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Cardiac Arrhythmias I: Atrioventricular Conduction Disturbances and Bradyarrhythmias Michael H. Lehmann, M.D. Clinical Professor of Internal Medicine Director,

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Presentation on theme: "Cardiac Arrhythmias I: Atrioventricular Conduction Disturbances and Bradyarrhythmias Michael H. Lehmann, M.D. Clinical Professor of Internal Medicine Director,"— Presentation transcript:

1 Cardiac Arrhythmias I: Atrioventricular Conduction Disturbances and Bradyarrhythmias Michael H. Lehmann, M.D. Clinical Professor of Internal Medicine Director, Electrocardiography Laboratory

2 Overview of Cardiac Arrhythmias

3 Why Are Arrhythmias Important? Symptoms span palpitations, lightheadedness, syncope (fainting) and cardiac arrest May be the first manifestation of heart disease May precipitate or exacerbate heart failure or ischemia Some arrhythmias can predispose to intracardiac clot formation and embolic events (stroke, myocardial infarction, peripheral emboli)

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5 EKG Assessment of Arrhythmias Is the rate slow ( 5 big boxes])? Is the rate fast (>100 beats/min [< 3 big boxes])? What drives the P waves? What drives the QRS complexes? What is the relationship between P’s and QRS’s?

6 Sites of Disturbances in Impulse Formation or Conduction Leading to Bradyarrhythmias SA Node AV Node His-Purkinje System

7 Components of Atrioventricular (AV) Conduction His- Purkinje System AV Node

8 Intraventricular Conduction Disturbances

9 Left bundle branch Left anterior fascicle Septal fascicle Left posterior fascicle Right bundle branch Intraventricular (His-Purkinje) Conduction System (AV node) His bundle

10 Rule for QRS Width: Any electrophysiologic process that engenders a departure from synchronous activation of the ventricles tends to widen the QRS

11 Normal synchronous overlapping activation of both ventricles: On time Asynchronous scenario I: Late Head start On time (or late) Asynchronous scenario II: QRS Narrow Wide QRS Width: Synchronous vs. Asynchronous Ventricular Activation

12 Generation of Narrow QRS Complex ( .10 sec [2.5 little boxes]) Intact Purkinje system assures synchronous, overlapping activation of right ventricle (RV) and left ventricle (LV) Horizontal plane with precordial leads: RV LV

13 Bundle Branch Blocks

14 Right Bundle Branch Block (RBBB) Late right ventricular activation, with slow muscle-to-muscle conduction RV is activated via the left bundle

15 QRS Distortion Induced by RBBB Note terminal rightward delay with QRS widening ( .12 sec [3 little boxes], with “complete” RBBB) rSR’ pattern Broad S wave Initial QRS inscription is normal due to normal LV activation

16 Note T wave pointing in direction opposite to late rightward component (2  repolarization effect) Complete RBBB Pattern V1 V6 rsR’ complex Broad S wave (Lead I similar)

17 Left Bundle Branch Block (LBBB) Delayed left ventricular activation, with slow muscle-to-muscle conduction LV is activated via the right bundle

18 QRS Distortion Induced by LBBB Broad monophasic R wave Entire QRS dominated by marked leftward delay and is wide ( .12 sec [3 little boxes], with “complete” LBBB) Broad S wave

19 Note absence of “septal-q” in V6; andT wave pointing in direction opposite to QRS (2  repolarization effect) Broad S wave Broad R wave (Lead I similar) Complete LBBB Pattern V1V6

20 Fascicular Blocks

21 Mean QRS Axis Quadrants in the Frontal Plane Lead I Lead AVF (+) ()() ()()

22 Frontal Plane Mean QRS Axis Designations I AVF r  S in Lead II for Left Axis Deviation

23 Left Anterior Fascicular (“/Hemi-”) Block (LAFB) Lead I Lead AVF 1) Initial QRS forces directed inferiorly to the right LV is activated via the left posterior fascicle 2) Bulk of QRS forces directed superiorly to the left Left Axis Deviation (to -45  or beyond) 3) Minimal or no QRS widening

24 Left Anterior Fascicular (“/Hemi-”) Block (LAFB) I II III Initial QRS forces directed rightward (negative in Lead I) and inferiorly (positive in Leads II and III rS qR Subsequent predominant forces directed leftward (positive in I) and superiorly (negative in II and III)

25 Left Posterior Fascicular (“/Hemi-”) Block (LPFB) Lead I LV is activated via the left anterior fascicle 1) Initial QRS forces directed superiorly to the left 2) Bulk of QRS forces directed inferiorly to the right Lead AVF Right Axis Deviation (beyond +90  ) 3) Minimal or no QRS widening

