12 Lead EKG Interpretation. Disclosures

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1 12 Lead EKG Interpretation Louann B. Bailey, DNP, APRN, FAANP ACNP BC I have no disclosures Disclosures 2 1

2 Objectives At the conclusion of this presentation the participant will be able to Outline a systematic approach to 12 lead ECG interpretation Demonstrate the process for determining axis List criteria for LVH, RVH, LBBB, RBBB, Bifasicular and trifasicular block, acute and chronic MI changes Define QTc significance Contrast features of VT vs SVT with aberrancy 3 Objectives At the conclusion of this presentation the participant will be able to Outline a systematic approach to 12 lead ECG interpretation Demonstrate the process for determining axis List criteria for LVH, RVH, LBBB, RBBB, Bifasicular and trifasicular block, acute and chronic MI changes Define QTc significance Contrast features of VT vs SVT with aberrancy 4 2

3 Section I Introduction Normal ECG, laying the ground work Section II Axis Section III Hypertrophy Section IV BBB, Bi trifasicular blocks 5 Section V Landscape of an MI Introduction Section VI QT abnormalities Section VII Other Cardiac conditions 6 3

4 Section I Normal ECG Laying the ground work Laying the ground work for 12 lead interpretation A tool, a sign, an extension of the history and physical examination Must take a sensible approach to analyze an ECG The ECG reflects the heart and all its functions 8 4

5 Systematic approach Compare with old ECG Look at Rate Look at Rhythm Look at Axis Look at Hypertrophy Look at I s Intervals, ischemia, injury, infarct 9 Laying the ground work cont. The ECG language is not difficult, just different Practice, Practice, Practice Obtain good, easy to understand resources 10 5

6 12 lead ECG A Normal ECG is dependent on intact plumbing, electrical, and structural components of the heart 11 ECG Dependent Factors Plumbing Electrical Structural 12 6

7 ECG Plumbing Coronary Arteries Right coronary Left Main Coronary Left anterior descending Circumflex artery

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9 17 ECG Electrical SA node: major electrical pacemaker Blood supply: Right coronary artery AV node: initiates ventricular contraction Blood supply: Right coronary artery and or circumflex 18 9

10 ECG Electrical Bundle of HIS: ventricular contraction Blood supply: Left anterior descending Purkinje fibers: ventricular contraction Blood supply: Left anterior descending 19 Electrical 20 10

11 ECG Structural Chambers Muscle Valves Nervous system Vascular Position of the heart and great vessels 21 Heart Valves and positions 22 11

12 23 Layers of the Heart 24 12

13 12 lead ECG A Normal ECG is dependent on intact plumbing, electrical, and structural components of the heart 25 Limb Leads View the frontal plane Include leads I, II, III, av R, av L and av F Provide inferior, superior, and lateral views of heart 26 13

14 View horizontal plane and include leads V 1, V 2, V 3, V 4, V 5, and V 6 Provide inferior, superior, and lateral views of heart Precordial Leads 27 Frontal/Limb leads Precordial leads Rhythm strip 28 14

15 Frontal leads Limb leads Vertical leads Precordial leads Horizontal leads Rhythm strip lead ECG An Abnormal ECG may result from disrupted plumbing, electrical, structure or a combination of all the above

16 Frontal/Limb Leads Precordial Leads Rhythm Strip 31 ECG Sensible Approach Rate Rhythm Axis Hypertrophy 4 I s Intervals, Ischemia, Injury, Infarction If possible, always have an old ECG for comparison 32 16

17 ECG Electrical There can be electrical activity and no mechanical response, but there can never be mechanical response without electrical activation Electrical activity precedes mechanical activity (contraction) 33 ECG Electrical There can be electrical activity and no mechanical response, but there can never be mechanical response without electrical activation Except in severe scleroderma Electrical activity precedes mechanical activity (contraction) 34 17

18 Electrophysiology of the Heart Properties of cardiac Muscle Myocardial cells: Make up bulk of heart muscle, actual contractile units. Specialized cells: Four specific properties that govern automaticity, excitability, conductivity and contractility. These cells make up the heart s electrical conduction system 35 Key Properties of Myocardial Cells Automaticity Can produce electrical activity without outside nerve stimulation Excitability Ability to respond to an electrical stimulus Conductivity Ability to transmit an electrical stimulus from cell to cell throughout myocardium Contractility Ability of myocardial cell to contract when stimulated by an electrical impulse 36 18

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20 Autonomic Nervous System 39 Electrophysiology of the Heart Autonomic Nervous System control Sympathetic nerves: supply primarily ventricles, chemical mediators are hormones norepinephrine and epinephrine (Tachy arrhythmias) Parasympathetic: supply primarily atria, stimulation of vagus nerve causes the release of the hormone acetylcholine (Brady arrhythmias) 40 20

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22 43 Cardiac cycle begins with RA and LA receiving blood from systemic and pulmonary circulations Rising pressure within atria forces tricuspid and mitral valves open I 44 22

23 Heartbeat initiated by an electrical impulse that arises from SA node Impulse travels through atria generates a positive waveform on ECG and contraction of atria I 45 Impulse slows as it passes through AV node from atria to ventricles Allows atria time to finish filling ventricles 46 23

24 Impulse then rapidly travels through His Purkinje system Seen as a flat line following P wave 47 Depolarization of septum and ventricular walls generates QRS complex and contraction of ventricles I 48 24

25 Repolarization of ventricles is represented on ECG by ST segment and T wave I 49 The Electrocardiogram What is important to know 25

