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Comprehensive ECG Guide

Cardiac cycle showing ECG in relation to pressures, volumes and heart sounds

The ECG in relation to the full cardiac cycle - Miller's Anesthesia, 10e

1. What is an ECG?

An ECG (electrocardiogram) measures differences in electrical potential generated by the heart at body surface electrodes. It gives direct information about rate, rhythm, and the time-dependent electrical vector of the heart. It also reveals the origin and conduction of the cardiac action potential through different regions of the heart.

Medical Physiology (Boron & Boulpaep), p. 730
Miller's Anesthesia, 10e, p. 1364

2. ECG Paper & Calibration

Parameter	Small box (1 mm)	Large box (5 mm)
Time	0.04 s	0.2 s
Voltage	0.1 mV	0.5 mV
5 large boxes	=	1.0 second

3. The Waveforms - What Each Represents

Wave / Interval	Electrical Event	Key Facts
P wave	Atrial depolarization	SA node fires → spreads to both atria; normal duration <120 ms
PR interval	AV node conduction delay	Normal 120-200 ms; represents delay before ventricular activation
QRS complex	Ventricular depolarization	Normal <120 ms; Purkinje → ventricular myocardium
ST segment	Early ventricular repolarization (plateau phase)	Should be isoelectric; deviation = ischemia/injury
T wave	Ventricular repolarization	Usually upright except aVR, V1
QT interval	Total ventricular action potential duration	Shortens with faster heart rate

The AV node creates a deliberate slowing of conduction - this is the PR interval - allowing atria to finish contracting before the ventricles begin. From the distal His bundle, impulses travel through the right and left bundle branches into the Purkinje system, then to individual ventricular cardiomyocytes.

Miller's Anesthesia, 10e, p. 1364

4. The 12 Leads - What They Look At

Limb leads (frontal plane):

I, II, III - bipolar limb leads
aVR, aVL, aVF - augmented unipolar limb leads

Precordial leads (horizontal plane):

V1-V2 - right ventricle / septal
V3-V4 - anterior wall
V5-V6 - lateral wall
II, III, aVF - inferior wall
I, aVL - high lateral wall

5. How to Read an ECG - Systematic Approach

Use a consistent sequence every time:

Step 1: Rate

Quick method: Count large boxes between two R waves. Rate = 300 ÷ (number of large boxes)
- 1 box = 300 bpm, 2 = 150, 3 = 100, 4 = 75, 5 = 60, 6 = 50
Precise method: R-R interval (seconds) → Rate = 60 ÷ R-R interval

Step 2: Rhythm

Ask three questions:

Where is the pacemaker? (Is there a P wave before every QRS?)
What is the conduction path? (Is PR normal? Is QRS narrow or wide?)
Is the rhythm regular?

Normal sinus rhythm: Regular rate 60-100 bpm, upright P in II, P:QRS = 1:1, normal PR (120-200 ms), narrow QRS (<120 ms).

Step 3: Axis (Frontal Plane)

Normal QRS axis: -30° to +90°

Axis	Meaning
-30° to +90°	Normal
More negative than -30°	Left axis deviation (LAD)
More positive than +110°	Right axis deviation (RAD)

Quick method: If QRS is positive in both Lead I and aVF → normal axis. If positive in I, negative in aVF → LAD. If negative in I, positive in aVF → RAD.

Step 4: P Wave

Present? Upright in II? One per QRS? Duration <120 ms?

Step 5: PR Interval

Normal: 120-200 ms (3-5 small boxes)
Short: WPW or junctional rhythm
Prolonged: AV block

Step 6: QRS Complex

Duration <120 ms = normal (narrow)
110-120 ms = incomplete bundle branch block
≥120 ms = complete bundle branch block or ventricular rhythm

Step 7: ST Segment & T Wave

Elevation or depression?
T wave morphology: upright, inverted, peaked?

Step 8: QT Interval

Corrected QT (QTc) = QT ÷ √(R-R interval)
Normal QTc: <440 ms (men), <460 ms (women)

6. Common Arrhythmias

Arrhythmia	Key ECG Features
Sinus tachycardia	Rate >100, normal P waves, regular, normal QRS
Sinus bradycardia	Rate <60, otherwise normal
Sinus arrhythmia	Rate varies with breathing (normal variant)
Atrial fibrillation (AF)	Absent P waves, irregularly irregular R-R, fibrillatory baseline
Atrial flutter	Sawtooth flutter waves at ~300/min, often 2:1 block (ventricular rate ~150)
SVT (AVNRT/AVRT)	Regular narrow complex tachycardia, P waves hidden or retrograde
Ventricular tachycardia (VT)	Wide complex (>120 ms), rate >100, AV dissociation
Ventricular fibrillation (VF)	Chaotic, no organized complexes - cardiac arrest
1st degree AV block	PR >200 ms, all P waves conduct
2nd degree (Mobitz I)	Progressive PR lengthening → dropped QRS (Wenckebach)
2nd degree (Mobitz II)	Fixed PR, intermittent dropped QRS without warning - more serious
3rd degree (complete) AV block	P waves and QRS completely dissociated, escape rhythm
LBBB	Wide QRS ≥120 ms, broad notched R in I/V5/V6, no septal q waves
RBBB	Wide QRS ≥120 ms, rSR' in V1 ("rabbit ears"), wide S in I/V6
WPW	Short PR (<120 ms), delta wave (slurred QRS upstroke), wide QRS

Conduction abnormalities are the first major category of arrhythmias. They can result from ischemia, fibrosis, infection, electrolyte imbalance, or drug toxicity.

