Most common ecg changes.along with images

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Most Common ECG Changes

A systematic approach to ECG interpretation requires analyzing rhythm, rate, PR/QRS/QT intervals, P waves, QRS axis & voltage, R-wave progression, Q waves, ST segments, T waves, and U waves. Below are the major ECG abnormalities with images from authoritative textbooks.

1. Normal ECG - Reference

Normal 12-lead ECG from a healthy subject. Sinus rhythm at 75 bpm, PR 160 ms, QRS 80 ms, QT 360 ms, mean QRS axis +70°.

Normal 12-lead ECG showing sinus rhythm at 75 bpm with normal R-wave progression (transition zone at V3/V4). (Harrison's Principles of Internal Medicine, 22E - Fig. 247-7)

2. P Wave Changes - Atrial Abnormalities

P wave changes: Normal vs Right atrial overload (tall peaked P wave in lead II) vs Left atrial abnormality (broad notched P in lead II, biphasic deep negative in V1)

Normal P wave vs. Right atrial overload ("P-pulmonale": peaked P ≥2.5 mm) vs. Left atrial abnormality ("P-mitrale": broad, notched P ≥120 ms in limb leads, biphasic with deep negative component in V1). (Harrison's Principles of Internal Medicine, 22E - Fig. 247-8)

Change	Appearance	Cause
Right atrial overload	Tall, peaked P wave ≥2.5 mm (lead II)	Pulmonary hypertension, COPD, tricuspid stenosis
Left atrial abnormality	Broad (≥120 ms), notched P in limb leads; biphasic P in V1	Mitral valve disease, hypertension, LVH
Absent P waves	Irregular baseline (fibrillation) or absent (junctional rhythm)	Atrial fibrillation, junctional rhythm

3. PR Interval Changes

Change	Normal = 120-200 ms	Cause
Short PR (<120 ms)	Delta wave present	WPW syndrome (accessory pathway)
Short PR, no delta wave	-	LGL syndrome, junctional rhythm
Prolonged PR (>200 ms)	1st degree AV block	Digoxin, inferior MI, vagal tone
Progressive PR lengthening until dropped beat	2nd degree Mobitz I (Wenckebach)	AV nodal disease
Fixed PR with dropped beats	2nd degree Mobitz II	Bundle branch / His-Purkinje disease
No P-QRS relationship	3rd degree (complete) AV block	Severe AV nodal or infranodal disease

4. QRS Changes - Axis, Voltage & Hypertrophy

LVH vs RVH QRS changes: LVH shows tall R in V5/V6 and deep S in V1/V2; RVH shows tall R in V1 and right axis deviation

QRS in hypertrophy. LVH: tall precordial voltages (SV1 + RV5 or RV6 >35 mm), ST depression and T-wave inversion in lateral leads ("strain" pattern). RVH: tall R in V1, right axis deviation, ST-T changes in right precordial leads. (Harrison's Principles of Internal Medicine, 22E - Fig. 247-9)

Key voltage criteria:

LVH: SV1 + RV5 or RV6 >35 mm; RaVL >20 mm (women) or >28 mm (men)
RVH: R ≥ S wave in V1 with right axis deviation; qR pattern in V1
Low voltage: QRS <5 mm in all limb leads - think pericardial effusion, emphysema, infiltrative disease

5. Bundle Branch Blocks

RBBB vs LBBB comparison in V1 and V6: RBBB shows rSR' in V1 with T inversion; LBBB shows wide QS in V1 and broad R in V6 with T inversion

RBBB vs. LBBB in leads V1 and V5/V6. Arrows show secondary T-wave inversions - discordant (opposite to last QRS deflection), which is expected. Concordant T-wave changes suggest primary ischemia superimposed on bundle branch block. (Harrison's Principles of Internal Medicine, 22E - Fig. 247-10)

Block	QRS Width	V1 Pattern	V5/V6 Pattern	T wave
RBBB	≥120 ms	rSR' ("rabbit ears")	qRS (deep S)	Inverted in V1-V2 (secondary)
LBBB	≥120 ms	Wide QS (entirely negative)	Broad, monophasic R	Inverted in V5-V6 (secondary)
RBBB + LAD	≥120 ms	rSR'	-	Bifascicular block (right bundle + left anterior fascicle)

6. ST Segment Changes - Ischemia and Infarction

Subendocardial ischemia (left): ST vector toward cavity, causing ST depression in overlying leads. Transmural ischemia (right): ST vector outward, causing ST elevation

Current-of-injury concept. A: Subendocardial ischemia causes ST depression in overlying leads (and ST elevation in aVR). B: Transmural (epicardial) ischemia causes ST elevation. (Harrison's Principles of Internal Medicine, 22E - Fig. 247-11)

ST Elevation Causes (Tintinalli's differential):

Acute STEMI (most important - urgent reperfusion)
Pericarditis (diffuse, saddle-shaped; accompanied by PR depression)
Early repolarization (common benign variant, concave up)
LVH strain pattern
LBBB / ventricular paced rhythm (discordant ST)
Brugada pattern (coved-type in V1-V2)
Takotsubo cardiomyopathy
Hypertrophic cardiomyopathy
Hypercalcemia / hyperkalemia (right precordial)
Hypothermia (with J/Osborn waves)

