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 TachycardiaFocal Atrial Tachycardia

CSOCSO

IVCIVC

RAFWRAFW

RAARAA LAALAA

LAFWLAFW

PVPV

SNSN

IIA A SS

CTCT

* * ** * *

SVCSVC

20 yr woman with post-partum congestive heart failure20 yr woman with post-partum congestive heart failure

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Adenosine InjectionAdenosine Injection

III

IIIaVRaVL

aVF

V1

V2

V3

V4

V5V6

I

II

IIIaVR

aVL

aVF

V1

V2

V3

V4

V5V6

Post- Adenosine InjectionPost- Adenosine Injection

Catheter location : Right atrial Catheter location : Right atrial appendageappendage

RAORAO LAOLAO

CT MAP

CS

His

CTMAP

CS

His

IIIII

aVL

I

MAP dist

MAP prox

CT 1,2

CT 5,6

CT 9,10

CT 15,16

CT 3,4

CT 7,8

CT 13,14

CS dist

CS prox

CT 11,12

Earliest Atrial Activation : Right Atrial AppendageEarliest Atrial Activation : Right Atrial Appendage

- 23 msec

IIIII

aVL

I

MAP distMAP prox

CT 1,2

CT 5,6

CT 9,10

CT 15,16

CT 3,4

CT 7,8

CT 13,14

CS distCS prox

CT 11,12

CT 17,18

CT 19,20

Sinus RhythmSinus RhythmAtrial TachycardiaAtrial Tachycardia

RF on 1.9 sec

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 Activation on Halo Catheter

II

aVF

V1

CS Os

TA 1,2

TA 3,4TA 5,6

TA 7,8

TA 9,10

TA 11,12

TA 13,14

TA 17,18TA 19,20

Typical = CounterclockwiseTypical = Counterclockwise

TA 19,20

CS Os

TA 9,10

TA 1,2

Activation on Halo Catheter Activation on Halo Catheter

Atypical = ClockwiseAtypical = Clockwise

II

aVF

V1

CS Os

TA 1,2

TA 3,4TA 5,6

TA 7,8

TA 9,10

TA 11,12

TA 13,14

TA 17,18 19,20

TA 19,20

CS Os

TA 9,10

TA 1,2

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 FibrillationTreatment

• 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 FibrillationCatheter 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

SUMMARYMechanisms of SVT

Atrial Tachycardia AVNRT AVRT

FPSP

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