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Electrocardiogram (ECG) - A Detailed Guide

What is an ECG?

"The ECG is a recording of the small extracellular signals produced by the movement of action potentials through cardiac myocytes." - Medical Physiology (Boron & Boulpaep)

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ECG Paper and Scale

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The Cardiac Conduction System and Its ECG Correlates

1. SA node fires - not visible on ECG (too small)
2. Depolarization spreads through both atria -> P wave
3. Signal slows at the AV node (safety valve, prevents too-fast ventricular rates) -> PR segment (isoelectric pause)
4. Signal travels through Bundle of His -> left and right bundle branches -> Purkinje fibers -> ventricular muscle -> QRS complex
5. Ventricles recover (repolarize) -> T wave

"The ECG cannot show the electrical activity of the SA node, AV node, Bundle of His, bundle branches, or Purkinje network." - Medical Physiology

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The ECG Waveforms in Detail

1. P Wave

• Represents: Atrial depolarization (right + left atria)
• Duration: 80-100 ms (< 0.10 sec, up to 2.5 small boxes)
• Amplitude: < 0.25 mV (2.5 mm)
• Shape: Smooth, rounded, upright in leads I, II, aVF
• Clinical significance: Widened P wave = delayed atrial conduction (e.g., left atrial enlargement). Peaked P wave = right atrial enlargement (P pulmonale). Absent P wave = atrial fibrillation, junctional rhythm.
• Note: Atrial repolarization is "buried" underneath the QRS complex and not visible on normal ECG.

2. PR Interval

• Definition: Time from the onset of P wave to the onset of QRS complex (includes the P wave + PR segment)
• Normal range: 120-200 ms (3-5 small boxes)
• Represents: Total conduction time through atrial muscle, AV node, and His-Purkinje system
• The PR segment (flat part after P wave, before QRS) corresponds specifically to AV nodal delay
• Prolonged PR (>200 ms): First-degree AV block (slow AV conduction, as from parasympathetic stimulation)
• Short PR (<120 ms): Pre-excitation syndromes (e.g., WPW) where an accessory pathway bypasses the AV node

3. QRS Complex

• Represents: Ventricular depolarization
• Duration: 60-100 ms (normal < 0.10 sec)
• Components:
  • Q wave: First downward deflection (small, septal depolarization, left to right)
  • R wave: First upward deflection (main ventricular depolarization, moving toward positive electrode)
  • S wave: Downward deflection after R wave
• Despite ventricles being much larger than atria, QRS duration is similar to P wave duration - because the Purkinje system has very fast conduction velocity
• Widened QRS (>120 ms): Bundle branch block, ventricular ectopy, hyperkalemia, drug toxicity
• Pathological Q waves (wide >40 ms, deep >25% of R wave): Prior myocardial infarction (scar tissue)

4. ST Segment

• Definition: Isoelectric segment from the end of QRS (J point) to the start of T wave
• Normal: Flat, at the isoelectric baseline (TP segment)
• J point: Junction between QRS and ST segment
• ST elevation (>1 mm in limb leads, >2 mm in precordial leads): STEMI (acute MI), pericarditis, early repolarization, Brugada syndrome
• ST depression: Ischemia (NSTEMI/unstable angina), digoxin effect, posterior MI

5. T Wave

• Represents: Ventricular repolarization
• Shape: Asymmetric (slow rise, rapid fall), normally upright in I, II, V4-V6
• Duration: ~160 ms
• Inverted T waves: Ischemia, ventricular hypertrophy, bundle branch block, myocarditis
• Peaked T waves: Hyperkalemia (earliest ECG change), hyperacute STEMI

6. QT Interval

• Definition: From onset of QRS to end of T wave (ventricular depolarization + repolarization)
• Normal: 350-440 ms; varies with heart rate
• Must use corrected QT (QTc) to account for rate: Bazett's formula = QT / √(RR interval)
  • Normal QTc: < 440 ms (men), < 460 ms (women)
• Prolonged QTc: Risk of torsades de pointes (dangerous polymorphic VT) - caused by drugs (e.g., amiodarone, quinidine, sotalol, haloperidol), electrolyte imbalances (hypokalaemia, hypomagnesaemia), congenital long QT syndrome
• Short QTc: Hypercalcaemia, digoxin effect

7. U Wave

• Represents: Possibly repolarization of papillary muscles (debated)
• Appearance: Small, low-amplitude wave after T wave, same direction as T wave
• Prominent U waves: Hypokalaemia (classic), bradycardia
• Inverted U waves: May indicate ischemia or hypertension

