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![QRS complex
Normal values
• Duration: < 2.5 mm.
• Morphology:
progression from Short
R and deep S (r/s) in V1
to tall R and short S in
V6 with small Q in V5-6.
Abnormalities:
1. Wide QRS complex
• Bundle branch block.
• Ventricular rhythm.
2. Tall R in V1
• RVH.
• RBBB.
• Posterior MI.
• WPW syndrome.
3. abnormal Q wave
[ > 25% of R wave]
• MI.
• Hypertrophic
cardiomyopathy.
• Normal variant.](https://image.slidesharecdn.com/shafeiecg-160117224331/75/Shafei-ecg-53-2048.jpg)
![NORMAL ST- SEGMENT
it's isoelectric.
[i.e. at same level of PR
or PQ segment at least
in the beginning]](https://image.slidesharecdn.com/shafeiecg-160117224331/75/Shafei-ecg-73-2048.jpg)
Uploaded byshafei lashin
Shafei ecg نسخة
This document provides an overview of the electrocardiogram (EKG/ECG). It describes what an EKG is and how it represents the electrical events of the cardiac cycle. Each electrical event produces a distinctive waveform that can provide insight into a patient's cardiac pathophysiology when studied. The document also discusses the normal components of the EKG waveform, including the P wave, PR interval, QRS complex, ST segment, T wave, and QT interval. It provides the normal values for each component and examples of abnormalities.
Shafei ecg نسخة
- 3. What is anEKG? •The electrocardiogram (EKG) is a representation of the electrical events of the cardiac cycle. •Each event has a distinctive waveform •the study of waveform can lead to greater insight into a patient’s cardiac pathophysiology.
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- 8. V1 V1 V2 V2 V3 V3 V4 V4 V5 V5 Horizontal plane -the six chest leads V6 V6 RA LA LV RV 6.5
- 9. 9 The 12-Leads The 12-leadsinclude: –3 Limb leads (I, II, III) –3 Augmented leads (aVR, aVL, aVF) 1942- Goldberger increased Wilson’s Unipolar lead voltage by 50% –6 Precordial leads (V1- V6) 1938 -AHA and Cardiac society of great Britain 1906 - William Einthoven diagnoses some heart problems , 1924 - the noble prize
- 10. 60 – 100times a minute 40 – 60 times a minute 20 – 40 times a minute
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- 12. Impulse Conduction &the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers The “PQRST”
- 14. Normal Components ofthe EKG Waveform
- 16. ECG RULES • ProfessorChamberlains 10 rules of normal:- 1. PR interval should be 120 to 200 milliseconds or 3 to 5 little squares 2. The width of the QRS complex should not exceed 110 ms, less than 3 little squares 3. The QRS complex should be dominantly upright in leads I and II 4. QRS and T waves tend to have the same general direction in the limb leads 5. All waves are negative in lead aVR 6. The R wave must grow from V1 to at least V4 ,The S wave must grow from V1 to at least V3 , and disappear in V6 7. The ST segment should start isoelectric 8. The P waves should be upright in I, II, and V2 to V6 9. There should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6 10. The T wave must be upright in I, II, V2 to V6
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- 19. STANDARDISATION ECG amplitude scale Normalamplitude 10 mm/mV Half amplitude 5 mm/mV Double amplitude 20 mm/mV
- 21. Why “1500 /X”? • Paper Speed: 25 mm/ sec • 60 seconds / minute • 60 X 25 = 1500 mm / minute • 60 X 5 = 300 big square / minute • Take 6 sec strip (30 large boxes) • Count the P/R waves X 10 OR
- 22. DR/ SHAFEI LASHEEN Step1: Calculate Rate when rhythm is regular – Find a R wave that lands on a bold line. – Count the # of large boxes to the next R wave. – HR = 300/ no large boxes between R-R interval – Count the # of small boxes to the next R wave – HR= 1500/ no small boxes between R-R interval R wave
- 23. DR/SHAFEI LASHEEN HR ifirregular rhythm – Count the # of R waves in a 6 second rhythm strip, then multiply by 10. – Reminder: all rhythm strips in the Modules are 6 seconds in length. Interpretation? 9 x 10 = 90 bpm 3 sec 3 sec
- 24. DR/ SHAFEI LASHEEN Step2: Determine rhythm • Look at the R-R distances (using a caliper or markings on a pen or paper). • Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular? Interpretation? Regular R R
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- 34. True LAD • Soagain, if lead I is positive and aVF is negative, we suspect LAD • To diagnose true LAD, we examine lead II: – If lead II is positive, axis = 0° to –30° – If lead II is negative , axis = –30° to –90°
- 35. Extreme RAD • Iflead I is negative AND aVF is also negative – extreme RAD • Clue: If aVR is positive = extreme RAD • This is seen with rare situations such as VT or Pacemakers • In general we should never have an axis over here!
