ECG Analysis

ECG Analysis

1. ECGs A systemic guide Peter Watson

2. Objectives Electrical conduction in the heart Lead placement ECG settings ECG components ECG waves ECG complexes Abnormalies seen with ECG components Systemically work through an example

3. Cardiac conducting system Cardiac depolarisation begins at the Sinoatrial node, then spreads to the Atrioventricular node, before travelling to the Bundle of HIS and the Purkinje fibres to complete an electrical cardiac cycle.

4. ECG Waves and Components

5. 12 Lead ECG Placement 10 electrodes required to produce 12-lead ECG 4 Electrodes on all 4 limbs (RA, LL, LA, RL) 6 Electrodes on precordium (V1–6) Monitors 12 leads (V1–6), (I, II, III) and (aVR, aVF, aVL) Allows interpretation of specific areas of the heart ◦ Inferior (II, III, aVF) ◦ Lateral (I, aVL, V5, V6) ◦ Anterior (V1–4)

6. Components of the ECG Rate Rhythm Axis P wave PR interval QRS complex QT interval & QTc ST segment T wave Other: Delta wave Epsilon waves Osborne waves U waves

7. ECG Worksheet

8. Normal ECG The normal ECG will display these characteristics: • Rate • 60- 99bpm • Rhythm • <10% variation in RR intervals) • Cardiac Axis • -30° – 90° • P Waves • 0.2-0.3mV • 0.06 – 0.12s • Upright in I, II, aVF, V2- V6 • Inverted in aVR • Varies in III, aVLSinus origin • PR Interval • 0.12 – 0.2s • Q Waves • Small in I, II, aVL, V5, V6 • QRS Complex • <0.12s • ST Segment • Isoelectric • T Waves • <2/3 height of preceding R wave • 0.5mm in I, II, III • <10mm in V1 – V6 • Same direction as preceding R wave • U Waves • <25% of T wave • Same direction as T wave • QTc • <440ms in males • <460ms in females

9. The Normal ECG

10. Standard ECG Settings Normal paper/monitor speed is 25mm/sec 1mm = 40msec (one small square) 5mm = 120msec (one big square) V = 10mm/mV V = 10mm/mV

11. Standard ECG Settings Normal paper/monitor speed is 25mm/sec Check the monitor/paper speed, this should be displayed on the ECG

12. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval QRS complex QT interval & QTc ST segment T wave Other waves

13. Rate Adults Bradycardia < 60bpm Normal 60-100bpm Tachycardia >100bpm Children Normal range of heart rate is age dependent

14. Rate Calculating rate: one ECG paper page at 25mm/sec = 10sec duration, thus count complexes and x6 = Rate OR For regular rhythms; Rate = 300 /(No. large squares in-between the complexes) For really fast rhythms; Rate = 1500/(No. small squares in-between the complexes)

15. Heart Rate: Children

16. Sinus Bradycardia Heart rate 35bpm

17. Sinus Tachycardia Heart rate 150bpm; Note P waves hidden in T waves

18. Normal Sinus Rhythm Heart rate 84

19. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval QRS complex QT interval & QTc ST segment T wave Other waves

20. Rhythm Rhythms rate? Tachy/Brady/Normal Are P waves present? Are P waves regular? Is there always one P waves followed by one QRS complex? Are QRS complexes regular morphology and regular timing? Is the PR interval regular? Is there AV association?

21. Rhythm Regular OR Irregular Irregularly Irregular Regularly Irregular There are two parts of the rhythm Atrial: P waves Ventricular: QRS complex For each component, ?Is the rhythm;

22. Are P-waves Present? ie. Is atrial activity present? Sinus P-waves are up in II and aVF P-wave duration <120ms Morphology - positive dome shaped in II an aVF If retrograde activation then P-waves in II and aVF are inverted “Saw-tooth” flutter waves with a rate of 300/min No P-waves -> AF or atrial asystole

23. Rhythm If P-waves aren’t present it maybe: sinus arrest atrial fibrillation

24. Rhythm If P-waves are present it maybe: sinus atrial junctional, OR retrograde

25. Rhythm - QRS complex duration If the rhythm originates above the AV node the QRS complex will be narrow <120msec, it will be propagated down the Bundles of His and through the heart as normal. If the rhythm originates below the AV node it will be propagated retrograde and antegrade and will appear broad >120msec. The further away from the AV node, the wider the QRS complex The exception to this is SVT with aberrant conduction

26. Rhythm Is the atrial activity related to ventricular activity? Is there a constant interval between p-waves and QRS complexes? Yes, then its likely the conduction between them is intact. OR Yes, but not with every atrial depolarisation. ie Atrial flutter with 2:1 block No, there is a conduction delay i.e. 2nd degree heart block, Mobitz I (Wenckebach) or Mobitz II

27. Bradycardia Is there always one P waves followed by one QRS complex? Yes Sinus Bradycardia Sinus node exit block Sinus pause/arrest Junctional escape rhythm

28. Sinus arrest with a ventricular escape rhythm Sinus pause / arrest (there is a single P wave visible on the 6-second rhythm strip). Broad complex escape rhythm with a LBBB morphology at a rate of 25 bpm. The LBBB morphology (dominant S wave in V1) suggests a ventricular escape rhythm arising from the right bundle branch.

