDo not develop

16. ELECTROLYTE DISTURBANCES ON ECG

Hyperkalemia (progressive changes with rising K+):

  1. Tall, peaked, narrow ("tented") T waves (earliest sign)
  2. PR prolongation
  3. P wave flattening/disappearance
  4. Wide QRS
  5. Sine wave pattern
  6. VF/asystole (at K+ > 7-8 mEq/L)

Hypokalemia:

  • Flattening of T waves
  • Prominent U waves (most characteristic)
  • ST depression
  • Prolonged QU interval (mistaken for long QT)
  • Risk of TdP at severe levels

Hypercalcemia:

  • Short QT interval (shortened ST segment)
  • Broad T waves
  • J waves (Osborn waves) at very high levels

Hypocalcemia:

  • Prolonged QT interval (prolonged ST segment)
  • Risk of TdP

Hypomagnesemia:

  • PR prolongation
  • Prolonged QT
  • T wave changes
  • Risk of TdP (often co-exists with hypokalemia)

17. DRUG EFFECTS ON ECG

DrugECG Effect
Digoxin"Reverse tick" ST depression, shortened QT, T wave inversion, PR prolongation, various arrhythmias
Beta-blockersBradycardia, PR prolongation
Class Ia antiarrhythmics (quinidine)QT prolongation, QRS widening
Class Ic (flecainide)QRS widening, PR prolongation
Class III (amiodarone, sotalol)QT prolongation
TCAs (tricyclics)Sinus tachycardia, QRS widening, QT prolongation, right axis deviation
AntipsychoticsQT prolongation
Fluoroquinolones / macrolidesQT prolongation

18. OTHER IMPORTANT ECG PATTERNS

Wolff-Parkinson-White (WPW)

  • Short PR interval (< 120 msec)
  • Delta wave (slurred upstroke of QRS)
  • Widened QRS
  • ST/T changes
  • Caused by accessory pathway (Bundle of Kent) bypassing AV node
  • Risk: pre-excited AF → VF (never use AV-nodal blocking drugs in AF with WPW)

Brugada Pattern

  • RBBB-like pattern + ST elevation in V1-V3 (downsloping/coved type)
  • Associated with sudden cardiac death in structurally normal heart
  • Accentuated by fever, sodium channel blockers, vagal tone

Pulmonary Embolism (PE)

  • Most common finding: Sinus tachycardia
  • Classic (but uncommon): S1Q3T3 - deep S in I, Q wave + T inversion in III
  • Right heart strain: RBBB, RAD, P pulmonale
  • T wave inversions in V1-V4

Pericarditis

  • Stage 1: Diffuse ST elevation (concave/saddle-shaped) + PR depression in all leads except aVR/V1 (PR elevated in aVR)
  • Stage 2: ST and PR return to baseline
  • Stage 3: Diffuse T wave inversion
  • Stage 4: ECG normalizes

Hypothermia

  • Sinus bradycardia
  • Osborn (J) waves - positive deflection at J point; most prominent in leads V4-V6
  • QT prolongation
  • Prolonged PR and QRS
  • Shivering artifact

Long QT Syndrome

  • Congenital (LQT1, LQT2, LQT3 - different triggers and T wave morphologies)
  • Acquired (drugs, electrolytes)
  • Risk: Torsades de Pointes (polymorphic VT) → syncope / sudden death

19. QUICK CLINICAL CLUES TABLE

ECG FindingThink Of
Delta wave + short PRWPW
Sawtooth waves at 300 bpmAtrial flutter
Irregularly irregular, no P wavesAtrial fibrillation
Progressive PR prolongation + dropped beatMobitz I (Wenckebach)
Fixed PR + sudden dropped beatMobitz II
P-QRS complete dissociationComplete heart block
RSR' in V1 + wide S in V6RBBB
Broad notched R in V5-V6, no Q in V6LBBB
S1Q3T3 + sinus tachycardiaPulmonary embolism
Diffuse ST elevation + PR depressionPericarditis
Tall peaked T wavesHyperkalemia
Prominent U wavesHypokalemia
Short QTHypercalcemia
Long QT + low K/MgTorsades risk
Osborn (J) wavesHypothermia
Reverse tick ST depressionDigoxin effect

20. KEY FORMULAS SUMMARY

FormulaUse
HR = 300 / (# large boxes)Quick rate estimation
HR = 60,000 / RR interval (msec)Precise rate
QTc = QT / √RRBazett's correction for QT
Sokolow-Lyon: SV1 + RV5/V6 > 35 mmLVH criterion
Pathological Q: width ≥ 0.04 sec, depth ≥ 25% RQ wave = infarction

Sources:
  • Goldman-Cecil Medicine, International Edition (Chapter 42 - Electrocardiography)
  • Medical Physiology (Boron & Boulpaep), Chapter 21 - Box 21-2, Table 21-5
  • Miller's Anesthesia, 10th Edition - Chapter 13 (Electrical Events and the ECG)
  • Roberts & Hedges' Clinical Procedures in Emergency Medicine - Electrocardiography chapter

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