Tomorrow i have therapy exam. Tell me all the ECG and disease related to it.

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I now have comprehensive content from the textbooks. Let me compile a thorough, exam-ready ECG guide.

📋 ECG & Related Diseases — Complete Therapy Exam Guide


1. ECG BASICS — WAVES, INTERVALS, SEGMENTS

ComponentNormal DurationWhat It Represents
P wave<120 msAtrial depolarization
PR interval120–200 msAV conduction time
QRS complex60–100 msVentricular depolarization
ST segmentIsoelectricEarly ventricular repolarization
T waveUprightVentricular repolarization
QT interval<440 ms (corrected)Total ventricular activity
U waveSmall, uprightPurkinje repolarization (prominent in hypokalemia)

2. MYOCARDIAL INFARCTION (MI)

Pathophysiology of ECG Changes

Three ionic events explain MI changes (Ganong's Review of Medical Physiology):
Defect in Infarcted CellsCurrent FlowECG Change in Overlying Leads
Rapid repolarization (K⁺ efflux)Out of infarctST elevation
Decreased resting membrane potential (K⁺ loss)Into infarctTQ depression → ST elevation
Delayed depolarizationOut of infarctST elevation

Temporal ECG Evolution of MI

TimeECG Change
Minutes–HoursHyperacute tall T waves → ST elevation (>1 mm in 2+ contiguous leads)
Hours–DaysQ waves appear; ST still elevated; T wave begins inverting
Days–WeeksDeep symmetric T wave inversion; ST returns to baseline
Weeks–Months (late)Persistent Q waves may remain; T wave may normalize
"The hallmark of acute MI is elevation of the ST segments in the leads overlying the area of infarction." — Ganong's

STEMI vs NSTEMI vs Unstable Angina

STEMINSTEMIUnstable Angina
ECGST elevation (>1 mm, ≥2 leads)ST depression, deep T inversionUsually normal or nonspecific
TroponinElevatedElevatedNormal
MechanismComplete occlusionIncomplete occlusion or collateralsNo necrosis

MI Localization by Leads

TerritoryCulprit ArteryLeads with ST Elevation
AnteriorLADV1–V4
LateralLCxI, aVL, V5–V6
InferiorRCA (90%)II, III, aVF
Posterior (inferobasal)RCA/LCxST depression V1–V3 (reciprocal); ST elevation V7–V9
Right ventricularProximal RCAST elevation V4R
Key exam point: ST depression in V1–V4 may represent posterior MI — obtain posterior leads (V7–V9). (Rosen's Emergency Medicine)

New LBBB + Chest Pain

A new LBBB with suspected ischemia is treated equivalent to STEMI — use the Sgarbossa criteria to detect AMI in LBBB:
  1. ST elevation ≥1 mm concordant with QRS → most specific
  2. ST depression ≥1 mm in V1–V3 concordant with QRS
  3. ST elevation ≥5 mm discordant with QRS (modified: ST/S ratio >0.25)

3. ARRHYTHMIAS

Supraventricular Arrhythmias

Atrial Fibrillation (AF)

  • ECG: Irregularly irregular R-R intervals; absent P waves; fibrillatory baseline (f waves, >350/min)
  • Rate: Ventricular rate 100–180 bpm (uncontrolled)
  • Risk: Stroke (use CHADS₂/CHA₂DS₂-VASc to assess)
  • Causes: HTN, valvular disease, hyperthyroidism, alcohol, heart failure

Atrial Flutter

  • ECG: Regular "sawtooth" flutter waves at ~300/min (F waves); typically 2:1 AV block → ventricular rate ~150 bpm
  • Distinction from AF: Flutter is regular with discrete F waves; AF is irregular

Multifocal Atrial Tachycardia (MAT)

  • ECG: ≥3 different P wave morphologies in a single lead; no consistent PP, PR, or RR intervals; irregularly irregular at 100–180 bpm
  • Confused with: AF
  • Cause: COPD (most common)

Paroxysmal Supraventricular Tachycardia (PSVT / AVNRT)

  • ECG: Narrow complex, regular tachycardia; P waves hidden in or just after QRS; rate 150–250 bpm
  • Mechanism: Reentry within AV node (AVNRT) or accessory pathway (AVRT)

4. AV CONDUCTION BLOCKS

DegreeECG FindingClinical Significance
1st degreePR > 200 ms; all P waves conductBenign; no treatment needed
2nd degree Mobitz I (Wenckebach)Progressive PR prolongation → dropped QRS; group beatingUsually AV node level; benign, may not progress
2nd degree Mobitz IIFixed PR; sudden non-conducted P wave; often with BBBBelow AV node; high risk of progression to complete block
2:1 AV blockEvery other P wave non-conductedDifficult to classify; narrow QRS → Mobitz I likely; wide QRS → Mobitz II likely
3rd degree (Complete heart block)Complete AV dissociation; P rate > ventricular escape rateMedical emergency; requires pacemaker
"Type II block, particularly if bundle branch block is present, often antedates progression to complete heart block."Washington Manual

5. BUNDLE BRANCH BLOCKS (BBB)

Right BBB (RBBB)