- 37. DR/ SHAFEI LASHEEN Rightaxis deviation
- 40. P-wave Normal values 1. upin all leads except AVR. 2. Duration. < 2.5 mm. 3. Amplitude. < 2.5 mm. Extreme RT. axis Abnormalities 1. Inverted P-wave • Junctional rhythm. 2. Wide P-wave (P- mitrale) • LAE 3. Peaked P-wave (P-pulmonale) • RAE 4. Saw-tooth appearance • Atrial flutter 5. Absent normal P wave • Atrial fibrillation
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- 44. DR/ SHAFEI LASHEEN Step3: Assess the P waves • Are there P waves? • Do the P waves all look alike? • Do the P waves occur at a regular rate? • Is there one P wave before each QRS? Interpretation? Normal P waves with 1 P wave for every QRS
- 46. PR Interval Measured fromthe beginning of the P wave to the beginning of the Q wave. Normal PR interval ranges from 0.12 to 0.20 second. PR interval
- 47. PR interval Definition: thetime interval between beginning of P-wave to beginning of QRS complex. Normal PR interval 3-5mm or 3-5 small squares on ECG graph (0.12-0.2 sec) Abnormalities 1. Short PR interval • WPW syndrome 2. Long PR interval • First degree heart block
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- 50. DR/ SHAFEI LASHEEN Step4: Determine PR interval • Normal: 0.12 - 0.20 seconds. (3 - 5 boxes) Interpretation? 0.12 seconds
- 52. QRS Complex Represents complete ventricular depolarization QRScomplex QRS Complex Variants QRS Complex
- 53. QRS complex Normal values •Duration: < 2.5 mm. • Morphology: progression from Short R and deep S (r/s) in V1 to tall R and short S in V6 with small Q in V5-6. Abnormalities: 1. Wide QRS complex • Bundle branch block. • Ventricular rhythm. 2. Tall R in V1 • RVH. • RBBB. • Posterior MI. • WPW syndrome. 3. abnormal Q wave [ > 25% of R wave] • MI. • Hypertrophic cardiomyopathy. • Normal variant.
- 54. Small voltage QRS •Defined as < 5 mm peak-to-peak in all limb leads or <10 mm in precordial chest leads. • causes — pulmonary disease, hypothyroidism, obesity, cardiomyopathy. • Acute causes — pleural and/or pericardial effusions
- 56. DR/ SHAFEI LASHEEN Step5: QRS duration • Normal: 0.04 - 0.12 seconds. (1 - 3 boxes) Interpretation? 0.08 seconds
- 58. Q Wave Represents the beginningof septal depolarization The first negative deflection off of the baseline Q Wave
- 59. Q WAVES • Qwaves <0.04 second. • That’s is less than one small square duration. • Height <25% or < 1/4 of R wave height.
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- 61. 61 61 Normal Q waves Noticethe small Normal Q in Lead I
- 62. Abnormal Q waves •The duration or width of Q waves becomes more than one small square on ECG graph. • The depth of Q wave becomes more than 25% of R wave. • The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy.
