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Ecg fundamentals

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Ecg fundamentals

  1. 1. ECG fundamentals Dr. Emad Efat Shebin El kom Chest hospital July 2016
  2. 2. What is an ECG?  The electrocardiogram (ECG) is a representation of the electrical events of the cardiac cycle.  Each event has a distinctive waveform  the study of waveform can lead to greater insight into a patient’s cardiac pathophysiology.
  3. 3. With ECGs we can identify  Arrhythmias  Myocardial ischemia and infarction  Pericarditis  Chamber hypertrophy  Electrolyte disturbances (i.e. hyperkalemia, hypokalemia)  Drug toxicity (i.e. digoxin and drugs which prolong the QT interval)
  4. 4. Depolarization • Contraction of any muscle is associated with electrical changes called depolarization • These changes can be detected by electrodes attached to the surface of the body
  5. 5. Pacemakers of the Heart • SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute. • AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute. • Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.
  6. 6. Height • 10mm = 1mV • Look for a reference pulse which should be the rectangular looking wave somewhere near the left of the paper. It should be 10mm (10 small squares) tall Electrical impulse that travels towards the electrode produces an upright (“positive”) deflection Calibration
  7. 7. Impulse Conduction & the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers
  8. 8. The “PQRST” P wave - Atrial depolarization T wave - Ventricular repolarization QRS - Ventricular depolarization
  9. 9. The PR Interval Atrial depolarization + delay in AV junction (AV node/Bundle of His) (delay allows time for the atria to contract before the ventricles contract)
  10. 10. NORMAL ECG
  11. 11. The ECG Paper • Horizontally – One small box - 0.04 s – One large box - 0.20 s • Vertically – One large box 0.5 mV ( 5 mm )
  12. 12. The 12-leads include: –3 Limb leads (I, II, III) –3 Augmented leads (aVR, aVL, aVF) –6 Precordial leads (V1- V6) ECG Leads ( The 12-Leads ):
  13. 13. ECG Leads Bipolar Leads: Two different points on the body (I, II, III) Unipolar Leads: One point on the body and a virtual reference point with zero electrical potential, located in the center of the heart (aVR, aVL, aVF)
  14. 14. Standard Limb Leads
  15. 15. Standard Limb Leads
  16. 16. Augmented Limb Leads
  17. 17. All Limb Leads
  18. 18. Precordial Leads
  19. 19. Precordial Leads
  20. 20. Arrangement of Leads on the ECG
  21. 21. Anatomic Groups (Septum)
  22. 22. Anatomic Groups (Anterior Wall)
  23. 23. Anatomic Groups (Lateral Wall)
  24. 24. Anatomic Groups (Inferior Wall)
  25. 25. Anatomic Groups (Summary)
  26. 26. Determine regularity  Look at the R-R distances (using a caliper or markings on a pen or paper).  Regular (are they equidistant apart)? And presence of same number of P waves and QRS complexes  Occasionally irregular? Regularly irregular? Irregularly irregular? Interpretation? Regular R R
  27. 27. Determining the Heart Rate Rule of 300/1500 6 Second Rule
  28. 28. Rule of 300 Count the number of “big boxes” between two QRS complexes, and divide this into 300. (smaller boxes with 1500) for regular rhythms. 300/R-R interval ( big boxes) or 1500/R-R interval (smaller boxes )
  29. 29. What is the heart rate? (300 / 6) = 50 bpm
  30. 30. 6 Second Rule Number of QRS in 6 seconds ( 30 large squares ) x 10 For irregular rhythms. This method can be used also with regular rhythm. the heart rate 9 x 10 = 90 bpm 3 sec 3 sec
  31. 31. The QRS Axis The QRS axis represents overall direction of the heart’s electrical activity. Normal QRS axis from -30° to +90°. -30° to -90° is referred to as a left axis deviation (LAD) +90° to +180° is referred to as a right axis deviation (RAD)
  32. 32. Normal QRS axis from -30° to +90°. QRS up in I and up in aVF = Normal
  33. 33. QRS up in I and up in aVF = Normal
  34. 34. Example Negative in I, positive in aVF  RAD
