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 150-250 bpm 1:1 AV conduction Reentrant, automatic or triggered 150-250 bpm 1:1 AV conduction Paroxysmal or “warm up” P wave morphology variable

Focal Atrial Tachycardia CSO IVC RAFW RAA LAA LAFW PV SN I A S CT * * * SVC

20 yr woman with post-partum congestive heart failure 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 II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Catheter location : Right atrial appendage RAO LAO CT MAP CS His

Earliest Atrial Activation : Right Atrial Appendage II III 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 - 23 msec

Atrial Tachycardia Sinus Rhythm RF on 1.9 sec I II III aVL 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 CT 17,18 CT 19,20 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 Typical = Counterclockwise V1 II aVF TA 19,20 TA 1,2 TA 9,10 TA 3,4 TA 5,6 TA 7,8 CS Os TA 9,10 TA 1,2 TA 11,12 TA 13,14 TA 17,18 TA 19,20 CS Os

Activation on Halo Catheter Atypical = Clockwise II aVF V1 CS Os TA 1,2 TA 3,4 TA 5,6 TA 7,8 TA 9,10 TA 11,12 TA 13,14 TA 17,18 19,20 TA 19,20 TA 9,10 CS Os 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 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: 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 Does seeing the next ECG help you

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 AT AVRT AVNRT Conduction down AP during tachycardia gives WIDE QRS complex

Atrial Fibrillation

RF Ablation in WPW

SUMMARY Mechanisms of SVT Atrial Tachycardia AVNRT AVRT SP FP Predictions about V:A time for DDX Circuits require two pathways with different conduction vel and different refractory periods Atrial Tachycardia 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