Download Supraventricular Arrhythmias - Aultman Cardiology Fellowship

Supraventricular Arrhythmias
Ira R. Friedlander, M.D.
8/26/14
Definition
• Rapid heart rhythm during which the
electrical impulse propagates down the
normal His Purkinje system similar to
normal sinus rhythm
• Distinct from ventricular tachycardia
which only originates in the ventricles
Mechanisms of Arrhythmia
• Automaticity
– Enhanced automaticity
– Abnormal automaticity
Mechanisms of Arrhythmia
• Triggered Activity
– Small depolarizations during or just after
repolarization (phases 3 or 4) which can
trigger a new depolarization.
Mechanisms of Arrhythmia
• Reentry-most common mechanism
– Short circuit that forms between two
“pathways” that are either anatomically or
functionally distinct
– Typically:
• Path 1: Slow conduction, short refractory period
• Path 2: Rapid conduction, long refractory
period
Reentry
Panel A: Most impulses conduct
down both pathways.
Panel B: Unidirectional block, due to
longer refractoriness in one pathway.
Panel C: Potential to have reentry
back up the previously refractory
pathway
Panel D: Reentry then can persist.
Supraventricular Arrhythmias
• Atrial arrhythmias (AT, AFL and AF)
• Atrioventricular nodal reentrant tachycardia
(AVNRT) and junctional ectopic tachycardia
(JET)
• Atrioventricular reentrant tachycardia (AVRT)
Wolf-Parkinson-White Syndrome
– Orthodromic AVRT
– Antidromic AVRT
SVT: Symptoms
• May be variable
–
–
–
–
–
–
Palpitations, chest pounding, neck pounding
Weakness/malaise
Dyspnea
Chest pain
Lightheadedness
Near syncope/syncope
• Symptoms usually abrupt in onset and termination
• May have history of symptoms since childhood or
have a positive FHx
SVT: Physical Exam
• In absence of tachycardia, usually
normal
• Rapid heart rate (150-250)
– May be irregular or regular (mechanism)
• BP may be low or with narrow pulse
pressure
• Neck veins may reveal cannon waves.
Sinus Rhythm
• Originates in sinus
node (automaticity)
• 50-100 bpm resting
• Up to 200 bpm
• Conduction through
normal AV axis
• P wave morphology
reflects site of onset
Atrial Tachycardia
• Ectopic atrial focus
– Reentrant, automatic or
triggered
•
•
•
•
150-250 bpm
1:1 AV conduction
Paroxysmal or “warm up”
P wave morphology
variable
Focal Atrial Tachycardia
RAA
LAA
SN * * *
CT
RAFW
PV
CSO
IVC
LAFW
20 yr woman with post-partum congestive heart failure
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Adenosine Injection
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Post- Adenosine Injection
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Catheter location : Right atrial
appendage
LAO
RAO
CT
MAP
CT
MAP
CS
CS
His
His
Earliest Atrial Activation : Right Atrial Appendage
I
II
III
aVL
MAP dist
MAP prox
CT 1,2
CT 3,4
CT 5,6
CT 7,8
CT 9,10
CT 11,12
CT 13,14
CT 15,16
CS dist
CS prox
- 23 msec
Atrial Tachycardia
I
II
III
aVL
MAP dist
MAP prox
CT 1,2
CT 3,4
CT 5,6
CT 7,8
CT 9,10
CT 11,12
CT 13,14
CT 15,16
CT 17,18
CT 19,20
CS dist
CS prox
RF on
1.9 sec
Sinus Rhythm
Atrial Flutter
• Reentrant circuit
localized to the RA
• 250-350 bpm
• 2:1 or variable AV block
• Classic “saw-tooth” P
waves
Activation on Halo Catheter
Typical = Counterclockwise
V1
II
aVF
TA 19,20
TA 9,10
TA 1,2
TA 1,2
TA 3,4
TA 5,6
TA 7,8
CS Os
TA 9,10
TA 11,12
TA 13,14
TA 17,18
TA 19,20
CS Os
Activation on Halo Catheter
Atypical = Clockwise
V1
II
aVF
