Transcript Supraventricular arrhythmias

Supraventricular arrhythmias
Jerry John
July 29, 2009
Objectives
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Supraventricular Arrhythmias
How do supraventricular arrhythmias manifest?
What are the common supraventricular arrhythmias?
What is the mechanism of atrioventricular arrhythmias?
Which drugs are used in the management of supraventricular
arrhythmias?
Which patients should be offered catheter ablation?
Atrial Fibrillation and Atrial Flutter
What are the incidence and prevalence of atrial fibrillation?
What are the major sequelae of atrial fibrillation?
What are the risk factors for stroke in atrial fibrillation?
What are the treatment options for patients with atrial
fibrillation?
History
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F > M (2:1) – AVNRT
M >F AVRT
Posture
Menses
3rd trimester pregnancy
Neck pulsations (“Frog sign”)
Age of onset (10 year difference AVNRT(39) vs. AVRT (26)
Thyroid symptoms
Acute precipiants (post op, PE, drug withdrawal,
ischemia)
JACC 2009; 53:2353-58
EKG
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AV node dependent (Y/N)
Re-entrant circuit (Y/N)
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P wave
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Circuit (Macro/Micro)
Anatomic (e.g. previous ASD repair, CVTI)
Accessory pathway ( WPW, Mahaim, etc. )
Rate
Morphology (Sinus/Retrograde/abnormal): look at the T waves and
the psuedo R (V1) and psedo S (inferior leads)
Conduction (2:1; 3:1, etc.)
Response to AV Block
VA conduction (i.e. R-P relationship): (short/long)
Initiation (PAC or PVC) & Termination (P wave or QRS)
Anatomy & Physiology
• SA node
– 1 mm subendocardial near RSPV
• AV node
– Decremental conduction properties
• His-Purkinje
• Accessory pathways
– No decremental conduction
– AV conduction 10-20 ms
ORT
AVNRT
Non paraoxysmal
junctional tach
Atach (reentry
or automaticity)
AV Node Depdendence (Y/N)
AV nodal dependent arrhythmias
• AVNRT (micro-reentrant circuit)
• AVRT (macro-reentrant circuit): anti/orthodromic
• JET (junctional ectopic tachycardia) - childhood and
associated with congenital heart disease
AV nodal independent arrhythmias
• Atrial tachycardia
• Inappropriate Sinus Tachycardia
• Sinus Node Reentrant Tachycardia
• Atrial flutter
• Atrial fibrillation
RP relationship
• Short “RP” Tachycardias:
Typical AVNRT
AVRT
• Long “RP” Tachycardias:
Atrial Tachycardia
Atypical AVNRT
AVRT with long retrograde conduction
PJRT
Where’s the P wave
• Valsalva
• Carotid sinus massage
– Slows SA nodal; and/or AV nodal conduction
• Adenosine
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Slows sinus rate
Increases AV nodal conduction delay
T ½ 5 seconds
6 or 12 mg bolus
Effect blocked by theophylline, methylxanthines
(caffeine); and potentiated by dipyridamole
P waves
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Rate
Morphology (Sinus/Retrograde/abnormal)
Conduction (2:1; 3:1, etc.)