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- 64. 64 64 Pathological Q wave Noticethe deep & wide Infarction Q in Lead I
- 65. Q wave inseptal hypertrophy
- 67. R Wave Indicates left ventricular depolarization Thefirst positive deflection off the baseline R Wave
- 68. Normal upward progressionof R wave from V1 to V6 V1 V2 V3 V4 V5 V6 The R wave in the precordial leads must grow from V1 to at least V4
- 71. T-wave Normal values. 1.amplitude: < 10mmin the chest leads. Abnormalities: 1. Peaked T-wave: • Hyper-acute MI. • Hyperkalemia. • Normal variant . 2. T- inversion: • Ischemia. • Myocardial infarction. • Myocarditis • Ventricular strain • BBB. • Hypokalemia. • Digoxin effect.
- 73. NORMAL ST- SEGMENT it'sisoelectric. [i.e. at same level of PR or PQ segment at least in the beginning]
- 74. Abnormalities 1. ST elevation: Morethan one small square • Acute MI. • Prinzmetal angina. • Acute pericarditis. • Early repolarization ST depression: More than one small square • Ischemia. • Ventricular strain. • BBB. • Hypokalemia. • Digoxin effect.
- 75. Abnormalities of ST-segment
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- 79. QT- interval Definition: Timeinterval between beginning of QRS complex to the end of T wave. Normally: At normal HR: QT ≤ 11mm (0.44 sec) Abnormalities: 1. Prolonged QT interval: hypocalcemia and congenital long QT syndrome. 2. Short QT interval: hypercalcemia.
- 80. DR/ SHAFEI LASHEEN QTcinterval @ HR 70 QT< 0.40 sec @ HR 80 QT< 0.38 sec @ HR 60 QT< 0.42 sec < 0.44 s > 0.44 s Normal Long QT A prolonged QT can be very dangerous. It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte abnormalities, CNS disease, post-MI, and congenital heart disease. Torsades de Pointes Long QT
- 81. EKG Intervals 1. P-wave< 0.110 sec (approximately 3 small boxes) 2. PR interval = beginning of the P-wave to the beginning of QRS. Normal = 0.120 – 0.200 sec 3. QRS interval = from the first deflection to return to the baseline. Normal < 0.120 sec 4. QT interval = beginning of the QRS to the END of the T-wave. Normal < 0.450 sec
- 83. U Wave Represents thelast phase of repolarization. The exact significance is unknown. Characteristic of hypokalemia. May predispose to ventricular arrhythmias. U Wave
- 84. DR/ SHAFEI LASHEEN ECGRhythm Interpretation Normal Sinus Rhythm
- 85. 1. Every QRSis preceded by a P-wave 2. P-waves appear normal, that is they are of sinus node origin: A. Normal Morphology: 1. P-wave duration < 0.12 sec (< 3 boxes) 2. P-wave height < 2.5 mm B. Normal Axis – upright P-waves in lead II Sinus Rhythm…or Not!
- 86. DR/ SHAFEI LASHEEN RhythmSummary • Rate 90-95 bpm • Regularity regular • P waves normal • PR interval 0.12 s • QRS duration 0.08 s Interpretation? Normal Sinus Rhythm
- 87. DR/ SHAFEI LASHEEN NSRParameters • Rate 60 - 100 bpm • Regularity regular • P waves normal • PR interval 0.12 - 0.20 s • QRS duration 0.04 - 0.12 s Any deviation from above is sinus Tachycardia, sinus bradycardia or an arrhythmia
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- 90. What types ofpathology can we identify and study from EKGs?
- 91. DR/ SHAFEI LASHEEN ArrhythmiaFormation Arrhythmias can arise from problems in the: • Sinus node • Atrial cells • AV junction • Ventricular cells
- 92. DR/ SHAFEI LASHEEN SANode Problems The SA Node can: • fire too slow • fire too fast SAN diseases Sinus Arrhythmia Sinus Bradycardia Sinus Tachycardia (Sinus Tachycardia may be an appropriate response to stress.)
