Supraventricular arrhythmias

Jerry JohnJuly 29, 2009

Objectives• 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

– 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

• AV node dependent (Y/N)• Re-entrant circuit (Y/N)

– Circuit (Macro/Micro)– Anatomic (e.g. previous ASD repair, CVTI)– Accessory pathway ( WPW, Mahaim, etc. )

• P wave– 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

AVNRT

Atach (reentry or automaticity)

ORT

Non paraoxysmal junctional tach

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 diseaseAV 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 TachycardiaAtypical AVNRTAVRT with long retrograde conductionPJRT

Where’s the P wave

• Valsalva• Carotid sinus massage

– Slows SA nodal; and/or AV nodal conduction

• Adenosine– 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

• 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)– 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 pre-excitation 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 TachycardiaThree 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

• < 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 V6Clockwise with reverse activation

• Atypical or type II atrial flutterAlso 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 23-26% 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 categories1. Lone atrial fibrillation: no structural

heart disease (usually <60 years)2. Paroxysmal : terminate spontaneously

<7 days 3. Persistent: fails to self-terminate within

7 days. Episodes may eventually terminate spontaneously, or they can be terminated by cardioversion.

4. 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

1. Rate control• AV nodal agents• AV node ablation and pacemaker

2. Rhythm control• Cardioversion: chemical or electrical; +/-

TEE• Anti-arrhythmics• Catheter Ablation• MAZE

3. Anticoagulation1. ASA2. ASA + clopidogrel3. Warfarin

Irregularly irregular rhythms

• MAT• Afib• ATach with variable conduction

Pregnancy and SVTs• 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.

• 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).

• 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.org2. Cardiac Arrhythmias by Eric N.

Prystowsky and George J. Klein