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ECG: From Basics to Clinical Interpretation

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1. Why the ECG Exists - The Underlying Biology

The Cardiac Conduction System

The cardiac conduction system can be affected by coronary artery disease. If blood supply is disrupted, dysrhythmias may affect heart rate or contraction sequence, leading to heart failure and death. - Gray's Anatomy for Students

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2. ECG Paper and Basic Setup

The Paper Grid

• Small squares: 1 mm wide = 0.04 seconds horizontally; 1 mm tall = 0.1 mV vertically
• Large squares: 5 mm wide = 0.20 seconds; 5 mm tall = 0.5 mV
• Standard paper speed: 25 mm/sec
• Standard calibration: 10 mm/mV (the calibration pulse at the start of the trace should be 10 mm tall)

The 12 Leads

• Bipolar: I (right arm → left arm), II (right arm → left leg), III (left arm → left leg)
• Augmented unipolar: aVR (right arm), aVL (left arm), aVF (left foot)

• V1: 4th intercostal space, right sternal border
• V2: 4th intercostal space, left sternal border
• V3: between V2 and V4
• V4: 5th intercostal space, midclavicular line
• V5: anterior axillary line (same level as V4)
• V6: midaxillary line (same level as V4-V5)

"Each lead is analogous to a different video camera angle 'looking' at the same events - atrial and ventricular depolarization and repolarization - from different spatial orientations." - Harrison's Principles of Internal Medicine 22e

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3. The Normal ECG Waveforms

P Wave

• Represents: Atrial depolarization (SA node → right atrium → left atrium)
• Normal: Upright in II, inverted in aVR; duration < 120 ms; amplitude < 2.5 mm
• The normal P in V1 is often biphasic - positive component = RA depolarization; small negative terminal component = LA depolarization
• Retrograde P waves (negative in II, positive in aVR) indicate ectopic atrial or junctional pacemaker

PR Interval

• Represents: Time from atrial depolarization onset to start of ventricular depolarization - includes the AV nodal delay
• Normal: 120-200 ms (3-5 small squares)
• Short PR (<120 ms): pre-excitation (WPW), junctional rhythm
• Long PR (>200 ms): 1st degree AV block

QRS Complex

• Represents: Ventricular depolarization

1. Phase 1 - Septal depolarization: Left-to-right, anteriorly → produces small "septal r" in V1, small "septal q" in V6
2. Phase 2 - Main ventricular depolarization: LV dominates, vector goes left and posteriorly → large S in V1, tall R in V6

• Q wave: First negative deflection before R
• R wave: First positive deflection
• S wave: Negative deflection after R
• Use uppercase for large (>5 mm), lowercase for small waves

• Duration: < 120 ms (< 3 small squares)
• Pathologic Q wave: depth > 1/4 of R wave, or width ≥ 40 ms in 2 contiguous leads

ST Segment

• Represents: Early ventricular repolarization (phase 2 of action potential)
• Normal: Isoelectric (at baseline)
• Deviation is the hallmark of ischemia/infarction (see section 7)

T Wave

• Represents: Ventricular repolarization (phase 3)
• Normal: Upright in I, II, V3-V6; may be inverted in aVR, aVL, V1, III
• Direction is normally same as the main QRS deflection ("concordant")

QT Interval

• Represents: Total ventricular repolarization
• Normal (corrected QTc): < 440 ms in men, < 460 ms in women
• Corrected using Bazett formula: QTc = QT / √RR
• Prolonged QTc → risk of Torsades de Pointes (polymorphic VT)
• Causes of long QT: drugs (antiarrhythmics, macrolides, antipsychotics), hypokalemia, hypomagnesemia, hypocalcemia, congenital

U Wave

• Small, rounded deflection after T wave
• Most visible in V2-V3
• Prominent U wave: hypokalemia, bradycardia
• Inverted U wave: ischemia, LVH