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Cardiac Cycle Correlation

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The 12-Lead ECG

Limb Leads (Frontal Plane)

Precordial Leads (Horizontal/Transverse Plane)

"Each lead is an axis in one of the two planes, onto which the heart projects its electrical activity... Each lead looks at the heart from a unique angle and plane." - Medical Physiology

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How to Calculate Heart Rate from ECG

• Count large boxes between two R waves (R-R interval)
• Rate = 300 / number of large boxes
  • 1 box = 300 bpm, 2 boxes = 150, 3 = 100, 4 = 75, 5 = 60, 6 = 50

• Count QRS complexes in a 10-second strip and multiply by 6

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Cardiac Axis

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Systematic Approach to Reading an ECG (Harrison's 14-Point Checklist)

1. Standardization / calibration / lead placement / artifacts
2. Rhythm (sinus vs. non-sinus)
3. Heart rate
4. PR interval / AV conduction
5. QRS interval (duration)
6. QT / QTc interval
7. Mean QRS electrical axis
8. P waves (morphology, regularity)
9. QRS voltages (hypertrophy criteria)
10. Precordial R-wave progression (V1 to V6)
11. Abnormal Q waves (infarction)
12. ST segments (elevation/depression)
13. T waves (inversion, peaking)
14. U waves

"Many mistakes in ECG interpretation are errors of omission. Therefore, a systematic approach is essential." - Harrison's Principles of Internal Medicine 22e

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Common ECG Abnormalities - Quick Summary

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Depolarization vs. Repolarization on ECG

• Depolarization waves (P wave, QRS complex): The recording is positive when the wavefront moves toward the positive electrode
• Repolarization waves (T wave): The recording is positive when repolarization moves away from the positive electrode - which in the normal heart actually moves in the same direction as depolarization (toward the epicardium), so the T wave is normally upright like the QRS

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• Guyton and Hall Textbook of Medical Physiology - Fundamentals of Electrocardiography
• Costanzo Physiology, 7th Edition - Electrocardiogram chapter
• Medical Physiology (Boron & Boulpaep) - ECG components and leads
• Goldman-Cecil Medicine - Electrocardiographic waves and standards
• Miller's Anesthesia, 10e - Electrical events and the ECG
• Harrison's Principles of Internal Medicine 22e - Clinical interpretation of the ECG

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ECG Abnormalities - A Detailed Guide

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CATEGORY 1: CONDUCTION ABNORMALITIES

A. AV Blocks

1st Degree AV Block (Panel A above)

• ECG: PR interval > 200 ms on every beat; all P waves conduct
• Mechanism: Slowed conduction through the AV node (no dropped beats)
• Causes: Vagal tone, beta-blockers, digoxin, inferior MI, myocarditis, normal variant in athletes
• Clinical: Usually benign; no treatment needed

2nd Degree AV Block - Mobitz Type I (Wenckebach) (Panel B above)

• ECG:
  • Progressive PR prolongation with each beat
  • Progressive shortening of the RR interval
  • Then a dropped QRS (P wave with no QRS)
  • "Group beating" pattern
• Mechanism: Block within the AV node itself
• Causes: Inferior MI, increased vagal tone, medications
• Clinical: Usually benign; progression to complete block uncommon

2nd Degree AV Block - Mobitz Type II (Panel C above)

• ECG:
  • PR interval constant (does not lengthen)
  • Sudden, unexpected dropped QRS without warning
  • Often accompanied by bundle branch block
• Mechanism: Block below the AV node (infranodal - His-Purkinje system)
• Causes: Anterior MI, fibrosis of conduction system
• Clinical: Serious - high risk of progression to complete heart block; often requires pacemaker

2:1 AV Block (Panel D above)

• ECG: Alternate P waves fail to conduct; every other QRS is dropped
• Distinction: Narrow QRS suggests Mobitz I (nodal), wide QRS + bundle branch block suggests Mobitz II (infranodal)

3rd Degree (Complete) AV Block (Panel E above)

• ECG:
  • Complete dissociation between P waves and QRS complexes
  • P waves fire at their own rate (faster)
  • QRS complexes fire at their own (escape) rate (slower)
  • "P waves march through" the QRS complexes
  • Escape rhythm: junctional (narrow QRS, 40-60 bpm) or ventricular (wide QRS, 20-40 bpm)
• Causes: Inferior MI (often reversible), anterior MI (often permanent), Lyme disease, congenital, drug toxicity
• Clinical: Requires urgent pacing

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B. Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