  35. 35. Causes of left axis deviation include: • Normal variation (physiologic, often with age) • Mechanical shifts, such as expiration, high diaphragm (pregnancy, ascites, abdominal tumor) • ventricular hypertrophy • Left bundle branch block • left anterior fascicular block • Congenital heart disease (e.g. atrial septal defect) • Emphysema • Hyperkalemia • Ventricular ectopic rhythms • Preexcitation syndromes • Inferior myocardial infarction • Pacemaker rhythm
  36. 36. Causes of right axis deviation include: • Normal variation (vertical heart with an axis of 90º) • Mechanical shifts, such as inspiration and emphysema • Right ventricular hypertrophy • Right bundle branch block • Right ventricular load, for example Pulmonary Embolism or Cor Pulmonale (as in COPD) • Left posterior fascicular block • Dextrocardia • Ventricular ectopic rhythms • Preexcitation syndromes • Lateral wall myocardial infarction
  37. 37. P wave • Always positive in lead I and II • Always negative in lead aVR • < 3 small squares in duration • < 2.5 small squares in amplitude • Commonly biphasic in lead V1 • Best seen in leads II
  38. 38. Right Atrial Enlargement • Tall (> 2.5 mm), pointed P waves (P Pulmonale) • Causes : pulmonary diseases (pulmonary embolism and pulmonary hypertension) - Congenital e.g. PS,ASD
  39. 39. • Wide more than 0.12 sec in duration (3 small squares) & Notched in ( II,I) or biphasic in ( V1) P wave (P ‘mitrale’ ) • Causes: Valvular e.g.: MR,AR,AS – HTN - Dilated cardiomyopathy Left Atrial Enlargement
  40. 40. • Inversion : A-V junctional rhythms -ve in lead II +ve in lead aVR • Absent : in some of A-V junctional rhythms. • Replaced : by fibrillatory or flutter waves ( AF and Atrial flutter respectively) Other abnormalities of P wave
  41. 41. • the PR interval is the period, measured from the beginning of the P wave (the onset of atrial depolarization ) until the beginning of the QRS complex (the onset of ventricular depolarization) • it is normally between 0.12 – 0.20 sec in duration ( 3-5 small squares). The PR interval
  42. 42. Short PR Interval 1. Low atrial or junctional rhythms. 2. WPW (Wolff-Parkinson- White) Syndrome: Accessory pathway (Bundle of Kent) allows early activation of the ventricle (delta wave, wide QRS and short PR interval)
  43. 43. Long PR Interval • First degree Heart Block
  44. 44. QRS Complexes • Comment on: ( axis, voltage, interval and abnormal Q ) • A) Voltage: • Normally : The amplitudes of all the QRS complexes in any of the six limb leads is > 5 mm • low voltage when: The amplitudes of all the QRS complexes in the limb leads is < 5 mm
  45. 45. QRS Complexes • Specific causes of low voltage include:  Pericardial effusion  Pleural effusion  Obesity  Emphysema  Pneumothorax  Constrictive pericarditidis  Previous massive MI  End-stage dilated cardiomyopathy  Infiltrative myocardial diseases — i.e. restrictive cardiomyopathy due to amyloidosis, sarcoidosis, haemochromatosis  Scleroderma  Myxoedema
  46. 46. QRS Complexes • High Voltage ( Ventricular hypertrophy): A. Left Ventricular Hypertrophy (LVH) (Exaggeration of normal) • S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm or > 7 large squares ( Voltage criteria ) • (±) the left ventricular ‘strain’ pattern : ST segment depression and T wave inversion in the left-sided leads • Concomitantly : left atrial enlargement may be present • N.B. LVH can be diagnosed if S in V1 > 5 large squares or R in V5 or V6 > 5 large squares ( Voltage criteria )
  47. 47. QRS Complexes • Causes of LVH:  Hypertension (most common cause), Aortic stenosis, Aortic regurgitation, Mitral regurgitation, Coarctation of the aorta, Hypertrophic cardiomyopathy
  48. 48. QRS Complexes
  49. 49. QRS Complexes • Right Ventricular Hypertrophy (RVH) (opposite normal)  Right axis deviation of +110° or more.  Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).  Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).  Right atrial enlargement (P pulmonale) may be present.  Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4)
  50. 50. QRS Complexes  Causes of Right Ventricular Hypertrophy (RVH) : Pulmonary hypertension, Mitral stenosis, Pulmonary embolism, Chronic lung disease (cor pulmonale), Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis), Arrhythmogenic right ventricular cardiomyopathy
  51. 51. QRS in LVH & RVH
