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ECG

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ECG Presentation,Nice Interpretation

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ECG

  1. 1. ECG BASICS By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associate Professor Medicine Email drbashir123@gmail.com
  2. 2.       From Right to Left Dr.Smitha associate prof gynae Dr Bashir associate professor Medicine Dr Udaman neurologist Dr Patnaik HOD ortho Dr Tin swe aye paeds
  3. 3.       From RT to Lt Professor Dr Datuk rajagopal N Dr Bashir associate professor medicine Dr Urala HOD gynae Dr Nagi reddy tamma HODopthomology Dr Setharamarao Prof ortho
  4. 4. ELECTROGRAPHY MADE EASY  ULTIMATE AIM TO HELP PATIENTS
  5. 5. ECG machine
  6. 6. Limb and chest leads  When an ECG is taken we put 4 limb leads or electrodes with different colour codes on upper and lower limbs one each at wrists and ankles by applying some jelly for close contact.  We also put six chest leads at specific areas over the chest  So in reality we see only 10 chest leads.
  7. 7. Position of limb and chest leads  Four limb leads  Six chest leads V1- 4th intercostal space to the right of sternum V2- 4th intercostal space to the left of sternum V3- halfway between V2 and V4 V4- 5th intercostal space in the left mid-clavicular line V5- 5th intercostal space in the left anterior axillary line V6- 5th intercostal space in the left mid axillary line      
  8. 8. Horizontal plane - the six chest leads LA RA V1 V2 LV RV V6 V3 V4 V5 V6 V5 V4 V1 V2 V3 6.5
  9. 9. Colour codes given by AHA
  10. 10. ECG Paper: Dimensions 5 mm 1 mm 0.1 mV 0.04 sec 0.2 sec Speed = rate Voltage ~Mass
  11. 11. ECG paper and timing   ECG paper speed Voltage calibration 1 mV = 25mm/sec = 1cm  ECG paper - standard calibrations – each small square = 1mm – each large square = 5mm  Timings – 1 small square – 1 large square – 25 small squares – 5 large squares = = = = 0.04sec 0.2sec 1sec 1sec
  12. 12.  After applying these leads on different positions then these leads are connected to a connector and then to ECG machine.  The speed of machine kept usually 25mm/second.calibration or standardization done while machine is switched on.
  13. 13. ECG paper 1 Small square = 0.04 second 2 Large squares = 1 cm 1 Large square = 0.2 second 5 Large squares = 1 second Time 6.1
  14. 14.  The first step while reading ECG is to look for standardization is properly done.  Look for this mark and see that this mark exactly covers two big squares on graph.
  15. 15. STANDARDISATION ECG amplitude scale Normal amplitude Half amplitude Double amplitude 10 mm/mV 5 mm/mV 20 mm/mV
  16. 16. ECG WAVES  You will see then base line or isoelectric line that is in line with P-Q interval and beginning of S-T segment.  From this line first positive deflection will arise as P wave then other waves as shown in next slide.  Small negative deflections Q wave and S wave also arise from this line.
  17. 17. ECG WAVES
  18. 18. The Normal ECG Normal Intervals: PR 0.12-0.20s QRS duration <0.12s QTc 0.33-0.43s
  19. 19. Simplified normal Position of leads on ECG graph  Lead 1# upward PQRS  Lead 2# upward PQRS  Lead 3# upward PQRS  Lead AVR#downward or negative PQRS  Lead AVL# upward PQRS  Lead AVF# upwards PQRS
  20. 20. Simplified normal Position of leads on ECG graph  Chest lead V1# negative or downward PQRS  Chest leads V2-V3-V4-V5-V6 all are upright from base line .The R wave slowly increasing in height from V1 to V6.  So in normal ECG you see only AVR and V1 as negative or downward defelections as shown in next slide.
  21. 21. Normal ECG Slide 13
  22. 22. NSR
  23. 23. P-wave  Normal P wave length from beginning of P wave to end of P wave is 2 and a half small square.  Height of P wave from base line or isoelectric line is also 2 and a half small square.
  24. 24. P-wave Normal values 1. up in all leads except AVR. 2. Duration. < 2.5 mm. 3. Amplitude. < 2.5 mm. 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
  25. 25. P wave height 2 and half small squares ,width also 2 and half small square Slide 9
  26. 26. Shape of P wave  The upward limb and downward limbs of P wave are equal.  Summit or apex of P wave is slightly rounded.
  27. 27. P pulmonale & P mitrale P pulmonale-Summit or apex of P wave becomes arrow like pointed or pyramid shape,the height also becomes more than two small squares from base line.  P waves best seen in lead 2 and V1.
  28. 28. P pulmonale & P mitrale P mitrale- the apex or summit of p wave may become notched .the notch should be at least more than one small square.  Duration of P becomes more than two and a half small squares.
  29. 29. Slide 14
  30. 30. Slide 16
  31. 31. Left Atrial Enlargement Criteria P wave duration in II >than 2 and half small squares with notched p wave or Negative component of biphasic P wave in V1 ≥ 1 “small box” in area
  32. 32. Right Atrial Enlargement Criteria P wave height in II >2 and half small squares and are also tall and peaked. or Positive component of biphasic P wave in V1 > 1 “small box” in area
  33. 33. Slide 15
  34. 34. Atrial fibrillation P waves thrown into number of small abnormal P waves before each QRS complex  The duration of R-R interval varies  The amplitude of R-R varies  Abnormal P waves don’t resemble one another.
