electrocardiogram

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  • It is now recognized that unstable angina (UA), non-Q-wave myocardial infarction (NQMI), and ST-segment elevation myocardial infarction (STE-MI) are all parts of the spectrum of clinical manifestations of acute coronary syndrome (ACS). The older terminology has now been replaced with terminology that divides ACS into non-ST-elevation ACS (NSTE-ACS) and ST-segment-elevation. All the slides in this teaching set deal with NSTE-ACS.
  • electrocardiogram

    1. 1. Fore word <ul><li>Dear Doctor, </li></ul><ul><li>This ECG presentation is an attempt to illustrate some of the </li></ul><ul><li>fundamentals in ECG interpretation. We have advanced level </li></ul><ul><li>courses also on ECG. In addition, we have several educational </li></ul><ul><li>resource materials in the form of PowerPoint based CD-Rom </li></ul><ul><li>presentations. Also are available several philosophical and </li></ul><ul><li>religious works of all time great masters, translated into simple </li></ul><ul><li>English and presented as PowerPoint slide shows on CD-Rom. </li></ul><ul><li>A list of such materials is appended. Pl. request for your copy of </li></ul><ul><li>any of them at a nominal cost of Rs.100/ per CD. </li></ul><ul><li>Wishing You a happy learning experience !! </li></ul>
    2. 2. The Objectives <ul><li>To sensitize doctors towards learning ECG </li></ul><ul><li>To explain the clinical concepts involved </li></ul><ul><li>To illustrate them with diagrams, drawings, tables </li></ul><ul><li>To show real life ECG charts and interpret </li></ul><ul><li>Differential diagnosis on similar looking ECG changes </li></ul><ul><li>Spot light on ECG and Ischemic Heart Disease </li></ul><ul><li>Not Included are </li></ul><ul><li>Electrophysiological basis of ECG changes </li></ul><ul><li>Details on arrhythmias, conduction disorders </li></ul><ul><li>Sensitivity and specificity of different patterns </li></ul><ul><li>Atypical presentations, combination of pathologies </li></ul><ul><li>Scoring systems and predictive values </li></ul>
    3. 3. ECG Resources consulted <ul><li>Alan Lindsay’s Cyber ECG learning center (on line) </li></ul><ul><li>Interactive Electrocardiography by Novartis – CD Rom </li></ul><ul><li>Frank H Netter's medical drawings </li></ul><ul><li>American Heart Association (AHA) sites </li></ul><ul><li>American Heart Lung and Blood Institute (AHLBI) sites </li></ul><ul><li>J.G. Webster’s Cyber ECG library </li></ul><ul><li>Braunwald’s text book of cardiology - 6 ed. 2004 </li></ul><ul><li>Goldberger’s text book on ECG </li></ul><ul><li>Our personal collection of interesting ECGs </li></ul>
    4. 4. ECG Graph Paper X- Axis time in seconds Y- Axis Amplitude in mill volts
    5. 5. <ul><li>X-Axis represents time - Scale X-Axis – 1 mm = 0.04 sec </li></ul><ul><li>Y-Axis represents voltage - Scale Y-Axis – 1 mm = 0.1 mV </li></ul><ul><li>One big square on X-Axis = 0.2 sec (big box) </li></ul><ul><li>Two big squares on Y-Axis = 1 milli volt (mV) </li></ul><ul><li>Each small square is 0.04 sec (1 mm in size) </li></ul><ul><li>Each big square on the ECG represents 5 small squares </li></ul><ul><li>= 0.04 x 5 = 0.2 seconds </li></ul><ul><li>5 such big squares = 0.2 x 5 = 1sec = 25 mm </li></ul><ul><li>One second is 25 mm or 5 big squares </li></ul><ul><li>One minute is 5 x 60 = 300 big squares </li></ul>ECG Graph Paper
    6. 6. ECG Complex P wave PR Interval QRS complex ST segment T Wave QT Interval RR Interval
    7. 7. ECG Complex <ul><li>P Wave is Atrial contraction – Normal 0.12 sec </li></ul><ul><li>PR interval is from the beginning of P wave to the beginning of QRS – Normal up to 0.2 sec </li></ul><ul><li>QRS is Ventricular contraction –Normal 0.08 sec </li></ul><ul><li>ST segment – Normal Isoelectic (electric silence) </li></ul><ul><li>QT Interval – From the beginning of QRS to the end of T wave – Normal – 0.40 sec </li></ul><ul><li>RR Interval – One Cardiac cycle 0.80 sec </li></ul>
    8. 8. Identify the ECG Complex 1 2 3 4 5 6 7 8
    9. 9. <ul><li>P wave : Atrial contraction 0.12 sec (3) </li></ul><ul><li>PR interval – P to begin. of QRS 0.20 sec (5) </li></ul><ul><li>QRS complex - Ventricular 0.08 sec (2) </li></ul><ul><li>ST segment - Electrical silence Isoelectric </li></ul><ul><li>T wave - repolarization 0.12 sec (3) </li></ul><ul><li>QRS interval – Ventricular cont. 0.08 sec (2) </li></ul><ul><li>QT interval - From Q to T end 0.40 sec (10) </li></ul><ul><li>TP segment - Electrical silence 0.20 sec (5) </li></ul>Identify the ECG Complex The Wave or Interval Duration # of Boxes
    10. 10. Let us Identify the waves 1 2 3 4 5 6 7 8
    11. 11. <ul><li>P wave – Atrial contraction = 0.12 sec (3 small boxes) </li></ul><ul><li>PR Interval – P + AV delay = 0.20 sec (5 small boxes) </li></ul><ul><li>Q wave – Septal = < 3 mm, < 0.04 sec (1 small box) </li></ul><ul><li>R wave – Ventricular contraction < 15 mm </li></ul><ul><li>S wave – complimentary to R < 15 mm </li></ul><ul><li>ST segment – Isoelectric – decides our fate </li></ul><ul><li>T wave – ventricular repolarization – friend of ST </li></ul><ul><li>TP segment – ventricular relaxation – shortened in tachycardia </li></ul>Let us Identify the waves
    12. 12. Important Precautions <ul><li>Correct Lead placement and good contact </li></ul><ul><li>Proper earth connection, avoid other gadgets </li></ul><ul><li>Deep inspiration record of L3, aVF </li></ul><ul><li>Compare serial ECGs if available </li></ul><ul><li>Relate the changes to Age, Sex, Clinical history </li></ul><ul><li>Consider the co-morbidities that may effect ECG </li></ul><ul><li>Make a xerox copy of the record for future use </li></ul><ul><li>Interpret systematically to avoid errors </li></ul>
    13. 13. Normal ECG
    14. 14. Normal ECG <ul><li>Standardization – 10 mm (2 boxes) = 1 mV </li></ul><ul><li>Double and half standardization if required </li></ul><ul><li>Sinus Rhythm – Each P followed by QRS, R-R constant </li></ul><ul><li>P waves – always examine for in L2, V1, L1 </li></ul><ul><li>QRS positive in L1, L2, L3, aVF and aVL. – Neg in aVR </li></ul><ul><li>QRS is < 0.08 narrow, Q in V5, V6 < 0.04, < 3 mm </li></ul><ul><li>R wave progression from V1 to V6, QT interval < 0.4 </li></ul><ul><li>Axis normal – L1, L3, and aVF all will be positive </li></ul><ul><li>ST Isoelectric, T waves ↑, Normal T ↓ in aVR,V1, V2 </li></ul>
    15. 15. Pediatric ECG
    16. 16. <ul><li>This is the ECG of a 6 year old child </li></ul><ul><li>Heart rate is 100 – Normal for the age </li></ul><ul><li>See V1 + V5 R >> 35 – Not LVH – Normal </li></ul><ul><li>T ↓ in V1, V2, V3 – Normal in child </li></ul><ul><li>Base line disturbances in V5, V6 – due to movement by child </li></ul>Pediatric ECG
