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)

5. 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?

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
Node
His-
Purkinje
System

8. Intraventricular Conduction Disturbances

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

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

11. QRS Width: Synchronous vs. Asynchronous Ventricular Activation
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:

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

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

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. 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)

20. Fascicular Blocks

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

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

23. 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

24. Left Anterior Fascicular (“/Hemi-”) Block (LAFB)qR rS rS I II
III
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)

25. 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

26. 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)

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

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

30. Bifascicular Block (RBBB + LPFB)
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
QRS  .12 sec
without a
typical BBB
pattern
Leads I & V1
inconsistent
with RBBB;
septal q in I
with LBBB

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
Node
His-
Purkinje
System

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]) .36 II P P P
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)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

38. 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

39. Ladder Diagram of AV Conduction
QRS P

40. 4:3 AV Wenckebach Sequence
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
7:6 Conduction Ratio
Note “atypical” PR & RR features

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

43. 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

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

45. 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
Favoring AV Node
Favoring His-Purkinje System
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
Rules-of-Thumb only

47. 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

48. (Dominant vs Subsidiary/Escape Pacemakers)
Pacemaker Hierarchy
(Dominant vs Subsidiary/Escape Pacemakers)
Intrinsic Rate of Firing SA
Node
(+Atria)
min1
AV Junction
(=AVN/His Bundle)
min1
Ventricles
(= Distal Purkinje System)
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
Narrow
QRS
Wide
QRS P’ P’
Sinus
Rhythm
Atrial
Junctional
Ventricular
(Retrograde P waves require
intact retrograde AVN cond.)

52. QRS Width: Synchronous vs. Asynchronous Ventricular Activation
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:

53. (Complete Heart Block)
Third Degree AV Block
(Complete Heart Block) II P P P P P 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

54. (Complete Heart Block)
Third Degree AV Block
(Complete Heart Block) V1 P P P P 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
No QRS complexes! P P P
(P) P

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. Sinus Arrhythmia Inspiration Expiration SA nodal acceleration
SA nodal deceleration

61. (Dominant vs Subsidiary/Escape Pacemakers)
Pacemaker Hierarchy
(Dominant vs Subsidiary/Escape Pacemakers)
Intrinsic Rate of Firing SA
Node
(+Atria)
min1
AV Junction
(=AVN/His Bundle)
min1
Ventricles
(= Distal Purkinje System)
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)
4:3 pattern P P P P
Missing
P wave
PP:
PP intervals shorten prior to block
Note unaffected, fixed PR intervals

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

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

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

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

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

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

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