29. Bradycardia Is there always one P waves followed by one QRS complex? No AV block: 2nd degree, Mobitz 1 (Wenkebach) 2nd degree, Mobitz 1I 2nd degree, Mobitz 1 or II with fixed ratio ie 2:1, 3:1 2nd degree, Mobitz 1 or II with high grade block ≥3:1 3rd degree/Complete Heart Block Ventricular escape rhythm

30. First Degree Heart Block

31. AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon) Progressive prolongation of the PR interval culminating in a non-conducted P wave T he PR interval is longest immediately before the dropped beat The PR interval is shortest immediately after the dropped beat

32. AV Block: 2nd degree, Mobitz II 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.

33. AV block: 3rd degree (complete heart block) In complete heart block, there is complete absence of AV conduction – none of the supraventricular impulses are conducted to the ventricles. Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).

34. Ventricular escape rhythm in sinus arrest

35. Rhythm - Narrow complex tachycardia Regular atrial Sinus tachycardia Atrial tachycardia Atrial flutter Inappropriate sinus tachycardia Sinus node re-entrant tachycardia Regular Atrioventricular Atrioventricular re-entry tachycardia (AVRT) AV nodal re-entry tachycardia Automatic junctional tachycardia Irregular atrial Atrial fibrillation Atrial flutter with variable block Multifocal atrial tachycardia

36. Narrow complex tachycardias AF Atrial flutter

37. AV nodal re-entry tachycardia (AVNRT) AKA supraventricular tachycardia typically paroxysmal, may be spontaneous or provoked Rapid Palpitation, may have pre-syncopal symptoms Tachycardia 140-280bpm and regular Occurs via a functional re-entry circuit within the AV node

38. AV nodal re-entry tachycardia (AVNRT) In AVNRT, there are two pathways within the AV node: The slow pathway  ( alpha ):  a slowly-conducting pathway with a short refractory period. The fast pathway ( beta ):  a rapidly-conducting pathway with a long refractory period. I f a premature atrial contraction (PAC)  arrives while the fast pathway is still refractory, the electrical impulse will be directed solely down the slow pathway (1). By the time the premature impulse reaches the end of the slow pathway, the fast pathway is no longer refractory (2) — hence the impulse is permitted to recycle retrogradely up the fast pathway, thus creating a circus movement Three Subtypes 1 Slow-Fast AVNRT (common type) no visible p waves 2 Fast-Slow AVNRT (Uncommon AVNRT) P waves visible after the QRS complexes 3 Slow-Slow AVNRT (Atypical AVNRT) P waves visible before the QRS complexes

39. AV nodal re-entry tachycardia (AVNRT) Slow-Fast (Typical) AVNRT: Narrow complex tachycardia at ~ 150 bpm. No visible P waves. There are pseudo R’ waves in V1-2.

40. Atrioventricular re-entry tachycardia (AVRT) AVRT is a form of paroxysmal supraventricular tachycardia, occurring in people with WPW syndrome. A reentry circuit is formed by the normal conduction system and the accessory pathway (Bundle of Kent) resulting in circus movement. During tachyarrythmias the features of pre-excitation are lost as the accessory pathway forms part of the reentry circuit. AVRT often triggered by premature atrial or premature ventricular beats. Tachyarrhythmias can be fatal with AVRT AVRT are further divided in to orthodromic or antidromic conduction based on direction of reentry conduction and ECG morphology.

