Bradycardia and Narrow Complex Tachycardia Smriti Banthia CCU Lecture Series

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 www.baptistoneword.org

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

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.

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.

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

WHAT IS THIS? Premature junctional complex Retrograde p wave

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

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

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

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

What is the rhythm? Afib ATRIAL FIBRILLATION

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

What’s wrong?

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

When Rx Coumadin? Afib

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

ACC/AHA Guidelines for Anticoagulation

Tachy-Brady Syndrome

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

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

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

AVNRT – Mechanism? APC blocked in fast pathway

Aflutter with variable conduction

MAT

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

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.

Atrial Tachycardia

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.

WHAT IS THIS? WPW

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

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

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

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