- 93. DR / SHAFEILASHEEN Rhythm #1 30 bpm• Rate? • Regularity? regular normal 0.10 s • P waves? • PR interval? 0.12 s • QRS duration? Interpretation? Sinus Bradycardia
- 94. DR/ SHAFEI LASHEEN Rhythm#2 130 bpm• Rate? • Regularity? regular normal 0.08 s • P waves? • PR interval? 0.16 s • QRS duration? Interpretation? Sinus Tachycardia
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- 97. Sick Sinus Syndrome Sinoatrial block (note the pause is twice the P-P interval) Sinus arrest with pause of 4.4 s before generation and conduction of a junctional escape beat Severe sinus bradycardia
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- 99. DR/ SHAFEI LASHEEN AtrialCell Problems • fire occasionally from a focus • fire continuously due to a looping re- entrant circuit Premature Atrial Contractions (PACs) Atrial Flutter
- 100. DR/ SHAFEI LASHEEN PrematureAtrial Contractions • Deviation from NSR – These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node.
- 101. DR/ SHAFEI LASHEEN Rhythm#3 70 bpm• Rate? • Regularity? occasionally irreg. 2/7 different contour 0.08 s • P waves? • PR interval? 0.14 s (except 2/7) • QRS duration? Interpretation? NSR with Premature Atrial Contractions
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- 105. DR/ SHAFEI LASHEEN Rhythm#5 100 bpm• Rate? • Regularity? irregularly irregular none 0.06 s • P waves? • PR interval? none • QRS duration? Interpretation? Atrial Fibrillation
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- 108. DR/ SHAFEI LASHEEN Rhythm#6 70 bpm• Rate? • Regularity? regular flutter waves 0.06 s • P waves? • PR interval? none • QRS duration? Interpretation? Atrial Flutter
- 109. DR/ SHAFEI LASHEEN AVJunctional Problems The AV junction can: • fire continuously due to a looping re- entrant circuit • block impulses coming from the SA Node Paroxysmal Supraventricular Tachycardia AV Junctional Blocks
- 110. DR/ SHAFEI LASHEEN Rhythm#7 74 148 bpm• Rate? • Regularity? Regular regular Normal none 0.08 s • P waves? • PR interval? 0.16 s none • QRS duration? Interpretation? Paroxysmal Supraventricular Tachycardia (PSVT)
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- 112. Junctional Premature Beat •single ectopic beat that originates in the AV node or • Bundle of His area of the condunction system • – Retrograde P waves immediately preceding the QRS • – Retrograde P waves immediately following the QRS • – Absent P waves (buried in the QRS)
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- 116. DR/ SHAFEI LASHEEN VentricularCell Problems Ventricular cells can: • fire occasionally from 1 or more foci • fire continuously from multiple foci • fire continuously due to a looping re- entrant circuit Premature Ventricular Contractions (PVCs) Ventricular Fibrillation Ventricular Tachycardia
- 117. DR/ SHAFEI LASHEEN VentricularConduction Normal Signal moves rapidly through the ventricles Abnormal Signal moves slowly through the ventricles
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- 119. DR/ SHAFEI LASHEEN Rhythm#4 60 bpm• Rate? • Regularity? occasionally irreg. none for 7th QRS 0.08 s (7th wide) • P waves? • PR interval? 0.14 s • QRS duration? Interpretation? Sinus Rhythm with 1 PVC
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- 126. DR/ SHAFEI LASHEEN 160bpm• Rate? • Regularity? regular none wide (> 0.12 sec) • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Tachycardia
- 127. Ventricular Fibrillation (VF) * ** * * ** ***