26 W i l l i a m E i n t h o v e n 51 ECG Paper Normal ECG Usually moves at a rate of 25mm/second There are horizontal lines, indicating time, five large boxes of 5mm each equal 25mm or 1 second of time There are vertical lines, indicating voltage, calibrated so that a 1mV standardization signal produces a deflection of exactly 10mm, (full standardization)

27 How things are measured

28 Limb Leads Precordial Leads 55 Limb Leads Precordial Leads Vertical Voltage Horizontal Time 56 28

29 Standardization Normal EKG Vertical lines indicating mv Horizontal lines indicating time

30 59 ECG Analysis Five Step Process is a logical and systematic process for analyzing ECG tracings I 60 30

31 Relationship of conduction to ECG measurement 61 Normal Sinus Rhythm Characteristics Rate: BPM Rhythm: Regular P waves: Upright and round, one preceding each QRS complex QRS complexes: Narrow, seconds in duration PR Interval: seconds in duration T waves: Upright and slightly asymmetrical I 62 31

32 Calculating Heart Rate Several methods can be used including: 6-Second Interval x 10 Method 300, 150, 100, 75, 60, 50 Method 1500 Method Rate Calculator I 63 3 second = 15 blocks 3 seconds 6 Seconds 6 seconds = 30 blocks 1 block 64 32

33 6-Second Interval x 10 Method Quick and easy and does not require tools or devices Not as accurate as other methods Multiply by 10 the number of QRS complexes found in a six second portion of ECG tracing I , 150, 100, 75, 60, 50 Method If the second R wave does not fall on a bold line the heart rate is approximated Example: if it falls between the 4 th and 5th bold line the heart rate is between 60 and 75 BPM 66 33

34 300, 150, 100, 75, 60, 50 Method If the second R wave falls in between two bold lines the heart rate can be more precisely determined using the identified values for each thin line I 67 Rate rulers 68 34

35 1500 Method Most accurate and requires no special tools but math calculation must be done to determine heart rate Cannot be used with irregular rhythms Count the number of small squares between two consecutive R waves and divide 1500 by that number I =

36 =

37 =

38 75 3 seconds =

39 77 3 seconds 4 X 20 = 80 Only 2 out of the 4 is generating a pulse 78 39

40 ECG Paper

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43 ECG Leads Direction an ECG waveform takes depends on whether electrical currents are traveling toward or away from a positive electrode I 85 ECG Leads Planes provide a crosssectional view of heart Frontal plane Horizontal plane I 86 43

44 87 Bipolar Leads Record difference in electrical potential between a positive and negative electrode Uses a third electrode called a ground Include leads I, II and III I 88 44

45 Limb Leads Lead I Positive electrode left arm (or under left clavicle) Negative electrode right arm (or below right clavicle) Ground electrode left leg (or left side of chest in midclavicular line just beneath last rib) Waveforms are positive 89 Limb Leads Lead II Positive electrode left leg (or on left side of chest in midclavicular line just beneath last rib) Negative electrode right arm (or below right clavicle) Ground electrode left arm (or below left clavicle) Waveforms are positive 90 45

46 Limb Leads Lead III Positive electrode left leg (or left side of the chest in midclavicular line just beneath last rib) Negative electrode left arm (or below left clavicle) Ground electrode right arm (or below right clavicle) Waveforms are positive or biphasic 91 Limb Leads Augmented Leads Includes av R, av L and av F Unipolar Enhanced by ECG machine because waveforms produced by these leads are normally small I 92 46

47 Limb Leads Lead av R Positive electrode placed on right arm Waveforms have negative deflection 93 Limb Leads Lead av L Positive electrode placed on left arm Waveforms have positive deflection 94 47

48 Limb Leads Lead av F Positive electrode located on left leg Waveforms have a positive deflection 95 Precordial Leads Includes leads V 1, V 2, V 3, V 4, V 5 and V 6 Positioned in order across the chest Unipolar Opposing pole is center of heart as calculated by ECG I 96 48

49 Essential parts of the ECG Frontal leads Precordial leads Bipolar leads Augmented leads Unipolar leads 97 Normal EKG Leads I, avl Lateral leads Leads V1, V2 Septal leads Leads V3, V4 Anterior leads Leads II, III, avf Inferior leads Leads V5, V6 Lateral leads 98 49

50 99 50

51 Section II Dysrhythmias 12 lead EKG lecture 1 Heart Rates Average adult has a heart rate of BPM Heart rate < 60 BPM called bradycardia Heart rate > 100 BPM called tachycardia I 12 lead EKG lecture 2 1

52 Sinus Bradycardia Slow rate that arises from SA node May or may not have an adverse affect on cardiac output In extreme cases it can lead to severe reductions in cardiac output and eventually deteriorate into asystole 12 lead EKG lecture 3 Sinus Arrest Transient failure of SA node to initiate a heart beat Can lead to a slow heart rate I 12 lead EKG lecture 4 2

53 AV Heart Blocks Blockage of the impulse traveling through the AV node can cause a slow heart rate 2 nd degree AV heart block 12 lead EKG lecture 5 AV Heart Blocks 3rd - degree AV heart block occurs with complete blockage of AV node I 12 lead EKG lecture 6 3

54 Rapid Atrial Rates With Slow Ventricular Rates Because of the rapid rate not all atrial impulses are conducted through to the ventricles A slower than normal ventricular rate can result if the number of atrial impulses reaching the ventricles falls to less than normal 12 lead EKG lecture 7 Atrial Flutter I 12 lead EKG lecture 8 4