  52. 52. QRS Complexes  B) Interval (duration): The width of the QRS complex should be less than 3 small squares (0.12 seconds ) Wide QRS Complex: • Bundle branch block • Hyperkalaemia • Pre-excitation (i.e. Wolff-Parkinson-White syndrome) • Hypothermia • Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants) • Ventricular pacing
  53. 53. QRS Complexes Right Bundle Branch Block ( R.B.B.B )  Criteria: • Broad QRS ≥ 0.12 sec ( 3 small squares ) • rsR’ with prominent final R in V1-3 (‘M-shaped’ QRS complex) • Wide final S wave in the lateral leads (I, aVL, V5-6) • ST depression and T wave inversion in the right precordial leads (V1-3)
  54. 54. QRS Complexes Right Bundle Branch Block ( R.B.B.B )  Causes of RBBB: ( Right ventricular hypertrophy / cor pulmonale, Pulmonary embolus, Ischaemic heart disease, Rheumatic heart disease, Myocarditis or cardiomyopathy, Degenerative disease of the conduction system, Congenital heart disease (e.g. atrial septal defect)  R.B.B.B is also called RSR pattern  Can occur in healthy people with normal QRS width ( partial RBBB )
  55. 55. QRS Complexes Left Bundle Branch Block( L.B.B.B )  Criteria: • Broad QRS ≥ 0.12 sec ( 3 small squares ) • Dominant S wave in V1 • Prominent (often notched ) R wave (M shaped ) in lateral leads (I, aVL, V5-V6) • the ST segments and T waves always go in the opposite direction to the main vector of the QRS complex
  56. 56. QRS Complexes Left Bundle Branch Block( L.B.B.B )  Causes : ( Aortic stenosis, Ischaemic heart disease, Hypertension, Dilated cardiomyopathy, Anterior MI, Primary degenerative disease (fibrosis) of the conducting system (Lenegre disease), Hyperkalaemia, Digoxin toxicity )  New onset LBBB with chest pain consider Myocardial infarction  Not possible to interpret the ST segment.
  57. 57. Q wave • The Q wave represents the normal left-to-right depolarisation of the interventricular septum • Non-pathological Q waves: Small ‘septal’ Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6) • A Q wave can be pathological if it is: Deeper than 2 small squares (0.2mV) and/or Wider than 1 small square (0.04s) and/or In a lead other than III or one of the leads that look at the heart from the left (I, II, aVL, V5 and V6) where small Qs (i.e. not meeting the criteria above) can be normal • Pathological Q waves usually indicate current or prior myocardial infarction.
  58. 58. Q wave
  59. 59. Poor R Wave Progression • R wave height ≤ 3 mm ( 3 small squares ) in V3. • The R wave height normally becomes progressively taller from leads V1 through V6.
  60. 60. Poor R Wave Progression • Causes:  Anterior MI  Left ventricular hypertrophy  Dilated cardiomyopathy  Inaccurate lead placement (e.g. transposition of V1 and V3)  WPW syndrome  LBBB, Left anterior fascicular block  Chronic lung disease, Left sided pneumothorax  May be a normal variant
  61. 61. ST Segment • The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave. • It represents the interval between ventricular depolarization and repolarization. • Elevation or depression of ST segment by 1 mm or more Variable Shapes Of ST Segment Elevations in AMI
  62. 62. ST Segment • Abnormalities: • ST Segment Elevation : • Acute myocardial infarction • Coronary vasospasm (Printzmetal’s angina) • Pericarditis • Ventricular aneurysm • Benign early repolarization • Left bundle branch block • Left ventricular hypertrophy • Brugada syndrome • Ventricular paced rhythm • Raised intracranial pressure
  63. 63. ST Segment • Acute ST elevation myocardial infarction (STEMI): There is usually reciprocal ST depression in the electrically opposite leads. Anterolateral STEMI elevation reciprocal ST depression
  64. 64. ST Segment Inferior MI elevation reciprocal ST depression
  65. 65. ST Segment • Pericarditis: • Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6). • Reciprocal ST depression and PR elevation in lead aVR (± V1). • Sinus tachycardia due to pain and/or pericardial effusion.
  66. 66. ST Segment Pericarditis elevation reciprocal ST depression
  67. 67. ST Segment Coronary Vasospasm (Prinzmetal’s angina): • ST elevation that is very similar to acute STEMI occurring during episodes of chest pain. • the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis. It may be impossible to differentiate these two conditions based on the ECG alone.