41. Type A WPW Delta wave, Dominant R wave in V1, associated with left side accessory pathway

42. Type B WPW Dominant S wave in V1, Delta wave, short PR interval, associated with right side accessory pathway

43. Orthodromic Atrioventricular re-entry tachycardia (AVRT) Orthodromic AVRT antegrade conduction is via the node and retrograde via the accessory pathway Rate 200-300bpm P waves buried in QRS QRS alterans ST depression T wave inversion

44. Orthodromic AVRT Narrow complex tachycardia 180bpm, no P waves

45. Atrioventricular re-entry tachycardia (AVRT) Antidromic AVRT antegrade conduction via the accessory pathway with retrograde conduction via the node Rate 200-300bpm Wide QRS Occurs in ~5% of WPW

46. Antidromic AVRT Regular broad complex tachycardia,

47. Rhythm - Broad complex tachycardia Regular Ventricular tachycardia Antidromic Atrioventricular re-entry tachycardia (AVRT) Supraventricular tachycardia with aberrant conduction Irregular Ventricular Fibrillation Polymorphic VT Torsades de Pointes AF with WPW SVT with aberrant conduction; ie RBBB

48. AF/Atrial Flutter in WPW Atrial fibrillation can occur in up to 20% of patients with WPW. Atrial flutter can occur in up to 7% of patients with WPW. The accessory pathway allows for rapid conduction directly to the ventricles bypassing the AV node. Rapid ventricular rates may result in degenerati on to VT or VF. Rate > 200 bpm Irregular rhythm Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway QRS Complexes change in shape and morphology Axis remains stable unlike Polymorphic VT

49. AF with WPW Very rapid 300bpm, 2 conducted beats in V1-3, lack of twisting seen in Torsades de Point

50. Monomorphic VT Ventricular Tachycardia (VT) is a broad complex tachycardia originating in the ventricles. Monomorphic VT is the most common. Reenty pathway develops due to prior ischaemia or infection causing abnormal myocardial scarring leading to two distinct conduction pathways with a conduction block and region of slow conduction, and is triggered by early or late depolarisation and then accelerated abnormal impulses generated in the ventricle >30sec sustained; <30sec non-sustained Patients maybe haemodynamically stable

51. Monomorphic VT Uniform QRS complexes, indeterminate axis, Very broad QRS ~200ms, Josephsons sign, notching near the nadir of the S wave

52. Increased risk of VT rather than SVT Clinical features ECG features Age >35years AV dissociation Smoker Fusion beats Ischaemic heart disease Captured beats Previous VT Left axis variation >30° favours VT Active angina QRS morphology in V1 Cannon “a” waves Variable intensity of S1 Unchanged intensity of S2 QRS with >140ms (<120ms SVT) Concordance of QRS vectors in pericardial leads Brugada’s sign Josephson’s sign

53. Brugada’s sign (red callipers) – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms. Josephson’s sign (blue arrow) – Notching near the nadir of the S-wave.

54. Polymorphic VT & Torsades de Pointes Polymorphic ventricular tachycardia (PVT) is a form of  ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration.  The commonest cause of PVT is myocardial ischaemia. Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation; it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.

55. Causes of Torsades de Point Hypomagnesia Hypocalcaemia Class I and Class II antiarrhytmic drugs Phenothiaxine Tricyclic antidepressants Congenital long QT syndrome Organophosphates Complete heart block Drug interaction of terfenidine with erythromycin

56. Polymorphic VT-TdP Sinus rhythm with inverted T waves, prominent U waves and a long Q-U interval due to severe hypokalaemia (K+ 1.7)

57. Torsades de Pointes “R on T” phenomenon causing Torsades de Pointes , which subsequently degenerates to VF

58. Ventricular fibrillation Ventricular fibrillation (VF) is the the most important shockable cardiac arrest rhythm. The ventricles suddenly attempt to contract at rates of up to 500 bpm. This rapid and irregular electrical activity renders the ventricles unable to contract in a synchronised manner, resulting in immediate loss of cardiac output. The heart is no longer an effective pump and is reduced to a quivering mess. Unless  advanced life support  is rapidly instituted, this rhythm is invariably fatal. Prolonged ventricular fibrillation results in decreasing waveform amplitude, from initial coarse VF to fine VF and ultimately degenerating into asystole due to progressive depletion of myocardial energy stores. ECG Chaos, no P wave, no QRS, no T wave, Rate 150-500bpm

59. TdP to Ventricular Fibrillation

60. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval QRS complex QT interval & QTc ST segment T wave Other waves

61. Cardiac Axis Cardiac depolarisation begins at the Sinoatrial node, then spreads to the Atrioventricular node, before travelling to the Bundle of HIS and the Purkinje fibres to complete an electrical cardiac cycle. The biggest wave height changes occur in leads inline with the cardiac depolarisation. The smallest wave height changes occur in those leads perpendicular to the cardiac depolarisation

62. Cardiac Axis Normal Axis   = QRS axis between -30°& +90° Left Axis Deviation = QRS axis <-30°. Right Axis Deviation = QRS axis >+90°. Extreme Axis Deviation = QRS axis between -90° & 180° (“Northwest Axis”).