    17. 17. Juvenile ECG
    18. 18. Be aware of normal ECG <ul><li>Normal Resting ECG – cannot exclude disease </li></ul><ul><li>Ischemia may be covert – supply / demand equation </li></ul><ul><li>Changes of MI take some time to develop in ECG </li></ul><ul><li>Mild Ventricular hypertrophy - not detectable in ECG </li></ul><ul><li>Some of the ECG abnormalities are non specific </li></ul><ul><li>Single ECG cannot give progress – Need serial ECGs </li></ul><ul><li>ECG changes not always correlate with Angio results </li></ul><ul><li>Paroxysmal events will be missed in single ECG </li></ul>
    19. 19. Normal Variations in ECG <ul><li>May have slight left axis due to rotation of heart </li></ul><ul><li>May have high voltage QRS – simulating LVH </li></ul><ul><li>Mild slurring of QRS but duration < 0.09 </li></ul><ul><li>J point depression, early repolarization </li></ul><ul><li>T inversions in V2, V3 and V4 – Juvenile T ↓ </li></ul><ul><li>Similarly in women also T↓ </li></ul><ul><li>Low voltages in obese women and men </li></ul><ul><li>Non cardiac causes of ECG changes may occur </li></ul>
    20. 20. Early Repolarization <ul><li>This ECG has all normal features </li></ul><ul><li>The ST-T (J) Junction point is </li></ul><ul><li>elevated. T waves are tall, May be inverted in LIII, The ST </li></ul><ul><li>segment initial portion is concave. This does not signify Ischemia </li></ul>
    21. 21. Pseudo Normalization Before Chest pain During Chest pain Chest pain Relieved T ↓ T ↓ T ↑
    22. 22. Rate Determination Next QRS QRS
    23. 23. Rate Determination BRADY T ACHY NORMA L No. of Big Boxes R – R Interval Rate Cal. Rate One 0.2 sec 60 ÷ 0.2 300 Two 0.4 sec 60 ÷ 0.4 150 Three 0.6 sec 60 ÷ 0.6 100 Four 0.8 sec 60 ÷ 0.8 75 Five 1.0 sec 60 ÷ 1.0 60 Six 1.2 sec 60 ÷ 1.2 50 Seven 1.4 sec 60 ÷ 1.4 43 Eight 1.6 sec 60 ÷ 1.6 37
    24. 24. What is the Heart Rate ? Answer on next slide
    25. 25. <ul><li>To find out the heart rate we need to know </li></ul><ul><ul><li>The R-R interval in terms of # of big squares </li></ul></ul><ul><ul><li>If the R-R intervals are constant </li></ul></ul><ul><li>In this ECG the R-R intervals are constant </li></ul><ul><li>R-R are approximately 3 big squares apart </li></ul><ul><li>So the heart rate is 300 ÷ 3 = 100 </li></ul>What is the Heart Rate ?
    26. 26. What is the Heart Rate ? Answer on next slide
    27. 27. What is the Heart Rate ? <ul><li>To find out the heart rate we need to know </li></ul><ul><ul><li>The R-R interval in terms of # of big squares </li></ul></ul><ul><ul><li>If the R-R intervals are constant </li></ul></ul><ul><li>In this ECG the R-R intervals are constant </li></ul><ul><li>R-R are approximately 4.5 big squares apart </li></ul><ul><li>So the heart rate is 300 ÷ 4.5 = 67 </li></ul>
    28. 28. What is the Heart Rate ? Answer on next slide
    29. 29. What is the Heart Rate ? <ul><li>To find out the heart rate we need to know </li></ul><ul><ul><li>The R-R interval in terms of # of Big Squares </li></ul></ul><ul><ul><li>If the R-R intervals are constant </li></ul></ul><ul><li>In this ECG the R-R intervals are not constant </li></ul><ul><li>R-R are varying from 2 boxes to 3 boxes </li></ul><ul><li>It is an irregular rhythm – Sinus arrhythmia </li></ul><ul><li>Heart rate is 300 ÷ 2 to 3 = 150 to 100 approx </li></ul>
    30. 30. + + + - - - ECG Bipolar Limb Leads R L F R F L
    31. 31. <ul><li>Standard ECG is recorded in 12 leads </li></ul><ul><li>Six Limb leads – L1, L2, L3, aVR, aVL, aVF </li></ul><ul><li>Six Chest Leads – V1 V2 V3 V4 V5 and V6 </li></ul><ul><li>L1, L2 and L3 are called bipolar leads </li></ul><ul><li>L1 between LA and RA </li></ul><ul><li>L2 between LF and RA </li></ul><ul><li>L3 between LF and LA </li></ul>ECG Bipolar Limb Leads
    32. 32. ECG Unipolar Limb Leads + + + Lead aVR Lead aVL Lead aVF R L F
    33. 33. <ul><li>Standard ECG is recorded in 12 leads </li></ul><ul><li>Six Limb leads – L1, L2, L3, aVR, aVL, aVF </li></ul><ul><li>Six Chest Leads – V1 V2 V3 V4 V5 and V6 </li></ul><ul><li>aVR, aVL, aVF are called unipolar leads </li></ul><ul><li>aVR – from Right Arm Positive </li></ul><ul><li>aVL – from Left Arm Positive </li></ul><ul><li>aVF – from Left Foot Positive </li></ul>ECG Unipolar Limb Leads
    34. 34. ECG Chest Leads
    35. 35. <ul><li>Precardial (chest) Lead Position </li></ul><ul><li>V1 Fourth ICS, right sternal border </li></ul><ul><li>V2 Fourth ICS, left sternal border </li></ul><ul><li>V3 Equidistant between V2 and V4 </li></ul><ul><li>V4 Fifth ICS, left Mid clavicular Line </li></ul><ul><li>V5 Fifth ICS Left anterior axillary line </li></ul><ul><li>V6 Fifth ICS Left mid axillary line </li></ul>ECG Chest Leads
    36. 36. Atrial Ectopics APC APC APC APC
    37. 37. <ul><li>Note the premature (ectopic) beats marked as </li></ul><ul><li>APC (Atrial Premature Contractions) </li></ul><ul><li>These occurred before the next expected QRS complex (premature) </li></ul><ul><li>Each APC has a P wave preceding the QRS of that beat – So impulse has originated in the atria </li></ul><ul><li>The QRS duration is normal < 0.08, not wide </li></ul>Atrial Ectopics
    38. 38. Atrial Fibrillation
    39. 39. <ul><li>Note ECG changes of Atrial Fibrillation </li></ul><ul><li>The heart rate is irregularly irregular </li></ul><ul><li>The R-R intervals are very different from beat to beat </li></ul><ul><li>There is narrow QRS tachycardia </li></ul><ul><li>There are no P waves – instead small fibrillary waves called ‘ f ’ waves are seen </li></ul>Atrial Fibrillation
    40. 40. Look at this ECG
    41. 41. Atrial Flutter Heart rate Rhythm P wave PR interval QRS in sec
    42. 42. <ul><li>Note ECG changes of Atrial Flutter </li></ul><ul><li>The heart rate is regular or variable </li></ul><ul><li>Atrial rate is 300 per minute </li></ul><ul><li>All P waves are not conducted to ventricles </li></ul><ul><li>The R-R intervals very depending on the AV conduction ratio </li></ul><ul><li>The QRS is narrow – < 0.12 sec </li></ul><ul><li>The P waves have a ‘saw toothed’ appearance called ‘F’ waves </li></ul>Atrial Flutter
    43. 43. Ventricular Ectopics VPC VPC VPC VPC
    44. 44. <ul><li>Note the premature (ectopic) beats marked as VPC (Ventricular Premature Contractions) </li></ul><ul><li>These occurred before the next expected QRS complex (premature) </li></ul><ul><li>Each VPC has no definite P wave preceding the QRS of that beat – So impulse has originated in the ventricles </li></ul><ul><li>The QRS complexes are wide with abnormal duration of > 0.12 and their shapes are bizarre </li></ul>Ventricular Ectopics