55 Atrial Fibrillation I 12 lead EKG lecture 9 Sinus Tachycardia Fast rate, > 100 BPM, arises from the SA node 12 lead EKG lecture 10 5

56 Tachycardia From an Ectopic Pacemaker Results from rapid depolarization that overrides the SA node Supraventricular tachycardia is term used for ectopic tachycardia arising from above the ventricles Atrial tachycardia Generally BPM Junctional tachycardia Generally BPM I 12 lead EKG lecture 11 Tachycardia From an Ectopic Site 12 lead EKG lecture 12 6

57 Tachycardia From an Ectopic Pacemaker Ventricular tachycardia arises in the ventricles and has a rate of BPM 12 lead EKG lecture 13 Rapid Atrial Rates With Fast Ventricular Rates In addition to having either a normal or slow ventricular rate in atria flutter the ventricular rate can also be fast I 12 lead EKG lecture 14 7

58 Rapid Atrial Rates With Fast Ventricular Rates In addition to having either a normal or slow ventricular rate in atria fibrillation the ventricular rate can also be fast I 12 lead EKG lecture 15 Summary Approach each ECG tracing analysis in a logical and systematic manner. Some dysrhythmias are of no problem to the patient whereas others are life threatening. Five steps to analyzing an ECG rhythm are determining the: 1. Heart rate 2. Regularity 3. Presence of and characteristics of P waves 4. Presence of and characteristics of QRS complexes 5. Presence of and characteristics of the PR intervals I 12 lead EKG lecture 16 8

59 Summary To determine the heart rate first check to see if the rate is slow, normal or fast. The 6-second interval x 10 method multiplies by 10 the number of QRS complexes found in a 6-second portion of the ECG tracing. The 300, 150, 100, 75, 60, 50 method involves locating an R wave on a bold line on the ECG paper, then finding the next consecutive R wave and using the 300, 150, 100, 75, 60, 50 values for subsequent bold lines to determine the rate. To use the 1500 method count the number of small squares between two consecutive R waves and divide 1500 by that number. I 12 lead EKG lecture 17 Summary A heart rate less than 60 beats per minute is called bradycardia. Slow heart rates are seen with sinus bradycardia, junctional escape rhythm, idioventricular rhythm, AV heart block and atrial flutter or fibrillation with slow ventricular response. A heart rate greater than 100 beats per minute is called tachycardia. Fast heart rates are seen with sinus tachycardia, atrial tachycardia, junctional tachycardia, ventricular tachycardia and atrial flutter or fibrillation with rapid ventricular response. I 12 lead EKG lecture 18 9

60 Heart Blocks Partial delays or complete interruptions in the cardiac conduction pathway between the atria and ventricles The degree of block defines the type and classification of heart block Q I 12 lead EKG lecture 19 Heart Blocks Common causes: Ischemia Myocardial necrosis Degenerative disease of the conduction system Congenital anomalies Drugs (especially digitalis preparations) I 12 lead EKG lecture 20 10

61 AV Heart Blocks 1 st -degree AV heart block 2 nd -degree AV heart block, Type I (Wenckebach) 2 nd -degree AV heart block, Type II 3 rd -degree AV heart block I 12 lead EKG lecture 21 1 st -Degree AV Heart Block Not a true block A consistent delay of conduction at the level of the AV node I 12 lead EKG lecture 22 11

62 1 st -Degree AV Heart Block Q 12 lead EKG lecture 23 1 st -Degree AV Heart Block 12 lead EKG lecture 24 12

63 1 st Degree AV Block PR intverval is regular but prolonged PR interval prolonged PR is

64 2 nd -Degree AV Heart Block, Type I Intermittent block at the level of the AV node Also referred to as Wenckebach 12 lead EKG lecture 27 2 nd -Degree AV Heart Block, Type I 12 lead EKG lecture 28 14

65 PR gets longer and longer till it drops a QRS 2 nd degree Type 1 2 nd -Degree AV Heart Block, Type II Intermittent block at the level of the bundle of His or bundle branches resulting in atrial impulses that are not conducted to the ventricles I 12 lead EKG lecture 30 15

66 2 nd -Degree AV Heart Block, Type I 12 lead EKG lecture 31 2 nd -Degree AV Heart Block, Type II 12 lead EKG lecture 32 16

67 3 rd -Degree AV Heart Block Complete block of conduction at or below the AV node Impulses from atria cannot reach ventricles 12 lead EKG lecture 33 3 rd -Degree AV Heart Block Atrial pacemaker site is the SA node Atrial rate 60 to 100 BPM Ventricular pacemaker site is an escape rhythm From AV junction rate 40 to 60 BPM From ventricles rate 20 to 40 BPM Q 12 lead EKG lecture 34 17

68 12 lead EKG lecture 35 18

69 Section III Axis Determination Objectives At the conclusion of this presentation the participant will be able to Outline a systematic approach to 12 lead ECG interpretation Demonstrate the process for determining axis List criteria for LVH, RVH, LBBB, RBBB, Bifasicular and trifasicular block, acute and chronic MI changes Define QTc significance Contrast features of VT vs SVT with aberrancy 2 1

70 ECG Lead System Standard 12 lead system Six limb leads or frontal leads Six precordial leads or horizontal leads (R wave Progression) Additional leads: 18 leads Posterior leads Right sided leads A point of view Depolarization towards that lead or the action potential 3 Limb Leads View the frontal plane Include leads I, II, III, av R, av L and av F Provide inferior, superior, and lateral views of heart 4 2