Response to AV Block
VA conduction (i.e. R-P relationship):
(short/long)
P waves
• (-) Inferior leads atrial activation from low to
high: AVNRT, atypical AVNRT; AVRT
• Right atrial focus:
1) (-/+) in aVL right atrium activated first and then
left atrium)
2) (-) or biphasic in V1
• Left atrial focus:
1) (-) or isoelectric in aVL
2) (+) V1 suggests back to front
Tachycardia onset
• Most SVTs triggered by a PAC
• If the PAC conducts with a long PR, dual AV
nodal physiology is suggested with the
conduction being through the slow pathway
• If a PVC initiates SVT, it is likely to be AV node
dependent
Tachycardia termination
• Ends with a P wave: suggests an AV nodal
dependent arrhythmia because the generation of
the P wave without a QRS suggests block in the AV
node… this is more likely to be AVNRT or AVRT
• AVNRT p waves however can be buried in the QRS if VA
conduction is very short
• Ends with a QRS : almost always atrial tachycardia
(some rare AV node dependent tachycardias can
terminate in this manner)
AVNRT
• Most common cause of a regular narrow complex
tachycardia
• Involves a slow and a fast pathway in the region
of the AV node
• Turn around point appears above the bundle of
His
• 160-190 bpm but may exceed 200 bpm
• Slow-fast form accounts for 90% of AVNRT
• Fast-slow or slow-slow AVNRT accounts for 10%
• Pseudo r’ in V1, pseudo S wave in 2,3,avf, and p
wave absence help distinguish AVNRT from AVRT
and atrial tachycardia
AVNRT
• Initiation and termination by APDs, VPDs or atrial
pacing during AVW
• Dual AVN physiology
• Initiation depends on critical A-H delay
• Concentric retrograde atrial activation(V-A -42 to 70
msec)
• Retrograde P wave within QRS with distortion of
terminal portion of the QRS
• Atrium, His bundle and ventricle not required , vagal
maneuvers slow and then terminate SVT
Atypical AVNRT
• Initiation and termination by APDs, VPDs, or
ventricular pacing during retrograde AVW
• Dual retrograde AVN physiology
• Initiation dependent on critical H-A delay
• Earliest retrograde activation at CS os
• Retrograde P wave with long R-P interval
• Atrium, His bundle, and ventricle not required,
vagal , maneuvers slow and then terminate SVT,
always in the retrograde slow pathway
AVNRT Treatment
• Low threshold for catheter ablation given long term
success rate > 90% and low risk of complications
• AV nodal blocking agents (diagnosis/treatment)
– Adenosine
– BB/CCB
– Digoxin
• Anti-arrhythmics (third choice)
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Procainamide
Amiodarone
Disopyramide
Flecainide/Propafenone
AVRT
• Activation sequence is ventricle via atria; therefore P wave
often in the ST or T
• Left lateral AP: (+) Delta V1; (-) Delta I
• Right sided AP: (-) Delta V1 {QS pattern}; (+) Delta I
• Concealed AP implies only retrograde conduction; i.e. no preexcitation and only orthodromic AVRT.
• Rapidly conducted Afib occurs may occur for 2 reasons: 1) AP
may have a short refractory period ; 2) AP does not exhibit
decremental conduction properties like the AV node
• Flecainide and Propafenone preferred as they prolong the
effective refractory period
BBB on tachycardia
• Interval development of BBB and increased
tachycardia cycle length suggests contralateral
AVRT
• Pre-existing BBB
• Rate related BBB: will look like a conventional BBB
• Accessory pathway
AVRT
• Use of Adenosine or Verapamil
• There is a small risk (3-5%) of preferential
conduction down the accessory pathway, and
ibutilide or procainamide, or electric
cardioversion should be immediately
available
Asymptomatic WPW
• 165 children (5-12 years) screened
• 60 randomized, 3 withdrew: 20 ablation and 27 no
ablation
• 1 child in ablation group had arrhythmia (5%) and 12
of 27 in control group ( 44% )
• 2 children in control group had VF and one died
Pappone et al; NEJM 2004;351:1197-05
AVRT Treatment
• Low threshold for catheter ablation given long term
success rate > 90% and low risk of complications
– Posteroseptal pathways have less success rates
– L sided
• AV nodal blocking agents (diagnosis/treatment)
– Adenosine
– BB orCCB in conjunction with Flecainide or Propafenone
Atrial tachycardia
• Older patients - related to atrial stretch or scarring
• If conduction to the ventricle via the AV node, variable AV
block may occur
• A bystander (accessory) pathway may be used to conduct
antegrade to the ventricles; i.e. the accessory pathway is not
what is causing the atria to beat so fast
• Tachycardia may be incessant: “the ventricle is a slave to the
atrium”
• Procainamide may be considered to achieve immediate
control
• AV nodal blocking agents and sotalol may be considered for