  35. 35. Slide 41
  36. 36. Atrial flutter  The P waves thrown into number of abnormal P waves before each QRS complex.  But these abnormal P waves almost resemble one another and are more prominent like saw tooth appearance.
  37. 37. Slide 40
  38. 38. Junctional rhythm  In Junctional rhythm the P waves may be absent or inverted.in next slide u can see these inverted P waves.
  39. 39. Slide 43
  40. 40. Paroxysmal atrial tachycardia  The P and T waves you cant make out separately  The P and T waves are merged in one  The R-R intervals do not vary but remain constant and same.  The heart rate being very high around 150 and higher.
  41. 41. Slide 39
  42. 42. NORMAL P-R INTERVAL  PR interval seconds.  That time 0.12 seconds to 0.2 is three small squares to five small squares.
  43. 43. PR interval Definition: the time 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
  44. 44. Short P-R interval  Short P-R interval seen in WPW syndrome or preexcitation syndrome or LG syndrome  P-R interval is less than three small squares.  The beginning of R wave slopes gradually up and is slightly widened called Delta wave.  There may be S-T changes also like ST depression and T wave inversion.
  45. 45. Slide 17
  46. 46. Lengthening of P-R interval  Occurs in first degree heart block.  The P-R interval is more than 5 small squares or > than 0.2 seconds.  This you will see in all leads and is same fixed lengthening .
  47. 47. Slide 44
  48. 48. Q WAVES Q waves <0.04 second.  That’s is less than one small square duration.  Height <25% or < 1/4 of R wave height.
  49. 49. Normal Q wave
  50. 50. 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.
  51. 51. Q wave in MI
  52. 52. Q wave in septal hypertrophy
  53. 53. QRS COMPLEX  QRS duration <0.11 s  That is less than almost three small squares  Some books write 2 and a half small squares.  Height of R wave is (V1-V6) >8 mm some say >10 mm chest leads (in at least one of chest leads).
  54. 54. 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.
  55. 55. 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. 56. Normal upward progression of 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
  57. 57. J point  The term J point means Junctional point at the end of S wave between S wave and beginning of S-T segment.
  58. 58. ST Q S J point
  59. 59. L V H-Voltage Criteria In adult with normal chest wall SV1+RV5 >35 mm or SV1 >20 mm or RV6 >20 mm
  60. 60. Left ventricular hypertrophy-Voltage Criteria  Count small squares of downward R wave in V1 plus small squares of R wave in V5 .  If it comes to more than 35 small squares then it is suggestive of LVH.
  61. 61. LEFT VENTRICULAR HYPERTROPHY
  62. 62. Right ventricular hypertrophy  Normally you see R wave is downward deflection in V1.but if you see upward R wave in V1 then it is suggestive of RVH etc.
  63. 63. Dominant or upward R wave in V1  Causes  RBBB  Chronic lung disease, PE Posterior MI WPW Type A Dextrocardia Duchenne muscular dystrophy
  64. 64. Right Ventricular Hypertrophy  WILL SHOW AS  Right axis deviation (RAD)  Precordial leads  In V1, R wave > S wave  In V6, S wave > R wave  Usual manifestation is pulmonary disease or  congenital heart disease
  65. 65. Right Ventricular Hypertrophy
  66. 66. Right ventricular hypertrophy  Right ventricular hypertrophy (RVH) increases the height of the R wave in V1. And R wave in V1 greater than 7 boxes in height, or larger than the S wave, is suspicious for RVH. Other findings are necessary to confirm the ECG diagnosis.
  67. 67. Right Ventricular Hypertrophy  Other findings in RVH include right axis deviation, taller R waves in the right precordial leads (V1-V3), and deeper S waves in the left precordial (V4-V6). The T wave is inverted in V1 (and often in V2).
  68. 68. Right Ventricular Hypertrophy  True posterior infarction may also cause a tall R wave in V1, but the T wave is usually upright, and there is usually some evidence of inferior infarction (ST-T changes or Qs in II, III, and F).
  69. 69. Right Ventricular Hypertrophy A large R wave in V1, when not accompanied by evidence of infarction, nor by evidence of RVH (right axis, inverted T wave in V1), may be benign “counterclockwise rotation of the heart.” This can be seen with abnormal chest shape.
  70. 70. Right Ventricular Hypertrophy Although there is no widely accepted criteria for detecting the presence of RVH, any combination of the following EKG features is suggestive of its presence:  Tall R wave in V1  Right axis deviation  Right atrial enlargement  Down sloping ST depressions in V1-V3 ( RV strain pattern)
  71. 71. Right Ventricular Hypertrophy
  72. 72. Left Ventricular Hypertrophy
  73. 73. Left Ventricular Hypertrophy
  74. 74. ECG criteria for RBBB  •(1) QRS duration exceeds 0.12 seconds or 2 and half small squares roughly in V1 and may also see it in V2.  •(2) RSR complex in V1 may extend to V2.
  75. 75. ECG criteria for RBBB  •ST/T must be opposite in direction to the terminal QRS(is secondary to the block and does not mean primary ST/T changes).  It you meet all above criteria it is then complete right bundle branch block.  In incomplete bundle branch block the duration of QRS will be within normal limits.
  76. 76. RBBB & MI  If abnormal Q waves are present they will not be masked by the RBBB pattern.  •This is because there is no alteration of the initial part of the complex RS (in V1) and abnormal Q waves can still be seen.
  77. 77. Significance of RBBB  RBBB is seen in : (1) occasional normal subjects  (2) pulmonary embolus  (3) coronary artery disease  (4) ASD  (5) active Carditis  (6) RV diastolic overload
  78. 78. Partial / Incomplete RBBB  is diagnosed when the pattern of RBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and a half small squares.