TA 19,20
TA 9,10
TA 1,2
TA 1,2
TA 3,4
TA 5,6
TA 7,8
CS Os
TA 9,10
TA 11,12
TA 13,14
TA 17,18
19,20
CS Os
Atrial Fibrillation
• Chaotic atrial rhythm due
to multiple reentrant
wavelets
• 350-500 bpm
• Ventricular rate irregular
and rapid due to variable
AV block
• HTN, valvular dz.,
metabolic dz., CMP,
EtOH
Atrial Fibrillation
• The rapid atrial activity results in:
– Increased risk of thrombus formation and stroke
– Rapid and irregular ventricular rate
• The treatment is aimed at:
– Decreasing the risk of stroke (coumadin, ASA)
– Decreasing the ventricular rate (beta-blockers,
calcium channel blockers, digoxin)
– Restoring the rhythm to sinus (drug therapy,
catheter ablation, surgical Maze)
Atrial Fibrillation
• Advantages of rhythm control:
– Abolition of symptoms
– Halting atrial enlargement
– Improvement in left ventricular function and
exercise capacity
• Disadvantages of rhythm control:
– Subjecting patients to drug therapy and/or
procedure that might be associated with
complications
Atrial Fibrillation
Treatment
• In patients with minimal symptoms and normal left
ventricular function:
– Coumadin/ASA
– Rate control (drugs, AVJ ablation + BV pacing)
• In patients with significant symptoms and/or left
ventricular dysfunction:
– Coumadin/ASA
– Rate control (drugs, AVJ ablation + BV pacing)
– Rhythm control (anti-arrhytmic drugs, catheter ablation)
Drug Therapy to Maintain Sinus Rhythm in Patients
with Recurrent Paroxysmal or Persistent Atrial Fibrillation
ACC/AHA/ESC Guidelines
Atrial Fibrillation
Catheter Ablation
Ablate PV potentials
PV Isolation
Pappone
(circumferential LA ablation)
AV Nodal Reentrant Tachycardia
Morphology and location of P wave relative to QRS distinct
27 y.o with palpitations
Pseudo R’ in V1 during tachycardia
NSR
AVNRT
Junctional Ectopic Tachycardia
Normal sinus rhythm
Junctional tachycardia
Wolff-Parkinson-White Syndrome
• Second electrical connection
exists between the atria and
ventricles (accessory
pathway)
– Resemble atrial tissue
– Results in a short PR and
– Delta wave (pre-excitation)
• Some AP conducts only
retrograde (concealed)
Arrythmias in WPW
• The most common arrhythmia is orthodromic AV
reentrant tachycardia (narrow QRS)
• Less common are pre-excited tachcyardias
(wide QRS)
–
–
–
–
Antidromic AV reentrant tachycardia
Atrial tachycardia/flutter with pre-excitation
AVNRT with pre-excitation
Atrial fibrillation with pre-excitation (most life
threatening due to rapid ventricular response)
Orthodromic AVRT
Conduction down AV axis during tachycardia gives NARROW QRS complex
Pre-excited Tachycardia
Mechanisms
AVRT
AT
AVNRT
Conduction down AP during tachycardia gives WIDE QRS complex
Atrial Fibrillation
RF Ablation in WPW
SUMMARY
Mechanisms of SVT
SP
Atrial Tachycardia
FP
AVNRT
AVRT
Differential Diagnosis of NCT
• Short RP
– AVRT
– AT
– Slow-Slow
AVNRT
• Long RP
– AT
– Atypical
AVNRT
– PJRT
• P buried in QRS
– Typical AVNRT
– AT
– JET
SUMMARY
• Obtain a 12 lead ECG. The location of the P wave will
dictate the differential diagnosis
• If hemodynamically unstable (chest pain, heart
failure, hypotension) CARDIOVERSION
• If hemodynamically stable AV NODAL AGENT
• Long term therapy depends on mechanism and can
be conservative, pharmacologic or invasive
• EP study often needed for definitive characterization
of mechanism and can cure most SVTs with 90%
success rate