  68. 68. ST Segment • Left Ventricular Aneursym: • ST elevation seen > 2 weeks following an acute MI. • Most commonly seen in the precordial leads. • May exhibit concave or convex morphology.
  69. 69. ST Segment • ST Depression: • Acute Coronary Syndrome (ACS): Unstable angina (UA) & Non- ST-elevation MI (NSTEMI) ( subendocardial ischaemia ) • Reciprocal change in STEMI • +ve stress E.C.G test • Strain pattern with LVH or RVH ( asymmetrical ) • 2ry ST-T changes with BBB & WPW pattern • Drugs e.g. Digoxin effect • Hypokalaemia • Posterior MI • Variant of normal
  70. 70. ST Segment • Subendocardial ischaemia: • ST depression is usually widespread — typically present in leads I, II, V4-6 and a variable number of additional leads. • ST depression localised to a particular territory (esp. inferior or high lateral leads only) is more likely to represent reciprocal change due to STEMI. The corresponding ST elevation may be subtle and difficult to see, but should be sought.
  71. 71. ST Segment • Digoxin Effect: • Down-sloping ST depression with a characteristic “sagging” appearance (see below). • Flattened, inverted, or biphasic T waves. • Shortened QT interval.
  72. 72. T wave • It represents part of ventricular repolarisation. • Generally follow the direction of the main deflection of QRS • Upright in all leads except aVR and V1 • Amplitude < 5 mm in limb leads, < 10 mm in precordial leads • T wave abnormalities: • Prominent T wave inversion • Tall +ve T wave • Biphasic T waves
  73. 73. T wave • Prominent T wave inversion ( or flat T wave ): • Strain pattern with LVH or RVH • 2ry ST-T changes with BBB & WPW pattern • Hypertrophic cardiomyopathy • subendocardial ischaemia • Evolving phase of MI • Pulmonary embolism • Drugs e.g. Digoxin effect • Normal finding in children • Hypokalaemia • Raised intracranial pressure
  74. 74. T wave • Tall +ve T wave: • The early stages of ST-elevation MI (STEMI) • Hyperkalaemia • Normal variant
  75. 75. T wave • Biphasic T waves: • There are two main causes of biphasic T waves: Myocardial ischaemia Hypokalaemia • The two waves go in opposite directions: Ischaemic T waves go up then down Hypokalaemic T waves go down then up
  76. 76. QT interval  Total duration of Depolarization and Repolarization  Measured from the start of the QRS complex to the end of the T wave.  QT interval decreases when heart rate increases  QT interval should be 0.36–0.44 (9–11 small squares)  Should not be more than half of the interval between adjacent R waves (RR interval).
  77. 77. QT interval 1. A prolonged QT: ( Hypokalaemia, Hypomagnesaemia, Hypocalcaemia, Hypothermia, Myocardial ischemia, Post-cardiac arrest, Raised intracranial pressure, Congenital long QT syndrome, DRUGS ) 2. A short QT: 1. familial/genetic: (short Q-T syndrome) 1. Digoxin toxicity 2. Hypercalcemia 3. Hyperthermia
  78. 78. U wave • The U wave is a small deflection immediately following the T wave, usually in the same direction as the T wave. • It is best seen in leads V2 and V3.They are thought to be due to repolarisation of the atrial septum • Prominent U waves can be a sign of hypokalaemia, hyperthyroidism
  79. 79. E.C.G sequence of MI 1. Acute phase:  ST segment elevation in 2 or more consecutive leads with reciprocal changes (Sometimes tall positive T wave )  At least 1mm ST elevation in limb leads and 2mm in precordial leads to be significant.  Pathological Q appear in leads that show ST elevation (8-48 h ) 2. Evolving phase: ST segment returns to the baseline with development of deep T wave inversion hours to days later in the same leads that show ST elevation 3. Chronic phase: Regression of ST-T changes pathological Q wave without ST-T changes that usually persists for months to years (old MI )
  80. 80. Again localization of leads in STEMI 1. Septal (V1-2) 2. Strict anterior (V3-4) 3. Anteroseptal ( V1 V4 ) 4. Lateral (I , aVL, V5-6) 5. Anterolateral ( V3 V6 ,I,aVL ) 6. Extensive anterior (V1 V6, I,aVL ) 7. Inferior (II, III, aVF)
  81. 81. Inferior Wall MI This is an inferior MI. Note the ST elevation in leads II, III and aVF.