  79. 79. In next slide you will see  ECG characteristics of a typical RBBB showing wide QRS complexes with a terminal R wave in lead V1 and slurred S wave in lead V6.  Also you see R wave has become upright in V1.QRS duration has also increased making it complete RBBB.
  80. 80.
  81. 81. ECG criteria for LBBB  (1)Prolonged QRS complexes, greater than 0.12 seconds or roughly 2 and half small squares in all leads almost.  (2)Wide, notched QRS (M shaped) V5, V6  (3)Wide, notched QS complexes are seen in V1 (due to spread of activation away from the electrode through septum + LV)  (4)In V2, V3 small r wave may be seen due to activation of para septal region
  82. 82. ECG criteria for LBBB  So look in all leads for QRS duration to make it complete LBBB or incomplete LBBB as u did in RBBB.  Look in V5 and V6 for M shaped pattern at summit or apex of R wave.  Look for any changes as S-T depression and T wave in inversion if any.
  83. 83. Significance of LBBB  LBBB is seen in : (1) Always indicative of organic heart disease  (2) Found in ischemic heart disease  (3) Found in hypertension.  MI should not be diagnosed in the presence of LBBB →Q waves are masked by LBBB pattern  Cannot diagnose the presence of MI with LBBB
  84. 84. Partial / Incomplete LBBB  is diagnosed when the pattern of LBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and half small squares.
  85. 85. NORMAL ST- SEGMENT it's isoelectric. [i.e. at same level of PR or PQ segment at least in the beginning]
  86. 86. NORMAL CONCAVITY OF S-T SEGMENT  It then gradually slopes upwards making concavity upwards and not going more than one small square upwards from isoelectric line or one small square below isoelectric line.  In MI this concavity may get lost and become convex upwards called coving of S-T segment.
  87. 87. Abnormalities ST elevation: More than one small square 1.     Acute MI. Prinzmetal angina. Acute pericarditis. Early repolarization ST depression: More than one small square      Ischemia. Ventricular strain. BBB. Hypokalemia. Digoxin effect.
  88. 88. Slide 11
  89. 89. Slide 12
  90. 90. Stress test ECG – note the ST Depression
  91. 91. Note the arrows pointing ST depression
  92. 92. ST depression & Troponin T positive is NON STEMI
  93. 93. Coving of S-T segment  Concavity upwards. lost and convexity appear facing
  94. 94. Diagnostic criteria for AMI • • • • • Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias
  95. 95. Abnormalities of ST- segment
  96. 96. Q waves in myocardial infarction
  97. 97. T-wave Normal values. 1.amplitude: < 10mm in the chest leads. . 2. T- inversion:  Abnormalities:  1. Peaked T-wave:  Hyper-acute MI.  Hyperkalemia.  Normal variant      Ischemia. Myocardial infarction. Myocarditis Ventricular strain BBB. Hypokalemia. Digoxin effect.
  98. 98. QT- interval Definition: Time interval between beginning of QRS complex to the end of T wave. Normally: At normal HR: QT ≤ 11mm (0.44 sec) Abnormalities: 1. 2. Prolonged QT interval: hypocalcemia and congenital long QT syndrome. Short QT interval: hypercalcemia.
  99. 99. QT Interval - Should be < 1/2 preceding R to R interval -
  100. 100. QT Interval - Should be < 1/2 preceding R to R interval - QT interval
  101. 101. QT Interval - Should be < 1/2 preceding R to R interval - QT interval
  102. 102. QT Interval - Should be < 1/2 preceding R to R interval R QT interval R
  103. 103. QT Interval - Should be < 1/2 preceding R to R interval R QT interval R
  104. 104. QT Interval - Should be < 1/2 preceding R to R interval R QT interval R
  105. 105. QT Interval - Should be < 1/2 preceding R to R interval 65 - 90 bpm R QT interval R
  106. 106. QT Interval - Should be < 1/2 preceding R to R interval 65 - 90 bpm R QT interval Normal QTc = 0.46 sec R
  107. 107. Atrioventricular (AV) Heart Block
  108. 108. Classification of AV Heart 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
  109. 109. AV Blocks  First Degree – Prolonged AV conduction time – PR interval > 0.20 seconds
  110. 110. 1st Degree AV Block Prolongation of the PR interval, which is constant All P waves are conducted
  111. 111. 1st degree AV Block: • Regular Rhythm • PRI > .20 seconds or 5 small squares and is CONSTANT • Usually does not require treatment PRI > .20 seconds
  112. 112. First Degree Block prolonged PR interval
  113. 113. Analyze the Rhythm
  114. 114. AV Blocks  Second Degree – Definition  More Ps than QRSs  Every QRS caused by a P
  115. 115. Second-Degree AV Block  There is intermittent failure of the supraventricular impulse to be conducted to the ventricles  Some of the P waves are not followed by a QRS complex.The conduction ratio (P/QRS ratio) may be set at 2:1,3:1,3:2,4:3,and so forth 
  116. 116. Second Degree – Types  Type I – Wenckebach phenomenon  Type II – Fixed or Classical
  117. 117. Type I Second-Degree AV Block: Wenckebach Phenomenon  ECG findings  1.Progressive lengthening of the PR interval until a P wave is blocked
  118. 118. 2nd degree AV Block (“Mobitz I” also called “Wenckebach”): • Irregular Rhythm • PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse) • PRI is NOT CONSTANT PRI = .24 sec PRI = .36 sec PRI = .40 sec QRS is “dropped” Pause 4:3 Wenckebach (conduction ratio may not be constant) Pattern Repeats………….