71 Frontal Leads 5 Bipolar Leads Record difference in electrical potential between a positive and negative electrode Uses a third electrode called a ground Include leads I, II and III I 6 3

72 Limb Leads Augmented Leads Includes av R, av L and av F Unipolar Enhanced by ECG machine because waveforms produced by these leads are normally small I 7 Limb Leads Lead av R Positive electrode placed on right arm Waveforms have negative deflection 8 4

73 Limb Leads Lead av L Positive electrode placed on left arm Waveforms have positive deflection 9 Limb Leads Lead av F Positive electrode located on left leg Waveforms have a positive deflection 10 5

74 Precordial Leads Includes leads V 1, V 2, V 3, V 4, V 5 and V 6 Positioned in order across the chest Unipolar Opposing pole is center of heart as calculated by ECG I 11 Precordial or Horizontal leads 12 6

75 Normal Sinus Rhythm 13 Additional Leads 14 7

76 Mean Electrical Axis Direction of the mean vector called the mean electrical axis Axis is defined in the frontal plane only 15 Ventricular Depolarization and Mean QRS Axis Interventricular septum depolarization represents the first cardiac vector associated with ventricular depolarization A sequence of vectors is produced as the Purkinje fibers carry the impulse from the endocardial lining of the RV and LV through the ventricular wall toward the epicardium 16 8

77 Position of the Mean QRS Axis Limb leads provide information about the frontal plane and are used to determine the position of the mean QRS axis Described in degrees within an imaginary circle drawn over the patient s chest I 17 Vectors of Limb Leads 18 9

78 12 Lead Point of View 12 lead records electrical activity between two points. There are two types of leads: Bipolar: Negative and positive lead (limb leads). Unipolar: Positive lead and neutral reference point (all other leads). 19 ECG Lead System Limb leads and Axis determination Axis: where the cardiac vector is headed Made up from the Einthoven triangle and bipolar standard limb leads 20 10

79 Limb Lead Vectors 21 Position of the Mean QRS Axis AV node is center of circle Intersection of all lines divides circle into equal, 30 degree segments Lead I starts at +0 degrees and is located at the three o clock position Lead av F starts at +90 degrees and is located at the six o clock position 22 11

80 23 Einthoven s Triangle 24 12

81 Position of the Mean QRS Axis Mean QRS axis normally points downward and to patient s left (between 0 and +90 degrees) 25 Determining Electrical Axis Use leads I and av F The two leads that can best detect variations in the heart s electrical axis I 26 13

82 27 Quick Axis Determination 28 14

83 Determining Electrical Axis I 29 Determining Electrical Axis Location of axis influenced by: Heart s position in the chest Heart size Patient s body size Conduction pathways Force of electrical impulses being generated 30 15

84 ECG Potential causes of Axis deviation Right axis deviation Normal RVH Conduction disturbances MI Valvular Disease Pulmonary HTN Congenital Pulmonary disease Left Axis deviation Normal LVH Conduction disturbances MI Valvular Disease Systemic HTN Congenital Other 31 Practice Makes Perfect Determine if the mean QRS is normal or if there is axis deviation 32 16

85 Practice Makes Perfect Determine if the mean QRS is normal or if there is axis deviation 33 Practice Makes Perfect Determine if the mean QRS is normal or if there is axis deviation 34 17

86 35 Left Axis Deviation 36 18

87 Right Axis Deviation 37 Section III Hypertrophy 19

88 Hypertrophy Condition in which muscular wall of the ventricle(s) becomes thicker than normal 39 Dilation or Enlargement Occurs as result of volume overload where chamber dilates to accommodate increased blood volume 40 20

89 Hypertrophy or Enlargement Enlargement associated with atria P wave changes used to identify atrial enlargement Hypertrophy associated with ventricles QRS complex changes used to identify ventricular hypertrophy I 41 ECG Structure Hypertrophy or enlargement Atrial and ventricular ECG will show changes in duration and amplitude of wave forms Electrical activity takes longer to activate muscle 42 21

90 Hypertrophy Atrial RAE Pulmonary HTN Pulmonary emboli COPD Tricuspid/Pulmonary valve disease Some congenital heart disease LAE Systemic HTN Aortic and Mitral disease Left ventricular failure 43 Duration seconds Amplitude mm First portion represents right atrial depolarization Terminal portion represents left atrial depolarization Normal P Wave 44 22

91 Leads II and V 1 used to assess atrial enlargement Atrial Enlargement I 45 Right Atrial Enlargement Increase in amplitude of the first part of the P wave 46 23

92 Left Atrial Enlargement Increased amplitude in the terminal portion of the P wave in V 1 Increased duration or width of the P wave I 47 Criteria for RAE & LAE 48 24

93 Different Looking Sinus P Waves Tall, rounded or peaked P waves may be seen with increased right atrial pressure and right atrial dilation Q

94 Right Atrial Enlargement

95 Right Atrial Enlargement 53 Different Looking Sinus P Waves Notched, wide (enlarged) or biphasic P waves may be seen in increased left atrial pressure and left atrial dilation Q 54 27

96 55 Left Atrial Enlargement 56 28

97 What s your diagnosis? 57 Left atrial enlargement 58 29

98 Ventricular Hypertrophy Commonly caused by chronic, poorly treated hypertension Because there is more muscle to depolarize there is more electrical activity occurring in the hypertrophied muscle Reflected by changes in the amplitude of portions of the QRS complex I 59 Ventricular Hypertrophy RVH Pulmonary HTN, COPD, PE Mitral valve disease Pulmonary valve stenosis VSD Congenital heart disease with right ventricular overload 60 30

