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ECG Reading: A Complete Guide

An ECG (electrocardiogram) records the heart's electrical activity from electrodes placed on the body surface. The fundamental principle: when a depolarization wave moves toward a positive electrode, it inscribes an upward (positive) deflection; when it moves away, it records a downward (negative) deflection.

The Basic ECG Waveform

Here is the standard ECG waveform with all labeled components:

ECG waveform showing P, Q, R, S, T, U waves with PR, QRS, ST, and QT intervals

Fig. 4.17 - The electrocardiogram measured from Lead II (Costanzo Physiology, 7th Ed.)

Harrison's ECG waveform showing P, QRS, ST, T, U waves and J point

Fig. 247-2 - Basic ECG waveforms and intervals including the J point (Harrison's, 22nd Ed.)

The Cardiac Conduction System (What the ECG Records)

The ECG captures this sequence of electrical events:

SA node (sinoatrial node, high right atrium) fires spontaneously - it is the dominant pacemaker
Wave spreads through both atria (Bachmann bundle speeds it to the left atrium)
Signal reaches the AV node - where there is a physiologic conduction delay
Exits into the Bundle of His → splits into right and left bundle branches → left bundle divides into left anterior and left posterior fascicles
Depolarization travels through the Purkinje system rapidly to ventricular myocardium (endocardium → epicardium)

"The depolarization wavefronts then spread through the ventricular wall, from endocardium to epicardium, triggering coordinated ventricular contraction." - Harrison's Principles of Internal Medicine, 22nd Ed.

Step-by-Step: What Each Wave/Segment Means

1. P Wave

Represents atrial depolarization
Duration reflects conduction time through the atria
Normal: upright in leads I and II; negative in aVR
The SA node-generated P wave is positive in Lead II and negative in aVR (the depolarization vector points down and leftward)
Atrial repolarization is buried under the QRS and not normally seen
Abnormal P wave? Broad/notched = left atrial enlargement; tall/peaked = right atrial enlargement; absent or inverted = ectopic/junctional rhythm

2. PR Interval

From the start of the P wave to the start of the QRS complex
Represents the time for the impulse to travel from atria → through the AV node → to the ventricles
The isoelectric (flat) portion within it (the PR segment) corresponds to AV nodal conduction delay
Normal: 120-200 ms (3-5 small squares at 25 mm/s)
Sympathetic stimulation shortens it; parasympathetic (vagal) stimulation prolongs it

Finding	Meaning
Short PR (<120 ms)	Pre-excitation (e.g., WPW syndrome) or junctional rhythm
Long PR (>200 ms)	1st degree AV block
Progressively lengthening → dropped beat	2nd degree AV block (Mobitz I / Wenckebach)
Fixed PR + random dropped beats	2nd degree AV block (Mobitz II)
No relationship between P and QRS	3rd degree (complete) AV block

3. QRS Complex

Represents ventricular depolarization
Q = first downward deflection; R = first upward deflection; S = downward deflection after R
Not every QRS has all three components - a large upward wave alone can be called an R wave
Normal duration: ≤100-110 ms (≤2.5 small squares)
The His-Purkinje system allows rapid ventricular spread, so QRS duration is similar to P wave duration despite the far larger ventricular mass

Finding	Meaning
Wide QRS >120 ms	Bundle branch block, hyperkalemia, drugs (Na-channel blockers), paced rhythm
Deep Q waves (>25% of R height, >40 ms)	Pathological - prior myocardial infarction
Tall R waves	Left or right ventricular hypertrophy
Low voltage	Pericardial effusion, emphysema, hypothyroidism

4. ST Segment

From end of QRS (the J point) to start of T wave
Corresponds to the plateau phase (phase 2) of the ventricular action potential - the isoelectric period between depolarization and repolarization
Normally at the baseline (isoelectric)

Finding	Meaning
ST elevation ≥1 mm	STEMI (myocardial infarction), pericarditis (diffuse saddle-shaped), Prinzmetal angina, Brugada pattern
ST depression	NSTEMI/unstable angina, subendocardial ischemia, digoxin effect (scooped)
Diffuse saddle-shaped elevation	Pericarditis