    45. 45. Ventricular Tachycardia
    46. 46. <ul><li>A wide QRS tachycardia is VT until proved </li></ul><ul><li>otherwise. Features suggesting VT include </li></ul><ul><li>Evidence of AV dissociation </li></ul><ul><li>Independent P waves (shown by arrows here) </li></ul><ul><li>Beat to beat variability of the QRS morphology </li></ul><ul><li>Very wide complexes (> 0.14 ms) </li></ul><ul><li>The QRS is similar to that in ventricular ectopics </li></ul><ul><li>Concordance (chest leads all positive or negative) </li></ul>Ventricular Tachycardia
    47. 47. The Six Limb Leads INFERIOR LEFT RIGHT FRONTAL PLANE
    48. 48. The 12 Camera Photography <ul><li>There SIX cameras photographing frontal plane </li></ul><ul><li>Lead 1 and aVL are horizontal left sided cameras </li></ul><ul><li>Lead 2, aVF, Lead 3 are vertical inferior cameras </li></ul><ul><li>aVR is horizontal Rt. sided camera (cavitary lead) </li></ul><ul><li>Lateral Leads – L1, aVL, V5 and V6 </li></ul><ul><li>Inferior Leads – L2, aVF, and L3 leads </li></ul><ul><li>Septal Leads – V1 and V2 </li></ul><ul><li>Anterior Leads – V3 and V4 </li></ul><ul><li>Anterio-lateral leads – V3, V4, V5, V6, L1 and aVL </li></ul>
    49. 49. The Six Chest Leads TRANSVERSE PLANE
    50. 50. <ul><li>There SIX cameras photographing in transverse or anterio-posterior plane </li></ul><ul><ul><li>V1 and V2 record events of septum </li></ul></ul><ul><ul><li>V3 and V4 record events of the anterior wall </li></ul></ul><ul><ul><li>V5 and V6 record events of left lateral wall </li></ul></ul><ul><li>To record right side events V2R to V6R are needed – In dextrocardia, in RV infarction </li></ul>The 12 Camera Photography
    51. 51. Cardiac Impulse
    52. 52. <ul><li>Cardiac impulse originates in the SA node </li></ul><ul><li>Traverses the atria simultaneously – no special conduction wires in atria – so the delay </li></ul><ul><li>Reaches AV node – the check post – so delay </li></ul><ul><li>Enters bundle of His and branches – through specialized conducting wires called Purkinje network - activates both ventricles – quick QRS </li></ul><ul><li>First the septum from L to R, then right ventricle and then the left ventricle and finally the apex </li></ul><ul><li>Then the ventricles recover for next impulse </li></ul>Cardiac Impulse
    53. 53. QRS Axis SE NE NW SW
    54. 54. QRS Axis <ul><li>The QRS electrical (vector) axis can have 4 directions </li></ul><ul><li>Normal Axis - when it is downward and to the left – southeast quadrant – from -30 to +90 degrees </li></ul><ul><li>Right Axis – when it is downward and to the right – southwest quadrant – from +90 to 180 degrees </li></ul><ul><li>Left Axis – when it is upward and to the left – Northeast quadrant –from -30 to -90 degrees </li></ul><ul><li>Indeterminate Axis – when it is upward & to the right – Northwest quadrant – from -90 to +180 </li></ul>
    55. 55. Axis Determination NORMAL RIGHT LEFT MEET LEAVE ALL UPRIGHT
    56. 56. Axis Determination Axis L I L III or aVF TIP Normal Positive Positive Both Up Right Negative Positive Meet Left Positive Negative Leave Indeterminate Negative Positive Meet
    57. 57. What is the Axis ? LEAD 1 LEAD 2 LEAD 3 aVR aVL aVF
    58. 58. ECG With Normal Axis <ul><li>Note the QRS voltages are positive and upright in the leads - L1, L2, L3 and aVF </li></ul><ul><li>L2, L3 and aVF tell that it is downward </li></ul><ul><li>L1, aVL tell that it is to the left </li></ul><ul><li>Downward and leftward is Normal Axis </li></ul><ul><li>Normal QRS axis </li></ul>
    59. 59. LEAD 1 LEAD 2 LEAD 3 What is the Axis ?
    60. 60. ECG With Right Axis <ul><li>Note the QRS voltages are positive and upright in leads L2, L3 </li></ul><ul><li>Negative in Lead 1 </li></ul><ul><li>L2, L3 tell that it is downward </li></ul><ul><li>L1 tells that it is not to the left but to right </li></ul><ul><li>Downward and rightward is Right Axis </li></ul><ul><li>See the Right –Meet criterion QRS in L1 and L3 meet </li></ul><ul><li>Right Axis Deviation - RAD </li></ul>
    61. 61. LEAD 1 LEAD 2 LEAD 3 aVR aVL aVF What is the Axis ?
    62. 62. ECG With Left Axis <ul><li>Note the QRS voltages are positive and upright in leads L1and aVL </li></ul><ul><li>Negative in L2, L3 and aVF </li></ul><ul><li>L1, aVL tell that it is leftward </li></ul><ul><li>L2, L3, and aVF tell that it is not down ward - instead it is upward </li></ul><ul><li>Upward and Leftward is Left Axis </li></ul><ul><li>See the Left - Leave criterion QRS in L1 and L3 leave each other </li></ul><ul><li>Left Axis Deviation - LAD </li></ul>
    63. 63. Atrial Waves
    64. 64. Right Atrial Enlargement
    65. 65. Right Atrial Enlargement P wave voltage is 4 boxes or 4 mm
    66. 66. <ul><li>Always examine Lead 2 for RAE </li></ul><ul><li>Tall Peaked P Waves, Arrow head P waves </li></ul><ul><li>Amplitude is 4 mm ( 0.4 mV) - abnormal </li></ul><ul><li>Pulmonary Hypertension, Mitral Stenosis </li></ul><ul><li>Tricuspid Stenosis, Regurgitation </li></ul><ul><li>Pulmonary Valvular Stenosis </li></ul><ul><li>Pulmonary Embolism </li></ul><ul><li>Atrial Septal Defect with L to R shunt </li></ul>Right Atrial Enlargement
    67. 67. Atrial Enlargements RIGHT ATRIAL ENLARGEMENT LEFT ATRIAL ENLARGEMENT
    68. 68. Left Atrial Enlargement
    69. 69. Left Atrial Enlargement P wave duration is 4 boxes-0.04 x 4 = 0.16
    70. 70. <ul><li>Always examine V 1 and Lead 1 for LAE </li></ul><ul><li>Biphasic P Waves, Prolonged P waves </li></ul><ul><li>P wave 0.16 sec, ↑ Downward component </li></ul><ul><li>Systemic Hypertension, MS and or MR </li></ul><ul><li>Aortic Stenosis and Regurgitation </li></ul><ul><li>Left ventricular hypertrophy with dysfunction </li></ul><ul><li>Atrial Septal Defect with R to L shunt </li></ul>Left Atrial Enlargement
    71. 71. Ventricular Hypertrophy <ul><li>Ventricular Muscle Hypertrophy </li></ul><ul><li>QRS voltages in V1 and V6, L 1 and aVL </li></ul><ul><li>We may have to record to ½ standardization </li></ul><ul><li>T wave changes opposite to QRS direction </li></ul><ul><li>Associated Axis shifts </li></ul><ul><li>Associated Atrial hypertrophy </li></ul>
    72. 72. Right Ventricular Hypertrophy
    73. 73. <ul><li>Tall R in V1 with R >> S, or R/S ratio > 1 </li></ul><ul><li>Deep S waves in V4, V5 and V6 </li></ul><ul><li>The DD is RVH, Posterior MI, Anti-clock wise rotation of Heart </li></ul><ul><li>Associated Right Axis Deviation, RAE </li></ul><ul><li>Deep T inversions in V1, V2 and V3 </li></ul><ul><li>Absence of Inferior MI </li></ul>Right Ventricular Hypertrophy
    74. 74. Is there any hypertrophy ?
