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Information and Knowledge for medical professionals about electrocardiography including rationale, standardization, and interpretation. This is part one of

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  1. 1. Electrocardiogram Basic Interpretation Diagnosis of Ischemic Heart Diseases Santi Silairatana, MD
  2. 2. Physiology of the Heart
  3. 3. Basic Function of the Heart O2 CO2
  4. 4. Electromechanical Coupling Mechanism ⇣ Propagation of electrical current in conducting tissues ⇣ Electrical Generation of electrical current Depolarization of myocardial cells Myocardial contraction ⇣ Increased intracardiac pressures ⇣ Blood flow in the circulation Mechanical ⇣
  5. 5. Specialized Tissue of the Heart Pacemaker cells & Conducting tissues Intercalated striated muscle
  6. 6. Primary Pacemaker of the Heart: Sinoatrial (SA) Node +20 mV 2 K+ channel opening Outward current iK 0 mV -20 mV 1 Rapid 
 Na+ channel 
 opening, INa -40 mV 4 -60 mV 3 Action ATPase potential pump threshold Na+-K+ Ca2+ channel opening Inward current ICa Na+ channel opening Inward current If
  7. 7. Cardiac Electrical Activity 1 2 3 4 5 Sinus node depolarization Spreading to atria via bundles Atrioventricular node depolarization Atrial contraction SA node 
 repolarization Spreading to His bundle Spreading to septum (LBB)
  8. 8. Cardiac Electrical Activity 6 7 8 9 10 Septal depolarization (Left —> Right) Purkinje fiber depolarization Ventricular myocardial depolarization Purkinje fiber repolarization Inner layer ventricular repolarization Outer layer ventricular
  9. 9. Electrocardiography
  10. 10. Electrocardiography A recording of cardiac electrical activity ! Amplitude Vector Time ! Willem Einthoven (1860-1927) using conductivity of the body to the electrodes
  11. 11. Electrocardiograph Paper Voltage 1mm 5mm 2x 1x 0.5x Sens 0.5x = 5 mm/mV Sens 1x = 10 mm/mV Sens 2x = 20 mm/mV Time Recorder speed = 25 mm/sec 5 mm = 1/5 sec (0.2 sec) 1 mm = 1/25 sec (0.04 sec)
  12. 12. Electrocardiograph Leads: Why Many? Left Right inferior Apex
  13. 13. Electrocardiograph Leads Use multiple leads (electrodes) to enhance MULTI-DIMENSION assessement of the cardiac activity
  14. 14. The Einthoven’s Triangle: Lead I, II, III I II III
  15. 15. Additional Limb Leads: aVR, aVL, aVF aVR aVL Wilson central 
 terminal aVF
  16. 16. Chest Leads: V3R, V4R, V1-V6, V7-9 Descending aorta Chest Leads V1 V2 Left 
 lung V3 V4 V5 V6 V6 LA Recordings of electrical activity in horizontal plane Right 
 lung RA LV RV Sternum V1 V2 V5 V3 V4
  17. 17. 12 Leads Electrocardiogram
  18. 18. Cardiac Physiology & ECG Correlations
  19. 19. Nomenclature of the ECG complex QRS complex T P ST 
 segment PR segment PR interval P duration QRS duration QT interval U
  20. 20. ECG Complex & the Sequence of Activation Ventricle SA AV node Atrium HB BB P
  21. 21. ECG and Electrical Vector
  22. 22. Atrial Depolarization V6 the first half: Right atrial depolarization the 2nd half: Left atrial depolarization V1 Normal P wave: 
 Duration: ≤0.12 sec Amplitude: <0.25 mV (2.5 mm) V3
