Explain me 10 changes of ecg

Reading File

Finding Sources

Reading File

Excellent - I now have rich textbook content from Harrison's Principles of Internal Medicine (22nd ed). Let me compile the comprehensive answer from what I've gathered.

10 Important ECG Changes

Based on Harrison's Principles of Internal Medicine, 22nd Edition and Medical Physiology (Boron & Boulpaep).

1. P-Wave Changes (Atrial Enlargement)

Right atrial overload produces tall, peaked P waves ≥ 2.5 mm (historically "P-pulmonale") - seen in right-sided pressure overload (e.g., pulmonary hypertension, tricuspid stenosis).

Left atrial abnormality produces a broad (≥120 ms), often notched P wave in limb leads, and a biphasic P wave in V1 with a prominent negative (terminal) component. Historically called "P-mitrale." Can occur with interatrial conduction delay even without true enlargement.

2. ST-Segment Elevation

Classic sign of acute myocardial infarction (STEMI). ST elevation in anatomically contiguous leads indicates acute transmural ischemia/injury. The elevated segment is concave-upward ("coved" or "tombstone" shape in severe cases). Also seen in:

Pericarditis (diffuse, saddle-shaped elevation)
Vasospastic (Prinzmetal) angina (transient, resolves with nitrates)
Brugada syndrome (right precordial V1-V2)

3. ST-Segment Depression

Indicates subendocardial ischemia or non-ST elevation ACS (NSTEMI/UA). Also seen in:

Reciprocal changes in STEMI in the opposite territory
Right or left ventricular hypertrophy ("strain" pattern)
Digitalis effect (produces a characteristic "scooped" or "hockey-stick" depression)

4. T-Wave Inversion

Reflects abnormal ventricular repolarization. Causes include:

Ischemia/NSTEMI - deep symmetric T-wave inversions (Wellens' pattern in V2-V3 indicates LAD critical stenosis)
Right/Left ventricular hypertrophy - in leads with dominant R waves ("strain" pattern)
Bundle branch blocks
Pulmonary embolism - T-wave inversions in V1-V4

Normally the mean T-wave vector should be roughly concordant (within ~45°) with the mean QRS vector in the frontal plane.

5. QRS Axis Deviation

The normal QRS axis is -30° to +90° in the frontal plane.

Left axis deviation (LAD): axis more negative than -30°. Causes include left anterior fascicular block, inferior MI, LVH, Wolff-Parkinson-White syndrome.
Right axis deviation (RAD): axis beyond +90°. Causes include RVH, left posterior fascicular block, pulmonary embolism (acute cor pulmonale), and normal variant in tall/thin individuals.

The axis can shift markedly in hypertrophy or conduction block.

6. Bundle Branch Blocks (QRS Widening ≥ 120 ms)

Right Bundle Branch Block (RBBB): rsR' ("rabbit ears") in V1, wide slurred S wave in lateral leads (I, V5-V6). QRS ≥ 120 ms.

Left Bundle Branch Block (LBBB): broad, notched R wave in lateral leads (I, aVL, V5-V6), deep S wave in V1. QRS ≥ 120 ms. New LBBB in the context of chest pain is treated as a STEMI equivalent.

Incomplete bundle branch blocks show similar morphology but QRS 100-119 ms.

7. LVH and RVH Voltage Changes

Left Ventricular Hypertrophy (LVH): increases amplitude of electrical forces directed leftward and posteriorly. Voltage criteria (e.g., Sokolow-Lyon: S in V1 + R in V5 or V6 ≥ 35 mm). Often accompanied by ST depression and T-wave inversions in lateral leads ("strain pattern").

Right Ventricular Hypertrophy (RVH): tall R wave in V1 (R ≥ S), right axis deviation, ST-T changes in right precordial leads. Due to pulmonic stenosis or pulmonary arterial hypertension.

8. QT Interval Prolongation

The QT interval reflects total ventricular repolarization duration. Rate-corrected QTc (Bazett formula) is normally:

Males: ≤440 ms
Females: ≤460 ms

Prolonged QT predisposes to torsades de pointes (polymorphic VT). Causes:

Drugs: antiarrhythmics (quinidine, sotalol, amiodarone, dofetilide), antibiotics (azithromycin, fluoroquinolones), antipsychotics
Electrolyte abnormalities: hypokalemia, hypomagnesemia, hypocalcemia
Congenital long QT syndrome

Prominent U waves (especially with hypokalemia) are also a marker of prolonged repolarization and torsades risk.

9. PR Interval Changes

Normal PR interval: 120-200 ms (3-5 small boxes).

Short PR (< 120 ms): seen in pre-excitation syndromes (Wolff-Parkinson-White - with delta wave), Lown-Ganong-Levine syndrome, or AV junctional/low atrial rhythms.
First-degree AV block: PR > 200 ms, every P followed by QRS.
Second-degree AV block (Mobitz I/Wenckebach): progressively lengthening PR until a QRS is dropped.
Second-degree AV block (Mobitz II): fixed PR with sudden non-conducted P waves - more ominous, may progress to complete block.
Third-degree (complete) AV block: no relationship between P waves and QRS; atria and ventricles beat independently.

10. Pathological Q Waves

A pathological Q wave is:

Width ≥ 40 ms (1 small box)
Depth ≥ 25% of the following R wave
Seen in ≥ 2 contiguous leads

They indicate prior transmural myocardial infarction (irreversible myocardial necrosis). Q waves develop hours to days after a STEMI and may persist permanently. Their location maps to the infarcted territory:

Inferior MI: Q waves in II, III, aVF
Anterior MI: Q waves in V1-V4
Lateral MI: Q waves in I, aVL, V5-V6

Quick Reference Summary

ECG Change	Key Feature	Classic Cause
P-wave changes	Tall/peaked or broad/notched	Atrial enlargement
ST elevation	≥1 mm in ≥2 contiguous leads	STEMI, pericarditis
ST depression	Horizontal/downsloping	NSTEMI, strain
T-wave inversion	Symmetric, deep	Ischemia, hypertrophy
Axis deviation	LAD or RAD	Block, hypertrophy, PE
Bundle branch block	QRS ≥ 120 ms	RBBB or LBBB pattern
LVH/RVH voltage	Tall R/deep S	Hypertrophy
QT prolongation	QTc > 440/460 ms	Drugs, electrolytes
PR interval changes	<120 or >200 ms	Pre-excitation, AV block
Pathological Q waves	Wide ≥ 40 ms, deep	Prior MI

Sources: Harrison's Principles of Internal Medicine, 22nd Edition (2025), p. 1913-1920; Medical Physiology (Boron & Boulpaep), pp. 731-732

This is a shared conversation. Sign in to Orris to start your own chat.