    75. 75. <ul><li>Criteria of RVH </li></ul><ul><li>Tall R in V1 with R >> S, or R/S ratio > 1 </li></ul><ul><li>Deep S waves in V4, V5 and V6 </li></ul><ul><li>The DD is RVH, Posterior MI, Rotation </li></ul><ul><li>Associated Right Axis Deviation, RAE </li></ul><ul><li>Deep T inversion in V1, V2 and V3 </li></ul><ul><li>Cause of RVH </li></ul><ul><li>Long standing Mitral Stenosis </li></ul><ul><li>Pulmonary Hypertension of any cause </li></ul><ul><li>VSD or ASD with initial L to R shunt </li></ul><ul><li>Congenital heart with RV over load </li></ul><ul><li>Tricuspid regurgitation, Pulmonary stenosis </li></ul>Criteria and Causes of LVH
    76. 76. What is in this ECG ?
    77. 77. ECG OF MS with RVH, RAE <ul><li>Classical changes seen are </li></ul><ul><li>Right ventricular hypertrophy </li></ul><ul><li>Right axis deviation </li></ul><ul><li>Right Bundle Branch Block </li></ul><ul><li>P – Pulmonale - Right Atrial enlargement </li></ul><ul><li>P – Mitrale – Left Atrial enlargement </li></ul><ul><li>If Atrial Fibrillation develops – ‘P’ disappears </li></ul>
    78. 78. Left Ventricular Hypertrophy
    79. 79. <ul><li>High QRS voltages in limb leads </li></ul><ul><li>R in Lead I + S in Lead III > 25 mm </li></ul><ul><li>S in V1 + R in V5 > 35 mm </li></ul><ul><li>R in aVL > 11 mm or S V3 + R aVL > 24 ♂, > 20 ♀ </li></ul><ul><li>Deep symmetric T inversion in V4, V5 & V6 </li></ul><ul><li>QRS duration > 0.09 sec </li></ul><ul><li>Associated Left Axis Deviation, LAE </li></ul><ul><li>Cornell Voltage criteria, Estes point scoring </li></ul>Left Ventricular Hypertrophy
    80. 80. What is in this ECG ?
    81. 81. <ul><li>Causes of LVH </li></ul><ul><li>Pressure overload - Systemic Hypertension, Aortic Stenosis </li></ul><ul><li>Volume overload - AR or MR - dilated cardiomyopathy </li></ul><ul><li>VSD - cause both right & left ventricular volume overload </li></ul><ul><li>Hypertrophic cardiomyopathy – No pressure or volume overload </li></ul><ul><li>Criteria of LVH </li></ul><ul><li>High QRS voltages in limb leads </li></ul><ul><li>R in Lead I + S in Lead III > 25 mm or S in V1 + R in V5 > 35 mm </li></ul><ul><li>R in aVL > 11 mm or S V3 + R aVL > 24 ♂, > 20 ♀ </li></ul><ul><li>Deep symmetric T inversion in V4, V5 & V6 </li></ul><ul><li>QRS duration > 0.09 sec, Associated Left Axis Deviation, LAE </li></ul>Causes and Criteria of LVH
    82. 82. LVH Types Volume Over Load Pressure Over Load
    83. 83. <ul><li>Pressure Over load </li></ul><ul><li>Like in hypertension, IHD </li></ul><ul><li>LV strain pattern – ST depression with T ↓ </li></ul><ul><li>in V5, V6, L1 and aVL leads </li></ul><ul><li>Volume Over load </li></ul><ul><li>Like in Mitral or Aortic regurgitation </li></ul><ul><li>Shows prominent positive T waves in </li></ul><ul><li>V5, V6, L1 and aVL </li></ul>LVH Types
    84. 84. Cardiac Conduction
    85. 85. Causes of Conduction Block <ul><li>Clinically normal individual </li></ul><ul><li>CAD, Acute MI, Remote MI, Pulmonay embolism </li></ul><ul><li>Aortic stenosis, SABE + abscesses in conduction </li></ul><ul><li>Cardiac trauma, Hyperkalemia, Rapid heart rates </li></ul><ul><li>Lenegre's disease (idiopathic fibrosis of conduction) </li></ul><ul><li>Lev's disease (calcification of the cardiac skeleton) </li></ul><ul><li>Cardiomyopathy - Dilated and Hypertrophic </li></ul><ul><li>Infiltrative Tumor – Chaga’s disease </li></ul><ul><li>Myxedema, Amyloidosis, Ventricular hypertrophy </li></ul>
    86. 86. Complete RBBB
    87. 87. Complete RBBB <ul><li>Complete RBBB has a QRS duration > 0.12 sec </li></ul><ul><li>R' wave in lead V1 (usually see rSR' complex) </li></ul><ul><li>S waves in leads I, aVL, V6, R wave in lead aVR </li></ul><ul><li>QRS axis in RBBB is -30 to +90 (Normal) </li></ul><ul><li>Incomplete RBBB has a QRS duration of 0.10 to 0.12 sec with the same QRS features as above </li></ul><ul><li>The &quot;normal&quot; ST-T waves in RBBB should be oriented opposite to the direction of the QRS </li></ul>
    88. 88. Interpret this ECG
    89. 89. Complete LBBB
    90. 90. Complete LBBB <ul><li>Complete LBBB has a QRS duration > 0.12 sec </li></ul><ul><li>Prominent S waves in lead V1, R in L I, aVL, V6 </li></ul><ul><li>Usually broad, Bizarre R waves are seen, M pattern </li></ul><ul><li>Poor R progression from V1 to V3 is common. </li></ul><ul><li>The &quot;normal&quot; ST-T waves in LBBB should be oriented opposite to the direction of the QRS </li></ul><ul><li>Incomplete LBBB looks like LBBB but QRS duration is 0.10 to 0.12 sec, with less ST-T change. </li></ul><ul><li>This is often a progression of LVH changes. </li></ul>
    91. 91. Interpret This ECG
    92. 92. Rate Dependent LBBB
    93. 93. <ul><li>Complete LBBB is sometimes rate dependent </li></ul><ul><li>See the LBBB pattern when the HR is 75 per minute </li></ul><ul><li>But, LBBB pattern disappeared when the HR is < 50 </li></ul><ul><li>Some times the LBBB appears and disappears with out any change in heart rate. This is called stuttering LBBB. It signifies underlying Ischemia. </li></ul><ul><li>Appearance of new LBBB in a patient with chest pain is enough evidence of MI. It presents primary T changes </li></ul>Rate Dependent LBBB
    94. 94. Blood Supply of Heart LCA RCA LAD LCX RCA
    95. 95. <ul><li>Heart has four surfaces </li></ul><ul><li>Anterior surface – LAD, Left Circumflex (LCx) </li></ul><ul><li>Left lateral surface – LCx, partly LAD </li></ul><ul><li>Inferior surface – RCA, LAD terminal portion </li></ul><ul><li>Posterior surface – RCA, LCx branches </li></ul><ul><li>Rt. and Lt. coronary arteries arise from aorta </li></ul><ul><li>They are 2.5 mm at origin, 0.5 mm at the end </li></ul><ul><li>Coronary arteries fill during diastole </li></ul><ul><li>Flow - epicardium to endocardium – poverty/plenty </li></ul>Blood Supply of Heart
    96. 96. Ischemia, Injury & Infarction <ul><li>Ischemia produces ST segment depression with or without T inversion </li></ul><ul><li>Injury causes ST segment elevation with or without loss of R wave voltage </li></ul><ul><li>Infarction causes deep Q waves with loss of R wave voltage. </li></ul>Myocardial Ischemia Myocardial Injury Myocardial Infarction
    97. 97. Ischemia and Infarction TRANSMURAL Injury ST Elevation
    98. 98. Ischemic Heart Disease (IHD) Blood supply Sub-endocardial Transmural Ischemia Transient loss Stable Angina Variant Angina Infarction Persistent loss NSTEMI ACS STEMI ACS ST Segment Depressed Elevated
    99. 99. Types of Angina CHRONIC STABLE ANGINA