Medical Physiology, p. 731

7. Ischemia and Infarction

Ischemia lowers the resting membrane potential and shortens the action potential duration, creating a voltage gradient between normal and ischemic zones - these "currents of injury" appear as ST deviation.

STEMI (ST-Elevation MI)

Territory	Leads with ST Elevation	Likely Vessel
Anterior	V1-V4	LAD
Lateral	I, aVL, V5-V6	LCx
Inferior	II, III, aVF	RCA (or LCx)
Posterior	Reciprocal ST depression V1-V3 (mirror)	RCA/LCx
Right ventricle	ST elevation in right-sided leads (V3R/V4R)	RCA proximal

Hyperacute T waves are the earliest sign of acute MI - tall, peaked, symmetric T waves preceding ST elevation.

Evolutionary changes of STEMI:

Hyperacute T waves (minutes)
ST elevation (minutes to hours)
Q wave formation (hours to days)
T wave inversion (hours to days)
Q waves may persist permanently

NSTEMI / Unstable Angina

ST depression and/or T wave inversions without ST elevation
Biomarkers (troponin) elevated in NSTEMI, normal in unstable angina
Subendocardial ischemia: ST depression in precordial leads + ST elevation in aVR
Harrison's Principles of Internal Medicine 22e, p. 1398-1400

8. Hypertrophy Patterns

Left Ventricular Hypertrophy (LVH)

Tall left precordial R waves + deep right precordial S waves
Sokolov-Lyon criterion: SV1 + (RV5 or RV6) >35 mm
Cornell criterion: RaVL >20 mm (women), >28 mm (men)
Repolarization abnormality: ST depression + T wave inversion in I, aVL, V5-V6 ("strain pattern")
LVH increases risk of cardiovascular morbidity, mortality, and sudden cardiac death

Right Ventricular Hypertrophy (RVH)

Right axis deviation
Tall R in V1 (R >S in V1)
T wave inversions in right precordial leads

Pulmonary Embolism (Acute Cor Pulmonale)

Sinus tachycardia (most common)
S1Q3T3 pattern: S wave in I, Q wave in III, T wave inversion in III
Right axis deviation, RBBB pattern, ST-T changes V1-V4
Harrison's Principles of Internal Medicine 22e, p. 1363-1368

9. Bundle Branch Blocks

Feature	RBBB	LBBB
QRS duration	≥120 ms	≥120 ms
V1	rSR' ("rabbit ears")	Broad QS or rS
V6	Wide slurred S	Broad tall R, no q
Axis	Normal or RAD	Normal or LAD
Clinical significance	Often benign; RV conduction delay	Always abnormal; structural disease

LBBB note: New LBBB in the context of chest pain should be treated as STEMI equivalent. LBBB also makes ST analysis unreliable - use Sgarbossa criteria if needed.

Fascicular Blocks

Left anterior fascicular block (LAFB): QRS axis more negative than -45° - most common cause of marked LAD
Left posterior fascicular block (LPFB): QRS axis >+110° to +120° - rare isolated finding, must exclude other causes of RAD
Harrison's Principles of Internal Medicine 22e, p. 1371-1393

10. Other Important ECG Patterns

Pattern	Key Finding	Association
Long QT	QTc >440-460 ms	Drug effect, hypokalemia, hypomagnesemia, congenital (LQTS); risk of Torsades de Pointes
Short QT	QTc <340 ms	Short QT syndrome; hypercalcemia
Brugada pattern	Coved ST elevation + RBBB morphology in V1-V2	Sudden cardiac death risk, especially in young Asian males
Delta wave (WPW)	Short PR + slurred QRS onset	Accessory pathway; risk of rapid AF degenerating to VF
Peaked T waves	Tall symmetric T waves	Hyperkalemia (earliest sign)
PR depression	Diffuse in multiple leads	Pericarditis (also with saddle-shaped ST elevation)
Electrical alternans	Beat-to-beat QRS axis alternation	Cardiac tamponade
Low voltage	QRS <5 mm in limb leads, <10 mm precordial	Pericardial effusion, emphysema, obesity, hypothyroidism

11. Electrolyte Effects on ECG

Electrolyte	Change	ECG Findings
Hyperkalemia	K+ rises	Peaked T → flat P → wide QRS → sine wave → VF
Hypokalemia	K+ falls	Flat T, prominent U wave, ST depression, long QU
Hypercalcemia	Ca2+ rises	Short QT
Hypocalcemia	Ca2+ falls	Long QT (prolonged ST segment)
Hypomagnesemia	Mg2+ falls	Long QT, Torsades risk

12. Quick Clinical Practice Framework

When you pick up an ECG, run through: Rate - Rhythm - Axis - P waves - PR - QRS - ST/T - QT

Ask yourself:

Is this a sinus rhythm?
Is the rate normal, fast, or slow?
Are complexes narrow or wide?
Is there ST deviation?
Are there any high-risk features (e.g. VT, complete heart block, STEMI, long QT)?

Sources:

Medical Physiology (Boron & Boulpaep), pp. 710-735
Miller's Anesthesia, 10e, pp. 1364-1368
Harrison's Principles of Internal Medicine 22e, pp. 1362-1400
Tintinalli's Emergency Medicine, Chapter 49

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