- 128. DR/ SHAFEI LASHEEN Rhythm#9 none• Rate? • Regularity? irregularly irreg. none wide, if recognizable • P waves? • PR interval? none • QRS duration? Interpretation? Ventricular Fibrillation
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- 134. AV Blocks AV NodeBundle of His Right Bundle Branch Left Bundle Branch Anterior Fascicle of Posterior Fascicle of Left Bundle Left Bundle
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- 136. Classification of AVHeart Blocks Degree AV Conduction Pattern 1St Degree Block Uniformly prolonged PR interval 2nd Degree, Mobitz Type I Progressive PR interval prolongation 2nd Degree, Mobitz Type II Sudden conduction failure 3rd Degree Block No AV conduction
- 137. DR/ SHAFEI LASHEEN 60bpm• Rate? • Regularity? regular normal 0.08 s • P waves? • PR interval? 0.36 s • QRS duration? Interpretation? 1st Degree AV Block
- 138. Second Degree AVBlock • Mobitz type I or Winckebach • Mobitz type II
- 139. DR/ SHAFEI LASHEEN Rhythm#11 50 bpm• Rate? • Regularity? regularly irregular nl, but 4th no QRS 0.08 s • P waves? • PR interval? lengthens • QRS duration? Interpretation? 2nd Degree AV Block, Type I
- 140. DR/ SHAFEI LASHEEN 40bpm• Rate? • Regularity? regular nl, 2 of 3 no QRS 0.08 s • P waves? • PR interval? 0.14 s • QRS duration? Interpretation? 2nd Degree AV Block, Type II
- 141. Third Degree AVBlock (Complete Heart Block) SA Node conducts at its AV Node conducts at its inherent rate of 60-100 BPM inherent rate of 40-60 BPM Two independent pacemakers
- 142. Third Degree AVBlock (Complete Heart Block) P P P P P P P P P QRS QRS QRS Atria AV Node Ventricles BLOCK
- 144. DR/ SHAFEI LASHEEN 40bpm• Rate? • Regularity? regular no relation to QRS wide (> 0.12 s) • P waves? • PR interval? none • QRS duration? Interpretation? 3rd Degree AV Block
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- 146. ECG assessment ST Elevationor new LBBB STEMI Non-specific ECG Unstable Angina ST Depression or dynamic T wave inversions NSTEMI
- 148. DR/ SHAFEI LASHEEN ECGRhythm Interpretation Acute Myocardial Infarction
- 149. DR/ SHAFEI LASHEEN STElevation and non-ST Elevation MIs
- 150. DR/ SHAFEI LASHEEN ECGChanges & the Evolving MI There are two distinct patterns of ECG change depending if the infarction is: –ST Elevation (Transmural or Q-wave), or –Non-ST Elevation (Subendocardial or non-Q-wave) Non-ST Elevation ST Elevation
- 151. DR/ SHAFEI LASHEE ECGChanges Ways the ECG can change include: Appearance of pathologic Q-waves T-waves peaked flattened inverted ST elevation & depression
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- 154. Sequence of changesin evolving AMI 1 minute after onset 1 hour or so after onset A few hours after onset A day or so after onset Later changes A few months after AMI Q R P Q TST R P Q ST P Q T ST R P S T P Q T ST R P Q T
- 155. DR/ SHAFEI LASHEEN Viewsof the Heart Some leads get a good view of the: Anterior portion of the heart Lateral portion of the heart Inferior portion of the heart
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- 164. Which part ofthe heart is affected ? I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 • Leads V1, V2, V3, and V4 = Anterior Wall MI
- 165. Anterior infarctionAnterior infarction III III aVR aVL aVF V1 V2 V3 V4 V5 V6 Left coronary Artery or LAD
- 166.
- 167. AWMI (pardee’s sign) Theconvex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the “Pardee’s sign”
- 168. DR/ SHAFEI LASHEEN STElevation (cont) Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.