99 LVH Systemic HTN Ventricular Hypertrophy continued Aortic Stenosis/insufficiency Hypertrophic cardiomyopathy (IHSS, HOCM) Cardiomyopathies 61 Criteria for RVH RAE RAD or indeterminate axis Incomplete RBBB (or an rsr in lead V1) Low voltage Persistent precordial S waves Right Ventricular strain (ST, T wave changes in right sided leads) Tall R wave in lead V

100 Right Ventricular Hypertrophy Most common characteristic in limb leads is right axis deviation I 63 Right Ventricular Hypertrophy In precordial leads R waves are more positive in leads which lie closer to lead V

101 ECG Example RVH 65 ECG Example RVH 66 33

102 What s the Diagnosis? 67 ECG Example RVH 68 34

103 What s your diagnosis? 69 What s your diagnosis? 70 35

104 What s your Diagnosis? 71 What s your Diagnosis? 72 36

105 Criteria for LVH Deepest S wave in lead V1 or V2, plus tallest R wave in lead V5 or V6 > 35mm R in lead avl > 12mm Patient > 35 years old Strain in left sided leads 73 Criteria of LVH by the Cornell Method Cornell Voltage Criteria S in V3 + R in avl > 28 mm (men) S in V3 + R in avl > 20 mm (women) 23% Sensitivity 96% Specificity 74 37

106 Left Ventricular Hypertrophy Increased R wave amplitude in precordial leads over LV S waves that are smaller in leads over LV (lead V 6 ) but larger in leads over RV (lead V 1 ) I 75 Other Criteria for LVH determination An R wave > 20 mm in any of the other inferior leads (II, III, avf) Deep S waves (> 20 25mm) in lead V1 or V2 An R wave > 25mm in lead V5 An R wave > 20mm in lead V

107 What s your Diagnosis 77 Example ECG LVH Deepest S wave in V1 or V2 + Tallest R wave in V 5 or V6 = 35 mm Tall R wave in avl > 12 mm S wave R wave 78 39

108 79 Example of LVH 80 40

109 What s your diagnosis? 81 What s your diagnosis? 82 41

110 Section IV LBBB, RBBB Bifascicular, Trifascicular Block Objectives At the conclusion of this presentation the participant will be able to Outline a systematic approach to 12 lead ECG interpretation Demonstrate the process for determining axis List criteria for LVH, RVH, LBBB, RBBB, Bifasicular and trifasicular block, acute and chronic MI changes Define QTc significance Contrast features of VT vs SVT with aberrancy 2 1

111 Bundle Branches Bundle of His divides into right and left bundle branches Left bundle branch divides into septal, anterior and posterior fascicles I 3 Conduction Abnormalities BBB Causes of BBB Arterial occlusion total Arterial occlusion partial Structural changes Helpful hints r/t BBB ST segment and the T wave are opposite deflection of QRS If T waves same deflection, may mean ischemia 4 2

112 Normal QRS Complex Narrow < 0.12 seconds in duration Electrical axis between 0 and +90 I 5 QRS Interval/Bundle Branch Block Assess QRS Duration 1. QRS duration can be measured from any of the 12 leads 2. All that matters is whether the QRS is normal or wide 3. Judge QRS prolongation from the lead where the QRS appears longest 6 3

113 QRS Interval/Bundle Branch Block Assess QRS Duration cont. 4. If the QRS is: < 0.12 seconds than the QRS is normal > 0.12 seconds than the QRS is wide (greater than half a large box) 5. The limits given do not hold for children 7 Bundle Branch Block Leads to one or both bundle branches failing to conduct impulses Produces delay in depolarization of the ventricle it supplies I 8 4

114 Bundle Branch Block Widened QRS complex RR configuration in chest leads I 9 QRS Interval/Bundle Branch Block QRS Widening Typical RBBB Typical LBBB Neither typical RBBB or LBBB IVCD 10 5

115 Key Leads 11 ECG Findings for BBB s 12 6

116 Conduction Abnormalities RBBB RBBB Thin fiber, runs along intraventricular septum to the base of the papillary muscle of the right ventricle. No sub divisions. Septal perforator of LAD 13 Right Bundle Branch Block Look for RR in leads V 1 or V

117 Conduction Abnormalities LBBB LBBB Divides two primary fascicles anterior and posterior branches, rare median branch Blood supply: LAFB ; septal perforator of LAD, LPFB ; PDA, or septal perforator 15 Left Bundle Branch Block Look for RR in leads V 5 or V

118 Criteria for RBBB ECG changes with RBBB QRS > 0.12 sec Rabbit ear rsr in V1 Wide S wave in V1 Slurred S wave in Lead I

119 19 ECG Findings RBBB 20 10

120 Criteria for LBBB ECG changes with LBBB QRS > 0.12 sec Absence of Q wave and presence of R wave usually notched in leads V1 & V6 rs or QS in V1 21 ECG Findings for LBBB 22 11

121 LBBB 23 ECG Findings for BBB s 24 12

122 10/11/

123

124 29 Section IV Continued Hemiblock Blocks 15

125 A Word about Hemiblocks LAHB M ore common than LPHB If net deflection of Lead II is Negative and more than -30degrees LPHB Distinctly uncommon Rarely isolated finding Often associated with accompanying RBBB Dramatically deepened S wave in Lead I More dangerous 31 Hemiblocks Occur when one of fascicles of LBB blocked Key to detecting is a change in the QRS axis I 32 16