  23. 23. Septal Depolarization In septal depolarization, electrical wavefront spreads 
 from Left —> Right V6 V1 V3
  24. 24. Ventricular Depolarization In ventricular depolarization, electrical wavefront spreads V6 from Right —> Left Anterior —> Posterior Medial —> Lateral V1 V3
  25. 25. Ventricular Repolarization V6 1 V3 2 In ventricular repolarization, electrical wavefront spreads 
 from Inner to outer
  26. 26. Systematic ECG Analysis & Interpretation
  27. 27. Rhythm: Sinus Rhythm QRS complexes preceded by P waves Relatively constant PP interval Each P waves are of the same configurations
  28. 28. Components of ECG “Read” 1 Rhythm 2 Rate 3 Axis 4 Chamber enlargement/hypertrophy 5 Intervals 6 Ischemia/infarction pattern
  29. 29. Heart (Atrial - Ventricular) Rate R RR interval 22 mm HR = 1500/22 = 68 bpm RR interval R R R 1 sec = 25 mm (small squares) or 5 large squares 60 sec = 1500 mm (small squares) or 300 large squares Heart rate (/min) = 1500/RR interval (small square) = 300/RR interval (Large square)
  30. 30. Heart Rate: Quick Look 0015010075 60 50 3 1 2 300/1 = 300 bpm 300/2 = 150 bpm 300/3 = 100 bpm 300/4 = 75 bpm 300/5 = 60 bpm 300/6 = 50 bpm 3 4 5 6 One big block = 1 sec (5 large boxes) HR = No. of QRS complexes in 6 sec x 10
  31. 31. QRS Axis: Normal Axis Extreme right axis deviation Left axis deviation -150o aVR -30o aVL 0o I Right axis deviation 120o III 60o II 90o aVF Normal axis
  32. 32. QRS Axis: Biphasic Method -150o aVR -30o aVL 0o I 120o III 60o II 90o aVF
  33. 33. QRS Axis: High QRS Amplitude Method -150o aVR -30o aVL 16 mm 0o I 13 mm 120o III 60o II 90o aVF 14 mm
  34. 34. Atrial Enlargement “P Pulmonale” Right atrial enlargement: 
 P wave amplitude > 2.5 mm “P Mitrale” Left atrial enlargement: 
 P wave duration > 3 mm (0.12 msec) Notching of P wave
  35. 35. S V1,2ϩR V6 Grant RϩS any precordial lead Hancock et al Ͼ40 mm Ͼ35 mm Grant66 R V5 : R V 6 Standardization and Interpretation of the ECG, Part V Ͼ1.0 e253 Holt67 R, any precordial lead Table 1. Ͼ26 mm McPhie70 S V2ϩR V4,5 Ͼ45 mm Wolff77 R V5 First AuthorVof Study R 6 Ͼ33 mm Wilson76 Ͼ25 mm Wilson76 Left Ventricular Hypertrophy Criteria for Left Ventricular Hypertrophy Amplitude Limb lead voltage Year of Study Publication Combinations of limb and precordial voltage (R I–S I)ϩ(S III–R III) Ͼ16 mm Lewis5 1914 RS aVFϩV2ϩV6 (Ͼ30 years) Ͼ59 mm Manning68 R IϩS III Ͼ25 mm Gubner6 1943 RS aVFϩV2ϩV6 (Ͻ30 years) Ͼ93 mm Manning68 RI Ͼ15 mm Gubner6 aVL (men) S V3ϩR 1943 Ͼ28 mm Casale8 R aVL Ͼ11 mm Sokolow7 aVL (women) S V3ϩR 1949 Ͼ20 mm Casale8 R aVF Ͼ20 mm Goldberger65 Total 12-lead voltage 1949 Ͼ175 mm Siegel74 Q or S aVR Ͼ19 mm Schack73 1950 Combinations of voltage and nonvoltage RϩS in any limb lead Ͼ19 mm Romhilt9 1968 Voltage-STT-LAA-axis-QRS duration Point score Romhilt9 Ͼ2436 mm/sec Molloy71 Ͼ1742 mm/sec Molloy71 Precordial lead voltage (R aVLϩS V3)ϫQRS duration Total duration Wilson76 12-lead voltageϫQRS 1944 S V1 Ͼ23 mm S V2 Ͼ25 mm S V1ϩR V5 Ͼ35 mm S V1ϩR Sokolow7 V5ϩS V5 1949 Ͼ25 Bozzi33 S V2ϩR V5,6 Ͼ45 mm S V1,2 Romhilt72ϩR V6ϩS V6 1969 Ͼ25 Bozzi33 S V1,2ϩR