5. T Wave

Represents ventricular repolarization
Normally upright in most leads (I, II, V3-V6), inverted in aVR
Corresponds to phase 3 of the action potential (active repolarization)

Finding	Meaning
Peaked tall T waves	Hyperkalemia (early), myocardial infarction (hyperacute)
Flat/inverted T waves	Ischemia, ventricular hypertrophy, bundle branch block
T wave inversions V1-V4	Right heart strain (PE), anterior ischemia

6. QT Interval

From start of QRS to end of T wave
Encompasses ventricular depolarization + repolarization
Normal upper limits: 460 ms in women, 450 ms in men (rate-corrected QTc)
QT varies inversely with heart rate - must correct using Bazett's formula: QTc = QT / √RR interval
Prolonged QT → risk of Torsades de Pointes (polymorphic VT) - causes include drugs (antiarrhythmics, antipsychotics, macrolides), electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), congenital LQTS

7. U Wave

Small deflection after the T wave, best seen in V2-V3
Thought to represent repolarization of the Purkinje system or papillary muscles
Prominent U waves: hypokalemia, bradycardia
Inverted U waves: may indicate ischemia

The 12 Leads: What They See

The 12-lead ECG gives 12 different "camera angles" of the same electrical events:

Limb Leads (Frontal Plane):

Lead	View
I	Lateral (left side)
II	Inferior
III	Inferior
aVR	Right shoulder (cavity view, everything inverted)
aVL	High lateral
aVF	Inferior

Precordial (Chest) Leads (Horizontal Plane):

Lead	View
V1-V2	Septal / right ventricle
V3-V4	Anterior wall
V5-V6	Lateral wall

A positive deflection occurs when depolarization moves toward the positive electrode of a lead.

Systematic ECG Reading: The RRIAPQRST Approach

Use this order every time to avoid missing anything:

Step	What to assess	Normal values
1. Rate	Count R-R intervals: 300/large squares between R waves	60-100 bpm
2. Rhythm	Regular vs. irregular; P before every QRS?	Regular sinus
3. Axis	Leads I and aVF (both positive = normal axis)	-30° to +90°
4. P waves	Morphology, upright in II, negative in aVR	Upright in II
5. PR interval	Onset P to onset QRS	120-200 ms
6. QRS complex	Duration, morphology, Q waves	≤110 ms
7. ST segment	Elevation or depression vs. baseline	Isoelectric
8. T waves	Upright vs. inverted, peaked vs. flat	Upright in I, II, V3-V6
9. QT interval	Measure QTc	<450 ms (men), <460 ms (women)
10. U wave	Present? Prominent?	Small, if seen

How to Calculate Heart Rate

Regular rhythm:

Count large squares between two R waves → divide 300 by that number
Or: count small squares between R waves → divide 1500 by that number

Example: R-R interval = 4 large squares → Heart rate = 300/4 = 75 bpm

Irregular rhythm (e.g., AF): Count QRS complexes in a 10-second strip × 6

Key Action Potential Correlations

The ECG waveforms directly reflect action potential phases:

ECG	Action Potential Phase	Ion Movement
QRS onset	Phase 0 (rapid upstroke)	Na⁺ influx
ST segment	Phase 2 (plateau)	Ca²⁺ influx balanced by K⁺ efflux
T wave	Phase 3 (repolarization)	K⁺ efflux

Drugs/conditions impairing Na⁺ influx (e.g., hyperkalemia, flecainide) → widen QRS
Drugs/conditions prolonging phase 2 or 3 (e.g., amiodarone, hypocalcemia) → lengthen QT
Factors shortening repolarization (e.g., hypercalcemia, digoxin) → shorten QT

Sources:

Harrison's Principles of Internal Medicine, 22nd Ed. (2025), Ch. 247
Goldman-Cecil Medicine International Edition, 2 Vol Set, Ch. 42
Costanzo Physiology, 7th Edition, Ch. 4
Braunwald's Heart Disease, 11th Ed.

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