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Complete ECG Analysis Guide: Basic to Advanced

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PART 1 - THE BASICS: Understanding the ECG

What is an ECG?

• P wave - atrial depolarization
• QRS complex - ventricular depolarization
• T wave - ventricular repolarization
• U wave - delayed repolarization of Purkinje fibers (may be seen in hypokalemia)

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The ECG Paper

• Vertical axis: 0.1 mV per mm
• Horizontal axis: 0.04 seconds per small box (1 mm), 0.2 seconds per large box (5 mm)
• 5 large boxes = 1 second

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The 12 Leads: What Each Sees

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PART 2 - THE SYSTEMATIC APPROACH (7-Step Method)

Step 1 - Rate

• Normal: 60-100 bpm
• Bradycardia: < 60 bpm
• Tachycardia: > 100 bpm

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Step 2 - Rhythm

1. Is there a P wave before every QRS?
2. Is there a QRS after every P wave?
3. Are P-P intervals regular?
4. Are R-R intervals regular?

• P wave before each QRS
• P wave upright in leads II, III, aVF
• PR interval 0.12-0.20 sec
• Regular rate 60-100 bpm

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Step 3 - Axis

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Step 4 - Intervals

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Step 5 - P Waves and Atrial Enlargement

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Step 6 - QRS Complex

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Step 7 - ST Segment and T Waves

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PART 3 - ARRHYTHMIAS

3.1 Sinus Arrhythmias

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3.2 Atrial Arrhythmias

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• Abnormal P wave morphology (ectopic atrial focus)
• QRST usually normal (same ventricular activation)
• Followed by a compensatory or non-compensatory pause
• Clinically benign in most individuals

• Rate: 150-220 bpm from a single atrial focus
• P waves present but different morphology from sinus
• May have AV block (especially in digitalis toxicity)

• Atrial rate: 200-350 bpm, typically ~300 bpm
• Classic sawtooth "flutter waves" at 300/min in leads II, III, aVF (negative) and V1 (positive)
• Usually 2:1 AV block → ventricular rate ~150 bpm (always suspect flutter when rate is exactly 150)
• Mechanism: large counterclockwise reentrant circuit in right atrium around cavo-tricuspid isthmus

• Atrial rate: 300-500/min, completely irregular and disorganized
• No distinct P waves - replaced by fibrillatory baseline
• Irregularly irregular R-R intervals (pathognomonic)
• Ventricular rate: 80-160 bpm
• Mechanism: multiple concurrent reentrant excitation waves in both atria; some paroxysmal AF from ectopic foci in pulmonary veins (Ganong's Review of Medical Physiology)

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3.3 AV Nodal Arrhythmias

• 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 (unless aberrant)
• Terminates with vagal maneuvers or adenosine

• Accessory pathway connects atria and ventricles
• Delta wave on baseline ECG: slurred upstroke of QRS, short PR (<0.12 sec), wide QRS
• Orthodromic AVRT: narrow complex (down accessory, up normal)
• Antidromic AVRT: wide complex (down normal, up accessory) - looks like VT!

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3.4 Heart Blocks (AV Blocks)

First-Degree AV Block

• Generally benign
• Causes: inferior MI, increased vagal tone, digoxin, electrolyte abnormalities
• No treatment needed for isolated first-degree block

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

• Level of block: AV node
• Associated with: right coronary artery territory MI (inferior leads II, III, aVF)
• Usually benign, may be transient
• Rarely requires pacing

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Second-Degree AV Block - Mobitz Type II

• Level of block: His-Purkinje system (below AV node)
• High risk of progression to complete heart block
• Permanent pacemaker usually required (Frameworks for Internal Medicine)

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Second-Degree AV Block - 2:1 Block

• Every other P wave is non-conducted
• Cannot distinguish Mobitz I from II electrocardiographically in pure 2:1 block
• PR interval of conducted beats helps: prolonged = more likely Mobitz I; normal = more likely Mobitz II

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Third-Degree (Complete) AV Block

• Atrial rate (P waves) is faster than the ventricular rate (QRS)
• Escape rhythm: junctional (narrow QRS, 40-60 bpm) or ventricular (wide QRS, 20-40 bpm)
• Causes: inferior MI (transient), anterior MI (permanent), Lyme disease, digoxin toxicity, fibrosis
• Treatment: atropine acutely; permanent pacemaker for persistent cases (Goldman-Cecil Medicine)

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3.5 Bundle Branch Blocks

• LBBB: W in V1, M in V6 (= "WilLiam")
• RBBB: M in V1, W in V6 (= "MaRRow")