V5,6 Ͼ35 mm S IIIϩmax R/S any lead (men) Murphy54 1984 Ͼ30 Gertsch32 S V1,2ϩR V6 Ͼ40 mm S IIIϩmax R/S any lead (women) Grant66 1957 Ͼ28 Gertsch32 RϩS any precordial lead Ͼ35 mm Criteria for use with right bundle-branch block Grant66 1957 Ͼ29 mm Vandenberg75 R V5 : R V 6 Ͼ1.0 Criteria for Mazzoleni69 use with left anterior fascicular block 1964 Max Holt67 R/S precordial lead (with LAD) 1962 R, any precordial lead Ͼ26 mm SV McPhie170 1958 Ͼ2 mm Vandenberg75 S V2ϩR V4,5 Ͼ45 mm R 77 WolffV5,6 1956 Ͼ15 mm Vandenberg75 R V5 Ͼ33 mm Ͼ40 mm Vandenberg75 R V6 Ͼ25 mm S IIIϩmax R/S precordial (with LAD) Wilson76 1944 RI Wilson76 1944 Ͼ11 mm Vandenberg75 Amplitudes are given in millimeters, where 1 mmϭ0.1 mV. LAD indicates left axis deviation. Combinations of limb and precordial voltage RS aVFϩV2ϩV6 (Ͼ30 years) Ͼ59 mm Manning68 1964
  36. 36. axis, left atrial abnormality, and QRS duration, in diagnosing LVH in the presence of LBBB; Identification of criteria that consistently outperform Table 2. Criteria for Right Ventricular Hypertrophy ic populations other (semi) cluding criteria and those that are only redundant; First Author sFor pediatric patients, possible improvement of criteria possible and Amplitude of Study based on current sampling technology, wider demo- 78 Tall R V1 Ͼ6 mm Myers specific indicagraphic groups, and the use of more leads; and Increased R:S ratio V1 Ͼ1.0 Myers78 g,The effectof day-to-day variation of voltage and other follow-up of Ͼ10 mm Myers78 Deep S V5 criteria on the validity of LVH criteria. 78 Reduced R:S V5 to R:S V1 (R 1ϩS III)–(S IϩR III) Ͻ0.04 Sokolow7 1949 Ͻ15 mm Lewis5 1914 Butler51 1986 Max HypertrophyϾ6 mm Right Ventricular R V , ϩmax S I, when used in Deep S V6 Ͼ3 mm Myers Tall R aVR Ͼ4 mm Sokolow7 ypicalRight Ventricular Hypertrophy of LVH Small S V1 Ͻ2 mm Myers78 t ventricular (RVH) causes a displacement 78 criteria of LVH hypertrophy5,6 Small R V Ͻ3 mm Myers e QRS vector toward the right and anteriorly and often 78 Reduced R:S ratio V5 Ͻ0.75 Myers , a delay in essuch as QRS the R-waveR:S ratio V right precordial leads. 78 peak in Reduced Ͻ0.4 Myers 6 S duration, in ever, considerable Reduced R:S ofto R:S V are often required to 7 degrees V RVH Ͻ0.04 Sokolow 5 1 BB; the balance of right and left ventricular vectors, ge (R 1ϩS III)–(S IϩR III) Ͻ15 mm Lewis5 tly outperform use the vector of left ventricular activation dominatesButler51 the Max R V1,2ϩmax S I, Ͼ6 mm undant; nce in the normal heart and even more so in the setting of aVL–S V1 ment of criteria H. wider demo-abilityR of the,6 ECG to detect RVH may be 7 Thus, the V1ϩS V5 Ͼ10.5 mm Sokolow cted to Ͼ0.035 sec Myers78 ds; and be low. R peak V1 (QRS duration ltage and criteria Ͻ0.12 derived from the amplitude of R umerous other mostly sec) Present Myers QR V1 the R-wave peak time in V have 78 S in leads I, V1, V6, and 1 proposed and areSupporting criteria shown in Table 2. They have been phy RSR V1 (QRS duration Present 12 Year of Study aVL–S V1 Publication R V1ϩS V5,6 Ͼ10.5 mm Sokolow7 1949 R peak V1 (QRS duration 1948 Ͻ0.12 sec) Ͼ0.035 sec Myers78 1948 Present Myers78 1948 1948 1948 QR V1 1948 Supporting criteria 1949 RSR V1 (QRS duration 1948 Ͼ0.12 sec) 1948 Present SϾR in I, II, III 1948 Present S I and Q III 1948 Present 1949 R:S V1ϾR:S V3,4 Present 1914 Negative T-wave V1 1986 through V3 Present P II amplitude 1949 Ͼ2.5 mm Amplitudes are given in millimeters, where 1 mmϭ0.1 mV. 1948 1948 and T-wave inversion in right precordial leads; as with LVH, these ST-T abnormalities are better referred to as “secondary