    100. 100. Types of Angina <ul><li>Chronic Stable Angina – Dynamic occlusion + Micro vascular dysfunction – Progressive </li></ul><ul><li>Micro vascular Angina – No flow limiting stenosis – Angio normal – less severe IHD </li></ul><ul><li>Unstable Angina – Dynamic occlusion + Micro vascular dysfunction + Active Thromb </li></ul><ul><li>Prinzemetal Angina – Occlusive spasm, No Micro vascular dys, No thrombus – ST ↑ </li></ul>
    101. 101. Micro Vascular Angina
    102. 102. <ul><li>Normal Coronary blood flow by angiogram </li></ul><ul><li>No significant CAD in epicardial blood vessels </li></ul><ul><li>Cardiac micro circulation is at fault </li></ul><ul><li>Poor collateral connections – younger age </li></ul><ul><li>More common in women – Syndrome X </li></ul><ul><li>ECG or TMT show ST - T changes repeatedly </li></ul><ul><li>Patient will be symptomatic for IHD </li></ul>Micro Vascular Angina
    103. 103. ST Segment Depression <ul><li>Upward sloping depression of ST segment is not indicative of IHD </li></ul><ul><li>It is called J point depression or sagging ST seg </li></ul><ul><li>Downward slopping or Horizontal depression of ST segment leading to T↓is significant of IHD </li></ul>
    104. 104. Lateral Wall Ischemia <ul><li>Note the classical ischemic ST depressions </li></ul><ul><li>ST ↓ are seen in V4,V5,V6 – lateral wall </li></ul><ul><li>His ST segments retuned to base line after sublingual nitroglycerine </li></ul><ul><li>His pain is precipitated by effort </li></ul><ul><li>Notice the tachycardia – heart rate = 140 </li></ul>
    105. 105. T wave inversion
    106. 106. <ul><li>Deep symmetric inverted T waves </li></ul><ul><li>In more than 2 precardial leads </li></ul><ul><li>85% of the patients with such T wave ↓had > 75% stenosis of the coronary artery </li></ul><ul><li>T wave ↓ are significantly associated with MI or death during follow up </li></ul>T Wave Inversion
    107. 107. Acute Coronary Syndromes Minor Plaque Disruption Non-Occlusive Thrombus Occlusive Thrombus Myocardial Infarction or Sudden Cardiac Death Asymptomatic Unstable Angina or Non-Q-MI Major Plaque Disruption Occlusive Thrombus Non-Vulnerable Atherosclerotic Plaque Vulnerable Atherosclerotic Plaque
    108. 108. ACUTE CORONARY SYNDROMES No ST Elevation ST Elevation Unstable Angina NQMI QWMI Myocardial Infarction NSTEMI
    109. 109. The Plaque – Clinical Effects Nature of the Plaque Clinical Presentation Picture Stable Plaque Silent or Stable Angina Vulnerable Plaque Stable Angina A Minor Plaque Disruption Unstable Angina B Major Plaque Rupture USA / NSTEMI C Non Occlusive Thrombus NSTEMI or STEMI D Occlusive Thrombus STEMI or Sudden Death
    110. 110. Pathogenesis of ACS <ul><li>Sequence of events </li></ul><ul><li>Plaque Rupture </li></ul><ul><li>Platelet Adhesion </li></ul><ul><li>Platelet Activation </li></ul><ul><li>Platelet Aggregation </li></ul><ul><li>Thrombotic Occlusion </li></ul>Anti-platelet drugs Platelet rupture Platelet Adhesion Platelet Activation Platelet Aggregation Thrombotic Occlusion
    111. 111. ACS Pathophysiology Plaque Rupture, Thrombosis, and Microembolization Quiescent plaque Platelet-thrombin micro-emboli Plaque rupture Process Plaque formation Inflammation Multiple factors ? Infection Plaque Rupture ? Macrophages Metalloproteinases Thrombosis Platelet Activation Thrombin Marker Cholesterol LDL, LP (a), HCy C-Reactive Protein sICAM Interleukin 6, TNF  sCD-40 ligand, SAA MDA Modified LDL, MMP-9, sICAM, D-dimer, Neopterin Complement, Fibrinogen, Troponin, CRP, CD40L Vulnerable plaque Macrophages Foam Cells Collagen  platelet activation TF  Clotting Cascade Lipid core Metalloproteinases Inflammation
    112. 112. QMI Thrombus Formation and ACS UA NQMI STE-MI Plaque Disruption/Fissure/Erosion Thrombus Formation Non-ST-Segment Elevation Acute Coronary Syndrome (ACS) ST-Segment Elevation Acute Coronary Syndrome (ACS) Old Terminology: New Terminology:
    113. 113. Management of ACS A = Aspirin, B = Beta-blocker, C = Clopidogrel, G = GPIIb/IIIa Inhibitor IHD type Drug Rx. Hep. /LMH ICU Care Lytic Rx P PTCA Stable Angina A+B No No No No Unstable Angina A+B+C Heparin No / Yes No No NSTEMI A+B+C+G LMH YES No No STEMI or QWMI A+B+C+G LMH YES YES YES
    114. 114. New Markers of CHD <ul><li>1. Markers of Plaque formation (Stable </li></ul><ul><li>Plaque) LDLc, LP(a),Homocysteine </li></ul><ul><li>2. Markers of Inflammation </li></ul><ul><li>(Vulnerable Plaque) </li></ul><ul><li>HS CRP – High Sensitivity C Reactive </li></ul><ul><li>Protein </li></ul><ul><li>sICAM – Soluble Intercellular Adhesion </li></ul><ul><li>Molecule </li></ul><ul><li>IL 6 – Interleukin 6 </li></ul><ul><li>TNF α - Tumor Necrosis Factor Alpha </li></ul><ul><li>SAA – Serum Amyloid Alpha </li></ul><ul><li>sCD 40 – serum CD 40 Ligand </li></ul>3. Markers of Plaque Rupture MDA Modified LDL – Oxidized LDL MMP-9 – Matrix Metallo Proteinase sICAM – Soluble Intercellular Adhesion Molecule 4. Markers of Thrombosis D-dimer, Complement Neopterin, Fibrinogen Troponins, CRP, CD 40 L
    115. 115. Lipid Profile Report We have 2 types of fats in our body – the cholesterol and the triglyceride LIPID TYPE LIPOPROTEIN Remarks Treatment TC = 250 HDL = 30 Abnormal Exercise LDL = 170 Abnormal STATINS VLDL = 50 Abnormal Diet TG = 350 VLDL = 235 Abnormal FIBRATE Chylomicron= 85 Abnormal Diet
    116. 116. CHD Risk Factors <ul><li>Diabetes Mellitus – FBG > 110, PPBG > 140 </li></ul><ul><li>Hypertension – SBP > 140, DBP > 90 </li></ul><ul><li>Dyslipidemia – LDL > 100, TG > 150, HDL < 50 </li></ul><ul><li>Overweight – BMI > 25, Waist girth > 34 ♀ 38 ♂ </li></ul><ul><li>Micro-albuminuria > 20 mg / L or GFR < 60 ml / min. </li></ul><ul><li>Male Sex up to age 55 yrs – Equal after 55 </li></ul><ul><li>Smoking, Alcohol, sedentary life, couch potatoes </li></ul><ul><li>Family H/o premature CAD – 1º blood relative < 50 </li></ul><ul><li>Presence of LVH by Echo or ECG </li></ul><ul><li>Emerging new risk factors – HCy, LP(a) </li></ul>
    117. 117. Complications of Acute MI Arrhythmia Extension / Ischemia Acute MI Heart Failure Expansion / Aneurysm RV Infarct Pericarditis Mechanical Mural Thrombus
    118. 118. Which BP Drug to Choose ? <ul><li>HT + DM ACEi, ARB </li></ul><ul><li>HT + IHD ACEi, Perindopril + BB (Meto, Carva) </li></ul><ul><li>HT + MRD ACEi + / or Methyl dopa (MD) </li></ul><ul><li>HT + CHF ARB, ACEi, Diuretics, No CCB </li></ul><ul><li>HT + Pregnancy MD or CCB (Amlo) No ACEi </li></ul><ul><li>HT + Asthma, COPD No beta blockers, Alpha blockers OK </li></ul><ul><li>HT + Tachycardia No CCBs, Give BB </li></ul><ul><li>HT + Dyslipidemia No Diuretics- give ACEi, ARB, CCB </li></ul><ul><li>HT in elderly, ISH Indapamide, Diuretics, CCB </li></ul>
