Chapt. 11,12,13 ECG ١ Dr. Foadoddini
ECG= Combination of Depol. And Repol. waves ٢ Dr. Foadoddini
ﻪﻌﻄﻗ Isoelectric ﻪﻠﺻﺎﻓ P ‐ R interval: bw A &V excitation Q ‐ T interval: V contraction ٣ Dr. Foadoddini
Biphasic record ٤ Dr. Foadoddini
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Importance of electrode location Depolrized zone Current lead Polarized (Rest) zone ٦ Dr. Foadoddini
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I + III = II Dr. Foadoddini ٨
Factors that change the direction of the mean electrical vector ٩ ٩ Dr. Foadoddini
The Nobel Prize in Physiology or Medicine 1924 Willem Einthoven ١٠ Dr. Foadoddini
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ECG Leads: placement of Recording Electrodes • ECG chest lead (unipolar leads) – These leads measure the electrical activity in a horizontal plane that perpendicular to the frontal plane ١٣ Dr. Foadoddini
Augmented vector ١٤ Dr. Foadoddini
Right to Left Base to Apex Endocard. to Eipcard. ١٥ Dr. Foadoddini
Normal range -20 to +100 ١٦ Dr. Foadoddini
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Q wave ٢٠ Dr. Foadoddini
ﻲﻜﻳﺮﺘﻜﻟا رادﺮﺑ ﺖﻬﺟ Long duration of action potential in septum and endocardium D R جاﻮﻣا رﺎﺸﺘﻧا ﺖﻬﺟ ﻦﻄﺑ رد ٢١ Dr. Foadoddini
Atrial Depol. And repol. ٢٢ Dr. Foadoddini
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Plotting the Mean Electrical Axis ٢٤ Dr. Foadoddini
Electrical Axis Deviation • Heart position • Hypertrophy • Block ٢٥ Dr. Foadoddini
Left axis deviation (Left ventricle hypertrophic) ٢٦ Dr. Foadoddini
Right axis deviation (right ventricle hypertrophic): Pulmonary valve stenosis Tetralogy of Fallot VSD High QRS ٢٧ Dr. Foadoddini
tetralogy of Fallot A: Pulmonary stenosis B: Overriding aorta C: ventricular septal defect (VSD) D: Right ventricular hypertrophy ٢٨ Dr. Foadoddini
Left axis deviation (Left bundle branch block) Long QRS ٢٩ Dr. Foadoddini
Right axis deviation (right bundle branch block) Long QRS ٣٠ Dr. Foadoddini
Short waves: short QRS ٣١ Dr. Foadoddini
QRS abnormalities: Change in voltage: Hypertrophy/Infarction Slow conduction Change in duration: Slow conduction/ Purkinje System Block destruction of cardiac muscle in various areas ٣٢ Dr. Foadoddini
Current of injury: Normal zone Injured zone Current lead ٣٣ Dr. Foadoddini
Current of injury: J point Isoelectric line ٣٤ Dr. Foadoddini
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New collateral coronary blood flow develops If the muscle does not die , it will continue to show an injury potential as long as the ischemia exists ٣٨ Dr. Foadoddini
Q wave: ٣٩ Dr. Foadoddini
Slow Conduction of the Depolarization Wave Shortened Depolarization in Portions of the Ventricular Muscle T- inversion Digitalin toxicity ٤٠ Dr. Foadoddini
Cardiac Arrhythmias 1. Abnormal rhythmicity of the pacemaker 2. Shift of the pacemaker from the sinus node to another place in the heart 3. Blocks at different points in the spread of the impulse through the heart 4. Abnormal pathways of impulse transmission through the heart 5. Spontaneous generation of spurious impulses in almost any part of the heart ٤١ Dr. Foadoddini
Tachycardia >100 Bradycardia <60 ٤٢ Dr. Foadoddini
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Atrioventricular Block ٤٤ Dr. Foadoddini
Atrial premature beat ٤٥ Dr. Foadoddini
A-V node premature beat ٤٦ Dr. Foadoddini
PVC ٤٧ Dr. Foadoddini
Paroxysmal Tachycardia ٤٨ Dr. Foadoddini
Long QT syndrome Ventricular action potentials QT ٤٩ Dr. Foadoddini
Re-entry Pathway around the circle is too long Velocity of conduction becomes decreased Refractory period of the muscle might become greatly shortened. ٥٠ Dr. Foadoddini
Reentry Mechanisms ٥١ Dr. Foadoddini
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Atrial fibrilation ٥٥ Dr. Foadoddini
Atrial flutter ٥٦ Dr. Foadoddini
Interpretation of Normal and Abnormal Cardiac Rhythm from ECG • Sinus rhythm = 60 – 100 beats/min • Bradycardia = heart rate < 60 beats/min • Tachycardia = heart rate >100 beats/min Atrial rate = 250-350 beats/min Ventricular rate = 100 – 200 beats/min Ventricular rate >250 beats/min ٥٧ Dr. Foadoddini
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