chronic treatment
Irregular SVT
• AV block
– Wenckebach
– Variable block (e.g. atrial tachycardias)
– 2:1 with typical flutter; odd multiples with atypical flutter
• Multifocal atrial tachycardia (MAT)
• Atrial Fibrillation (with or w/o pre-excitation)
Focal Atrial Tachycardia
• Incessant or paroxysmal atrial rhythms
120-250 bpm
• Demographic profile similar to reentrant
AT, but less likely to have cardiac surgery
• Typically 1:1 conduction
• P wave morphology different from sinus
• Typically terminate or transiently suppress
with adenosine
• Centrifugal activation
• Cannot be entrained
Focal Atrial Tachycardia
Three Subgroups:
1. Cristal Tachycardia
- Initiated and terminated with PES
- Arise along crista
- P wave similar to NSR
- Terminates with adenosine
2. Repetitive monomorphic AT
- Repetitive runs of nonsustained AT
- Suppress with adenosine
- Variable locations
3. Automatic AT
- Incessant AT
- Transient suppression with adenosine
Junctional Tachycardia
• Nonparoxysmal Junctional Tachycardia
• Junctional Ectopic Tachycardia
• Congenital Automatic Junctional Tachycardia
Nonparoxysmal Junctional
Tachycardia
• 70-120 bpm
• Generally regular with VA conduction
• Seen with dig toxicity, ischemia, COPD,
metabolic disturbances, carditis and after
cardiac surgery
• Mechanism is triggered activity due to DADs
Junctional Ectopic Tachycardia
(JET)
• Following surgery for congenital heart disease
• 3% of VSD repairs, 10% of TGV, 7% of TOF and
2% of Fontan
• Perinodal trauma
• Procainamide and cooling, amiodarone
Congenital Automatic Junctional
Tachycardia
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< 1% of pediatric SVTs
Average HR 230 bpm (140-370)
Infants < 6 months old
High mortality. Less malignant older the
child is
• Triggered activity, enhanced automaticity
• Amiodarone, ablation with PM
PJRT
• Orthodromic reciprocating tachycardia
• Earliest retrograde activation in proximal CS
• Tachycardia terminates with adenosine with
retrograde AP block
• HIS refractory PVC advances atrial activation
Atrial Flutter
• Typical or type I atrial flutter:
Counter clockwise atrial activation
manifested as - P waves in II,III,avf and + in VI
with transition to - P in V6
Clockwise with reverse activation
• Atypical or type II atrial flutter
Also called as fib flutter
• In the absence of AFib symptomatic Aflutter is often
amenable to ablation (success rates >90%)
Afib
• What are the incidence and prevalence of
atrial fibrillation?
• What are the major sequelae of atrial
fibrillation?
• What are the risk factors for stroke in atrial
fibrillation?
• What are the treatment options for patients
with atrial fibrillation?
Afib epidemiology
• Age adjusted incidence has been increasing from 1980 to
2000: 3.2 million in 1980; 5.1 million in 2000
• The detection of Afib requires symptoms and
asymptomatic PAF may go undetected.. Current
estimates at the Mayo Clinic would suggest 2.3 million
Americans.
• Afib prevalence increases with age: 0.1% <55 years; at
9% in octogenerians.
• At younger ages (<70), Afib has a greater prevalence
among males (5.8%) than females (2.8%) based on data
from CHS
• The lifetime risk based on the Framingham cohort is 2326% among 40 year olds.
Circulation 2006; 114(2):119-125. ;Am J Cardiol 1994; 74:236-241).; JAMA 2004;
292:2471-2477; JACC 2007; 49:565-571).
Afib epidemiology
• Age alone does not explain the increased incidence: an
increase in obesity accounted for 60% of the age adjusted
increase in AF incidence
• HTN and Diastolic dysfunction
• Obesity has been associated with new onset Afib in the
Framingham and other cohorts
• OSA, Etoh, Anger, ethnicity, and genetic influences have
been reported to be associated with incident Afib.
• Appropriately treated OSA reduces AFib recurrence after
cardioversion
• AA race is associated with less Afib than whites.
• Afib and CAD are co-existent
• Rheumatic heart disease and valvular heart disease
Circulation 2006; 114(2):119-125. ;Am J Cardiol 1994; 74:236-241).; JAMA 2004;
292:2471-2477; JACC 2007; 49:565-571; Circ 2003; 107:2589-2594).
Afib categories
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Lone atrial fibrillation: no structural heart
disease (usually <60 years)
Paroxysmal : terminate spontaneously <7 days
Persistent: fails to self-terminate within 7 days.
Episodes may eventually terminate
spontaneously, or they can be terminated by
cardioversion.
Permanent : > 1 year and CV not attempted or
failed.
Episodes > 30 seconds unrelated to a reversible
cause (cardiac surgery, pericarditis, MI,
hyperthyroidism, PE)
What are the major sequelae of atrial
fibrillation?
