Section 3 and 4. Objectives. Bundle Branches 10/9/2018. LBBB, RBBB Bifascicular, Trifascicular Block

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1 Section 3 and 4 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, RAE, LAE LBBB, RBBB, Bifasicular and trifasicular block, acute and chronic MI changes Define QTc significance Contrast features of VT vs SVT with aberrancy 2 Bundle of His divides into right and left bundle branches Left bundle branch divides into septal, anterior and posterior fascicles Bundle Branches I 3 1

2 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 Narrow < 0.12 seconds in duration Electrical axis between 0 and +90 Normal QRS Complex 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 2

3 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 Widened QRS complex RR configuration in chest leads Bundle Branch Block I 9 3

4 QRS Interval/Bundle Branch Block QRS Widening Typical RBBB Typical LBBB Neither typical RBBB or LBBB IVCD 10 Key Leads 11 ECG Findings for BBB s 12 4

5 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 2 14 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 5

6 Left Bundle Branch Block Look for RR in leads V 5 or V 6 16 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

7 19 ECG Findings RBBB 20 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 7

8 ECG Findings for LBBB 22 LBBB 23 LBBB 24 8

9 ECG Findings for BBB s r R r R S waves S waves RBBB 27 9

10 10/9/ Lead I and V6 look similar T wave opposite of the QRS Lead I and V6 look similar T wave opposite of the QRS LBBB pattern 30 10

11 10/9/ Section IV Continued Hemiblock Blocks 11

12 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 34 Hemiblocks Occur when one of fascicles of LBB blocked Key to detecting is a change in the QRS axis I 35 Identifying Hemiblocks What to look for in what leads Fasicular Blocks LAFB LPFB Leads I and avl qr rs II, III, avf rs qr 36 12

13 10/9/2018 Hemiblock Anatomy 37 Left Anterior Hemiblock I

14 10/9/2018 Small q wave Lead I Tall R wave avl Left Posterior Hemiblock I 42 14

15 10/9/ r S R r q R q S R q

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

17 RBBB RBBB r, S r, S RBBB with LAFB 49 Trifascicular Block (TFB) TFB refers to presence of conduction disease in all three fascicles RBB LAF LPF 50 Incomplete TFB Fixed block of two fascicles with evidence of delayed conduction in the remaining fascicle (1 st or 2 nd degree AV block) Fixed block of one fascicle (RBBB) with intermittent failure of the other two fascicles (alternating LAFB/LPFB) 51 17

18 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 52 Main Causes Ischemic Heart disease HTN AS AWMI Primary degenerative disease of the conducting system (Lenergre s disease) Congenital heart disease Hyperkalemia Digoxin Toxicity

19 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 Complete Tirfascicular Block RBBB LAD LAFB 3 rd degree AV block 57 19

20 Section 5 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 OAAPN SWM First part of QRS complex First downward deflection from baseline Q Wave I OAAPN SWM

21 Flat line that follows the QRS complex and connects it to T wave ST Segment I OAAPN SWM Slightly asymmetrical and oriented in same direction as preceding QRS complex T Wave OAAPN SWM Ischemia, Injury, and Infarction Occurs with interruption of coronary artery blood flow Often a progressive process OAAPN SWM I A 2

22 Landscape of an MI Changes in the 12 lead that may indicate : Ischemia Injury Infarct Must have changes in two or more contiguous leads OAAPN SWM OAAPN SWM ECG Indicators I OAAPN SWM

23 Myocardial Ischemia Characteristic signs: OAAPN SWM Occurs because ischemic tissue does not repolarize normally T Wave Inversion I OAAPN SWM T Wave Inversion I OAAPN SWM

24 May be seen in early stages of acute myocardial infarction Within a short time (two hours) T waves invert Peaked T Waves OAAPN SWM ST Segment Depression May or may not include T wave inversion I OAAPN SWM Flat ST Segment Depression Results from Non STEMI OAAPN SWM

25 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) OAAPN SWM OAAPN SWM Inferior and Lateral Ischemia OAAPN SWM

26 ST Segment Elevation Earliest reliable sign that myocardial infarction has occurred I OAAPN SWM 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 OAAPN SWM OAAPN SWM

27 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 OAAPN SWM Pathologic Q Waves Indicate presence of irreversible myocardial damage or myocardial infarction I OAAPN SWM 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 OAAPN SWM

28 Landscape of an MI cont. Myocardial Injury 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 OAAPN SWM 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 OAAPN SWM 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 OAAPN SWM

29 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 OAAPN SWM 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 OAAPN SWM 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 OAAPN SWM

30 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 OAAPN SWM What is your diagnosis? OAAPN SWM What is your diagnosis? Acute Inferior Wall MI OAAPN SWM

31 What is your diagnosis? OAAPN SWM What is your diagnosis? Acute Inferior lateral MI OAAPN SWM What is your diagnosis? OAAPN SWM

32 What is your diagnosis? Acute Inferior MI OAAPN SWM 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-V4 OAAPN SWM What is your diagnosis? OAAPN SWM

33 What is your diagnosis? Acute Anterior Lateral MI OAAPN SWM What is your diagnosis? OAAPN SWM What is your diagnosis? Acute Anterior Lateral MI with Tombstone T waves OAAPN SWM