63. How to calculate the Cardiac Axis There are several ways to calculate the cardiac axis: Quadrant Method - Leads 1 & aVF 3Lead analysis - Leads 1 & aVF Isoeletric Lead analysis Reaching and Leaving - Leads I & II Calculated method or Sam the Axis Man

64. Quadrant Method Using Leads I and aVF if positive in Lead I the axis is towards Lead I if positive in Lead aVF the axis is towards aVF This would be a normal axis between 0-90°

65. Watsons’ Thumbs Up Quadrant method Hold the ECG and look at it Your left hand should be closest to Lead I, and right hand closer to Lead aVF than your left hand Point you Left thumb up or down corresponding to Lead I Point you Right thumb up or down corresponding to Lead aVF

66. Watsons’ Thumbs Up Quadrant method Both thumbs up - good ie. normal axis Left thumb up (+QRS in Lead I, -QRS in aVF) Left axis deviation Right thumb up (-QRS in Lead I, +QRS in aVF) Right axis deviation Both thumbs down - bad really bad ie. NW axis

67. 3 lead analysis Buy adding in Lead II to the Quadrant method allows for more specific analysis of axis

68. 3 lead analysis

69. Isoelectric Lead The Lead with the least electric activity (equaphasic) has an axis at 90° to the axis

70. Reaching and Leaving This is a quick glance technique only. Are Leads I & II Reaching towards each other? ie the QRS of Lead I is predominately negative and Lead II is predominately positive = RAD Are Leads I & II Leaving each other? ie the QRS of Lead I is predominately positive and Lead II is predominately negative = LAD

71. Calculated Method Measure Lead I’s overall height = R-S (mm) Measure Lead aVF overall height = R-S (mm) Place into this formula Axis = tan - (Lead I R-S)/(Lead aVF)* *If both leads I and aVF are positive, this figure stands works for the cardiac axis If not, add 90° to the calculated figure

72. Sam- the Supper Axis Man plot the net deflection (R-S) of Lead I plot the net deflection (R-S) of Lead aVF The intersection of these two lines is the cardiac axis https://lifeinthefastlane.com/super-axis-man/

73. Normal Axis Lead I and aVF positive (and Lead II); Not reaching Not leaving; Two thumbs up aVL is isoelectric (-30°) thus axis is 60° Tan - Lead I R-S (8-3=5) / Lead aVF R-S (8-0=8) =+55°

74. Right Axis Deviation Lead I negative and aVF (and Lead II) positive; Reaching Not leaving; Right thumb up aVR is isoelectric (-150°) thus axis is +120° Tan - Lead I R-S (0-4=4) / Lead aVF R-S (12-1=11) [+90°] =-124°

75. Right Axis Deviation Right ventricular hypertrophy Acute right ventricular strain , e.g. due to pulmonary embolism Lateral STEMI Chronic lung disease, e.g. COPD Hyperkalaemia Sodium-channel blockade, e.g. TCA poisoning Wolff-Parkinson-White syndrome Dextrocardia Ventricular ectopy Secundum ASD – rSR’ pattern Normal paediatric ECG Left posterior fascicular block – diagnosis of exclusion Vertically orientated heart – tall, thin patient Wrong limb leads

76. Left Axis Deviation Lead I positive and aVF (and Lead II) negative; Not reaching but leaving; Left thumb up aVR is isoelectric (-150°) thus axis is -60° Tan - Lead I R-S (0-4=4) / Lead aVF R-S (12-1=11) [+90°]=-124°

77. Left Axis Deviation Left ventricular hypertrophy Left bundle branch block Inferior MI Ventricular pacing /ectopy Wolff-Parkinson-White Syndrome Primum ASD – rSR’ pattern Left anterior fascicular block – diagnosis of exclusion Horizontally orientated heart – short, squat patient

78. Extreme Axis Deviation Lead I and aVF (and Lead II) negative; Not reaching and leaving; Both thumbs down isoelectric? Tan - Lead I R-S (5-15=10) / Lead aVF R-S (10-0=10) [+90°+90°]=-135°

79. Extreme Axis Deviation Ventricular rhythms – e .g.VT, AIVR, vent ricular ectopy Hyperkalaemia Severe right ventricular hypertrophy

80. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval QRS complex QT interval & QTc ST segment T wave Other waves

81. Normal P waves Smooth contour Upright in lead II Inverted in aVR Biphasic in V1 ≤120msec duration (≤ 3 small squares wide) ≤ 2.5 mm in limb leads <1.5mm in precordial leads Axis 0 to 75°; upright in Leads I, & II and inverted in aVR Atrial activity is best seen in leads II and V1

82. P wave abnormalities P mitrale  (bifid P waves), seen with left atrial enlargement. P pulmonale  (peaked P waves), seen with right atrial enlargement. P wave inversion, seen with ectopic atrial and junctional rhythms. Variable P wave morphology, in multifocal atrial rhythms.