  119. 119. Type II Second-Degree AV Block: Mobitz Type II  ECG findings 1.Intermittent or unexpected blocked P waves you don’t know when QRS drops  2.P-R intervals may be normal or prolonged,but they remain constant  4. A long rhythm strip may help 
  120. 120. Second Degree AV Block Mobitz type I or Winckebach Mobitz type II
  121. 121. Type 1 (Wenckebach) Progressive prolongation of the PR interval until a P wave is not conducted. Type 2 Constant PR interval with unexpected intermittent failure to conduct
  122. 122. Mobitz Type I
  123. 123. MOBITZ TYPE 1
  124. 124. 2nd degree AV Block (“Mobitz II”): • Irregular Rhythm • QRS complexes may be somewhat wide (greater than .12 seconds) • Non-conducted sinus impulses appear at unexpected irregular intervals • PRI may be normal or prolonged but is CONSTANT and fixed • Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart block (3rd degree block) • It’s appearance in the setting of an acute MI identifies a high risk patient • Cause: anterioseptal MI, •Treatment: may require pacemaker in the case of fibrotic conduction system PRI is CONSTANT Non-conducted sinus impulses “2:1 block” “3:1 block”
  125. 125. Analyze the Rhythm
  126. 126. Second Degree Mobitz – Characteristics – Atrial rate > Ventricular rate – QRS usually longer than 0.12 sec – Usually 4:3 or 3:2 conduction ratio (P:QRS ratio)
  127. 127. Analyze the Rhythm
  128. 128. Mobitz II   Definition: Mobitz II is characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave will be constant for each QRS . EKG Characteristics:Atrial and ventricular rate is irregular. P Wave: Present in two, three or four to one conduction with the QRS. PR Interval constant for each P wave prior to the QRS. QRS may or may not be within normal limits.
  129. 129. Mobitz Type II
  130. 130. Mobitz Type II Sudden appearance of a single, nonconducted sinus P wave...
  131. 131. Advanced Second-Degree AV Block Two or more consecutive nonconducted sinus P waves
  132. 132. Complete AV Block – Characteristics  Atrioventricular dissociation  Regular P-P and R-R but without association between the two  Atrial rate > Ventricular rate  QRS > 0.12 sec
  133. 133. 3rd Degree (Complete) AV Block EKG Characteristics: No relationship between P waves and QRS complexes Relatively constant PP intervals and RR intervals Greater number of P waves than QRS complexes
  134. 134. Complete heart block P waves are not conducted to the ventricles because of block at the AV node. The P waves are indicated below and show no relation to the QRS complexes. They 'probe' every part of the ventricular cycle but are never conducted.
  135. 135. 3rd degree AV Block (“Complete Heart Block”) : • Irregular Rhythm • QRS complexes may be narrow or broad depending on the level of the block • Atria and ventricles beat independent of one another (AV dissociation) • QRS’s have their own rhythm, P-waves have their own rhythm • May be caused by inferior MI and it’s presence worsens the prognosis •Treatment: usually requires pacemaker QRS intervals P-wave intervals – note how the P-waves sometimes distort QRS complexes or T-waves
  136. 136. Third-Degree (Complete) AV Block
  137. 137. Third-Degree (Complete) AV Block The P wave bears no relation to the QRS complexes, and the PR intervals are completely variable
  138. 138. 30 AV Block         AV dissociation atria and ventricles beating on their own no relation between P’s & QRS’s Atrial rate is different from ventricular ventricular rate: 30-60 bpm Rhythm is regular for both QRS can be narrow or wide depends on site of pacemaker!
  139. 139. Key points         Wenckebach look for group beating & changing PR Mobitz II look for reg. atrial rhythm & consistent PR 3o block atrial & ventricular rhythm regular 􀂾 rate is different!!! no consistent PR
  140. 140. Left Anterior Fascicular Block  Left axis deviation , usually -45 to -90 degrees  QRS duration usually <0.12s unless coexisting RBBB  Poor R wave progression in leads V1-V3 and deeper S waves in leads V5 and V6  There is RS pattern with R wave in lead II > lead III S wave in lead III > lead II    QR pattern in lead I and AVL,with small Q wave No other causes of left axis deviation
  141. 141. LBB LPIF Lead I Left Anterior Hemiblock (LAHB): 1. Left axis deviation (> -30 degrees) will be noted and there will be a prominent S-wave in Leads II, and III 1. LASF 2. Lead III Lead AVF
  142. 142. Left Posterior Fascicular Block  Right axis deviation  QR pattern in inferior leads (II,III,AVF) small q wave  RS patter in lead lead I and AVL(small R with deep S)
  143. 143. Lead I LBB LPIF Left Posterior Hemiblock (LPHB): 1. 1. Right axis deviation and there will be a prominent S-wave in Leads I. Q-waves may be noted in III and AVF. Notes on (LPHB): • QRS is normal width unless BBB is present • If LPHB occurs in the setting of an acute MI, it is almost always accompanied by RBBB and carries a mortality rate of 71% LASF 2. Lead III Lead AVF
  144. 144. Bifascicular Bundle Branch Block RBBB with either left anterior or left posterior fascicular block  Diagnostic criteria  1.Prolongation of the QRS duration to 0.12 second or longer  2.RSR’ pattern in lead V1,with the R’ being broad and slurred  3.Wide,slurred S wave in leads I,V5 and V6  4.Left axis or right axis deviation 
  145. 145. Trifascicular Block  The combination of RBBB, LAFB and long PR interval  Implies that conduction is delayed in the third fascicle
  146. 146. Indications For Implantation of Permanent Pacing in Acquired AV Blocks     1.Third-degree AV block, Bradycardia with symptoms Asystole e.Neuromuscular diseases with AV block (Myotonic muscular dystrophy) 2.Second-degree AV block with symptomatic bradycardia
  147. 147. Cardiac Pacemakers  Definition – Delivers artificial stimulus to heart – Causes depolarization and contraction  Uses – Bradyarrhythmias – Asystole – Tachyarrhythmias (overdrive pacing)
  148. 148. Cardiac Pacemakers  Types – Fixed    Fires at constant rate Can discharge on T-wave Very rare – Demand   Senses patient’s rhythm Fires only if no activity sensed after preset interval (escape interval) – Transcutaneous vs Transvenous vs Implanted
  149. 149. Cardiac Pacemakers
  150. 150. Cardiac Pacemakers  Demand Pacemaker Types – Ventricular  Fires ventricles – Atrial Fires atria  Atria fire ventricles  Requires intact AV conduction 