• Causes: Congenital (ASD), pulmonary embolism, RVH, ischemic heart disease, or normal variant
• Right bundle block more commonly seen without underlying organic disease than LBBB

Left Bundle Branch Block (LBBB)

• Causes: Always consider organic disease - coronary artery disease, hypertensive heart disease, aortic valve disease, cardiomyopathy
• New LBBB in context of chest pain was formerly considered a "STEMI equivalent"
• LBBB makes it very difficult to diagnose ischemia on ECG (use Sgarbossa criteria for MI in LBBB)

Fascicular Blocks (Hemiblocks)

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CATEGORY 2: ISCHEMIA AND INFARCTION

Ischemic ST Changes

• A (subendocardial ischemia): ST vector points inward toward the cavity -> overlying leads show ST depression
• B (transmural/epicardial ischemia): ST vector points outward -> overlying leads show ST elevation

STEMI - Regional Distribution

ECG Evolution of STEMI (Temporal Changes)

Pathological Q Waves

• Width > 40 ms (1 small box) AND depth > 25% of R wave amplitude
• Indicate myocardial necrosis (scar)
• Small q waves in lateral leads (I, aVL, V5-V6) are normal (septal depolarization)

Wellens Sign

• Deep, symmetric T-wave inversions in V1-V4 (or biphasic T in V2-V3)
• Suggests critical LAD stenosis (proximal)
• Associated with severe anterior wall ischemia without infarction

De Winter T Waves

• ST depression at J point + tall, symmetric upright T waves in precordial leads
• STEMI equivalent - proximal LAD occlusion; no ST elevation present

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CATEGORY 3: CHAMBER ENLARGEMENT AND HYPERTROPHY

Atrial Abnormalities

Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)

• S in V1 + R in V5 or V6 > 35 mm; OR
• R in aVL > 11 mm; OR
• R in I + S in III > 25 mm

• Left axis deviation
• "LV strain" pattern: ST depression + T-wave inversion in I, aVL, V5-V6 (lateral leads)
• Prolonged QRS duration (< 120 ms but approaching it)
• Left atrial enlargement pattern

Right Ventricular Hypertrophy (RVH)

• Right axis deviation (> +90°)
• Dominant R wave in V1 (R > S in V1) - various morphologies: R, RS, or qR
• Deep S waves in V5, V6 (prominent S across lateral leads)
• "RV strain" pattern: T-wave inversions in V1-V3 (right precordial leads)
• ST depression in right precordial leads

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CATEGORY 4: ARRHYTHMIAS

A. Supraventricular Arrhythmias

Sinus Tachycardia

• Rate > 100 bpm; normal P wave precedes every QRS
• Causes: pain, fever, anxiety, hyperthyroidism, PE, anemia

Atrial Fibrillation (AF)

• ECG:
  • No identifiable P waves - replaced by irregular fibrillatory (f) baseline
  • Irregularly irregular QRS complexes
  • Narrow QRS (unless aberrant conduction or bundle branch block)
  • Ventricular rate 100-160 bpm if uncontrolled
• Causes: Hypertension, heart failure, valvular disease, hyperthyroidism, alcohol ("holiday heart"), post-cardiac surgery
• Risk: Stroke (thrombus in left atrial appendage)

Atrial Flutter

• ECG:
  • Sawtooth ("flutter") waves at ~300 bpm in leads II, III, aVF
  • Regular QRS with fixed ratio conduction: 2:1 (ventricular rate ~150), 3:1, 4:1
  • 2:1 flutter is the most common and classic
• Mechanism: Re-entrant circuit in right atrium around tricuspid valve annulus

SVT (AVNRT / AVRT)

• ECG:
  • Narrow-complex tachycardia, regular, rate 150-250 bpm
  • P waves absent, buried in QRS, or immediately after QRS (retrograde)
  • Sudden onset and termination ("paroxysmal")

B. Pre-excitation Syndromes

Wolff-Parkinson-White (WPW)

• ECG:
  • Short PR interval (< 120 ms)
  • Delta wave - slurred upstroke at the beginning of QRS
  • Wide QRS (> 120 ms, due to fusion of normal and accessory pathway conduction)
  • Secondary ST-T changes (discordant)
• Mechanism: Accessory pathway (Bundle of Kent) bypasses the AV node, causing early ventricular pre-excitation
• Risk: If AF develops in WPW, rapid conduction over the accessory pathway can cause ventricular fibrillation (life-threatening)

C. Ventricular Arrhythmias

Premature Ventricular Contractions (PVCs)