83. Left atrial enlargement (“P mitrale”) Bifid / notched P waves in lead II P wave > 3 small squares wide Classically caused by mitral stenosis

84. Right atrial enlargement (“P pulmonale”) Peaked P waves in lead II >2.5mm tall Indicates right heart dilatation, e.g. due to cor pulmonale

85. Biatrial atrial enlargement (“P pulmonale”) Peaked P waves in lead II > 2.5 mm tall Indicates right heart dilatation, e.g. due to cor pulmonale

86. Flutter Waves Seen with atrial flutter “Sawtooth” pattern at 300 bpm (one wave per large square) Best appreciated by turning the ECG upside down

87. Fibrillatory Waves Seen with atrial fibrillation Irregular, chaotic waveform May be coarse or fine Best seen in V1 Not always visible (may just have a irregular baseline) Coarse AF Fine AF

88. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval QRS complex QT interval & QTc ST segment T wave Other waves

89. PR interval The PR Interval indicates atrioventricular conduction time. The interval is measured from where the P wave begins until the beginning of the QRS complex. This represents the conduction though the AV node Normal duration 120-200msec <120msec suggests pre-excitation (eg. WPW)or AV nodal (junctional rhythm)

90. How to interpret the PR interval

91. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval Q waves QRS complex QT interval & QTc ST segment T wave Other waves

92. QRS complex Composed of Q waves, R waves and S waves Normal duration 70-100ms QRS duration can indicate the origin of each complex ie sinus, atrial, junctional, ventricular Narrow complexes originate above the ventricles Broad complexes originate from the ventricles or are due to conduction delays. Large voltage? Hypertrophy Low voltage? Impedance (fat, fluid)

93. Normal Q waves Produced by depolarisation of the interventricular septum Any negative deflection prior to the R wave Features of normal (“septal”) Q waves: < 1 mm wide < 2 mm deep Absent in V1-3 NB. Larger Q waves are permitted in leads III and aVR as a normal variant

94. Pathological Q Waves Indicate previous myocardial infarction Features: > 1 mm wide (>40msec) > 2 mm deep Seen in V1-3

95. Pathological Q Waves Differential Diagnosis include: Myocardial infarction Cardiomyopathies - HCM (“dagger Q waves”), infiltrative myocardial disease Rotation of the heart - extreme clock/anticlockwise rotation Lead placement errors

96. Pathological Q waves This ECG demonstrates Q waves in the inferior leads indicating a prior inferior infarct.

97. Dagger-like Q waves Hypertrophic (Obstructive) Cardiomyopathy HCM (HOCM); Dagger-like “septal Q waves” in the lateral leads.

98. R waves First positive deflection following the P wave Represents the early ventricular depolarisation R waves: Increase in height from V1-5 then decrease in V6 Abnormalities include: Dominant R Wave in V1 Dominant R wave in aVR Poor R wave progression

99. Dominant R waves in V1 Normal in children and young adults Right Ventricular Hypertrophy (RVH) Pulmonary Embolus Persistence of infantile pattern Left to right shunt Right Bundle Branch Block (RBBB) Posterior Myocardial Infarction (ST elevation in Leads V7, V8, V9) Wolff-Parkinson-White (WPW) Type A Incorrect lead placement (e.g. V1 and V3 reversed) Dextrocardia Hypertrophic cardiomyopathy Dystrophy Myotonic dystrophy Duchenne Muscular dystrophy

100. Paediatric ECG Dominant R waves in V1

101. Right Bundle Branch Block Dominant R waves in V1-6

102. Dominant R wave in aVR Poisoning with sodium-channel blocking drugs (e.g. TCAs) Dextrocardia Incorrect lead placement (left/right arm leads reversed) Commonly elevated in ventricular tachycardia (VT)

103. Sodium Channel Blockade Dominant ‘R wave in aVR . Marked Tachycardia R/S ratio ~0.7 This patient had taken 300 tablets of Amitryptaline 10mg, and had received IV NaHCO3

104. Dextrocardia Positive QRS complexes (with upright P and T waves) in aVR . Negative QRS complexes (with inverted P and T waves) in lead I . Marked right axis deviation . Absent R-wave progression in the chest leads (dominant S waves throughout)

105. Poor R Wave Progression Prior anteroseptal MI LVH WPW Dextrocardia Left bundle branch block or left anterior fascicular block Tension pneumothorax with mediastinal shift Congenital heart disease Inaccurate lead placement esp. in obese women May be a normal variant