  151. 151. Cardiac Pacemakers  Demand Pacemaker Types – Atrial Synchronous  Senses atria  Fires ventricles – AV Sequential Two electrodes  Fires atria/ventricles in sequence 
  152. 152. Cardiac Pacemakers  Problems – Failure to capture  No response to pacemaker artifact  Bradycardia may result  Cause: high “threshold”  Management – Increase amps on temporary pacemaker – Treat as symptomatic bradycardia
  153. 153. Cardiac Pacemakers  Problems – Failure to sense  Spike follows QRS within escape interval  May cause R-on-T phenomenon  Management – Increase sensitivity – Attempt to override permanent pacer with temporary – Be prepared to manage VF
  154. 154. Implanted Defibrillators  AICD – Automated Implanted CardioDefibrillator  Uses – Tachyarrhythmias – Malignant arrhythmias   VT VF
  155. 155. Implanted Defibrillators  Programmed at insertion to deliver predetermined therapies with a set order and number of therapies including: – pacing – overdrive pacing – cardioversion with increasing energies – defibrillation with increasing energies – standby mode  Effect of standby mode on Paramedic treatments
  156. 156. Implanted Defibrillators  Potential Complications – Fails to deliver therapies as intended   worst complication requires Paramedic intervention – Delivers therapies when NOT appropriate   broken or malfunctioning lead parameters for delivery are not specific enough – Continues to deliver shocks   parameters for delivery are not specific enough and device senses a reset may be shut off (not standby mode) with donut-magnet
  157. 157. Sinus Exit Block  Due to abnormal function of SA node  MI, drugs, hypoxia, vagal tone  Impulse blocked from leaving SA node  usually transient  Produces 1 missed cycle  can confuse with sinus pause or arrest
  158. 158. Sinus block
  159. 159. ARRTHYMIAS AND ECTOPIC BEATS
  160. 160. Recognizing and Naming Beats & Rhythms Atrial Escape Beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal normal ("sinus") beats sinus node doesn't fire leading to a period of asystole (sick sinus syndrome) p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. It is therefore called an "atrial" beat
  161. 161. Recognizing and Naming Beats & Rhythms Junctional Escape Beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction. The beat is therefore called a "junctional" or a “nodal” beat
  162. 162. Recognizing and Naming Beats & Rhythms Ventricular Escape Beat QRS is wide and much different ("bizarre") looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a “ventricular” beat there is no p wave, indicating that the beat did not originate anywhere in the atria actually a "retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles
  163. 163. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms Electrical Impulse Cardiac Conduction Tissue Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Tissues with these type of circuits may exist: • in microscopic size in the SA node, AV node, or any type of heart tissue • in a “macroscopic” structure such as an accessory pathway in WPW
  164. 164. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms Premature Beat Impulse Cardiac Repolarizing Tissue Conduction (long refractory period) Tissue Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery 1. An arrhythmia is triggered by a premature beat 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only
  165. 165. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms Cardiac Conduction Tissue Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery 3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
  166. 166. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms Cardiac Conduction Tissue Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery 4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit
  167. 167. Recognizing and Naming Beats & Rhythms Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles) : • A ventricular ectopic focus discharges causing an early beat • Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre" • QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant) • In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion • PVC’s are sometimes described by lay people as “skipped heart beats” R on T phenom em on M u lt if o c a l P V C 's C o m p e n s a to ry p a u s e a fte r th e o c c u r a n c e o f a P V C
  168. 168. Recognizing and Naming Beats & Rhythms Characteristics of PVC's • PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave) • T-waves for PVC’s are usually large and opposite in polarity to terminal QRS • Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle • Every other beat being a PVC (bigeminy) may indicate coronary artery disease • Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s The classic PVC – note the compensatory pause Interpolated PVC – note the sinus rhythm is undisturbed
  169. 169. Recognizing and Naming Beats & Rhythms PVC's are Dangerous When: • They are frequent (> 30% of complexes) or are increasing in frequency • The come close to or on top of a preceding T-wave (R on T) • Three or more PVC's in a row (run of V-tach) • Any PVC in the setting of an acute MI • PVC's come from different foci ("multifocal" or "multiformed") These dangerous phenomenon may preclude the occurrence of deadly arrhythmias: • Ventricular Tachycardia • Ventricular Fibrillation The sooner defibrillation takes place, the increased likelihood of survival “R on T phenomenon” time sinus beats V-tach Unconverted V-tach r V-fib
  170. 170. Recognizing and Naming Beats & Rhythms Notes on V-tach: • Causes of V-tach • Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause) • Typical V-tach patient • MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm) •V-tach complexes are likely to be similar and the rhythm regular • Irregular V-Tach rhythms may be due to to: • breakthrough of atrial conduction • atria may “capture” the entire beat beat • an atrial beat may “merge” with an ectopic ventricular beat (fusion beat) Fusion beat - note pwave in front of PVC and the PVC is narrower than the other PVC’s – this indicates the beat is a product of both the sinus node and an ectopic ventricular focus Capture beat - note that the complex is narrow enough to suggest normal ventricular conduction. This indicates that an atrial impulse has made it through and conduction through the ventricles is relatively normal.