  82. 82. Inferior Wall MI Now how about the inferior portion of the heart? Limb Leads Augmented Leads Precordial Leads Leads II, III and aVF
  83. 83. Anterolateral MI This person’s MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6, I, and aVL)
  84. 84. Lateral MI So what leads do you think the lateral portion of the heart is best viewed? Limb Leads Augmented Leads Precordial Leads Leads I, aVL, and V5- V6
  85. 85. Anterior MI Remember the anterior portion of the heart is best viewed using leads V1- V4. Limb Leads Augmented Leads Precordial Leads
  86. 86. E.C.G Signs of Pulmonary embolism 1. Sinus tachycardia: 8-73%. 2. RBBB (complete/incomplete): 6-67%. 3. Rightward axis shift : 3-66%. 4. P Pulmonale : 6-33%. 5. Inverted T-waves in right chest leads: 50%. 6. S1Q3T3 pattern: 11-50% (S1-60%, Q3-53% ,T3-20%). 7. Clockwise rotation:10-56%. 8. AF or A flutter: 0-35%. 9. No ECG changes: 20-24%.
  87. 87. E.C.G Signs of Pulmonary embolism Heart rate of 100/min & S1Q3T3 & inverted or flattened T waves in leads V1 through V3.
  88. 88. Hyperkalemia (according to K serum level )
  89. 89. Arrhythmias 1. Regular Tachyarrhythmias ( HR >100 beats/minute ):  Sinus tachycardia ( S.T )  Paroxysmal supraventricular tachycardia (PSVT)  Ventricular tachycardia ( VT) Wide QRS  Atrial flutter ( usually regular tachycardia but may be with normal or slow regular HR, or irregular HR with variable heart block ) 2. Regular Bradyarrhythmias (HR < 60 beats/minute ):  Sinus bradycardia ( SB )  Nodal rhythm  Partial heart block  Complete heart block
  90. 90. Arrhythmias 3. Irregular rhythm ( with tachycardia, bradycardia or within normal HR ):  Atrial fibrillation ( A.F ) may be irregular tachycardia, irregular bradycardia or with controlled ( within normal ) rate.  Premature beats ( may occur with sinus tachycardia, sinus bradycardia or with normal rate.  Partial irregular ( variable ) heart block ( bradycardia ).  PSVT & Atrial flutter with variable heart block ( usually tachycardia ).  Ventricular Fibrillation N.B. all arrhythmias are arrow QRS complex except with ventricular origin (Ventricular premature beats , Ventricular tachycardia and sometimes with complete heart block ) Wide QRS complex.
  91. 91. Arrhythmias Regular Tachyarrhythmias : 1. Sinus tachycardia ( S.T ) ( like normal but rapid ): Regular sinus rhythm. Each normal P is followed by a normal QRS complex. Rapid HR ( 100-180 beats/m )
  92. 92. Arrhythmias 2. Paroxysmal supraventricular tachycardia (PSVT) : ( Very rapid > 140/ min ), usually no P wave )  Rapid HR ( 100-250 beats/m ), regular QRS complexes of normal morphology  P wave are either a) Abnormal (deformed or has different shape) atrial tachycardia or b) Inverted ( retrograde ) or usually absent ( buried in QRS ) junctional tachycardia
  93. 93. Arrhythmias 3. VT ( ventricular tachycardia ) : ( wide rapid regular )  QRS complexes are wide ( usually > 0.14 sec ), bizarre shaped with rapid HR ( 120-250 beats/m )  P wave are of normal ( 60-100/m) rate and usually obscured by QRS complexes but sometimes may be superimposed on QRS complexes with A-V dissociation.
