1 / 66

Supraventricular arrhythmias

Supraventricular arrhythmias. Jerry John July 29, 2009. Objectives. Supraventricular Arrhythmias How do supraventricular arrhythmias manifest? What are the common supraventricular arrhythmias? What is the mechanism of atrioventricular arrhythmias?

leena
Télécharger la présentation

Supraventricular arrhythmias

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Supraventricular arrhythmias Jerry John July 29, 2009

  2. 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?

  3. 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

  4. 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)

  5. 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

  6. ORT AVNRT Non paraoxysmal junctional tach Atach (reentry or automaticity)

  7. 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

  8. RP relationship • Short “RP” Tachycardias: Typical AVNRT AVRT • Long “RP” Tachycardias: Atrial Tachycardia Atypical AVNRT AVRT with long retrograde conduction PJRT

  9. 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

  10. 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)

  11. 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

  12. 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

  13. 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)

  14. 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

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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

  21. 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

  22. 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

  23. 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

  24. 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)

  25. 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

  26. Focal Atrial Tachycardia Three Subgroups: • Cristal Tachycardia - Initiated and terminated with PES - Arise along crista - P wave similar to NSR - Terminates with adenosine • Repetitive monomorphic AT - Repetitive runs of nonsustained AT - Suppress with adenosine - Variable locations • Automatic AT - Incessant AT - Transient suppression with adenosine

  27. Junctional Tachycardia • Nonparoxysmal Junctional Tachycardia • Junctional Ectopic Tachycardia • Congenital Automatic Junctional Tachycardia

  28. 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

  29. 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

  30. 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

  31. PJRT • Orthodromic reciprocating tachycardia • Earliest retrograde activation in proximal CS • Tachycardia terminates with adenosine with retrograde AP block • HIS refractory PVC advances atrial activation

  32. 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%)

  33. 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?

  34. 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).

  35. 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).

  36. Afib categories • 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)

More Related