106. Left Bundle Branch Block Note the poor R wave progression in the precordial leads

107. QRS Bundle Branch Blocks Left BBB depolarised from RV via the right bundle then to the LV via the left bundle Right BBB RV depolarisation is delayed, and spreads form left to right

108. Left Ventricular Hypertrophy LV hypertrophies in response to pressure overload such as AS, AR, hypertension, HCM, MR. This l eads to: Increased R wave amplitude in the left-sided (lateral) ECG leads (I, aVL and V4-6) Increased S wave depth in the right-sided leads (III, aVR, V1-3). The thick LV wall leads to prolonged depolarisation (increased R wave peak time) and delayed repolarisation (ST and T-wave abnormalities) in the lateral leads.

109. Left Ventricular Hypertrophy LVH criteria: Sokolov-Lyon criteria (S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm). Increased R wave peak time >50msec in V5-6 ST depression, T wave inversion, ‘strain’ pattern in I, aVL, and V5-6

110. Right Ventricular Hypertrophy RV hypertrophies in response to pressure overload such as pulmonary hypertension, PS, PR, MS, PE, Chronic lung disease ( cor pulmonale), Congential heart disease, VSD, ARVD. This l eads to: Right axis deviation Dominant R wave in V1 >7mm Dominant S wave in V6 >7mm QRS <120msec May see p pulmonale, RV strain pattern in V1-4, II, III, & aVF, S1S2S3 pattern, Deep S waves in lateral leads (I, aVL, V5-6)

111. Right Ventricular Hypertrophy Right axis deviation, Dominant R in V1 (>7mm), Dominant S in V6 (>7mm), Right ventricular strain pattern with ST depression and T wave inversion in V1-4

112. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval Q waves QRS complex QT interval & QTc ST segment T wave Other waves

113. QT and QTc The QT interval indicates ventricular activity, both depolarization and repolarization. QT is inversely proportional to heart rate. Measure the QT interval from the beginning of the QRS complex to the end of the T wave. Males 440msec Females 460msec QT>500msec risk of Torsades de Pointes

114. QT and QTc Bazett’s formula : QTC = QT / √ RR Fredericia’s formula : QTC = QT / ∛RR Framingham formula : QTC = QT + 0.154 (1 – RR) Hodges formula : QTC = QT + 1.75 (heart rate – 60) Guestimate: if the QT is less than half the RR interval it’s probably normal

115. Prolonged QTc Hypokalaemia, hypomagnesia, hypocalcaemia Hypothermia Myocardial ischaemia Post cardiac arrest Raised ICP Congenital long QT syndrome eg, Jervelle and Lange–Neilson syndrome (associated with deafness) Drugs: Antiarrhythmics; flecainide, quinidine, sotalol, procainamide, amiodarone Gastric motility promoter; cisapride, domperidone Antibiotics; clarithromycin, erythromycin Antipsychotics; chlorpromazine, haloperidol

116. Hypomagnesia QTc 510msec

117. QT Normogram Risk of TdP is determined by considering both the absolute QT interval and the simultaneous heart rate A QT interval-heart rate pair that plots above the line indicates that the patient is at risk of TdP.

118. Quetiapine toxicity QT 560msec, HR 120 Despite the QT prolongation, the risk of TdP is decreased due to the concurrent tachycardia.

119. Short QTc Hypercalcaemia Short QT syndrome Short QT syndrome is a recently-discovered arrhythmogenic disease associated with paroxysmal atrial and ventricular fibrillation, syncope and sudden cardiac death. Due to a potassium channelopathy Digoxin effect

120. Congenital Short QTc Very short QTc (280ms) with tall, peaked T waves

121. Digoxin effect QT 260msec QTc 310msec Note the reverse tick appearance in the lateral leads

122. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval Q waves QRS complex QT interval & QTc ST segment T wave Other waves

123. ST segment The ST segment begins at the end of the QRS complex and continues to beginning of the T wave. 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. The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.

