1 / 73

Cardiac Arrhythmias I : Atrioventricular Conduction Disturbances and Bradyarrhythmias

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

daniel_millan
Télécharger la présentation

Cardiac Arrhythmias I : Atrioventricular Conduction Disturbances and Bradyarrhythmias

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

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)

  4. EKG Assessment of Arrhythmias • Is the rate slow (< 60 beats/min [> 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?

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

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

  7. Intraventricular Conduction Disturbances

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

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

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

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

  12. Bundle Branch Blocks

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

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

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

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

  17. 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

  18. Complete LBBB Pattern V1 V6 Broad R wave (Lead I similar) Broad S wave Note absence of “septal-q” in V6; andT wave pointing in direction opposite to QRS (2 repolarization effect)

  19. Fascicular Blocks

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

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

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

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

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

  25. Left Posterior Fascicular (“/Hemi-”) Block (LPFB) rS qR qR II III I 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)

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

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

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

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

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

  31. 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

  32. AV Block

  33. Components of AV Conduction AV Node His- Purkinje System

  34. AV Block - Definitions • First Degree: Prolonged conduction time • Second Degree: Intermittent non-conduction • Third Degree: Persistent non-conduction

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

  36. Second Degree AV Block - Type I (Wenkebach or Mobitz I Block) II P P P P Block • 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

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

  38. Ladder Diagram of AV Conduction QRS P

  39. 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

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

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

  42. Second Degree AV Block - Type II (Mobitz II) II P P P P P P Block Block • 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

  43. Second Degree AV Block - Type II P P P P P Block 4:3 conduction ratio

  44. 2:1 Second Degree AV Block - Type I or Type II? II P P P P P P Is site of block within theAV nodeorHis-Purkinje System?

  45. 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 EKG/Clinical Clues to site of2:1 Second Degree AV block Favoring AV Node Favoring His-Purkinje System Rules-of-Thumb only

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

  47. Pacemaker Hierarchy (Dominant vs Subsidiary/Escape Pacemakers) Intrinsic Rate of Firing SA Node (+Atria) 60-100 min1 40-60 min1 AV Junction (=AVN/His Bundle) Ventricles (= Distal Purkinje System) 30-40 min1

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

  49. 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” )

More Related