  • QRS > 120 ms
  • V1: rSR' (M-shaped / "rabbit ears")
  • V6: Wide, slurred S wave
  • Causes: Normal variant, pulmonary embolism (acute RBBB), congenital, degenerative, MI

Left BBB (LBBB)

  • QRS > 120 ms
  • V1: Broad rS or QS complex
  • V5–V6: Broad, notched R wave (no septal Q waves)
  • Clinical: New LBBB = rule out acute MI; causes ventricular dyssynchrony and can worsen heart failure
  • Prevalence: Up to 25% of heart failure patients have LBBB

Fascicular Blocks (Hemiblocks)

BlockAxisECG Features
Left anterior fascicular block (LAFB)−45° to −90° (left axis deviation)Small R in II, III, aVF; tall R in I, aVL
Left posterior fascicular block (LPFB)+120° or more (right axis deviation)Must exclude RVH, PE, lateral MI

6. ELECTROLYTE DISTURBANCES & ECG

Hyperkalemia (DANGEROUS — potentially lethal)

K⁺ LevelECG Change
Mildly elevatedTall, peaked (tented) T waves — first change
Moderately elevatedPR prolongation, widening QRS, atrial paralysis
Severely elevatedSine wave pattern → ventricular fibrillation → asystole

Hypokalemia

  • Prolonged PR interval
  • Prominent U waves (key finding)
  • Late T wave inversion in precordial leads
  • T and U waves may merge → apparent QTc prolongation

Hypercalcemia

  • Shortened QT interval

Hypocalcemia

  • Prolonged QT interval (T wave unchanged, ST lengthened)

7. WPW (WOLFF-PARKINSON-WHITE) SYNDROME

  • Mechanism: Accessory pathway (Bundle of Kent) bypasses AV node → ventricular pre-excitation
  • ECG Triad:
    1. Short PR interval (<120 ms)
    2. Delta wave (slurred upstroke of QRS)
    3. Wide QRS
  • Risk: AF with rapid conduction through accessory pathway → ventricular fibrillation
  • Treatment: Avoid AV nodal blockers (digoxin, verapamil, adenosine) in AF + WPW

8. PERICARDITIS

  • ECG (4 stages):
StageECG
Stage I (acute)Diffuse ST elevation (concave/saddle-shaped) in most leads; PR depression
Stage IIST normalizes; PR depression persists
Stage IIIT wave inversion
Stage IVECG normalizes
  • Key distinguishing feature from MI: ST elevation is diffuse (not localized to a territory); PR depression present; no reciprocal ST depression (except aVR)

9. PULMONARY EMBOLISM (PE)

  • Most common ECG: Sinus tachycardia (nonspecific but most frequent)
  • Classic (but uncommon): S1Q3T3 — S wave in lead I, Q wave + T wave inversion in lead III
  • New RBBB (right heart strain)
  • Right axis deviation
  • ST changes suggesting RV strain

10. OTHER DISEASE-SPECIFIC ECG PATTERNS

ConditionKey ECG Finding
Left ventricular hypertrophy (LVH)Sokolow-Lyon: S in V1 + R in V5/V6 ≥35 mm; strain pattern (ST depression + T inversion in lateral leads)
Right ventricular hypertrophy (RVH)Right axis deviation; tall R in V1; deep S in V5–V6
Long QT syndromeQTc >440 ms (male) / >460 ms (female); risk of torsades de pointes
Brugada syndromePseudo-RBBB + ST elevation in V1–V3 (coved/saddleback pattern); risk of sudden death
HyperkalemiaPeaked T waves → sine wave
HypothermiaOsborn (J) waves at the QRS-ST junction; bradycardia
Digitalis toxicity"Reverse tick" / scooped ST depression; prolonged PR; various arrhythmias
Pneumothorax (left-sided)Mimics anterior MI — rightward axis shift, decreased precordial R-wave voltage
Takotsubo cardiomyopathyST elevation or deep T wave inversions without obstructive CAD; associated with emotional stress
Acute myocarditisSimilar to MI (ST elevation + troponin rise); requires coronary imaging to differentiate

11. QUICK EXAM MEMORY TRICKS

FindingDiagnosis
Irregularly irregular, no P wavesAF
Sawtooth at 300/minAtrial Flutter
Short PR + delta wave + wide QRSWPW
Diffuse ST elevation + PR depressionPericarditis
Peaked T → wide QRS → sine waveHyperkalemia
Prominent U wavesHypokalemia
S1Q3T3 + new RBBBPE
Osborn J wavesHypothermia
New LBBB + chest painTreat as STEMI (Sgarbossa criteria)
rSR' in V1, wide S in V6RBBB
Broad notched R in V5–V6LBBB

Sources: Ganong's Review of Medical Physiology 26th Ed. | Rosen's Emergency Medicine | Goldman-Cecil Medicine | Washington Manual of Medical Therapeutics | Tintinalli's Emergency Medicine
Good luck on your exam tomorrow! This covers the core ECG-disease relationships you're most likely to be tested on in a therapy/internal medicine context.
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