ST Depression Causes:

NSTEMI / subendocardial ischemia
Reciprocal changes in STEMI
Digoxin effect (classically "reverse tick" or "hockey stick")
Hypokalemia (with prominent U waves)
Right ventricular strain / cor pulmonale
LVH strain

7. Anterior Wall Ischemia - T Wave Inversions (Wellens' Pattern)

Anterior wall ischemia with deep, symmetric T wave inversions in V1-V6 (Wellens' pattern)

Severe anterior wall ischemia showing deep, symmetric T-wave inversions across V1-V6 (Wellens' syndrome - critical LAD stenosis). Present in ~15% of unstable angina patients. (Harrison's Principles of Internal Medicine, 22E - Fig. 247-12)

8. Evolving MI - Q Waves and ST Sequence

Sequential ECG changes in anterior MI (top) and inferior MI (bottom): hyperacute T waves → ST elevation → Q waves → T wave inversion → Q wave persists

Sequence of changes in anterior (top) and inferior (bottom) ST-elevation Q-wave infarction. Anterior STEMI: ST elevation in I, aVL, V1-V6 with reciprocal depressions in II, III, aVF. Inferior STEMI: ST elevation in II, III, aVF with reciprocal depressions in V1-V3. (Harrison's Principles of Internal Medicine, 22E - Fig. 247-13)

Q wave criteria for infarction:

Width ≥40 ms (one small square)
Depth ≥25% of the R wave in that lead
Present in ≥2 contiguous leads

9. ST-T Changes in LBBB (Sgarbossa Criteria)

Five ECG waveforms showing discordant ST depression (A), discordant ST elevation (B) = normal in LBBB; concordant ST elevation (C) = strongly suggests AMI; concordant ST depression (D) = suggests AMI; excessive discordant ST elevation >5mm (E) = weakly suggests AMI

Sgarbossa criteria in LBBB: A=discordant ST depression (normal), B=discordant ST elevation (normal), C=concordant ST elevation (strongly suggests AMI), D=concordant ST depression (suggests AMI), E=>5 mm discordant ST elevation (weakly suggests AMI). (Tintinalli's Emergency Medicine)

10. QT Interval Changes

Normal QTc (corrected): <440 ms in men, <460 ms in women (Bazett formula)

Change	Causes
Prolonged QTc	Hypokalemia, hypomagnesemia, hypocalcemia; drugs (sotalol, amiodarone, quinidine, haloperidol, erythromycin); congenital long QT syndrome; hypothyroidism
Short QTc (<360 ms)	Hypercalcemia, digoxin effect, short QT syndrome
Torsades de pointes	Runs of polymorphic VT in the setting of long QT - characteristic twisting of QRS around baseline

11. Common Electrolyte & Metabolic ECG Patterns

Condition	ECG Changes
Hyperkalemia	Peaked, tent-shaped T waves → Prolonged PR → Widened QRS → Sine wave → Asystole
Hypokalemia	Flattened T waves, prominent U waves, ST depression, QT prolongation
Hypercalcemia	Short QT interval, shortened ST segment
Hypocalcemia	Prolonged QT (lengthened ST segment)
Digoxin effect	"Reversed tick" or "hockey stick" ST depression, short QT, PR prolongation
Hypothermia	J (Osborn) waves at QRS-ST junction, bradycardia, long QT
Pulmonary embolism	Sinus tachycardia (most common), S1Q3T3 pattern, new RBBB, right axis deviation, T inversions V1-V4
Pericarditis	Diffuse saddle-shaped ST elevation + PR depression in most leads; PR elevation in aVR

Quick Reference Summary

ECG Component	Key Abnormality	Think of
P wave	Peaked (≥2.5 mm)	Right atrial overload
P wave	Broad, notched; biphasic V1	Left atrial abnormality
PR interval	Short + delta wave	WPW
PR interval	Prolonged / varying	AV blocks
QRS	Wide rSR' in V1	RBBB
QRS	Wide QS in V1, monophasic R in V6	LBBB
QRS	High voltage + strain	LVH
ST segment	Elevation (convex up) + chest pain	STEMI - emergent!
ST segment	Diffuse saddle-shaped elevation	Pericarditis
ST segment	Depression	NSTEMI, digoxin, strain
T wave	Deep symmetric inversions V1-V6	Wellens' (critical LAD stenosis)
T wave	Peaked, tent-shaped	Hyperkalemia
Q wave	Wide, deep, ≥2 contiguous leads	Prior MI
QT	Prolonged	Drug effect, electrolytes, long QT syndrome
U wave	Prominent	Hypokalemia, antiarrhythmics

Sources: Harrison's Principles of Internal Medicine 22E (2025), Tintinalli's Emergency Medicine, Goldberger AL et al: Goldberger's Clinical Electrocardiography, Tintinalli's ECG figures.

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