• Worsened heart failure
• Afib begets afib leading to electrical and
structural remodeling
• Tachycardia induced cardiomyopathies
• Stroke
• Decreased quality of life and exercise
tolerance
• Acute hemodynamic compromise
CHADS2
• . Risk of Stroke: (CHAD score ranges from 0-6; 2
points for prior TIA or stroke, 1 for HTN, CHF, DM,
Age>75, JAMA 2001; 285:28 64-70). Annual risk of
stroke: (non-rheumatic Afib)
• 0=1.9%
• 1=2.8%
• 2=4.0%
• 3=5.9%
• 4=8.5%
• 5=12.5%
• 6=18.2%
Afib treatment options
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Rate control
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AV nodal agents
AV node ablation and pacemaker
2. Rhythm control
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Cardioversion: chemical or electrical; +/- TEE
Anti-arrhythmics
Catheter Ablation
MAZE
3. Anticoagulation
1. ASA
2. ASA + clopidogrel
3. Warfarin
Irregularly irregular rhythms
• MAT
• Afib
• ATach with variable conduction
Pregnancy and SVTs
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50% have SV ectopics
Sustained arrhythmia rare (2-3/1000)
Symptomatic increase in 20%
Risk to mother and fetus
No controlled study and there would be
none
• AA drugs toxic and should be reserved for
only highly symptomatic patients
• Role of RF ablation
Antiarrhythmic drugs in Pregnancy
Radiofrequency Catheter Ablation
• Who should be referred?
• What arryhthmias should be referred for
ablation?
• What are the success rates?
• What are the risks of ablation?
Who should be referred?
• Symptomatic patients
– AVNRT (>90% succes rates)
– WPW and symptomatic AVRT (CCB ; BB and Dig not
appropriate as sole therapy) (>90%)
– Aflutter(>90%)
– AFib (40-70%)
• High risk for sudden death
– AFib with WPW and cycle length <250 ms
• Not amenable to catheter ablation
– MAT
– Reversible causes (thryotoxicosis; PE; post-op)
Question 1
• A 35-year old woman with unrepaired Ebstein's anomaly is evaluated in
the emergency department for recurrent tachycardia episodes. Several
episodes occur while she is being evaluated. She notes that she feels
somewhat lightheaded.
• The patient's blood pressure is 110/60 mm Hg. She is acyanotic and
afebrile. Cardiac examination demonstrates a brief systolic murmur along
the lower left sternal border, which increases with inspiration. The jugular
venous pressure is elevated.
• The electrocardiogram shows a short PR interval, an abnormal initial
portion of the QRS complex, and right bundle branch block. The
tachycardia is wide-complex and regular at a rate of 190/min.
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What is the most appropriate acute treatment of choice?
A Adenosine
B Procainamide
C Digoxin
D Direct-current cardioversion
Question 2
• A 26-year-old nurse is evaluated in the emergency department after an
episode of syncope. While working in the intensive care unit, she
developed tachycardia and then lost consciousness. She admits to having
a stressful day and having had more caffeine than normal. She has had
brief episodes of tachypalpitations in the past but no prior syncope.
• Physical examination is unremarkable and the patient is in sinus rhythm.
The chest radiograph is unremarkable. The electrocardiogram initially
demonstrates sinus rhythm and is unremarkable. Ten minutes later, the
patient develops an episode of brief tachycardia. Shortly after the
tachycardia episode, a repeat electrocardiogram is performed and is
shown (Figure 122).
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What is the most likely diagnosis in this patient?
A Atrioventricular nodal reentrant tachycardia
B Accelerated idioventricular tachycardia
C Atrioventricular reentrant tachycardia
D Multifocal atrial tachycardia
Question 3
• A 68-year-old woman comes to the emergency department because of a
racing heart for the past 2 hours. She reports a 2-year history of similar
episodes, for which her physician instructed her to cough or strain. The
episodes usually terminate after a few minutes of following her
physician's instructions, but the current episode is persisting. She does
not have chest pain, and she has no other cardiac history.
• The physical examination demonstrates a blood pressure of 110/60 mm
Hg, heart rate of 165/min, respiratory rate of 20/min, clear lungs, and no
murmurs or gallop. After the carotids are auscultated and the presence of
bruit excluded, carotid sinus massage is attempted, but the tachycardia
persists. The electrocardiogram obtained in the emergency department is
shown .
• Which is the drug of choice for terminating this patient's arrhythmia?
• A Metoprolol
• B Verapamil
• C Adenosine
• D Digoxin
References
1. www.blaufuss.org
2. Cardiac Arrhythmias by Eric N. Prystowsky
and George J. Klein