126 Identifying Hemiblocks What to look for in what leads Fasicular Blocks LAFB LPFB Leads I and avl qr rs II, III, avf rs qr 33 Hemiblock Anatomy 34 17

127 Left Anterior Hemiblock I

128 10/11/2017 Small q wave Lead I Tall R wave avl

129 Left Posterior Hemiblock I

130 41 Identifying Hemiblocks What to look for in what leads Fasicular Blocks LAFB LPFB Leads I and avl qr rs II, III, avf rs qr 42 21

131

132 RBBB RBBB r, S r, S RBBB with LAFB 45 Trifascicular Block (TFB) TFB refers to presence of conduction disease in all three fascicles RBB LAF LPF 46 23

133 Incomplete TFB Fixed block of two fascicles with evidence of delayed conduction in the remaining fascicile (1 st or 2 nd degree AV block) Fixed block of one fascicle (RBBB) with intermittent failure of the other two fasciciles (alternating LAFB/LPFB) 47 Complete TFB Complete TFB produces 3 rd degree AV block with features of bifascicular block This is due to escape rhythms that may arise from either LAF or LPF 48 24

134 Main Causes Ischemic Heart disease HTN AS AWMI Primary degenerative disease of the conducting system (Lenergre s disease) Congenital heart disease Hyperkalemia Digoxin Toxicity

135 Incomplete TFB RBBB: look at lead I and V1, V6 LAD: Lead I is +, Lead avf is LAFB: Tall qr in I and avl, rs in II, III, avf 1 st degree AV block: prolonged PR

136 Complete Tirfascicular Block RBBB LAD LAFB 3 rd degree AV block 53 27

137 Section V Landscape of an MI Objectives At the conclusion of this presentation the participant will be able to Outline a systematic approach to 12 lead ECG interpretation Demonstrate the process for determining axis List criteria for LVH, RVH, LBBB, RBBB, Bifasicular and trifasicular block, acute and chronic MI changes Define QTc significance Contrast features of VT vs SVT with aberrancy 2 1

138 Q Wave First part of QRS complex First downward deflection from baseline I 3 ST Segment Flat line that follows the QRS complex and connects it to T wave I 4 2

139 T Wave Slightly asymmetrical and oriented in same direction as preceding QRS complex 5 Ischemia, Injury, and Infarction Occurs with interruption of coronary artery blood flow Often a progressive process I 6 A 3

140 Landscape of an MI Changes in the 12 lead that may indicate : Ischemia Injury Infarct Must have changes in two or more contiguous leads 7 8 4

141 ECG Indicators I 9 Myocardial Ischemia Characteristic signs: 10 5

142 Occurs because ischemic tissue does not repolarize normally T Wave Inversion I 11 T Wave Inversion I 12 6

143 Peaked T Waves May be seen in early stages of acute myocardial infarction Within a short time (two hours) T waves invert 13 ST Segment Depression May or may not include T wave inversion I 14 7

144 Flat ST Segment Depression Results from Non STEMI 15 Landscape of an MI Ischemia: T wave inversion ST segment depression Other causes of T wave inversion Cardiac: BBB Ventricular hypertrophy Pericarditis Non cardiac: Electrolyte disorders Shock Positional changes CNS disorders(subarachnoid hemorrhage) 16 8

145 17 Inferior and Lateral Ischemia 18 9

146 ST Segment Elevation Earliest reliable sign that myocardial infarction has occurred I 19 Landscape of an MI cont. Injury: ST elevation Indicates acute injury: 1mm or > in limb leads 2mm or> in precordial leads Other causes: Pericarditis Ventricular aneurysm 20 10

147 21 Landscape of an MI cont. Necrosis (infarction): Q wave Q wave: indicates dead tissue, results in a negative deflection. Significant or pathologic Q waves are wide and deep. A Q wave is at least 0.04 in duration(1mm) and 25% of the entire QRS complex. Other causes: Ventricular hypertrophy Diffuse myocardial disease Fascicular blocks Small Q waves may be present in presence of Non STEMI 22 11

148 Pathologic Q Waves Indicate presence of irreversible myocardial damage or myocardial infarction I 23 Landscape of an MI cont. Myocardial ischemia Results from temporary interruption of blood flow Least acute phase Electrically irritable, prone to dysrhythmias Alters repolarization of ischemic cells Appears on ECG as ST segment or T wave changes Reversible with prompt treatment 24 12

149 Myocardial Injury Landscape of an MI cont. Results from prolonged interruption of oxygen and nutrients Causes tissue damage Appears on ECG as ST elevation > 1mm with or without loss of R wave Reversible with prompt treatment 25 Landscape of an MI cont. Myocardial Infarction Results from cell destruction Causes electrically inert tissue, non-conducted electrical impulses Prevents depolarization/repolarazation of myocardial cells ECG is abnormal with evidence of abnormal Q waves, ST or T wave abnormalities Irreversible due to scar tissue 26 13