• ECG:
  • Wide, bizarre QRS (> 120 ms) appearing early
  • Compensatory pause follows
  • No preceding P wave
  • T wave in opposite direction to QRS
• Isolated PVCs: usually benign; frequent or runs of PVCs need evaluation

Ventricular Tachycardia (VT)

• ECG:
  • Wide-complex tachycardia (QRS > 120 ms), rate 100-250 bpm
  • Regular or slightly irregular
  • AV dissociation (P waves independent of QRS) - pathognomonic when present
  • Fusion beats and capture beats confirm VT
  • Concordance across precordial leads (all positive or all negative)
• VT vs SVT with aberrancy: AV dissociation, extreme axis, RS > 100 ms, fusion beats all favor VT

Ventricular Fibrillation (VF)

• ECG: Chaotic, irregular, disorganized electrical activity; no recognizable QRS, ST, or T waves
• No effective cardiac output; cardiac arrest
• Requires immediate defibrillation

Torsades de Pointes

• ECG: Polymorphic VT where QRS complexes appear to "twist" around the isoelectric baseline
• Associated with prolonged QTc
• Can degenerate into VF
• Causes: Long QT syndrome (drugs, electrolytes)

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CATEGORY 5: ELECTROLYTE DISTURBANCES

Hyperkalemia (Progressive Changes with Rising K+)

Hypokalemia

• Flattened or inverted T waves
• Prominent U waves (U wave > T wave in same lead)
• ST depression
• Prolonged QU interval (often mistaken for prolonged QT)
• Severe: widened QRS, prolonged PR

Hypercalcemia

• Short QT interval (shortened ST segment)
• Osborn (J) waves occasionally
• Bradycardia in severe cases

Hypocalcemia

• Prolonged QT interval (elongated ST segment)

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CATEGORY 6: MISCELLANEOUS ECG ABNORMALITIES

Pericarditis

• ECG:
  • Diffuse ST elevation (concave/saddle-shaped, unlike the convex shape of STEMI) in most leads
  • PR depression in leads I, II, V4-V6 (and PR elevation in aVR) - classic sign
  • No reciprocal ST changes (unlike STEMI)
  • Evolves: ST elevation -> ST normalizes -> T-wave inversions
• Cause: Viral (most common), autoimmune, post-MI (Dressler's)

Pulmonary Embolism

• ECG:
  • Sinus tachycardia (most common finding)
  • S1Q3T3 pattern - S wave in lead I, Q wave in III, T-wave inversion in III
  • Right axis deviation
  • New RBBB (complete or incomplete)
  • T-wave inversions in V1-V4 (right heart strain)
  • These changes are nonspecific; normal ECG does not exclude PE

Hypothermia

• Osborn (J) waves - positive deflection at the junction of QRS and ST segment (J point), most prominent in V4-V6 and inferior leads
• Bradycardia; prolonged PR, QRS, QT intervals
• "Shivering artifact" on baseline

Brugada Syndrome

• ECG:
  • ST elevation in V1-V3 with a characteristic coved (Type 1) or saddle-back (Type 2) shape
  • Incomplete or complete RBBB appearance
  • Normal QT interval
• Clinical: Risk of sudden cardiac death from polymorphic VT/VF
• Associated with sodium channel mutation (SCN5A); often unmasked by fever, drugs

Digoxin Effect

• "Reverse tick" or "Salvador Dali moustache" appearance of ST segment
• ST depression with downward-concave "scooped" morphology in lateral leads
• Shortened QT interval
• T-wave flattening or inversion
• Bradycardia, prolonged PR

Digoxin Toxicity

• Almost any arrhythmia, but especially: PAT with block, bidirectional VT, AV blocks, junctional rhythms
• Combination of increased automaticity + slowed conduction is the hallmark

Long QT Syndrome (LQTS)

• QTc > 440 ms (men) or > 460 ms (women)
• Congenital (LQT1, LQT2, LQT3 - different genes, different triggers)
• Acquired: drugs (antiarrhythmics, antipsychotics, antibiotics like azithromycin), hypokalemia, hypomagnesemia, hypothyroidism
• Risk: Torsades de pointes -> syncope -> VF -> sudden death

Cardiac Tamponade

• ECG:
  • Sinus tachycardia
  • Low voltage QRS across all leads
  • Electrical alternans - alternating QRS height with each beat (pathognomonic for tamponade when combined with low voltage and tachycardia)
• Mechanism: Swinging motion of heart within pericardial fluid

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Summary Quick Reference Table

