ECG — Comprehensive Overview

What Is an ECG?

The electrocardiogram (ECG/EKG) records tiny potential differences on the body surface that reflect the sequence of depolarization and repolarization of the myocardium. Because different regions of the heart activate at different times (atria before ventricles, specific ventricular sequences), measurable voltage gradients arise between body-surface electrodes. — Costanzo Physiology, 7th Ed.

The Standard 12-Lead ECG

A standard recording runs for 10 seconds at 25 mm/s and 10 mm/mV. Each small box = 0.04 sec (40 ms); each large box = 0.2 sec (200 ms).

Lead groups:

Group	Leads	Territory viewed
Limb leads	I, II, III	Frontal plane
Augmented limb	aVR, aVL, aVF	Frontal plane (augmented)
Precordial	V1–V6	Horizontal plane

Under normal sinus rhythm, P waves and QRS complexes are upright in I, II, III, aVF and inverted in aVR. — Goldman-Cecil Medicine

ECG Waveforms — What Each Represents

ECG diagram from Costanzo Physiology showing PQRST complex with labeled PR interval, ST segment, and QT interval

Schematic of cardiac conduction system from Harrison's showing P, QRS, ST, T, U waves with PR, QRS, and QT intervals labeled

Wave / Segment	Electrical Event
P wave	Atrial depolarization; duration reflects atrial conduction time
PR interval	Onset of atrial depolarization → onset of ventricular depolarization (includes AV node conduction)
PR segment	Isoelectric; represents AV nodal conduction delay only
QRS complex	Ventricular depolarization (Q = initial septal; R = main ventricular; S = terminal basal/posterior)
ST segment	Between end of QRS (J point) and start of T wave; normally isoelectric; represents early ventricular repolarization
T wave	Ventricular repolarization
QT interval	QRS onset → T wave end; total ventricular depolarization + repolarization time
U wave	Small deflection after T; thought to represent repolarization of Purkinje fibers or papillary muscles; prominent in hypokalemia

Atrial repolarization is not visible on a normal ECG — it is buried within the QRS complex. — Costanzo Physiology

Normal Intervals

(From Goldman-Cecil Medicine, Table 42-1)

Parameter	Normal Range
Heart rate	50–100 bpm
P wave duration	< 120 ms
PR interval	90–200 ms
QRS duration	75–110 ms
QTc (males)	390–450 ms
QTc (females)	390–460 ms
QRS axis	−30° to +90°

Heart rate calculation: HR (bpm) = 60,000 ÷ RR interval (ms)

Systematic Approach to ECG Interpretation

(Goldman-Cecil Medicine, Table 42-2)

Rate — estimate heart rate
Rhythm — regular vs. irregular
P waves — present? morphology? 1:1 relationship with QRS?
Pauses / premature beats — any?
Intervals — measure PR, QRS duration, QT; calculate QTc
Axis — estimate QRS axis in frontal plane
P wave morphology — duration, axis
QRS progression — R-wave progression V1→V6; transition zone (normally V3–V4)
ST segments — elevation or depression in regional groupings (inferior: II, III, aVF; anterior: V2–V4; lateral: I, aVL, V5–V6)
T waves — inversion, hyperacuity

Key Abnormalities at a Glance

Rhythm Disturbances

Finding	Interpretation
No P waves, irregularly irregular RR	Atrial fibrillation
Sawtooth baseline ~300/min, regular RR	Atrial flutter
Wide QRS, no preceding P waves	Ventricular tachycardia
Short PR + delta wave + wide QRS	Wolff-Parkinson-White

Conduction Blocks

Finding	Interpretation
PR > 200 ms	1st-degree AV block
Progressively lengthening PR → dropped QRS	2nd-degree AV block, Mobitz I (Wenckebach)
Constant PR, intermittent dropped QRS	2nd-degree AV block, Mobitz II
Complete AV dissociation	3rd-degree (complete) AV block
QRS ≥ 120 ms, RsR' in V1, slurred S in I/V6	Right bundle branch block (RBBB)
QRS ≥ 120 ms, broad notched R in I/V6, no septal q	Left bundle branch block (LBBB)

Ischemia / Infarction

Pattern	Territory
ST elevation + Q waves in II, III, aVF	Inferior MI (RCA)
ST elevation in V1–V4	Anterior MI (LAD)
ST elevation in I, aVL, V5–V6	Lateral MI (LCx)
ST elevation in aVR + diffuse depression	Left main / proximal LAD occlusion
Reciprocal ST depression in V1–V3 + tall R	Posterior MI

AMI is classified by ECG into STEMI (ST-segment elevation MI) or NSTEMI (no ST elevation). Right-sided ECG leads should be obtained to detect RV infarction when inferior ST elevation is present. — Tintinalli's Emergency Medicine

QTc Prolongation

Caused by electrolyte abnormalities (hypokalemia, hypomagnesemia), drugs (antiarrhythmics, antipsychotics, antibiotics), or congenital long QT syndrome. Predisposes to torsades de pointes.

Axis Deviation

Axis	Degrees	Causes
Normal	−30° to +90°	—
Left axis deviation (LAD)	−30° to −90°	Left anterior fascicular block, inferior MI, LVH
Right axis deviation (RAD)	+90° to +180°	RVH, lateral MI, left posterior fascicular block, normal in children

To estimate axis quickly: find the lead in which QRS is most isoelectric — the axis is perpendicular to that lead.

Precordial Lead Progression

Normal R-wave progression: small r in V1 → progressively taller R waves → transition (R = S) at V3–V4 → large R in V6. Poor R-wave progression (R stays small through V4–V5) suggests anterior infarction or LVH.

This overview covers the essentials. If you need deeper coverage of any specific area — a particular arrhythmia, a specific conduction block, ischemia patterns, pediatric ECG, or drug-induced changes — just ask.

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