150 Landscape of an MI cont. Diagnosis of infarcts Importance of lead grouping Inferior wall MI: Leads II, III, avf High Lateral wall MI: Leads I, avl Low Lateral wall MI: Leads V5, V6 Anterior wall MI: V1-V4 Septal wall MI: V1, V2 Posterior wall MI: V7- V9, or mirror changes V1-V3 Right ventricular wall MI: V2R, V3R, V4R 27 Landscape of an MI cont. Review Coronary Anatomy Right Coronary Artery 55% supply to SA node 90% supply to AV node RA and RV Posterior wall of left ventricle Inferior wall of left ventricle Posterior interventricular septum Left posterior fasicle 28 14

151 Landscape of an MI cont. Review Coronary Anatomy Left Anterior Descending Anterior wall of left ventricle Apex of heart Anterior interventricular septum RBB LAF LPF Bundle of His 29 Landscape of an MI cont. Review Coronary Anatomy Left Circumflex 45% of blood SA node 10% of blood to AV node LA Lateral wall of left ventricle Posterior wall of left ventricle Small percentage of population the CX is dominant and supplies the entire left posterior ventricle and interventricular septum 30 15

152 Landscape of an MI Most common and complications Inferior MI Leads II, III, avf Characterized first by hypodynamic response (bradycardia and hypotension) Transient AV HB Papillary muscle dysfunction leading to Valvular insufficiency CHF A-Fib/A-Flutter Increase parasympathetic tone 31 What is your diagnosis? 32 16

153 What is your diagnosis? Acute Inferior Wall MI 33 What is your diagnosis? 34 17

154 What is your diagnosis? Acute Inferior lateral MI 35 What is your diagnosis? 36 18

155 What is your diagnosis? Acute Inferior MI 37 Landscape of an MI Most common and complications Anterior MI Hyperdynamic response (tachycardia and hypertension) Decreased LV Function CHF Pulmonary Edema Cardiogenic shock Multifascicular BBB and AV blocks Ventricular aneurysm Increased sympathetic stimulation Leads V1-V

156 What is your diagnosis? 39 What is your diagnosis? Acute Anterior Lateral MI 40 20

157 What is your diagnosis? 41 What is your diagnosis? Acute Anterior Lateral MI with Tombstone T waves 42 21

158 What is your diagnosis? 43 What is your diagnosis? Q waves Acute Anterior MI with q waves in V1, V2, V3, V

159 What is your diagnosis? 45 What is your diagnosis? ST Elevation ST Elevation ST Elevation ST Elevation Q waves ST Elevation Q waves Acute Anterior Lateral MI with q waves in V1 V

160 Landscape of an MI Most common and complications Lateral Wall MI 1 st and 2 nd degree blocks CHF Atrial arrhythmias Posterior wall involvement Changes in Leads I, avl, V5, V6 Reciprocal Changes II, III, avf 47 What is your diagnosis? 48 24

161 What is your diagnosis? Acute Lateral MI with reciprocal changes in inferior anterior leads 49 What is your diagnosis? 50 25

162 What is your diagnosis? Acute Lateral MI with reciprocal changes inferiorly 51 What is your diagnosis? 52 26

163 What is your diagnosis? Acute Anterior lateral MI with reciprocal changes in inferior leads 53 What is your diagnosis? 54 27

164 What is your diagnosis? Acute Anterior lateral MI with reciprocal changes in inferior leads 55 Other MI s Septal Wall Leads involved: V1 V2 Reciprocal leads: II, III, avf Complications: BBB, hemiblocks 56 28

165 Other MI s Posterior MI Indicative leads: Posterior leads with ST, T wave changes (mirror changes, increase in R wave in V1 2 Reciprocal changes: V1 2 Complication: same as Inferior MI 57 Posterior Myocardial Infarction Involve posterior surface of the heart Look for reciprocal changes in leads V 1 and V

166 What is your diagnosis? 59 What is your diagnosis? Acute Inferior Posterior MI with lateral involvement Likely the circumflex region and dominant left circ 60 30

167 What is your diagnosis? 61 What is your diagnosis? Posterior leads Acute Inferior Posterior MI 62 31

168 Additional Leads 63 Other MI s Right Ventricular Infarct Indicative leads: V 3-6R (II, III, avf) Reciprocal leads: I avl Complications: Right ventricular failure, same as inferior wall MI 64 32

169 Right sided leads 65 What is your diagnosis? 66 33

170 What is your diagnosis? Acute Inferior, RV infarct 67 What is your diagnosis? 68 34

171 What is your diagnosis? Acute Inferior MI with RV involvement 69 ECG Sensible Approach Rate Rhythm Axis Hypertrophy 4 I s Intervals, Ischemia, Injury, Infarction If possible, always have an old ECG for comparison 70 35

172 Section VI and VII QT Abnormalities Other Cardiac Conditions and EKG Abnormalities Objectives At the conclusion of this presentation the participant will be able to Outline a systematic approach to 12 lead ECG interpretation Demonstrate the process for determining axis List criteria for LVH, RVH, LBBB, RBBB, Bifasicular and trifasicular block, acute and chronic MI changes Define QTc significance Contrast features of VT vs SVT with aberrancy 2 1

173 Causes of Regular, Wide Complex Tachycardia Ventricular Tachycardia SVT with preexisting BBB SVT with aberrant conduction 3 HIS DEBS H ypoxia I schemia S ympathomimetic disturbances D rugs E lectrolytes B rady S tretch 4 2

174 VT vs. SVT with aberrancy IT is more likely VT if: Absence of typical RBBB or LBBB Extreme axis deviation (northwest axis) Very broad complexes (> 160 ms) Capture beats Fusion beats Positive or negative concordance throughout chest leads RSR complexes with a taller left rabbit ear. This is the most specific finding in favor of VT 5 Capture Beats 6 3