  171. 171. Recognizing and Naming Beats & Rhythms Premature Atrial Contractions (PAC’s): • An ectopic focus in the atria discharges causing an early beat • The P-wave of the PAC will not look like a normal sinus P-wave (different morphology) • QRS is narrow and normal looking because ventricular depolarization is normal • PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s) • PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco • PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy • PAC’s may also precede PSVT PAC Non conducted PAC Non conducted PAC distorting a T-wave
  172. 172. Recognizing and Naming Beats & Rhythms Premature Junctional Contractions (PJC’s): • An ectopic focus in or around the AV junction discharges causing an early beat • The beat has no P-wave • QRS is narrow and normal looking because ventricular depolarization is normal • PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm PJC
  173. 173. Recognizing and Naming Beats & Rhythms Multifocal Atrial Tachycardia (MAT): • Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles • QRS complexes are almost identical to the sinus beats • Rate is usually between 100 and 200 beats per minute • The rhythm is always IRREGULAR • P-waves of different morphologies (shapes) may be seen if the rhythm is slow • If the rate < 100 bpm, the rhythm may be referred to as “wandering pacemaker” • Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF • Treatments: Ca++ channel blockers,  blockers, potassium, magnesium, supportive therapy for underlying causes mentioned above (antiarrhythmic drugs are often ineffective) Note different P-wave morphologies when the tachycardia begins Note IRREGULAR rhythm in the tachycardia
  174. 174. Recognizing and Naming Beats & Rhythms Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) : • A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted normally to the ventricles (usually initiated by a PAC) • QRS complexes are almost identical to the sinus beats • Rate is usually between 150 and 250 beats per minute • The rhythm is always REGULAR • Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope (d Q) • Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter • May be terminated by carotid massage • u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction • Treatment: ablation of focus, Adenosine (d AV conduction), Ca++ Channel blockers Rhythm usually begins with PAC Note REGULAR rhythm in the tachycardia
  175. 175. Sinus arrest or exit block
  176. 176. PAC
  177. 177. 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)
  178. 178. Junctional Escape Beat
  179. 179. Junctional Rhythm  Rate: 40 to 60 beats/minute (atrial and ventricular)  •Rhythm: regular atrial and ventricular rhythm  •P wave: usually inverted, may be upright; may precede,  follow or be hidden in the QRS complex; may  be absent  •PR interval: not measurable or less than .20 sec.
  180. 180. Junctional Rhythm
  181. 181. MaligMalignant PVC patterns  Frequent PVCs Multiform PVCs  Runs of consecutive PVCs  R on T phenomenon – PVC that falls on a T  wave  PVC during acute MI
  182. 182. Types of PVCs  Uniform Multiform  PVC rhythm patterns  – Bigeminy – PVC occurs every other complex  – Couplets – 2 PVCs in a row  – Trigeminy – Two PVCs for every three complexes 
  183. 183. Junctional Escape Rhythm
  184. 184. Ventricular tachycardia (VTach) 3 or more PVCs in a row at a rate of 120 to 200 bts/min-1 Ventricular fibrillation (VFib)  No visible P or QRS complexes. Waves appear as fibrillating waves
  185. 185. Torsades de Pointes  Type of VT known as “twisting of the points.”  Usually seen in those with prolonged QT intervals caused by
  186. 186. Why “1500 / X”?  Paper Speed: 25 mm/ sec  60 seconds / minute  60 X 25 = 1500 mm / minute OR  Take 6 sec strip (30 large boxes)  Count the P/R waves X 10
  187. 187. Atrial Fibrillation:
  188. 188. Regular “Irregular” Premature Beats: PVC – Widened QRS, not associated with preceding P wave – Usually does not disrupt P-wave regularity – T wave is “inverted” after PVC – Followed by compensatory ventricular pause
  189. 189. Notice a Pattern in the PVC’s?
  190. 190. Identifying AV Blocks: Name 1°: Conduction P=R PR-Int > .20 R-R Rhythm Regular 2°:Mobitz P > R I Progressive Irregular 2°:Mobitz P > R II Constant Regular 3°: Grossly Irregular Regular P>R (20-40 bpm)
  191. 191. Most Important Questions of Arrhythmias  What is the mechanism? – Problems in impulse formation? (automaticity or ectopic foci) – Problems in impulse conductivity? (block or re-entry)  Where is the origin? – Atria, Junction, Ventricles?
  192. 192. QRS Axis Check Leads: 1 and AVF
  193. 193. Interpreting Axis Deviation:  Normal Electrical Axis: – (Lead I + / aVF +)  Left Axis Deviation: – Lead I + / aVF – – Pregnancy, LV hypertrophy etc  Right Axis Deviation: – Lead I - / aVF + – Emphysema, RV hypertrophy etc.
