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Electrocardiogram (ECG) Analysis: Comprehensive Clinical Notes

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PART 1: THE NORMAL ECG

1.1 Basic Principles

• Paper speed: 25 mm/s → 1 small box = 0.04 s; 1 large box = 0.2 s
• Amplitude calibration: 1 mV = 10 mm (2 large boxes)
• Isoelectric line: baseline between beats; deviations indicate electrical activity

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1.2 ECG Waveforms and Intervals

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1.3 Detailed Waveform Analysis

P Wave

• Produced by right atrial depolarization (first 40 ms) followed by left atrial depolarization
• Normal morphology: smooth, rounded, upright in leads I, II, aVF
• Inverted P in aVR (normal)
• Biphasic (±) in V1 — initial positive = RA, terminal negative = LA

PR Interval

• Reflects conduction through the AV node, Bundle of His, and bundle branches
• Short PR (< 120 ms): pre-excitation (WPW), junctional rhythm, LGL syndrome
• Long PR (> 200 ms): first-degree AV block

QRS Complex

• Q wave: initial septal depolarization (left → right); normal Q < 40 ms, < 25% of R height
• R wave: main ventricular depolarization; normal progression V1→V6 (R grows, S shrinks)
• S wave: terminal basal depolarization
• Transition zone: where R = S, normally V3–V4

ST Segment

• Represents the period when all ventricular cells are depolarized
• Should be isoelectric
• Measured from J point

T Wave

• Normally asymmetric (slow rise, rapid fall)
• Inverted T in aVR and V1 is normal
• Peaked T in V1: right atrial enlargement or hyperkalemia clue

QT Interval / QTc

• Corrected using Bazett's formula: QTc = QT / √RR (all in seconds)
• Prolonged QTc → risk of Torsades de Pointes

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1.4 Cardiac Axis

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PART 2: PATHOLOGICAL ECG CHANGES

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PART 2A: ATRIAL HYPERTROPHY / ENLARGEMENT

2A.1 Right Atrial Enlargement (RAE) — "P Pulmonale"

• P wave amplitude ≥ 2.5 mm (tall, peaked) in leads II, III, aVF
• P wave duration usually normal (≤ 120 ms)
• May also appear as tall initial positivity in V1
• P wave axis often rightward (> +75°)

• Cor pulmonale (chronic lung disease, pulmonary hypertension)
• Tricuspid stenosis or regurgitation
• Pulmonary stenosis
• Right heart failure

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2A.2 Left Atrial Enlargement (LAE) — "P Mitrale"

• Broad, notched P wave ≥ 120 ms in limb leads (I, II, aVL) — the "M-shaped" or bifid P
• Biphasic P wave in V1 with a broad, deep terminal negative component
  • Terminal negative portion: depth × duration ≥ 1 mm × 40 ms (Morris index ≥ 0.04 mm·s)
• P wave axis often leftward
• P-wave terminal force in V1 is the most sensitive criterion

• Mitral stenosis (classic "P-mitrale")
• Mitral regurgitation
• Left heart failure / LVH
• Hypertension
• Can occur with LA conduction delay without true anatomical enlargement

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2A.3 Biatrial Enlargement

• Broad AND tall P waves: duration ≥ 120 ms AND amplitude ≥ 2.5 mm
• Or: tall P waves in inferior leads + wide negative terminal component in V1

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PART 2B: VENTRICULAR HYPERTROPHY

2B.1 Right Ventricular Hypertrophy (RVH)

• Pulmonary hypertension (primary or secondary)
• Pulmonary stenosis
• Tetralogy of Fallot
• Chronic obstructive pulmonary disease (COPD)
• Mitral stenosis (with pulmonary HTN)

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2B.2 Left Ventricular Hypertrophy (LVH)

• Left axis deviation (−30° to −90°)
• Prolonged QRS (100–110 ms), broad R wave peak time > 50 ms in V5/V6
• ST depression + T-wave inversion in I, aVL, V5–V6 → LV "strain" pattern (systolic overload)
• Repolarization abnormality: asymmetric ST-T in V5–V6

• Voltage criteria: 3 pts
• LV strain pattern: 3 pts
• LAE: 3 pts
• LAD ≥ −30°: 2 pts
• QRS duration ≥ 90 ms: 1 pt
• Intrinsicoid deflection V5/V6 ≥ 50 ms: 1 pt
• ≥ 5 points = definite LVH; 4 points = probable LVH

• Systemic hypertension (most common)
• Aortic stenosis / aortic regurgitation
• Hypertrophic cardiomyopathy (HOCM)
• Coarctation of the aorta

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PART 3: PATHOLOGICAL ECTOPIC BEATS AND RHYTHMS

3.1 Ectopic Beats — Overview

• Supraventricular (atrial or junctional) — narrow QRS (< 120 ms)
• Ventricular — wide QRS (≥ 120 ms)

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3.2 Premature Atrial Complexes (PACs)

• Premature P' wave with abnormal morphology (different from sinus P)
• Usually narrow QRS (< 120 ms) — same as conducted sinus beats
• Incomplete compensatory pause (the SA node is reset)
• If P' falls too early → aberrant conduction (wide QRS) or blocked PAC (no QRS)

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3.3 Premature Ventricular Complexes (PVCs)