    119. 119. What is in this ECG
    120. 120. Unstable Angina <ul><li>Presence of one or more of the three features, </li></ul><ul><li>Crescendo Angina- more severe, prolonged, or frequent. Decrease in exercise capacity </li></ul><ul><li>New onset (1 month) & brought on by minimal exertion. Not relieved by Nitrates </li></ul><ul><li>Angina at rest as well as with minimal exertion. There are 3 classes – 1 to 3 </li></ul><ul><li>This may progress to NSTEMI or STEMI </li></ul>
    121. 121. Look at This ECG
    122. 122. Prinzemetal Angina <ul><li>Transient ST-segment elevation during chest pain due to coronary vasospasm – variant angina </li></ul><ul><li>ECG with ST ↑. Becomes normal soon, No Q wave </li></ul><ul><li>Intermittent chest pain </li></ul><ul><ul><li>often repetitive, usually at rest, early morning </li></ul></ul><ul><li>Other vasospasms - syncope, Raynaud’s, migraine </li></ul><ul><li>β blockers contraindicated. CCB, α blockers Rx. </li></ul>
    123. 123. Interpret this ECG
    124. 124. NSTEMI <ul><li>Non ST ↑ MI or NSTEMI, Non Q MI </li></ul><ul><li>Or also called sub-endocardial Infarction </li></ul><ul><li>Non transmural, restricted to the sub-endocardial region - there will be no ST ↑ or Q waves </li></ul><ul><li>ST depressions in anterio-lateral & inferior leads </li></ul><ul><li>Prolonged chest pain, autonomic symptoms like nausea, vomiting, diaphoresis </li></ul><ul><li>Persistent ST-segment ↓even after resolution of pain </li></ul>
    125. 125. What are these ECGs
    126. 126. STEMI and QWMI <ul><li>STEMI and QWMI </li></ul><ul><li>ST ↑ signifies severe transmural myocardial injury – This is early stage before death of the muscle tissue – the infarction </li></ul><ul><li>Q waves signify muscle death – They appear late in the sequence of MI and remain for a long time </li></ul><ul><li>Presence of either is an indication for thrombolysis </li></ul>
    127. 127. Evolution of Acute MI <ul><li>A – Normal ST segment and T waves </li></ul><ul><li>B – ST mild ↑ and prominent T waves </li></ul><ul><li>C – Marked ST ↑ + merging upright T </li></ul><ul><li>D – ST elevation reduced, T ↓, Q starts </li></ul><ul><li>E – Deep Q waves, ST segment returning to baseline, T wave is inverted </li></ul><ul><li>F – ST became normal, T Upright, Only Q+ </li></ul>
    128. 128. Critical Narrowing of LAD
    129. 129. Holter & TMT in CAD
    130. 130. Holter & TMT in CAD <ul><li>Holter is an ambulatory ECG, BP monitor </li></ul><ul><li>Look at the Stress Test – Deep ST ↓ </li></ul><ul><li>The Holter recordings show the changing patterns in ST segments and Heart rate during different activities </li></ul><ul><li>Worst ST changes during vigorous physical activity like playing tennis </li></ul>
    131. 131. Normal Q waves Notice the small Normal Q in Lead I
    132. 132. Normal Q Waves <ul><li>The normal Q wave in lead I is due to septal depolarization </li></ul><ul><li>It is small in amplitude – less than 25% of the succeeding R wave, or less than 3 mm </li></ul><ul><li>Its duration is < 0.04 sec or one small box </li></ul><ul><li>It is seen in L1 and some times in V5, V6 </li></ul>
    133. 133. Pathological Q wave Notice the deep & wide Infarction Q in Lead I
    134. 134. <ul><li>The pathological Q wave of infarction in the respective leads is due to dead muscle </li></ul><ul><li>It is deep in amplitude – more than 25% of the succeeding R wave, or more than 4 mm </li></ul><ul><li>Its duration is > 0.04 sec or > 1 small box </li></ul><ul><li>It is seen in Leads facing the infarcted muscle mass </li></ul>Pathological Q wave
    135. 135. Q wave of Cardiomyopathy
    136. 136. Q Wave of Cardiomyopathy <ul><li>In idiopathic hypertrophic cardiomyopathy the septal Q wave in lead 1 is deep and prolonged because of excessive septal thickness. Similar to MI Q wave, </li></ul><ul><li>but </li></ul><ul><li>There will be marked LVH evidence and </li></ul><ul><li>The R wave amplitude is very tall unlike in infarction – where R waves are reduced </li></ul>
    137. 137. Serial ECG changes of MI
    138. 138. Serial ECG Changes of MI <ul><li>Normal ECG does not exclude MI or IHD </li></ul><ul><li>First few hours of MI – Hyper acute T with ST segment elevation starting </li></ul><ul><li>Drop in R wave voltage and ST elevation </li></ul><ul><li>Significant Q, R wave none, ST ↑, T ↓ </li></ul><ul><li>No R, Marked Q, ST baseline, T↓ </li></ul><ul><li>Small R starts, Q remains, ST normal, T↓ </li></ul><ul><li>In some Q waves disappear, R improves, ECG becomes nearly normal. </li></ul>
    139. 139. Blood Supply - MI - Leads ANTERIOR LATERAL INFERIOR POSTERIOR LAD LAD or LCx RCA RCA + LCx V1, V2, V3, V4 V5, V6, L1, aVL L2, L3, aVF V1, V2 Mirror
    140. 140. What are the Investigations ? <ul><li>Resting 12 Lead ECG, Chest X-Ray </li></ul><ul><li>Tread Mill Test (TMT) – Provocative stress tests </li></ul><ul><li>Troponins (bed side), LDH, CPK isoenzymes </li></ul><ul><li>Echocardiography and Doppler </li></ul><ul><li>Calcium scoring and CT angiography </li></ul><ul><li>Exercise Echo, Dobutamine challenge echocardiography </li></ul><ul><li>Perfusion – Stress Thalium, Sistemibi, Dipyridamole </li></ul><ul><li>3D Coronary Cartography (CCG), PET scan </li></ul><ul><li>Coronary Angiography (Gold Standard) </li></ul>
    141. 141. Acute Anterior MI
    142. 142. Acute Anterior Wall MI <ul><li>Due to occlusion of the proximal LAD </li></ul><ul><li>Significant Q waves, ST elevation and T inversions in Leads V2, V3 and V4 </li></ul><ul><li>Q waves and T inversion in L1 </li></ul><ul><li>If only V1 and V2 show the changes it is called septal MI </li></ul><ul><li>Associated with abnormal conduction </li></ul><ul><li>Septal perforation with acquired VSD is a rare complication </li></ul>
    143. 143. Very Striking
    144. 144. Hyper Acute MI <ul><li>Note the hyper acute elevation of ST </li></ul><ul><li>The R wave is continuing with ST and the complexes are looking rectangular </li></ul><ul><li>Some times tall and peaked T waves in the precardial leads may be the only evidence of impending infarct </li></ul><ul><li>Sudden appearance LBBB indicates MI </li></ul><ul><li>MI in Dextro-cardia – right sided leads are to be recorded </li></ul>
    145. 145. <ul><li>Note the ST ↑ in V1, V2, V3 </li></ul><ul><li>T ↓ in V1 to V5 </li></ul><ul><li>R wave voltages of all lateral leads well preserved </li></ul><ul><li>No ST ↑ in the Lateral leads </li></ul>What is striking ?