26 Left Posterior Fascicular (“/Hemi-”) Block (LPFB) rSqR I II III Initial QRS forces directed leftward (positive in Lead I) and superiorly (negative in Leads II and III Subsequent predominant forces directed rightward (negative in I) and inferiorly (positive in II and III)

27 Bifascicular Block (RBBB + LAFB) LV is activated via the left posterior fascicle RV is activated from the left Site of RBBB Site of LAFB

28 Bifascicular Block (RBBB + LAFB) Note RBBB pattern plus left axis deviation of “unblocked” portion of QRS (initial.06 sec =1.5 little boxes)

29 Site of RBBB LV is activated via the left anterior fascicle Site of LPFB RV is activated from the left Bifascicular Block (RBBB + LPFB)

30 Note RBBB pattern plus right axis deviation of “unblocked” portion of QRS (initial.06 sec =1.5 little boxes)

31 Non-Specific Intraventricular Conduction Block Leads I & V1 inconsistent with RBBB; septal q in I inconsistent with LBBB QRS .12 sec without a typical BBB pattern

32 Causes of Intraventricular Conduction Disturbances Ischemic heart disease or cardiomyopathic scarring Degenerative changes in the conduction system Antiarrhythmic drugs that depress the inward sodium current Hyperkalemia (  K  ) Myocardial infection, infiltration (e.g., tumor) Trauma (e.g., cardiac surgery) Congenital abnormality

33 AV Block

34 Components of AV Conduction His- Purkinje System AV Node

35 AV Block - Definitions First Degree: Prolonged conduction time Second Degree: Intermittent non-conduction Third Degree: Persistent non-conduction

36 First Degree AV Block (PR >.20 sec [1 big box]) II PPP.36 Site of delay most commonly the AV node, but may be localized to the His-Purkinje system

37 Second Degree AV Block - Type I (Wenkebach or Mobitz I Block) PPP P Block II Example of 3:2 conduction ratio; general pattern, n:n-1 Note PR  prior to block and  post-block Characteristic of AV nodal site of block

38 II Block P PP P P 4:3 conduction ratio Note first RR longer than second RR Second Degree AV Block - Type I (Wenkebach or Mobitz I Block)

39 Ladder Diagram of AV Conduction P QRS

40 Schema of a “Typical” 4:3 AV Wenckebach Sequence Second RR (VV) shortens due to diminution in the increment of AV prolongation Pause encompassing blocked beat < 2 x PP

41 Second Degree AV Block - Type I V1 7:6 Conduction Ratio Note “atypical” PR & RR features

42 Second Degree AV Block - Type I (Repetitive Cycles) “Group beating” (“Regularly irregular” rhythm) II 4:3

43 II P PPPPP Second Degree AV Block - Type II (Mobitz II) Example of 3:2 conduction ratio; general pattern, n:n-1 Note fixed PR for all conducted beats Characteristic of His-Purkinje system site of block Block

44 Second Degree AV Block - Type II PP PPP 4:3 conduction ratio Block

45 II PPPP P P 2:1 Second Degree AV Block - Type I or Type II? Is site of block within the AV node or His-Purkinje System?

46 EKG/Clinical Clues  to site of 2:1 Second Degree AV block QRS narrow Improves with exercise (catecholamine-facilitated conduction) Observed in setting of increased vagal tone (e.g., sleep) or AV nodal depressant drugs QRS wide (BBB patterns) Unchanged (possibly even precipitated) during exercise May improve with heart rate slowing during increased vagal tone Favoring AV NodeFavoring His-Purkinje System  Rules-of-Thumb only

47 II PPPPP PPPP 3:1 conduction ratio, with ventricular rate in the 30’s Advanced Second Degree AV Block (Block of  2 Consecutive P Waves)

48 Pacemaker Hierarchy (Dominant vs Subsidiary/Escape Pacemakers) SA Node (+Atria) AV Junction (=AVN/His Bundle) Ventricles (= Distal Purkinje System) Intrinsic Rate of Firing min  min  min  1

49 Site of AV Block vs. Escape Rhythm AV Node: Junctional or ventricular His-Purkinje System: Ventricular

50 Junctional and ventricular (= “idioventricular”) escape beats or rhythms Are suppressed (inhibited) as long as their intrinsic rates are overdiven by a faster pacemaker tissue or rhythm process capturing the heart Become manifest (“escape” from suppression) in the absence of faster competing rhythms But, firing of these pacemakers at rates faster than their upper-limit escape rates is abnormal (i.,e., “accelerated rhythm” or relative “tachycardia” )

51 EKG Appearance of Escape Beats Sinus Rhythm AtrialJunctionalVentricular (Retrograde P waves require intact retrograde AVN cond.) P’ Narrow QRS Wide QRS