175

176

177 11 Northwest Axis 12 6

178 Indeterminate Axis or Northwest Axis 13 SVT or AV nodal re entry tachycardia (AVNRT) Classified based on site of origin (atria or AV node) or regularity (regular or irregular) QRS width not helpful and influenced by preexisting BBB, Rate related aberrant conduction or accessary pathways

179 Classification of SVT by site of Origin Atrial Regular ST Atrial Tach Atrial Flutter Inappropriate ST SN re entrant tach Irregular Atrial Fibrillation Atrial Flutter with variable block Multifocal atrial Tach Atrioventricular AV re entry tach (AVRT) AV nodal re entry Tach (AVNRT) Automatic Junctional tachycardia 15 AVNRT Most common cause of palpitations in pts with structurally normal hearts Occurs spontaneously or upon provocation (caffeine, ETOH, Beta agonists, sympathomimetics (amphetamines) More common in women and may occur in young healthy patients Sudden onset of rapid, regular palpitations SOB Pts with CAD may c/o angina Tachy rate bpm Generally well tolerated May cease spontaneously and abruptly

180 10/11/2017 Typical ECG findings Regular tachy bpm QRS complexes usually narrow (< 120 msec) unless pre existing BBB ST segment depression may be seen without CAD QRS alternans P waves if visible exhibit retrograde conduction with P wave inversion in leads II, III, avf P waves may be buried in the QRS Slow Fast AVNRT 9

181 Typical AVNRT Narrow complex Tachycardia No visible P waves There are pseudo R waves in V

182 Fast Slow AVNRT Narrow complex Tachycardia Retrograde P waves are visible after each QRS complex 21 Pre Excitation & Accessory Pathways Activation of the ventricles due to impulse bypassing the AV node via an accessary pathway Abnormal conduction pathways Impulses conduct either antergrade towards the ventricle or retrograde, away or in both directions Majority conduct in both directions Reentry circuit involving accessary pathways termed Atrioventricular reentry tachycardias (AVRT)

183 Wolf Parkinson White (WPW) PR interval < 120 ms Delta wave: slurring slow rise of initial portion of the QRS QRS prolongation > 110 ms ST segment and T wave discordant changes Pseudo infraction pattern can be seen in up to 70% of patients (pseudo q waves, or prominent R wave in V1 V3 mimicking posterior infarction)

184 Other Pre Excitation Syndromes Lown Ganong Levine (LGL) syndrome Accessary pathway composed of James Fibres ECG PR interval < 120 ms Normal QRS morphology The term should not be used in the absence of paroxysmal tachycardia Existence is disputed and may not exist 25 Delta wave Sinus rhythm with a very short PR interval Broad QRS with slurred upstroke (delta wave) Dominant R wave V1 Tall R wave and inverted T wave in V1 3 mimicking RVH Negative Delta wave in avl (pseudo infarction pattern)

185 Common causes of QT Prolongation Drugs Type IA, III Antiarrythmic Tricyclic antidepressants Phenothiazines Electrolyte disturbances Hypokalelmia Hypomagnesemia Hypocalcaemia CNS disturbances Stroke ICB or Brainstem bleed Coma

186 29 Common causes of ST Depression Ischemia Strain Digitalis effect Hypokalemia/hypomagnesemia Rate related changes Any combination of the above 30 15

187 Common causes of Tall R wave in V1 WPW RBBB RVH Posterior MI Normal variant 31 Common causes of Nonspecific ST-T wave Abnormalities Ischemia LVH Cardiomyopathy MVP Drug effect Lyte abnormalities CNS disorder Hyperventilation Severe medical illness Severe emotional stress Exercise Hypoxemia Acidosis Temp extremes Other causes 32 16

188 Other Cardiac Conditions Many conditions cause changes to the ECG Electrolyte abnormality Ischemia Infarction Inflammation Medications 33 ECG Changes in Pericarditis T wave initially upright and elevated but then during recovery phase it inverts ST segment elevated and usually flat or concave 34 17

189 Pericardial Effusion Can occur with pericarditis Can cause lowvoltage QRS complexes in all leads and electrical alternans 35 Electrical Alternans QRS complexes change in height with each successive beat 36 18

190 Pulmonary Embolism Acute blockage of one of the pulmonary arteries Leads to obstruction of blood flow to the lung segment supplied by the artery Produces large S wave in lead I, deep Q wave in lead III, inverted T wave in lead III Called the S1 Q3 T3 pattern 37 A 38 19

191 S1 Q3 T3 Sinus Tach RBBB T wave inversions in right precordial leads (V1 3) as well Lead III 39 Pulmonary Embolism 40 20

192 Electrolyte Imbalances Increases or decreases in potassium and calcium serum levels can have a profound effect on the ECG 41 Hyperkalemia Key characteristics include: T wave peaking Flattened P waves 1 st -degree AV heart block Widened QRS complexes Deepened S waves Merging of S and T waves 42 21

193 43 Hyperkalemia

194 Suspect Hyperkalemia New bradycardia New AV block especially with CKD or ESRD taking ACE I or potassium sparing meds 45 Hypokalemia Key ECG characteristics include: ST segment depression Flattening of the T wave Appearance of U waves 46 23

195

196 49 Hypocalcemia QT interval slightly prolonged 50 25

197

198 Systematic approach Compare with old ECG Look at Rate Look at Rhythm Look at Axis Look at Hypertrophy Look at I s Intervals, ischemia, injury, infarct 53 27

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