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3.6 Ventricular Arrhythmias

• Wide, bizarre QRS (> 0.12 sec), not preceded by a P wave
• Followed by full compensatory pause (SA node not reset)
• T wave opposite in polarity to QRS
• If PVCs appear every other beat = bigeminy; every 3rd beat = trigeminy; consecutive pairs = couplets

• Rate: > 100 bpm (usually 140-250), wide QRS (> 0.12 sec)
• AV dissociation (P waves march through independently) = diagnostic of VT
• Fusion beats (sinus + ventricular = hybrid QRS) = diagnostic of VT
• Capture beats (sinus impulse successfully captures ventricle = narrow QRS amid wide ones) = diagnostic of VT

• Completely chaotic, disorganized electrical activity
• No identifiable QRS complexes, P waves, or T waves
• "Coarse" VF = larger amplitude; "fine" VF = nearly flat
• Immediately life-threatening; requires immediate defibrillation

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PART 4 - ISCHEMIA AND INFARCTION

4.1 The ECG Progression of STEMI

• Tall, peaked, symmetric T waves (often first sign)

• Convex ("tombstone") ST elevation ≥ 1 mm in limb leads, ≥ 2 mm in precordial leads in ≥ 2 contiguous leads
• Reciprocal ST depression in opposite leads

• Pathological Q waves: > 1 mm wide or > 25% of QRS height

• T waves invert in the leads showing ST elevation

• Q waves may persist indefinitely (scar)

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4.2 STEMI by Territory

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4.3 Special STEMI Patterns

• Upsloping ST depression with tall, peaked T waves in precordial leads V1-V6
• ST elevation in aVR
• Treat as STEMI equivalent

• Type A: Biphasic T waves (upright then inverted) in V2-V3
• Type B: Deep symmetric T wave inversions in V2-V3
• Do NOT stress test; high risk for massive anterior MI

• Concordant ST elevation ≥ 1 mm in leads with positive QRS (+5 points)
• Concordant ST depression ≥ 1 mm in V1-V3 (+3 points)
• Discordant ST elevation ≥ 5 mm (+2 points)
• Score ≥ 3 = high specificity for acute MI

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PART 5 - HYPERTROPHY

Left Ventricular Hypertrophy (LVH)

• 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
• Strain pattern: ST depression and T-wave inversion in V5-V6, I, aVL (lateral "strain")

Right Ventricular Hypertrophy (RVH)

• Tall R wave in V1 (R > S in V1)
• Right axis deviation (> +90°)
• ST depression and T-wave inversion in V1-V4 (right "strain")
• Causes: pulmonary hypertension, cor pulmonale, severe pulmonary stenosis, PE (acute)

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PART 6 - METABOLIC AND DRUG CHANGES

Hyperkalemia (progressive changes with rising K+)

Hypokalemia

• Flattened T waves
• U waves become prominent (U > T in same lead)
• ST depression
• Prolonged QU interval (often misread as long QT)

Hypercalcemia

• Shortened QT interval
• Short ST segment

Hypocalcemia

• Prolonged QT interval (long ST segment)

Digoxin effect (not toxicity)

• "Reverse tick" or "sagging" ST depression (scooped ST depression)
• Shortened QT
• T-wave flattening or inversion

Digoxin toxicity

• Any arrhythmia, especially PAT with block, junctional tachycardia, bidirectional VT
• PVCs (bigeminy very common)

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PART 7 - OTHER IMPORTANT CONDITIONS

Pericarditis

Pulmonary Embolism

• S1Q3T3: S wave in lead I, Q wave and T-wave inversion in lead III
• Sinus tachycardia (most common finding)
• New RBBB or right heart strain pattern
• T-wave inversions in V1-V4
• Right axis deviation

Brugada Syndrome

• Type 1 (diagnostic): Coved ST elevation ≥ 2 mm with T-wave inversion in V1-V2 (unprovoked or with sodium channel blockers)
• Type 2: Saddle-back ST elevation in V1-V2 (not diagnostic alone)
• Associated with sudden cardiac death from VF in structurally normal hearts
• More common in males, South/Southeast Asians

Long QT Syndrome

• QTc > 450 ms (men), > 470 ms (women), or > 500 ms (high risk)
• Risk of torsades de pointes (polymorphic VT)
• Causes: congenital (LQTS1, 2, 3) or acquired (drugs - quinidine, sotalol, erythromycin, antipsychotics; hypokalemia, hypomagnesemia)

Hypothermia

• Osborn (J) wave: Positive deflection at the J-point (junction of QRS and ST segment), best seen in inferior and lateral leads
• Shivering artifact
• Bradycardia, prolonged intervals
• Osborn wave size correlates with depth of hypothermia