52 Normal synchronous overlapping activation of both ventricles: On time Asynchronous scenario I: Late Head start On time (or late) Asynchronous scenario II: QRS Narrow Wide QRS Width: Synchronous vs. Asynchronous Ventricular Activation

53 Third Degree AV Block (Complete Heart Block) PP PPP P P waves at 60 beats/min QRS complexes (junctional escape rhythm) at 45 beats/min Atrial and ventricular activity are completely unrelated Junctional escape rhythm suggests AV nodal site of block II

54 Third Degree AV Block (Complete Heart Block) V1 PP PP P P waves at beats/min QRS complexes (ventricular escape rhythm) at 35 beats/min Atrial and ventricular activity are completely unrelated Ventricular escape rhythm suggests His-Purkinje site of block

55 Ladder Diagram of AV Dissociation During Third Degree AV Block Faster atrial rate Slower ventricular (escape) rhythm Note that impulses block anterogradely and retrogradely within the AV conduction system

56 Unreliability of Ventricular Escape Rhythm in Third Degree AV Block PP (P) P P P PPPP P P No QRS complexes! P P P (P) P 15 s

57 Physiologic AV Block First and second degree AV block may occur physiologically at an AV Nodal level: –in response to premature atrial impulses or atrial tachyarrhythmias –in settings of increased vagal tone (e.g., sleep, Valsalva maneuver, well-trained athletes) BUT… persistent 3rd degree AV block is never physiologic

58 Causes of NON-Physiologic AV Block Ischemic heart disease, cardiomyopathy and degenerative changes Drugs that depress AV conduction –AV Node: digoxin, beta blockers, calcium channel blockers, amiodarone –His-Purkinje System: Antiarrhythmic drugs that depress the inward sodium current Myocardial infection, infiltration (e.g., tumor) Trauma (e.g., surgery; therapeutic ablation) Congenital abnormalities

59 Sinus Bradyarrhythmias

60 InspirationExpiration SA nodal accelerationSA nodal deceleration Sinus Arrhythmia

61 Pacemaker Hierarchy (Dominant vs Subsidiary/Escape Pacemakers) SA Node (+Atria) AV Junction (=AVN/His Bundle) Ventricles (= Distal Purkinje System) Intrinsic Rate of Firing min  min  min  1

62 Sinus Bradycardia II P wave upright in leads I and II, just as in normal sinus rhythm

63 Causes of Sinus Bradycardia Increased vagal tone Drugs: beta blockers, calcium channel blockers, amiodarone, digoxin (indirect effect) Myocardial ischemia/infarction Hypothyroidism “Sick sinus syndrome” - degenerative/fibrotic atrial process

64 Sequence of P Wave Generation Sinus Node SA Junction Atrium (P wave) Non-visible process on the EKG

65 Sinoatrial (SA) Exit Block - Definitions First Degree: Prolonged SA conduction time (non-detectable on EKG; no missing P waves) Second Degree: Intermittent non-conduction (intermittent absence of P waves) Third Degree: Persistent non-conduction (complete absence of P waves; escape rhythms only)

66 Second Degree SA Exit Block - Type I (Wenkebach) P P P P 4:3 pattern Missing P wave PP intervals shorten prior to block Note unaffected, fixed PR intervals PP:

67 Schema of a Typical 4:3 Second Degree SA Exit Block (Type I) Sequence Second PP (AA) shortens due to diminution in the increment of SA-A prolongation Pause encompassing blocked beat < 2 x normal PP Sinus Node SA Junct. A

68 Second Degree SA Exit Block - Type II PP: PP PP P One P wave abruptly “drops out” on time Missing P wave

69 X2X X PP PP P PPP 2:1 SA Exit Block (Every Other P wave is “Dropped”) Atrial rate is abruptly cut in half Resolution of block P

70 PPP’ Sinus bradycardia  Sinus arrest  Slow junctional escape rhythm ( with retrograde p waves) Sinus Arrest

71 Tachycardia-Bradycardia (Form of “Sick Sinus”) Syndrome Atrial Flutter Sinus arrestJunctional escape (tardy) Atrial Flutter terminates

72 Sinus Arrest  Asystole Sinus rhythm Sinus brady.  Sinus arrest  V. escape rhythm Failure of V. escape rhythm  Asystole P P P PP P P P

73 Causes of SA Exit Block and Sinus Pauses/Arrest Increased vagal tone (very intense for sinus arrest) Drugs: beta blockers, calcium channel blockers, amiodarone, digoxin (indirect effect) Myocardial ischemia/infarction Sick sinus syndrome Sequela of open heart surgery


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