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
Taken from www.baptistoneword.org
Zimetbaum PJ, Josephson ME. NEJM, 2003
Pacemaker?
• 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
WHAT NEXT?
52 year-old obese man who presents with
cellulitis. Above seen on telemetry during
hospitalization.
Page…. HR 30. WHAT NEXT?
WHAT IS THIS?
Premature
junctional
complex
Retrograde p
wave
WHAT NEXT?
Mobitz II – 2nd Degree AV Block
80 year-old man presents with
syncope.
What’s the rhythm?
NSR with first degree AV block
Pause duration to meet criteria
for pacemaker implantation?
3 seconds
Post cath, holding groin pressure.
Pt dizzy now. WHAT NEXT?
Sinus Bradycardia.
Vagal response.
Give Atropine.
What is the rhythm?
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
• 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?
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
WHAT NEXT???
32 year-old female with palpitations
After Adenosine 6mg IV
Retrograde p
waves
CSM/Vagal Maneuvers
Adenosine
BB/CCB
Ablation
AVNRT – Mechanism?
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?
•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
Concealed penetration into the
pathway.
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