1. Bradycardia and Narrow Complex Tachycardia
Smriti Banthia
CCU Lecture Series

2. Conduction System Anatomy
Sinus node is supplied by the RCA in 60% of people and by the LCX in 40%.
AV node is supplied by the RCA in 90% and by the LCX in 10% of patients.
Right bundle supplied by LAD
Left bundle supplied by branches of the RCA and LAD
Zimetbaum PJ, Josephson ME. NEJM, 2003
Taken from

3. Pacemaker? Progressive shortening of PP interval before it blocks
SA Exit Block Type I – progressive shortening of PP interval before it blocks; pause is less than 2 of the preceding PP intervals; PP interval following pause is greater than PP interval before pause; no need for PPM unless symptomatic.
Progressive shortening of PP interval before it blocks
Pause is less than 2 of the preceding PP intervals

4. Pacemaker? SA Block Type II – Pause approximately 2x PP interval
Type II SA Block- Pause approximately 2x PP interval; no need for PPM unless symptomatic.

5. WHAT NEXT?
2nd degree AV block- Mobitz I – progressive lengthening of PR interval followed by a dropped p wave. Usually due to AV nodal delay but can be his bundle disease if advanced disease. NO need for PPM. Rx the OSA!
52 year-old obese man who presents with cellulitis. Above seen on telemetry during hospitalization.

6. Page…. HR 30. WHAT NEXT?
CHB – needs PPM

7. WHAT IS THIS?
Premature junctional complex
Retrograde p wave

8. WHAT NEXT? Mobitz II – 2nd Degree AV Block
80 year-old man presents with syncope.

9. NSR with first degree AV block
What’s the rhythm?
NSR with first degree AV block

10. Pause duration to meet criteria for pacemaker implantation?
Include slide on other criteria for PPM implantation
3 seconds

11. Post cath, holding groin pressure. Pt dizzy now. WHAT NEXT?
Sinus Bradycardia. Vagal response. Give Atropine.

12. What is the rhythm?
Afib
ATRIAL FIBRILLATION

13. Management of AF Maintenance of normal sinus rhythm
No treatment
Pharmacologic therapy (AAD, anticoagulants)
Non-pharmacologic therapy (Ablation, PPM)
• Ventricular rate control
Pharmacologic therapy (BB, CCB, Digoxin)
Non-pharmacologic therapy (AVN ablation)
• Reduction of thromboembolic risk

14. What’s wrong?

15. AFIB AND STROKE • AF increases stroke risk ~ 17x Rheumatic heart Dz
Leading cause of stroke from embolism
• AF increases stroke risk
~ 17x Rheumatic heart Dz
~ 5x in non-valvular
Risk of stroke ~ 5%/yr
• Proportion of strokes attributable to AF increases with age

16. When Rx Coumadin?
Afib

18. Problem: What about pt with prior hx of CVA but no other RF
Problem: What about pt with prior hx of CVA but no other RF? Classified as moderate risk when in fact may be high risk…. Thus, the ACC/AHA guidelines differ in the following way…
ASA 325 daily
ASA or Coumadin
Coumadin INR 2-3

19. ACC/AHA Guidelines for Anticoagulation

20. Tachy-Brady Syndrome

21. 32 year-old female with palpitations
WHAT NEXT???
32 year-old female with palpitations

22. A small R’ is seen is lead V1 with pseudo-S waves in the inferior leads that are absent after termination of the arrhythmia. These represent retrograde atrial activation with a very short RP interval.
After Adenosine 6mg IV

23. Retrograde p waves
CSM/Vagal Maneuvers
Adenosine
BB/CCB
Ablation

24. AVNRT – Mechanism?
APC blocked in fast pathway

26. Aflutter with variable conduction

27. MAT

28. Aflutter with 4:1 Block
Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the right atrium
EKG Characteristics: Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm
Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node, resulting in ventricular rates of either 150 or 75 bpm

29. Unmasking of Flutter Waves
In the presence of 2:1 AV block, the flutter waves may not be immediately apparent. These can be brought out by administration of adenosine.

30. Atrial Tachycardia

31. Atrial tachycardia
P wave upright lead V1 and negative in aVL consistent with left atrial focus.
P wave negative in V1 and upright in aVL consistent with right atrial focus.
Adenosine may help with diagnosis if AV block occurs and continued arrhythmia likely atrial tachycardia
70-80% will also terminate with adenosine.

32. WHAT IS THIS?
WPW

33. A. Emergent cardioversion for polymorphic VT.
B. I.V. procainamide
C. I.V. lidocaine
D. diltiazem drip to obtain rate control.

34. WPW epidemiology Present in 0.3% of the population
Risk of sudden death 1 per 1000 patient-years
Sudden death due to atrial fibrillation with rapid ventricular conduction
Atrial fibrillation often induced from rapid ORT
ORT(orthodromic reciprocating tachycardia

35. Atrial Fibrillation and WPW
AV nodal blocking agents may paradoxically increase conduction over accessory pathway by removing concealed retrograde penetration into accessory pathway.
Concealed penetration into the pathway causes intermittent block of pathway conduction

36. Management of Atrial Fibrillation with WPW
Avoid AV nodal blockers
IV procainamide to slow accessory pathway conduction
Amiodarone if decreased LVEF
DC cardioversion if symptomatic with hypotension