    146. 146. Acute Anterio-Lateral MI
    147. 147. Acute Anterio-lateral MI <ul><li>Due to occlusion of the marginal branch or the main trunk of Left Circumflex artery </li></ul><ul><li>Or due to occlusion of the diagonal branch of Left anterior descending artery </li></ul><ul><li>Significant Q waves, ST elevation and T inversions in Lead 1, aVL, V5 and V6 </li></ul><ul><li>This is the most common form of MI </li></ul>
    148. 148. Severe Chest Pain – Why ?
    149. 149. Acute Anterio-lateral MI <ul><li>Note the marked ST elevations in chest leads V2 to V5 and also ST↑ in L1 & aVL </li></ul><ul><li>T inversions have not appeared as yet </li></ul><ul><li>R wave voltages have dropped markedly in V3, V4, V5 and V6 </li></ul><ul><li>Small R in L1 and aVL. </li></ul>
    150. 150. What changes we see ?
    151. 151. <ul><li>Note the marked ST elevations in chest leads V2 to V5, also ST ↑ in L1 & aVL </li></ul><ul><li>T inversions have not appeared as yet </li></ul><ul><li>R wave voltages have merged with ST ↑ markedly in V3, V4, V5 and V6 </li></ul><ul><li>In addition complimentary St ↓in L2, L3 </li></ul>Acute Anterio-lateral MI
    152. 152. Why Acute changes disappeared ? r TPA
    153. 153. Thrombolysed Anterio-lateral MI <ul><li>Note the ST elevations in chest leads V2 to V5 are returned toward baseline </li></ul><ul><li>Deep T ↓ have appeared in all leads </li></ul><ul><li>R wave voltages have improved in V2 to V5 </li></ul><ul><li>No residual Q waves seen </li></ul><ul><li>This patient was thrombolysed within 2 hours and MI has become stable – Golden period </li></ul><ul><li>Thrombolytics – UK, SK, TPA, r-TPA </li></ul>
    154. 154. Guess How Old is this MI !
    155. 155. Stable Anterio-lateral MI <ul><li>The coved ST ↑ in chest leads V2 to V5 almost returned to baseline </li></ul><ul><li>T ↓ are becoming less marked in all leads </li></ul><ul><li>R wave voltages improved well in V4 to V5 </li></ul><ul><li>No residual Q waves seen </li></ul><ul><li>This ECG is 4 weeks after the Acute MI </li></ul>
    156. 156. Acute Inferior wall MI
    157. 157. <ul><li>Due to occlusion of the right coronary artery </li></ul><ul><li>Significant Q waves, ST elevation and T inversions in Lead II, Lead III, aVF, </li></ul><ul><li>This is the associated with arrhythmias </li></ul>Acute Inferior wall MI
    158. 158. Which wall MI ?
    159. 159. <ul><li>Note the ST elevations in Inferior leads- namely L2, L3 and aVF </li></ul><ul><li>T inversions yet to appear </li></ul><ul><li>aVL lead shows complimentary ST ↓and T inversion </li></ul>Acute Inferior wall MI
    160. 160. What is striking ? Acute Inf Post
    161. 161. <ul><li>Note the ST elevations in Inferior leads- namely L2, L3 and aVF </li></ul><ul><li>Hyper acute T waves merging with ST </li></ul><ul><li>V1, V2, aVL lead shows rsR’ pattern with ST ↓and T inversion – Inferior MI </li></ul><ul><li>Associated RBBB also is present – QRS is wide > 0.12 sec </li></ul>Acute Inferior wall MI
    162. 162. Where are the ST ↑ ? Inf Lysed
    163. 163. Inferior Wall MI - Thrombolysed <ul><li>A case of inferior wall MI </li></ul><ul><li>Thrombolysed with in 2 hours </li></ul><ul><li>ST segments returned to base line </li></ul><ul><li>Deep T inversions signify residual ischemia </li></ul><ul><li>This patient became stable </li></ul>
    164. 164. What Can We Infer ?
    165. 165. Old Inferior wall MI <ul><li>This is months after the acute event </li></ul><ul><li>Patient suffered inferior MI </li></ul><ul><li>Residual QS waves in L3 and aVF </li></ul><ul><li>T inversions in L3 and aVF </li></ul><ul><li>ST segments are isoelectric </li></ul><ul><li>L3 t inversion became normal </li></ul><ul><li>Chest leads R wave voltages are good </li></ul>
    166. 166. Acute True Posterior MI
    167. 167. <ul><li>Due to occlusion of the distal Left circumflex artery or posterior descending or distal right coronary artery </li></ul><ul><li>Mirror image changes or reciprocal changes in the anterior precardial leads </li></ul><ul><li>Lead V1 shows unusually tall R wave (it is the mirror image of deep Q) </li></ul><ul><li>V1 R/S > 1, Differential Diagnosis - RVH </li></ul>Acute True Posterior MI
    168. 168. Decipher V1, V2, V3
    169. 169. <ul><li>V2, V3 show tall R waves, Even V1 shows R </li></ul><ul><li>V2, V3, V1 leads R/s ratio is >> 1 </li></ul><ul><li>These R waves are the mirrored MI – Qs </li></ul><ul><li>These leads show deep ST depression </li></ul><ul><li>This ST ↓is in fact the mirrored ST↑of MI </li></ul><ul><li>The same leads show sharp T waves </li></ul><ul><li>These are the mirrored T inversions of MI </li></ul>Acute True Posterior MI
    170. 170. Identify the Double wall MI
    171. 171. Inferio-Posterior MI <ul><li>V1, V2 show tall R waves </li></ul><ul><li>V1, V2 leads R/s ratio is >> 1 </li></ul><ul><li>These R waves are the mirrored MI – Qs </li></ul><ul><li>This ST↓ is in fact the mirrored ST ↑ of MI </li></ul><ul><li>The T ↓ are the mirrored T inversions of MI </li></ul><ul><li>L2, L3 and aVF show gross ST ↑ - Inferior MI </li></ul><ul><li>V4R, V5R show ST elevations – RV – MI too. </li></ul>
    172. 172. New or Old – What MI ?