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4. Heart Rate Calculation

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

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5. Electrical Axis

Quick Axis Check (Lead I + aVF method):

Common causes:

• LAD: Left ventricular hypertrophy, left anterior fascicular block (most common cause of marked LAD; axis < -45°), inferior MI, WPW
• RAD: Right ventricular hypertrophy, left posterior fascicular block, lateral MI, pulmonary embolism, normal variant in young/thin patients

"Left anterior fascicular block (QRS axis more negative than -45°) is probably the most common cause of marked left axis deviation in adults." - Harrison's 22e

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6. Systematic Interpretation - The 14-Parameter Approach

1. Standardization/calibration - Is the calibration pulse correct (10 mm = 1 mV)? Any artifacts? Lead placement errors?
2. Rhythm - Sinus or non-sinus? Regular or irregular?
3. Heart rate - Calculate using R-R intervals
4. PR interval - AV conduction time (normal 120-200 ms)
5. QRS interval - Narrow (<120 ms) or wide (≥120 ms)?
6. QT/QTc - Measure and correct for rate
7. Mean QRS electrical axis - Use hexaxial diagram
8. P waves - Morphology: size, shape, relationship to QRS
9. QRS voltages - Increased (hypertrophy) or decreased (effusion, obesity, emphysema)?
10. Precordial R-wave progression - Normally increases from V1 to V5; poor progression suggests anterior MI
11. Abnormal Q waves - Width ≥ 40 ms or depth > 1/4 R in ≥2 contiguous leads = pathological
12. ST segments - Elevation or depression vs. baseline?
13. T waves - Direction, symmetry, height
14. U waves - Prominent or inverted?

"Many mistakes in ECG interpretation are errors of omission. Therefore, a systematic approach is essential." - Harrison's Principles of Internal Medicine 22e

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7. Key Clinical Patterns

A. Chamber Hypertrophy

• Increased voltage (Sokolow-Lyon criteria: S in V1 + R in V5/V6 ≥ 35 mm)
• Left axis deviation
• ST depression + T-wave inversion in lateral leads (I, aVL, V5-V6) - "strain" pattern
• Broad, notched P wave in limb leads ± biphasic P in V1 (left atrial enlargement, often accompanies LVH)

• Tall R wave in V1 (R > S in V1)
• Right axis deviation (usually >+110°)
• ST depression + T-wave inversion in V1-V3 (right "strain" pattern)
• Often with right atrial enlargement (tall, peaked P wave in II ≥ 2.5 mm - "P pulmonale")

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B. Bundle Branch Blocks

• RSR' ("rabbit ears" or "M" pattern) in V1-V2 - the classic finding
• Wide, slurred S wave in I, aVL, V5-V6
• ST depression + T inversion in V1-V2

• Broad, notched R in I, aVL, V5-V6 ("M" or plateau shape)
• Absent septal q in lateral leads
• QS or rS in V1
• Secondary ST-T changes opposite to main QRS direction (discordant)
• LBBB makes ischemia very difficult to interpret (see Sgarbossa criteria for suspected STEMI in LBBB)

• Left anterior fascicular block (LAFB): Marked LAD (axis < -45°), small r in II, III, aVF; small q in I, aVL; QRS duration minimally prolonged
• Left posterior fascicular block (LPFB): Marked RAD (axis > +110°); rare in isolation; must exclude RVH, lateral MI, pulmonary disease

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C. AV Conduction Abnormalities

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D. Myocardial Ischemia and Infarction

• ST vector shifts toward ischemic epicardium → ST elevation in leads facing the injured zone
• Reciprocal ST depression in opposite leads
• Followed (hours to days) by T-wave inversion, then Q wave development

• ST vector toward subendocardium → ST depression in overlying leads
• ST elevation in aVR (global subendocardial ischemia = left main or proximal LAD lesion)