124. ST segment changes and Coronary arteries

125. ST Elevation Causes of ST elevation Acute myocardial infarction Coronary vasospasm (Printzmetal’s angina) Pericarditis Benign early repolarization Left bundle branch block Left ventricular hypertrophy Ventricular aneurysm Tako-Tsubo cardiomyopathy Brugada syndrome Ventricular paced rhythm Raised intracranial pressure Less Common Causes of ST segment Elevation Pulmonary embolism and acute cor pulmonale (usually in lead III) Acute aortic dissection (classically causes  inferior STEMI  due to RCA dissection) Hyperkalaemia Sodium-channel blocking drugs (secondary to QRS widening) J-waves  (hypothermia, hypercalcaemia) Following electrical cardioversion Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease

126. Benign Early Repolarisation Widespread modest (<25% Twave height) STE, Notching at the J point, Concordant T waves, No reciprocal changes, Fish-hook pattern in V4

127. Extensive Anterior AMI ST elevation in V1-6 plus I and aVL (most marked in V2-4). Minimal reciprocal ST depression in III and aVF. Q waves in V1-2, reduced R wave height (a Q-wave equivalent) in V3-4. There is a premature ventricular complex (PVC) with “R on T’ phenomenon at the end of the ECG; this puts the patient at risk for malignant ventricular arrhythmias.

128. Pericarditis Generalised ST elevation , Presence of PR depression , Normal T wave amplitude , ST segment / T wave ratio > 0.25 , Absence of “fish hook” appearance in V4

129. ST Depression ST depression can be either upsloping, downsloping, or horizontal. Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia ( according to t he 2007 Task Force Criteria ). Upsloping ST depression in the precordial leads with prominent “De Winter’s” T waves is highly specific for occlusion of the LAD. Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction. Posterior MI manifests as horizontal ST depression in V1-3 and is associated with upright T waves and tall R waves.

130. ST Depression Myocardial ischaemia / NSTEM I; LMCA, Triple vessel disease. Reciprocal change in STEMI; Inferior STEMI produces reciprocal ST depression in aVL (± lead I). Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II). Reciprocal ST depression in V1-3 occurs with posterior infarction Posterior MI De Winters T waves Digoxin effect Hypokalaemia: widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval. Supraventricular tachycardia Right bundle branch block (RBBB): Right ventricular hypertrophy: Left bundle branch block Left ventricular hypertrophy Ventricular paced rhythm Supraventricular Tachycardia(e.g. AVNRT) rate-related widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). resolves with treatment.

131. Posterior MI ST depression in V2-3. Tall, broad R waves (> 30ms) in V2-3. Dominant R wave (R/S ratio > 1) in V2, Upright terminal portions of the T waves in V2-3

132. Sgarbossa Criteria for LBBB/paced rhythms Modified Sgarbossa Criteria: ≥ 1 lead with ≥1 mm of concordant ST elevation ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave. These criteria are specific, but not sensitive for myocardial infarction. A total score of  ≥ 3 is reported to have a specificity of 90% for diagnosing myocardial infarction. But Low sensitivity (20%)

133. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval Q waves QRS complex QT interval & QTc ST segment T wave Other waves

134. T wave The T wave is the positive deflection after each QRS complex and represents ventricular repolarisation . Upright in all leads except aVR and V1 Amplitude < 5mm in limb leads, < 15mm in precordial leads

135. T wave Abnormalities Hyperacute “Peaked" T waves: Early STEMI, (De Winters T waves), Prinzmetal angina Inverted T waves: Paediatric, MI, BBB, Ventricular Hypertrophy “strain pattern”, PE, HCM, Raised ICP Biphasic T waves: MI, Hypokalaemia Wellens’ Syndrome; type I, and type II (LAD critical stenosis) ‘Camel Hump’ T waves; prominent U waves, hidden P waves Flattened T waves; Ischaemia, hypokalaemia

136. De Winters T waves T waves are tall and peaked , and preceded by an area of up-sloping ST segment depression in most of the precordial leads (esp V2 – V5). There is no ST elevation in these leads but there is subtle ST elevation in aVR. strongly suggestive of an acute left anterior descending coronary artery occlusion.

137. Wellens Syndrome Note the Biphasic T wave in V2

138. Hypertrophic Cardiomyopathy Deep T-waves in all of the precordial leads.

139. Bilateral Pulmonary Embolism T wave inversion in the inferior and right pericardial leads

140. U waves The U wave is a small (0.5 mm up to 2mm) deflection immediately following the T wave Inversely proportional to the heart rate, more visible when HR <65 bpm. U wave is usually in the same direction as the T wave. U wave is best seen in leads V2 and V3.