    173. 173. Old Inferio-Posterior MI <ul><li>V2 shows residual R waves of Posterior MI </li></ul><ul><li>V2 lead R/s ratio is > 1 </li></ul><ul><li>The R waves are the mirrored old Qs of MI </li></ul><ul><li>This ST↓ is no longer seen – stabilized MI </li></ul><ul><li>L3 & aVF show deep QS of old Inferior MI </li></ul><ul><li>The T ↓ in L3, aVF signify old inferior MI </li></ul>
    174. 174. Look at the Right Chest Leads R R R R R R
    175. 175. Dextrocardia and MI <ul><li>Note the ECG carefully – It is an eye opener </li></ul><ul><li>55 years ♀ is sent for ECG by another doctor </li></ul><ul><li>She has dextrocardia of which she is unaware </li></ul><ul><li>She has typical clinical features of acute MI </li></ul><ul><li>Routine chest leads placed on left chest showed no evidence of MI at all </li></ul><ul><li>ECG with chest leads on the right chest – V2R to V6R - typical acute anterio-septal MI </li></ul>
    176. 176. Will Right Ventricular MI occur ?
    177. 177. Right Ventricular MI <ul><li>Note the ECG carefully – It is an eye opener </li></ul><ul><li>65 yrs ♂ has typical clinical features of acute MI </li></ul><ul><li>Routine chest leads placed on left chest showed no MI - but limb leads showed acute Inferior MI </li></ul><ul><li>ECG with chest leads on the right chest – V2R to V6R show typical changes of acute MI of the Right Ventricle. RV MI is associated with Inferior wall MI </li></ul><ul><li>His serum troponins were very high </li></ul><ul><li>Angio showed 95% block of the RCA </li></ul>
    178. 178. Electrical Alternans
    179. 179. <ul><li>Note the typical ECG changes </li></ul><ul><li>Every alternate QRS complex has a small and a large amplitude but of sinus origin </li></ul><ul><li>The heart rate is 110 per minute </li></ul><ul><li>There are P waves preceding all QRS waves </li></ul><ul><li>This is a feature of pericardial effusion with cardiac tamponade </li></ul>Electrical Alternans
    180. 180. Ventricular Bigeminy Normal VPC VPC Normal
    181. 181. <ul><li>Note this typical ECG of bigeminy </li></ul><ul><li>Each normal sinus originated ventricular complex with narrow QRS is followed by a </li></ul><ul><li>Premature beat with wide and bizarre looking QRS of ventricular origin </li></ul><ul><li>Similarly Trigeminy, Quadrigeminy </li></ul><ul><li>These ectopics signify heart failure </li></ul><ul><li>In this ECG there are features of Inferior MI </li></ul>Ventricular Bigeminy
    182. 182. Myxedema 50 Heart rate Rhythm P wave PR interval QRS in sec
    183. 183. Myxedema <ul><li>Note the ECG changes </li></ul><ul><li>Bradycardia – HR of 55 per minute </li></ul><ul><li>Low voltages of all complexes </li></ul><ul><ul><li>Less than 5 mm Limb leads </li></ul></ul><ul><ul><li>Less than 8 mm chest leads </li></ul></ul><ul><li>DD of low voltage complexes </li></ul><ul><li>Pericardial effusion, Constrictive pericarditis </li></ul><ul><li>Severe Emphysema </li></ul><ul><li>Pneumothorax or left sided pleural effusion </li></ul>
    184. 184. S.A.H. ECG changes
    185. 185. S.A.H – ECG changes <ul><li>Striking ECG changes of Non Cardiac origin </li></ul><ul><li>Incredible deep and symmetric T Inversions </li></ul><ul><li>In young person with massive Sub Arachnoid Haemorrhage </li></ul><ul><li>He has no cardiac disease </li></ul><ul><li>Presumably due to autonomic dysfunction </li></ul><ul><li>Intense Head ache, Has very high B.P </li></ul><ul><li>Lumbar Puncture clinches the issue </li></ul>
    186. 186. Hyperkalemia
    187. 187. <ul><li>This is a 58 yr old man's with CRF </li></ul><ul><li>Serum K was 7.6 m mol/L. (Normal upto 4.2) </li></ul><ul><li>Hyperkalaemia ECG changes are </li></ul><ul><li>Small or absent P waves </li></ul><ul><li>Atrial fibrillation (not in this ECG) </li></ul><ul><li>Wide QRS </li></ul><ul><li>Shortened or absent ST segment </li></ul><ul><li>Wide, tall and tented T waves </li></ul>Hyperkalemia
    188. 188. Hypokalemia
    189. 189. <ul><li>This 22 year lady had prolonged vomiting </li></ul><ul><li>Her serum K was 1.8 mmol/L. </li></ul><ul><li>Normal 3.2 to 4.2 </li></ul><ul><li>Hypokalaemia ECG changes are </li></ul><ul><li>Small or absent T waves or inverted T </li></ul><ul><li>Prominent U waves (see pointer) </li></ul><ul><li>T wave is the tent house of K </li></ul><ul><li>More K – tall T, less K flat or inverted T </li></ul>Hypokalemia
    190. 190. Wandering base line <ul><li>In non co-operative child </li></ul><ul><li>Excessive movements of limbs </li></ul><ul><li>Movement disorders of CNS </li></ul><ul><li>Not properly earthed machine </li></ul><ul><li>Additional wet ground earth helps </li></ul>
    191. 191. Muscle Tremor <ul><li>Limb movements cause baseline fluctuations </li></ul><ul><li>Tense muscles cause tremor of baseline </li></ul><ul><li>Hairy chest interferes with proper contact of chest leads – better to shave the area if needed. </li></ul><ul><li>Reassurance, starting recording a few minutes after the leads are placed – reduce muscle tension </li></ul>
    192. 192. AC Interference <ul><li>Any electrical gadgets in the same line may interfere </li></ul><ul><li>Like Mixie, Motor, Musical tube lights etc </li></ul><ul><li>Proper earthing is essential </li></ul><ul><li>Dedicated direct line for ECG power point </li></ul><ul><li>Use battery mode, Artifacts are quite misleading </li></ul>
    193. 193. Our Other Resources <ul><li>We have also an advanced course on ECG </li></ul><ul><li>We have several other educative CMEs prepared </li></ul><ul><li>Please refer to the list at the beginning of this book </li></ul><ul><li>We have several religious and philosophical texts sung, translated and made as PowerPoint slides </li></ul><ul><li>Please request what ever you want </li></ul><ul><li>CME talk can also be given if you intimate ahead </li></ul><ul><li>The charge of Rs.100/- per CD is nominal and to cover the incidental costs only </li></ul>
    194. 194. THIS IS NOT THE END <ul><li>This only a beginning and certainly not the end </li></ul><ul><li>We look forward for more learning experiences </li></ul><ul><li>Please write to us what you felt about this ECG </li></ul><ul><li>Contact address and phone are in the beginning </li></ul><ul><li>Thank YOU and </li></ul><ul><li>With Warm Regards, </li></ul><ul><li>Dr.Sarma. </li></ul>

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