  194. 194. NW Axis (No Man’s Land) Both I and aVF are – Check to see if leads are transposed (- vs +) Indicates: – Emphysema – Hyperkalemia – VTach
  195. 195. Determining Regions of CAD: ST-changes in leads… RCA: Inferior myocardium – II, III, aVF LCA: Lateral myocardium – I, aVL, V5, V6 LAD: Anterior/Septal myocardium – V1-V4
  196. 196. Regions of the Myocardium: Lateral I, AVL, V5-V6 Inferior II, III, aVF Anterior / Septal V1-V4
  197. 197. Sinus Arrhythmia
  198. 198. Sinus Arrest/Pause
  199. 199. Sinoatrial Exit Block
  200. 200. Premature Atrial Complexes (PACs)
  201. 201. Wandering Atrial Pacemaker (WAP)
  202. 202. Supraventricular Tachycardia (SVT)
  203. 203. Wolff-Parkinson-White Syndrome (WPW)
  204. 204. Atrial Flutter
  205. 205. Atrial Fibrillation (A-fib)
  206. 206. Premature Junctional Complexes (PJC)
  207. 207. Junctional Rhythm
  208. 208. Junctional Rhythm
  209. 209. Accelerated Junctional Rhythm
  210. 210. Junctional Tachycardia
  211. 211. Premature Ventricular Complexes (PVC's) Note – Complexes not Contractions
  212. 212. PVC’s  Uniformed/Multiformed  Couplets/Salvos/Runs  Bigeminy/Trigeminy/Quadrageminy
  213. 213. Uniformed PVC’s
  214. 214. R on T Phenomena
  215. 215. Multiformed PVC’s
  216. 216. PVC Couplets
  217. 217. PVC Salvos and Runs
  218. 218. Bigeminy PVC’s
  219. 219. Trigeminy PVC’s
  220. 220. Quadrageminy PVC’s
  221. 221. Ventricular Escape Beats
  222. 222. Idioventricular Rhythm
  223. 223. Ventricular Tachycardia (VT)  Rate: 101-250 beats/min  Rhythm: P regular waves: absent  PR interval: none  QRS duration: > 0.12 sec. often difficult to differentiate between QRS and T wave Note: Monomorphic - same shape and amplitude
  224. 224. Ventricular Tachycardia (VT)
  225. 225. V Tach
  226. 226. Torsades de Pointes (TdeP)  Rate: 150-300 beats/min  Rhythm: P regular or irregular waves: none  PR interval: none  QRS duration: > 0.12 sec. gradual alteration in amplitude and direction of the QRS complexes
  227. 227. Torsades de Pointes (TdeP)
  228. 228. Ventricular Fibrillation (VF)  Rate: CNO as no discernible complexes  Rhythm: P rapid and chaotic waves: none  PR interval: none  QRS duration: none Note: Fine vs. coarse?
  229. 229. Ventricular Fibrillation (VF)
  230. 230. Ventricular Fibrillation (VF)
  231. 231. Asystole (Cardiac Standstill)  Rate: none  Rhythm: P none waves: none  PR interval: not measurable  QRS duration: absent
  232. 232. Asystole (Cardiac Standstill)
  233. 233. Asystole The Mother of all Bradycardias
  234. 234. Atrial Pacemaker (Single Chamber) pacemaker •Capture?
  235. 235. Ventricular Pacemaker (Single Chamber) pacemaker
  236. 236. Dual Paced Rhythm pacemaker
  237. 237. Pulseless Electrical Activity (PEA)  The absence of a detectable pulse and blood pressure  Presence of electrical activity of the heart as evidenced by ECG rhythm, but not VF or VT + = 0/0 mmHg
  238. 238. ventricular bigeminy  The ECG trace below shows ventricular bigeminy, in which every other beat is a ventricular ectopic beat. These beats are premature, wider, and larger than the sinus beats.
  239. 239. ventricular bigeminy
  240. 240. ventricular trigeminy;  The occurrence of more than one type of ventricular ectopic impulse morphology is evidence of multifocal ventricular ectopics. In this example, the ventricular ectopic beats are both wide and premature, but differ considerably in shape
  241. 241. ventricular trigeminy
  242. 242. ventricular trigeminy
  243. 243. MYOCARDIAL INFARACTION
  244. 244. Diagnosing a MI To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. 12-Lead ECG Rhythm Strip
  245. 245. ST Elevation One way to diagnose an acute MI is to look for elevation of the ST segment.
  246. 246. ST Elevation (cont) Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.
  247. 247. Anterior Myocardial Infarction If you see changes in leads V1 - V4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.
  248. 248. Putting it all Together Do you think this person is having a myocardial infarction. If so, where?
  249. 249. Interpretation Yes, this person is having an acute anterior wall myocardial infarction.
  250. 250. Putting it all Together Now, where do you think this person is having a myocardial infarction?
  251. 251. Inferior Wall MI This is an inferior MI. Note the ST elevation in leads II, III and aVF.
  252. 252. Putting it all Together How about now?
  253. 253. Anterolateral MI This person’s MI involves both the anterior wall (V2V4) and the lateral wall (V5-V6, I, and aVL)!