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• Harrison's Principles of Internal Medicine 22e - Myocardial ischemia, bundle branch blocks, hypertrophy
• Goldman-Cecil Medicine - ECG waves, conduction abnormalities, BBB table
• Washington Manual of Medical Therapeutics - AV blocks classification
• Medical Physiology (Boron & Boulpaep) - WPW, pre-excitation
• Miller's Anesthesia 10e - Cardiac rhythm disorders
• Tintinalli's Emergency Medicine - Atrial flutter/fibrillation, ECG in emergency

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CT Scan - Abnormal Findings (Concise Guide)

CT Basics: Understanding Density (Hounsfield Units)

• Hyperdense = brighter than surrounding tissue (blood, calcification, contrast, bone)
• Hypodense = darker than surrounding tissue (air, fat, edema, necrosis, CSF)
• Isodense = same density as surrounding tissue (can be missed - e.g., subacute SDH)

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CT HEAD - Abnormal Findings

1. Intracranial Hemorrhages

Key: Subacute SDH (1-3 weeks) becomes isodense with brain - easy to miss. Bilateral isodense SDH may appear as "pseudonormalization." Look for effacement of sulci and midline shift.

2. Ischemic Stroke

• Acute (< 6 hrs): CT may be normal or show subtle hypodensity; CT is used mainly to exclude hemorrhage before thrombolysis
• Early signs:
  • Loss of gray-white differentiation (insular ribbon sign, loss of basal ganglia outline)
  • Hyperdense MCA sign - clot visible as hyperdense middle cerebral artery
  • Sulcal effacement
• Established (> 24 hrs): Well-defined wedge-shaped hypodense area in a vascular territory
• Chronic: Encephalomalacia (very dark/hypodense area), ex-vacuo dilatation of nearby ventricle

3. Brain Tumors

• Primary (e.g., glioblastoma): Heterogeneous mass with surrounding vasogenic edema (finger-like hypodensity in white matter), ring enhancement on contrast, mass effect, midline shift
• Metastases: Multiple enhancing nodules at gray-white junction, marked surrounding edema
• Meningioma: Extraaxial, isodense or hyperdense, homogeneous enhancement, dural tail, may have calcification

4. Cerebral Edema / Raised ICP

• Loss of cortical sulci
• Effacement of basal cisterns (compressed by swelling)
• Compressed ventricles
• Midline shift (brain pushed toward opposite side)
• Tonsillar herniation: Cerebellar tonsils displaced below foramen magnum

5. Hydrocephalus

• Obstructive (non-communicating): Dilated ventricles proximal to obstruction; normal/small distal ventricles; periventricular lucency ("transependymal edema") in acute cases
• Communicating: All ventricles dilated; sulci may be enlarged (NPH) or effaced (SAH-related)

6. Cerebral Contusion

• Heterogeneous hyperdense (blood) and hypodense (edema) areas, typically anterior temporal or posterior frontal lobes ("coup-contrecoup")
• May be normal initially with delayed bleed

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CT CHEST - Abnormal Findings

1. Pulmonary Parenchyma

2. Pleural Space

3. Pulmonary Vasculature

4. Mediastinum

5. Cardiac (CT Coronary/Cardiac)

• Coronary artery calcification - Calcium score (Agatston score); predictor of cardiovascular risk
• Pericardial effusion - Fluid around heart (HU variable by content)
• Pericardial thickening/calcification - Constrictive pericarditis

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CT ABDOMEN & PELVIS - Abnormal Findings

1. Liver

2. Gallbladder & Biliary

3. Pancreas

4. Spleen

• Splenomegaly: > 13 cm; causes include portal hypertension, hematological disease, infection
• Splenic laceration/hematoma: Hypodense (old blood) or hyperdense (fresh blood) areas within spleen; subcapsular collection
• Infarct: Wedge-shaped peripheral hypodensity, no enhancement

5. Kidneys

6. Bowel

7. Aorta (Abdomen)

8. Pelvis (Common Findings)

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CT SPINE - Abnormal Findings (Brief)

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Quick Summary by CT Density

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• Bradley & Daroff's Neurology in Clinical Practice - CT physics, Hounsfield units
• Tintinalli's Emergency Medicine - Intracranial injury CT findings
• Rosen's Emergency Medicine - Head CT findings, acute emergencies
• Murray & Nadel's Textbook of Respiratory Medicine - CT chest patterns
• Fuster & Hurst's The Heart - Thoracic CT/CTA
• Harrison's Principles of Internal Medicine 22e - Ischemia, hemorrhage imaging