141. Prominent U waves U wave >2mm or >25% of the T wave Prominent with bradycardia, severe hypokalaemia Maybe seen with: hypocalcaemia, hypomagnesia, hypothermia Raised ICP LVH HCM Drugs: Digoxin, Phenothiazides, Class Ia (quinidine, procainamide) and Class III (sotalol, amiodarone) antiarrhythmics

142. Inverted U waves U wave inversion in leads with upright T wave A negative U wave is highly specific for the presence of heart disease The main causes of inverted U waves are: Coronary artery disease Hypertension Valvular heart disease Congenital heart disease Cardiomyopathy Hyperthyroidism Unstable angina

143. Sinus Bradycardia Prominent U waves in this patient with anorexia nervosa

144. NSTEMI Subtle U wave inversion the lateral leads (I, V5-6)

145. Step-by-Step ECG Analysis Rate Rhythm Axis P wave PR interval Q waves QRS complex QT interval & QTc ST segment T wave Other waves

146. Other Waves Delta Wave Epsilon Waves Osborne Waves

147. Delta Waves Slurred upstroke of the QRS complex Often associated with a short PR interval <120msec Most commonly seen in WPW syndrome Broad QRS (>100msec)

148. Wolff-Parkison-White Syndrome Delta Waves (slurred upstroke of her QRS) are the cardinal sign of WPW, and most obvious in leads V1 & V2. The minor ST changes seen resolved promptly.

149. Epsilon Waves The epsilon wave is a small positive deflection (‘blip’) buried in the end of the QRS complex. Characteristic finding in arrhythmogenic right ventricular dysplasia (ARVD).

150. Osborne Waves Osborne Waves (J wave) is a positive deflection at the J point (negative in aVR and V1) It is usually most prominent in the precordial leads Most commonly seen in hypothermia Also seen in hypercalcaemia, Head injury, raised ICP, secondary to medications, idiopathic VF.

151. Hypothermia The ECG rhythm is slow and irregularly irregular.Atrial fibrillation. The other marked ECG feature is an extra positive deflection immediately after the main QRS seen most obviously in leads V3-V6 and leads II & III. These are J or Osborne waves. Put together with slow AF the ECG pattern is one of moderate to severe hypothermia. This patient’s temperature measured at 29.5 C

152. Work through this example, step-by-step?

153. 39 year old man with chest pain after going to the gym Rate = 9-10/10seconds = 54-60/min

154. 39 year old man with chest pain after going to the gym Rhythm = Sinus Every QRS is preceded by a P-wave P-waves appear normal; normal axis normal morphology Therefore, sinus origin

155. 39 year old man with chest pain after going to the gym Axis +QRS in Lead 1 -QRS in aVF +/-QRS in Lead II = 60° Normal Axis ~ 60°

156. 39 year old man with chest pain after going to the gym P waves present, regular, followed by a QRS duration = 60-80ms, morphology = normal

157. 39 year old man with chest pain after going to the gym PR interval ≤ 200ms

158. 39 year old man with chest pain after going to the gym Q waves None visible

159. 39 year old man with chest pain after going to the gym QRS duration ≤ 120ms

160. 39 year old man with chest pain after going to the gym LV Hypertrophy if, SV1 + (RV5 or RV6) > 35mm SV1 + RV5 19mm X

161. 39 year old man with chest pain after going to the gym RV Hypertrophy if R/S ratio V5 or V6 < 1 X Or R/S ratio V1 > 1 Or S1S2S3 pattern R/S ratio V5 or V6 < 1 X R/S ratio V1 > 1 X S1S2S3 pattern X

162. 39 year old man with chest pain after going to the gym ST Duration & morphology appear normal

163. 39 year old man with chest pain after going to the gym T waves Duration & morphology appear normal

164. 39 year old man with chest pain after going to the gym QT Duration ~400ms QTc =QT / ∛ RR RR QT =0. 4/ ∛ 1.2 =376ms

165. 39 year old man with chest pain after going to the gym Additional Waves Hmm.....Is that a U wave? And that? And that?

166. 39 year old man with chest pain after going to the gym Interpretation: Sinus Bradycardia with associated U waves No signs of acute ischaemia or dysrhythmia

167. 39 year old man with chest pain after going to the gym Implication: Not uncommon ECG finding in healthy individuals Look for other source of pain

168. Objectives Covered Electrical conduction in the heart Lead placement ECG settings ECG components ECG waves ECG complexes Abnormalies seen with ECG components

169. Questions?

170. References http://www.newhealthadvisor.com/Tachycardia-in-Children.html https://prepgenie.com.au/gamsat/importance-of-graphs-and-data-tables-in-gamsat-biology-questions/ https://thephysiologist.org/study-materials/the-normal-ecg/ https://lifeinthefastlane.com/ecg-library/accelerated-junctional-rhythm/ https://ekg.academy http://www.ems12lead.com/2010/12/23/why-learn-axis/ http://alstrainingresources.com/education/ecg-image-library/junctional-rhythm/ http://www.dallasheart.com/page2/page42/page43/page43.html http://hqmeded-ecg.blogspot.com.au/2012/04/is-this-simple-right-bundle-branch.html