  94. 94. Arrhythmias 4. Atrial flutter : ( Saw-tooth appearance, usually regular tachycardia, exclusion. DD from AF )  P wave is replaced by flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF . may be more easily spotted by turning the ECG upside down!  Atrial rate = 250-350/m with a ventricular rate that is often fraction of the atrial rate ( 1/2, 1/4 , etc )  Atrial rate = 1500/ F-F interval ( small squares ) or simply ( no of F waves before QRS +1) X HR ( ventricular rate )
  95. 95. Arrhythmias Regular Bradyarrhythmias : 1. Sinus bradycardia ( like normal but slow ): Regular sinus rhythm. Each normal P is followed by a normal QRS complex. Slow HR (< 60 beats/m)
  96. 96. Arrhythmias 2. Nodal ( junctional ) rhythm : ( Slow, no or retrograde P wave ). QRS complexes are regular, narrow, slow ( usually 40-60 beats/m ) of normal morphology. P wave is either : a) absent b) Inverted (retrograde)
  97. 97. Arrhythmias 3. Heart block : a) First degree HB: constant prolongation of P-R interval > 0.20 sec (> 5 small squares ) b) Second degree HB 2 subtypes: Mobitz type I HB ( Wenckebach ): Progressive prolongation of the PR interval from beat to beat until a dropped or non conducted beat then the sequence is repeated.
  98. 98. Arrhythmias Mobitz type II HB :  Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I).  The PR interval in the conducted beats remains constant.  The block may be fixed ( 2:1, 3:1 ) or variable.
  99. 99. Arrhythmias c) Third degree HB ( complete HB ): ( No relation between QRS and P waves)  QRS may be normal width or abnormally wide of slow regular rate ( 30- 60 beats/m)  P waves are of normal regular rate and may be superimposed on QRS complex and T wave. Atrial rate is almost always faster than ventricular rate. P-R interval is constantly changing. There is complete A-V dissociation.
  100. 100. Arrhythmias  1St & 2nd degree HB are considered incomplete or partial HB.
  101. 101. Arrhythmias 3. Irregular rhythm : 1) A.F.: ( irregular) • Irregularly irregular rhythm. No P waves. • Variable ventricular rate. QRS complexes usually rapid ( 100- 200 beats/m) but may be slow from drug toxicity e.g. digitalis or disease of A-V junction or controlled by drugs e.g. digitalis. • Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm). • Fibrillatory waves may mimic P waves leading to misdiagnosis.
  102. 102. Arrhythmias 2. Premature beats = Extrasystole: • Comes prematurely followed by compensatory pause. • Premature peats may occur with sinus tachycardia, sinus bradycardia or with normal heart rate. Atrial premature beats ( APB ) ( Like normal but comes early followed by slight compensatory pause ) A premature abnormal ( deformed or has different shape ) P wave with different PR interval followed by normal QRS complex followed by slight compensatory pause.
  103. 103. Arrhythmias Ventricular premature beats ( VPB ) ( wide, bizarre, comes early and followed by full compensatory pause) Abnormal ( Wide > 0.12 sec, bizarre ) premature QRS complex not preceded by P wave followed by full compensatory pause. The T wave is of opposite direction to QRS . ( uniform VPBs : the same shape in a single lead, multiform VPBs : different shapes in the same lead ).
  104. 104. Arrhythmias Ventricular premature beats ( VPB ) N.B. When a VPB occurs regularly after each normal beat Ventricular bigemini ( common with digitalis toxicity )
  105. 105. Arrhythmias Ventricular premature beats ( VPB ) When the rhythm is two normal beats followed by a VPB ventricular trigemini
  106. 106. Arrhythmias Ventricular premature beats ( VPB ) When two VPBs in a row ventricular couplet
  107. 107. Arrhythmias 1. When a APB occurs regularly after each normal beat Atrial bigemini 2. When the rhythm is two normal beats followed by a APB Atrial trigemini 3. When two APBs in a row Atrial couplet 1 2 3
  108. 108. Arrhythmias none• Rate? • Regularity? irregularly irregular none wide, if recognizable • P waves? • PR interval? none • QRS duration? Ventricular Fibrillation
  109. 109. ECG RULES • Professor Chamberlains 10 rules of a normal ECG, a foundation to ECG interpretation used all over the world to this date.
  110. 110. RULE 1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
  111. 111. RULE 2 The width of the QRS complex should not exceed 110 ms, less than 3 little squares
  112. 112. RULE 3 The QRS complex should be dominantly upright in leads I and II
  113. 113. RULE 4 QRS and T waves tend to have the same general direction in the limb leads
  114. 114. RULE 5 All waves are negative in lead aVR
  115. 115. RULE 6 The R wave must grow from V1 to at least V4 The S wave must grow from V1 to at least V3 and disappear in V6
  116. 116. RULE 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated
  117. 117. RULE 8 The P waves should be upright in I, II, and V2 to V6
  118. 118. RULE 9 There should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6
  119. 119. RULE 10 The T wave must be upright in I, II, V2 to V6

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