  37. 37. PR Interval QRS complex PR 
 P segment PR interval Prolonged PR (>200 msec): 
 First degree AV block Normal Value: 
 0.12-0.20 msec (3-5 small squares) The PR interval is the time from the onset of the P wave to the start of the QRS complex. It reflects conduction through the Atrioventricular (AV) junction Shorted PR (<120 msec): 
 Pre-excitation syndrome
  38. 38. QT Interval QRS complex U QT interval • The QT interval should be measured in either lead II or V5-6 • Several successive beats should be measured, with the maximum interval taken • Large U waves (> 1mm) that are fused to the T wave should be included in the measurement • Smaller U waves and those that are separate from the T wave should be excluded QT interval upper normal limit (sec) 1.5 T Heart rate (bpm) 40 0.5 1.2 50 0.46 1 60 0.44 0.86 ST 
 segment Measure RR interval (sec) 70 0.4 0.8 75 0.38 0.75 80 0.37 0.67 90 0.35 0.6 100 0.34 0.5 120 0.31 0.4 150 0.25
  39. 39. Rate Corrected QT (QTc) Estimation of QT interval 
 at a heart rate of 60 bpm Bazett’s formula: QTC = QT / √ RR Fredericia’s formula: 
 QTC = QT / RR 1/3 Framingham formula: 
 QTC = QT + 0.154 (1 – RR) Hodges formula: 
 QTC = QT + 1.75 (heart rate – 60) Prolonged QTc (>440 msec): 
 Hypokalemia Hypomagnesemia Hypocalcemia Hypothermia Myocardial ischemia Post-cardiac arrest Increased intracranial pressure Congenital long QT syndrome Drugs Short QTc (300-350 msec): 
 Hypercalcemia Congenital short QT syndrome Digoxin effect
  40. 40. ECG in Diagnosis of Ischemic Heart Diseases
  41. 41. Coronary Arteries for Myocardial Blood Supply RCA LCX LAD
  42. 42. Acute Transmural Myocardial Infarction
  43. 43. ECG Change in Acute Transmural Myocardial Infarction Ischemia/Infarction of myocardium ⇣ Failure of Na+-K+ ATPase pump
 and protein channel ⇣ Decreased membrane potential during action potential ⇣ Electrical gradient and current flow to infarct area
  44. 44. ECG Criteria of Acute STEMI ST segment amplitude (mm) J point Leads Male Female Age <40 Age >40 V2 V3 2.5 2 1.5 V3R V4R 1 0.5 0.5 V7-V9 0.5 0.5 0.5 Others 1 1 1
  45. 45. ST Elevation VS Early Repolarization Notching or slurring at the J-point Concordant asymmetrical T wave Concave upward ST elevation; <2 mm
  46. 46. ECG Evolution in Acute Transmural Myocardial Infarction Normal ECG Minutes to Hours Hours to day ST elevation and Peaked T wave Deepens Q wave ! “Hyperacute 
 ST elevation” Days to weeks Return of ST segment ! Inverted T wave ST segment elevation Persistent Q wave decreases Months on T wave returns Q wave persists