1. Hyperacute T waves (minutes) - tall, broad, peaked T waves
2. ST elevation (minutes-hours)
3. T-wave inversion (hours-days)
4. Pathological Q waves (hours-days, may persist permanently)

"When the acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves." - Harrison's 22e

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E. Common Arrhythmias - ECG Recognition

• Sinus tachycardia: Rate >100, normal P morphology, regular
• Sinus bradycardia: Rate <60, normal P morphology
• Sinus arrhythmia: Regular P-QRS but RR varies with respiration (normal in young patients)

• PAC (premature atrial complex): Premature P wave (may be abnormal shape), narrow QRS (unless aberrant), followed by incomplete compensatory pause
• Atrial flutter: Sawtooth flutter waves (F waves) at ~300 bpm, typically with 2:1, 3:1, or 4:1 block; regular or regularly irregular
• Atrial fibrillation: Absent P waves, chaotic fibrillatory baseline, irregularly irregular narrow QRS

• Narrow QRS; P absent, buried in QRS, or retrograde (inverted in II, III, aVF)
• Rate 40-60 bpm (junctional escape) or >60 bpm (accelerated junctional)

• PVC (premature ventricular complex): Wide, bizarre QRS > 120 ms, no preceding P, T wave opposite main deflection, full compensatory pause
• Ventricular tachycardia (VT): ≥3 consecutive wide complex beats at >100 bpm; AV dissociation (P marching through, capture/fusion beats) confirms VT
• Ventricular fibrillation (VF): Chaotic, irregular broad deflections; no organized QRS; cardiac arrest

• Short PR (<120 ms)
• Delta wave (slurred initial QRS upstroke)
• Wide QRS
• Secondary ST-T changes
• At-risk for rapid AF conducting down the accessory pathway → VF

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F. Other Important Patterns

• Most common: Sinus tachycardia
• Classic (but insensitive): S1Q3T3 pattern - deep S in I, Q wave and T inversion in III
• New RBBB or right axis shift
• T-wave inversions V1-V4 (right heart strain)
• AF may occur

1. Tall, peaked, narrow ("tented") T waves (K⁺ ~5.5-6.5)
2. PR prolongation, P wave flattening (K⁺ ~6.5-7.0)
3. Wide QRS (K⁺ ~7.0+) - sine wave pattern
4. VF / asystole (K⁺ > 8-9)

• Prominent U waves (U > T in same lead)
• ST depression, T-wave flattening
• Long QU interval (mistaken for long QT)

• Diffuse (saddle-shaped) ST elevation in multiple leads (not conforming to one coronary territory)
• PR depression (most specific sign)
• Reciprocal changes only in aVR and V1

• Coved-type ST elevation ≥2 mm in V1-V2 with RBBB morphology
• Risk of sudden cardiac death from VF, especially at rest/during fever

• Scooped ("reverse tick" / "Salvador Dali mustache") ST depression - most noticeable in V5-V6
• Shortened QT
• Digitalis toxicity: almost any arrhythmia possible (PAT with block is classic)

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8. Computerized ECG Interpretation

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Summary: Stepwise Approach to Any ECG

1. Calibration check (10 mm = 1 mV; 25 mm/s)
2. Rhythm: P present? Regular? P:QRS ratio?
3. Rate: count R-R intervals
4. PR interval (normal 120-200 ms)
5. QRS width (narrow <120 ms or wide ≥120 ms?)
6. QTc (correct for rate; normal <440 ms men, <460 ms women)
7. Axis (Lead I + aVF; hexaxial diagram)
8. P wave morphology (size, shape)
9. QRS voltages (high = hypertrophy; low = effusion/COPD)
10. R-wave progression across chest leads (V1→V6)
11. Abnormal Q waves (pathological ≥40 ms or >25% R height)
12. ST segments (elevation/depression; shape)
13. T waves (axis, symmetry, height)
14. U waves (prominent or inverted?)
→ Correlate with CLINICAL CONTEXT always

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