  254. 254. I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 The ST segment should start isoelectric except in V1 and V2 where it may be elevated
  255. 255. Characteristic changes in AMI      ST segment elevation over area of damage ST depression in leads opposite infarction Pathological Q waves Reduced R waves Inverted T waves
  256. 256. ST elevation hyperacute phase • Occurs in the early stages R ST P Q • Occurs in the leads facing the infarction • Slight ST elevation may be normal in V1 or V2
  257. 257. Deep Q wave • Only diagnostic change of myocardial infarction R ST • At least 0.04 seconds in duration P T Q • Depth of more than 25% of ensuing R wave
  258. 258. T wave changes • Late change R • Occurs as ST elevation is returning to normal ST P • Apparent in many leads T Q
  259. 259. Bundle branch block Anterior wall MI I II III aVR aVL aVF V1 V2 V3 Left bundle branch block V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
  260. 260. Sequence of changes in evolving AMI R R T R ST ST P P P QS T Q 1 minute after onset Q 1 hour or so after onset A few hours after onset R ST P P T Q A day or so after onset ST T P T Q Later changes Q A few months after AMI
  261. 261. Anterior infarction Anterior infarction I II III Left coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
  262. 262. Inferior infarction Inferior infarction I II III Right coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
  263. 263. Lateral infarction Lateral infarction I II III Left circumflex coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
  264. 264. Diagnostic criteria for AMI • • • • • Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias
  265. 265. Surfaces of the Left Ventricle  Inferior - underneath  Anterior - front  Lateral - left side  Posterior - back
  266. 266. Inferior Surface   Leads II, III and avF look UP from below to the inferior surface of the left ventricle Mostly perfused by the Right Coronary Artery
  267. 267. Inferior Leads – II – III – aVF
  268. 268. Anterior Surface    The front of the heart viewing the left ventricle and the septum Leads V2, V3 and V4 look towards this surface Mostly fed by the Left Anterior Descending branch of the Left artery
  269. 269. Anterior Leads – V2 – V3 – V4
  270. 270. Lateral Surface    The left sided wall of the left ventricle Leads V5 and V6, I and avL look at this surface Mostly fed by the Circumflex branch of the left artery
  271. 271. Lateral Leads V5, V6, I, aVL
  272. 272. Posterior Surface    Posterior wall infarcts are rare Posterior diagnoses can be made by looking at the anterior leads as a mirror image. Normally there are inferior ischaemic changes Blood supply predominantly from the Right Coronary Artery
  273. 273. RIGHT Inferior II, III, AVF Posterior V1, V2, V3 LEFT Antero-Septal V1,V2, V3,V4 Lateral I, AVL, V5, V6
  274. 274. ST Segment Elevation The ST segment lies above the isoelectric line:  Represents myocardial injury  It is the hallmark of Myocardial Infarction  The injured myocardium is slow to repolarise and remains more positively charged than the surrounding areas  Other causes to be ruled out include pericarditis and ventricular aneurysm
  275. 275. ST-Segment Elevation
  276. 276. T wave inversion in an evolving MI
  277. 277. The ECG in ST Elevation MI
  278. 278. The Hyper-acute Phase Less than 12 hours     “ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction” (Quinn, 1996) The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal Usually occurs within a few hours of infarction May vary in severity from 1mm to ‘tombstone’ elevation
  279. 279. The Fully Evolved Phase 24 - 48 hours from the onset of a myocardial infarction  ST segment elevation is less (coming back to baseline).  T waves are inverting.  Pathological Q waves are developing (>2mm)
  280. 280. The Chronic Stabilised Phase  Isoelectric ST segments  T waves upright.  Pathological Q waves.  May take months or weeks.
  281. 281. Reciprocal Changes  Changes occurring on the opposite side of the myocardium that is infarcting
  282. 282. Reciprocal Changes ie S-T depression in some leads in MI
  283. 283. Non ST Elevation MI  Commonly ST depression and deep T wave inversion  History of chest pain typical of MI  Other autonomic nervous symptoms present  Biochemistry results required to diagnose MI  Q-waves may or may not form on the ECG
  284. 284. Changes in NSTEMI
  285. 285. + + + + _ _ _ _ _ _ _ _ _ + + + + + + + + + _ + __ + + Action potentials and electrophysiology + Na _ _ _ _ _ _ _ + + + + + _ + + _ _ + + + + + _ _ _ _ _ _ + _ _ _ + + + + + _ + + _ + + + + + _ _ _ _ _ _ + K _ _ _ _ _ + + _ _ + _ + + + + + + _ _ _ _ _ _ _ _ _ + + + + + + + K Resting Depolarised Ca + Na ++ in(slow) in K ++ Ca + out Plateau Repolarised 3.2
  286. 286. LVH and strain pattern Ventricular Strain Strain is often associated with ventricular hypertrophy Characterized by moderate depression of the ST segment.
  287. 287. Non-ischaemic ST segment changes: in patient taking digoxin (top) and in patient with left ventricular hypertrophy (bottom) Channer, K. et al. BMJ 2002;324:1023-1026 Copyright ©2002 BMJ Publishing Group Ltd.
  288. 288. Examples of T wave abnormalities Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026
  289. 289. 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
  290. 290. Bundle Branch Block
  291. 291. Left Bundle Branch Block  Widened QRS (> 0.12 sec, or 3 small squares)  Two R waves appear – R and R’ in V5 and V6, and sometimes Lead I, AVL.  Have predominately negative QRS in V1, V2, V3 (reciprocal changes).
  292. 292. Right Bundle Branch Block
  293. 293. Where’s the MI?
  294. 294. Where’s the MI?
  295. 295. Where’s the MI?
  296. 296. Final one…
  297. 297. Which one is more tachycardic during this exercise test?
  298. 298. Any Questions?
  299. 299. I hope you have found this session useful.

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