- 169. What part ofthe heart is affected ? I, aVL, V5 and V6 Lateral wall of left ventricle I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
- 170. Lateral infarction Lateral infarction III III aVR aVL aVF V1 V2 V3 V4 V5 V6 Left circumflex coronary artery
- 171. DR/ SHAFEI LASHEEN AnterolateralMI This person’s MI involves both the anterior wall (V2- V4) and the lateral wall (V5-V6, I, and aVL)!
- 172. DR/ SHAFEI LASHEEN Infarct:Is the ST elevation or depression? Yes! Elevation in V2-V6, I and avL. Depression in II, III and avF.
- 174. What part ofthe heart is affected ? II, III, aVF = Inferior Wall I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
- 175. Inferior infarction Inferior infarction III III aVR aVL aVF V1 V2 V3 V4 V5 V6 Right coronary artery
- 176. DR SHAFEI LASHEE InferiorWall MI This is an inferior MI. Note the ST elevation in leads II, III and aVF.
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- 181. inferior/posterior STEMI withRV involvement
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- 185. 45 yo female1 week post-op with shortness of breath
- 186. Findings • Accelerated junctional rhythm •Right axis deviation • “S1Q3T3” pattern • Clinical history and EKG most consistent with acute PE
- 188. DR/ SHAFEI LASHEEN Non-STElevation Infarction ST depression & T-wave inversion The ECG changes seen with a non-ST elevation infarction are: Before injury Normal ECG ST depression & T-wave inversion ST returns to baseline, but T-wave inversion persists Ischemia Infarction Fibrosis
- 189. ST Depression orDynamic T wave Inversions
- 190. DR/ SHAFEI LASHEEN Non-STElevation Infarction Here’s an ECG of an evolving non-ST elevation MI: Note the ST depression and T-wave inversion in leads V2-V6. Question: What area of the heart is infarcting? Anterolateral
- 192.
- 193. DR/ SHAFEI LASHEEN Hypertrophy Inthis step of the 12-lead ECG analysis, we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied. We want to determine if there are any of the following: – Right atrial enlargement (RAE) – Left atrial enlargement (LAE) – Right ventricular hypertrophy (RVH) – Left ventricular hypertrophy (LVH)
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- 196. DR/ SHAFEI LASHEEN –To diagnose RAE you can use the following criteria: • II P > 2.5 mm, or • V1 or V2 P > 1.5 mm Right atrial enlargement
- 197. DR/ SHAFEI LASHEEN Leftatrial enlargement – To diagnose LAE you can use the following criteria: • II > 0.04 s (1 box) between notched peaks, or • V1 Neg. deflection > 1 box wide x 1 box deep
- 199. 199 199 Ventricular Hypertrophy • VentricularMuscle Hypertrophy • QRS voltages in V1 and V6, L 1 and aVL • We may have to record to ½ standardization • T wave changes opposite to QRS direction • Associated Axis shifts • Associated Atrial hypertrophy
- 200. DR/ SHAFEI LASHEEN LeftVentricular Hypertrophy
- 201. DR// SHAFEI LASHEEN LeftVentricular Hypertrophy Why is left ventricular hypertrophy characterized by tall QRS complexes? LVH ECHOcardiogram Increased QRS voltage As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage.
- 202. Criteria for LVH •Sokolow-Lyon – S v1+R v5/v6>35mm – R I+S III>25mm – R avl>11mm • Cornell – S v3+R avl >28 (men) >20 (women) • Romhilt-Estes – LV strain 3 – LAE 3 – LAD 2 – QRS duration 1 – R v5/v6>3 3 – Sv1/v2>3 3 – Largest R or S>2 3 5 or more points suggests LVH
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- 207. DR/ SHAFEI LASHEEN BundleBranch Blocks
- 208. DR / SHAFEILASHEE Right Bundle Branch Blocks What QRS morphology is characteristic? For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2).
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- 210. DR/SHAFEI LASHEEN Left BundleBranch Blocks What QRS morphology is characteristic? For LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2).
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