  47. 47. required during mechanical revascularization procedures, either by PCI or by coronary artery bypass grafting (CABG). Elevated cTn values may be detected following Anterior Myocardial Infarction • results from occlusion of Left Anterior Descending (LAD) artery • ST segment elevation with Q wave formation in the precordial leads (V1-V6) ± the high lateral leads (I and aVL) • Reciprocal ST depression in the inferior leads (II, III, aVF) Septal Leads: 
 V1-V2 Anterior Leads: 
 V3-V4 Lateral Leads: 
 V5-V6, I, aVL Anteroseptal: 
 V1-V4 Anterolateral: 
 V3-V6, I, aVL Extensive anterior/anterolateral: 
 V1-V6, I + aVL
  48. 48. Acute Transmural Infarction: Anteroseptal Wall
  49. 49. Acute Transmural Infarction: Anterolateral Wall
  50. 50. Acute Transmural Infarction: Extensive Anterolateral Wall
  51. 51. Prediction of the Site of LAD Occlusion: Proximal VS Distal Basal septal involvement: 
 ST elevation in aVR ST elevation in V1 >2.5 mm Complete RBBB ST depression in V5 High lateral involvement: 
 ST elevation/Q wave in aVL ST depression ≥1 mm in II, III, aVF
  52. 52. Proximal LAD Occlusion
  53. 53. Proximal LAD Occlusion Reciprocal ST depression in II, III, aVF High lateral involvement
  54. 54. Acute Transmural Infarction: Inferior Wall • accounts for 40-50% of all myocardial infarctions • Generally have a more favorable prognosis than anterior myocardial infarction (2-9%) • Up to 40% with a concomitant RV infarction • Up to 20% with significant bradycardia due to 2nd or 3rd degree AV block and higher mortality (>20%) • may be associated with posterior wall infarction
  55. 55. Acute Transmural Infarction: Infero-posterior Wall How to recognize an inferior STEMI
 ST elevation in leads II, III and aVF Progressive development of Q waves in II, III, aVF Reciprocal ST depression in aVL (± lead I)
  56. 56. Acute Transmural Infarction: Inferior Wall
  57. 57. Prediction of the Culprit Artery: RCA VS LCX Left Circumflex involvement: 
 ST elevation in lead II = lead III No reciprocal ST depression in lead I Signs of ST elevation in V5-V6, I , and aVL Right Coronary involvement: 
 ST elevation in Lead III > lead II Reciprocal ST depression in lead I ST elevation in V1 and V3R-V4R
  58. 58. Acute Inferior STEMI: RCA as the Culprit Reciprocal ST depression in lead I and aVL ST segment elevation in lead II = lead III
  59. 59. Acute Inferior STEMI: LCX as the Culprit Isoelectric ST segment in lead I ST segment elevation in lead II = lead III
  60. 60. Acute Inferior STEMI: LAD as the Culprit
  61. 61. Left Ventricular Aneurysm ECG features of LV aneurysm: 
 ST elevation seen >2 weeks after acute MI Most commonly seen in the precordial leads Convex or concave morphology Presence of Q wave or QS pattern Relatively small T wave
  62. 62. Acute Non-transmural Myocardial Infarction
  63. 63. ECG Change in Acute Non-transmural Myocardial Infarction Horizontal ST segment 
 depression >1 mm Down slope ST segment depression J point >1 mm Symmetrical T wave inversion
  64. 64. Acute Nontransmural Myocardial Infarction
  65. 65. Acute Nontransmural Myocardial Infarction
  66. 66. Acute Nontransmural Myocardial Infarction
  67. 67. Thank You