34 What is your diagnosis? OAAPN SWM What is your diagnosis? Q waves Acute Anterior MI with q waves in V1, V2, V3, V4 OAAPN SWM What is your diagnosis? OAAPN SWM

35 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 V4 OAAPN SWM 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 OAAPN SWM What is your diagnosis? OAAPN SWM

36 What is your diagnosis? Acute Lateral MI with reciprocal changes in inferior anterior leads OAAPN SWM What is your diagnosis? OAAPN SWM What is your diagnosis? Acute Lateral MI with reciprocal changes inferiorly OAAPN SWM

37 What is your diagnosis? OAAPN SWM What is your diagnosis? Acute Anterior lateral MI with reciprocal changes in inferior leads OAAPN SWM What is your diagnosis? OAAPN SWM

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

39 Posterior Myocardial Infarction Involve posterior surface of the heart Look for reciprocal changes in leads V 1 and V 2 OAAPN SWM What is your diagnosis? OAAPN SWM What is your diagnosis? Acute Inferior Posterior MI with lateral involvement Likely the circumflex region and dominant left circ OAAPN SWM

40 What is your diagnosis? OAAPN SWM What is your diagnosis? Posterior leads Acute Inferior Posterior MI OAAPN SWM Additional Leads OAAPN SWM

41 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 OAAPN SWM Right sided leads OAAPN SWM What is your diagnosis? OAAPN SWM

42 What is your diagnosis? Acute Inferior, RV infarct OAAPN SWM What is your diagnosis? OAAPN SWM What is your diagnosis? Acute Inferior MI with RV involvement OAAPN SWM

43 ECG Sensible Approach Rate Rhythm Axis Hypertrophy 4 I s Intervals, Ischemia, Injury, Infarction If possible, always have an old ECG for comparison OAAPN SWM

44 Section 6 and 7 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 OAAPN SWM Causes of Regular, Wide Complex Tachycardia Ventricular Tachycardia SVT with preexisting BBB SVT with aberrant conduction OAAPN SWM

45 HIS DEBS H ypoxia I schemia S ympathomimetic disturbances D rugs E lectrolytes B rady S tretch OAAPN SWM 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 OAAPN SWM Capture Beats OAAPN SWM

46 OAAPN SWM OAAPN SWM OAAPN SWM

47 OAAPN SWM OAAPN SWM Northwest Axis OAAPN SWM

48 Indeterminate Axis or Northwest Axis OAAPN SWM 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 OAAPN SWM Classification of SVT by site of Origin Atrial Atrioventricular Regular ST Atrial Tach Atrial Flutter Inappropriate ST SN re entrant tach AV re entry tach (AVRT) AV nodal re entry Tach (AVNRT) Automatic Junctional tachycardia Irregular Atrial Fibrillation Atrial Flutter with variable block Multifocal atrial Tach OAAPN SWM

49 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 OAAPN SWM 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 OAAPN SWM Slow Fast AVNRT OAAPN SWM

50 Typical AVNRT Narrow complex Tachycardia No visible P waves There are pseudo R waves in V1 2 OAAPN SWM OAAPN SWM Fast Slow AVNRT Narrow complex Tachycardia Retrograde P waves are visible after each QRS complex OAAPN SWM

51 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) OAAPN SWM 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) OAAPN SWM OAAPN SWM

52 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 OAAPN SWM 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 OAAPN SWM 2018 Negative Delta wave in avl (pseudo infarction pattern) 26 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 OAAPN SWM

53 OAAPN SWM OAAPN SWM Common causes of ST Depression Ischemia Strain Digitalis effect Hypokalemia/hypomagnesemia Rate related changes Any combination of the above OAAPN SWM

54 Common causes of Tall R wave in V1 WPW RBBB RVH Posterior MI Normal variant OAAPN SWM 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 OAAPN SWM Other Cardiac Conditions Many conditions cause changes to the ECG Electrolyte abnormality Ischemia Infarction Inflammation Medications OAAPN SWM

55 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 OAAPN SWM Pericardial Effusion Can occur with pericarditis Can cause lowvoltage QRS complexes in all leads and electrical alternans OAAPN SWM Electrical Alternans QRS complexes change in height with each successive beat OAAPN SWM

56 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 OAAPN SWM A OAAPN SWM S1 Q3 T3 Sinus Tach RBBB T wave inversions in right precordial leads OAAPN (V1 3) SWM as 2018 well Lead III

57 Pulmonary Embolism OAAPN SWM Electrolyte Imbalances Increases or decreases in potassium and calcium serum levels can have a profound effect on the ECG OAAPN SWM 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 OAAPN SWM

58 OAAPN SWM Hyperkalemia OAAPN SWM Suspect Hyperkalemia New bradycardia New AV block especially with CKD or ESRD taking ACE I or potassium sparing meds OAAPN SWM

59 Hypokalemia Key ECG characteristics include: ST segment depression Flattening of the T wave Appearance of U waves OAAPN SWM OAAPN SWM OAAPN SWM

60 OAAPN SWM Hypocalcemia QT interval slightly prolonged OAAPN SWM OAAPN SWM

61 OAAPN SWM 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 OAAPN SWM