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PART 8 - QUICK REFERENCE SUMMARY TABLE

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PART 9 - CLINICAL MEMORY AIDS

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Structure of the Heart

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1. Overview and Location

• A base (broad top, facing upward and to the right) - where the great vessels attach
• An apex (pointed tip, facing downward and to the left) - at approximately the 5th intercostal space in the midclavicular line

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2. The Pericardium - Outer Covering

Fibrous Pericardium

• Outermost, tough connective tissue layer
• Cone-shaped bag with its base on the diaphragm, apex continuous with the adventitia of the great vessels
• Attached to the posterior sternum by sternopericardial ligaments
• Prevents cardiac overdistention and keeps the heart in position in the thoracic cavity

Serous Pericardium

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3. The Wall of the Heart - Three Layers

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4. The Four Chambers

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Right Atrium (RA)

• Thin-walled receiving chamber
• Receives deoxygenated blood from the body via:
  • Superior vena cava (from head, neck, arms)
  • Inferior vena cava (from trunk, legs, abdominal organs)
  • Coronary sinus (venous drainage from heart muscle itself)
• Contains the fossa ovalis - a depression on the interatrial septum, remnant of the foramen ovale (fetal opening between atria)
• Contains the SA node at the junction of the right atrial appendage and superior vena cava
• Contains the AV node in the floor of the right atrium near the interatrial septum

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Right Ventricle (RV)

• Triangular in shape, anteriorly positioned (directly behind the sternum)
• More trabeculated (muscular ridges) inner wall than the left
• Contains a moderator band (carrying bundle branch fibers)
• Has a muscular outflow tract called the infundibulum (conus arteriosus)
• Pumps blood to the lungs via the pulmonary trunk (low-pressure circuit)
• Separated from the RA by the tricuspid valve
• Separated from the pulmonary artery by the pulmonary valve

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Left Atrium (LA)

• Thin-walled, located posteriorly behind the right atrium
• Receives oxygenated blood from the lungs via four pulmonary veins (two right, two left)
• Has a narrow, tubular left atrial appendage (important site for thrombus formation in AF)
• The mitral valve separates it from the left ventricle

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Left Ventricle (LV)

• Thickest-walled chamber - the primary pump of the body
• Positioned posteriorly and to the left
• Smooth septum (no trabeculae in contrast to RV)
• Contains papillary muscles (anterolateral and posteromedial) connected to valve leaflets via chordae tendineae
• Has a membranous and muscular interventricular septum dividing it from the RV
• Pumps blood to the entire body via the aorta (high-pressure circuit)
• Separated from the LA by the mitral valve
• Separated from the aorta by the aortic valve

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5. The Four Heart Valves

AV Valves (Tricuspid and Mitral)

• Connected to papillary muscles via chordae tendineae ("heartstrings")
• During ventricular contraction, papillary muscles also contract, pulling the chordae taut - this prevents the leaflets from prolapsing backward into the atria (preventing regurgitation)
• Opening is driven by pressure difference between atria and ventricles during diastole

Semilunar Valves (Pulmonary and Aortic)

• Each cusp is shaped like a half-moon (semilunar)
• Have three pockets (sinuses) - blood fills these pockets during diastole, pushing cusps together to close the valve
• No papillary muscles or chordae tendineae

Valve Wall Layers (Histology)

1. Fibrosa - dense collagen, load-bearing layer
2. Spongiosa - loose connective tissue, acts as shock absorber
3. Ventricularis (semilunar valves) or Atrialis (AV valves) - elastic tissue facing blood flow

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6. Blood Flow Through the Heart

Body (deoxygenated blood)
        ↓
Superior + Inferior Vena Cava
        ↓
RIGHT ATRIUM  →  [Tricuspid Valve]  →  RIGHT VENTRICLE
        ↓
[Pulmonary Valve]  →  Pulmonary Trunk  →  Lungs
        ↓
Pulmonary Veins (oxygenated blood)
        ↓
LEFT ATRIUM  →  [Mitral Valve]  →  LEFT VENTRICLE
        ↓
[Aortic Valve]  →  Aorta  →  Body

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7. The Cardiac Conduction System

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8. Coronary Blood Supply

• Coronary arteries course along the epicardial surface first, then penetrate the myocardium
• Blood flows predominantly during diastole (not systole), because during systole the contracting myocardium compresses the intramural vessels
• Resting coronary blood flow ≈ 225 mL/min (4-5% of cardiac output)
• During heavy exercise, coronary flow can increase 3-4 fold
• Venous drainage: most of the LV drains via the coronary sinus → right atrium; RV drains via small anterior cardiac veins → directly into right atrium

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9. Summary Table - Heart Chambers at a Glance