• Wide, bizarre QRS ≥ 120 ms
• No preceding P wave (or retrograde P after QRS)
• Full compensatory pause (SA node not reset)
• T wave in opposite direction to the main QRS deflection (discordant T)
• Fusion beats: occur when a PVC coincides with a sinus impulse

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3.4 Supraventricular Tachycardias (SVT)

Sinus Tachycardia

• Rate 100–180 bpm; normal P waves precede each QRS; physiological

Atrial Flutter

• Rate: Atrial rate ~300 bpm; ventricular rate typically 150 bpm (2:1 block)
• Sawtooth flutter waves (F waves) in leads II, III, aVF — no isoelectric baseline
• Regular R-R intervals (if fixed block ratio)
• Narrow QRS unless aberrant conduction

Atrial Fibrillation (AF)

• Absent P waves replaced by chaotic fibrillatory (f) waves, best seen V1
• Irregularly irregular R-R intervals
• Narrow QRS (unless pre-existing BBB or aberrant conduction)
• Rate: 100–180 bpm (uncontrolled)

AV Nodal Re-entrant Tachycardia (AVNRT)

• Most common paroxysmal SVT
• Rate: 150–250 bpm
• Narrow QRS (< 120 ms)
• P waves buried in or just after QRS (retrograde P' — negative in II, III, aVF)
• Pseudo-r' in V1 or pseudo-s in inferior leads

WPW / Accessory Pathway Tachycardia

• Delta wave (slurred upstroke of QRS) during sinus rhythm
• Short PR (< 120 ms)
• Wide QRS due to ventricular pre-excitation
• Risk: AF with rapid conduction → VF

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3.5 AV Blocks

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3.6 Ventricular Tachycardia (VT) and Fibrillation (VF)

Ventricular Tachycardia (VT)

• ≥ 3 consecutive PVCs at rate > 100 bpm
• Wide QRS (≥ 120 ms), bizarre morphology
• AV dissociation (P waves independent of QRS) — pathognomonic
• Capture beats: occasional narrow QRS from sinus capture
• Fusion beats: partial sinus capture
• Monomorphic VT: uniform QRS morphology
• Polymorphic VT: varying QRS morphology

1. No RS complex in any precordial lead → VT
2. RS interval > 100 ms in any precordial lead → VT
3. AV dissociation → VT
4. Morphology criteria (LBBB/RBBB pattern) → VT

Torsades de Pointes

• Polymorphic VT with twisting QRS axis around baseline
• Occurs with prolonged QTc
• Causes: drugs (antiarrhythmics, antipsychotics, antibiotics), hypokalemia, hypomagnesemia, congenital long QT

Ventricular Fibrillation (VF)

• Chaotic, irregular waveform — no identifiable QRS, P, or T
• Immediately life-threatening → defibrillation required

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3.7 Bundle Branch Blocks

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PART 4: ECG IN ACUTE CORONARY SYNDROME (ACS)

4.1 ACS Spectrum Overview

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4.2 ECG Evolution in STEMI

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4.3 ST Elevation — Diagnostic Criteria (STEMI)

• ≥ 1 mm (0.1 mV) in ≥ 2 contiguous limb leads
• ≥ 2 mm in ≥ 2 contiguous precordial leads (V1–V4)
• ≥ 1.5 mm in V2–V3 in women

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4.4 Localization of Infarction

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4.5 Pathological Q Waves

• Duration ≥ 40 ms (≥ 1 small box)
• Depth ≥ 25% of the R wave in the same lead
• Present in ≥ 2 contiguous leads
• May represent transmural scar (old MI) but can also occur in LBBB, LVH, WPW, HOCM

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4.6 NSTEMI / Unstable Angina

• Horizontal or downsloping ST depression ≥ 0.5–1 mm in ≥ 2 contiguous leads
• T-wave inversion (symmetric, deep) — Wellens' syndrome: critical LAD stenosis
• Transient ST elevation possible (vasospasm / Prinzmetal's)
• Normal ECG in ~30% of NSTEMI — does NOT exclude diagnosis

• Type A: Biphasic T waves in V2–V3 (less common, ~25%)
• Type B: Deep, symmetric T-wave inversions in V2–V3 (more common, ~75%)
• Pain-free at time of ECG recording

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4.7 De Winter T Waves (STEMI Equivalent)

• ST depression at J point + tall, symmetric, hyperacute T waves in precordial leads
• No ST elevation
• Represents proximal LAD occlusion — treat as STEMI equivalent
• Seen in ~2% of LAD occlusions

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4.8 Sgarbossa Criteria (STEMI in LBBB)

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4.9 Right Ventricular Infarction (RVI)

• Complicates inferior STEMI (proximal RCA occlusion)
• Right-sided leads are essential:
  • ST elevation ≥ 1 mm in V4R = diagnostic
• Clinical triad: hypotension + elevated JVP + clear lung fields (Kussmaul's sign)
• Important: Avoid nitrates (preload-dependent RV)

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QUICK REFERENCE SUMMARY

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Sources: Harrison's Principles of Internal Medicine, 21st Edition (pp. 6787, 6796); Braunwald's Heart Disease; AHA/ACC STEMI Guidelines 2013 (updated 2015); ESC ACS Guidelines 2023.