Avrt and avnrt

INTRODUCTION

1. AVNRT & AVRT DR RAMDHAN KR KAMAT PG (MD MEDICINE) JLNMCH BHAGALPUR

2. AVNRT Most common form of PSVTs, accounting for nearly two-thirds of cases. synonyms   AV junctional reentrant tachycardia. Reciprocal or reciprocating AV nodal reentrant tachycardia. Junctional reciprocating tachycardia .

3. Commonest cause of palpitations in patients with structurally normal hearts. AVNRT is typically paroxysmal and may occur spontaneously or provocation). It is more common in women than men (~ 75% of cases occurring in women) complain of the sudden onset of rapid, regular palpitations , presyncope . angina. The patient may complain of shortness of breath , anxiety and occasionally polyuria . The tachycardia typically ranges between 140-280 bpm and is regular in nature.  It may cease spontaneously (and abruptly) or continue indefinitely until medical treatment is sought. The condition is generally well tolerated and is rarely life threatening in patients with pre-existing heart disease. AVNRT

4. SYMPTOMS Palpitations Dizziness Dyspnea Chest pain Fatigue Syncope polyuria    

5. The  slow pathway  ( alpha ) :  a slowly-conducting pathway with a short refractory period. The  fast pathway  ( beta ):  a rapidly-conducting pathway with a long refractory period. AVNRT

6. AV NODAL REENTRANT TACHYCARDIA

7. AVNRT has been traditionally classified as: Slow–fast ( T ypical AVNRT) , F ast–slow or Slow-slow ( Atypical AVNRT) The fast pathway of the re-entry circuit runs superiorly and anteriorly in the triangle of Koch, whereas the slow pathway runs inferiorly and posteriorly close to the coronary sinus ostium .

8. AVNRT Typical AVNRT Slow–fast In the slow–fast form of AVNRT, the onset of atrial activation appears early, at the onset or just after the QRS complex Maintaining an atrial -His/His- atrial ratio AH/HA.> 1. AH/HA ratio > 3, and a VA interval measured from the onset of ventricular activation on surface ECG to the earliest deflection of the atrial activation in the His bundle electrogram <60 ms, or VA interval measured at the high right atrium< 95 ms are diagnostic of the slow–fast AVNRT type. VA conduction time Traditionally, a VA interval measured from the onset of ventricular activation on surface ECG to the earliest deflection of the atrial activation in the His bundle electrogram VA< 60 ms , or a VA interval measured at the high right atrium < 95 ms , has been considered as diagnostic for the slow–fast form of AVNRT.

9. Slow-Fast AVNRT (common type ) .

10. Slow-Fast (Typical) AVNRT: Narrow complex tachycardia at ~ 150 bpm . No visible P waves. There are pseudo R’ waves in V1-2. RP <PR

11. Atypical AVNRT Fast–slow . In the fast–slow form of AVNRT (5–10% of all AVNRT cases ), retrograde conduction is slower than antegrade conduction. The VA interval is > 60 ms . In the majority of fast–slow cases, the site of the earliest atrial activation is posterior to the AV node near the orifice of the coronary sinus

12. Accounts for 10% of AVNRT Associated with Fast AV nodal pathway for anterograde conduction and Slow AV nodal pathway for retrograde conduction. Due to the relatively long ventriculo-atrial interval, the retrograde P wave is more likely to be visible after the corresponding QRS. Fast-Slow AVNRT (Uncommon AVNRT)

13. Slow–slow AVNRT 1-5% AVNRT Associated with Slow AV nodal pathway for anterograde conduction and Slow left atrial fibres as the pathway for retrograde conduction. In the slow–slow form, the AH/HA ratio is >1 but the VA interval is >60 ms, suggesting that two slow pathways are utilized for both anterograde and retrograde activations. Usually, but not always, the earliest atrial activation is at the posterior septum (coronary sinus ostium ). ECG features: Tachycardia with a P-wave appearing “before” the QRS complex. Confusing as a P wave appearing before the QRS complex in the face of a tachycardia might be read as a sinus tachycardia.

14. TREATMENT: ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA Acute Treatment Treatment is directed at altering conduction within the AV node. Vagal stimulation , such as Valsalva maneuver or carotid sinus massage , can slow conduction in the AV node sufficiently to terminate AVNRT. In patients in whom physical maneuvers do not terminate the tachyarrhythmia, the administration of adenosine, 6–12 mg IV, . Intravenous beta blockade ( metoprolol 5mg over 3-5 minx 3 doses then 1.25-5mg q6h ) or calcium channel blocker ( verapamil 5-10 mg over 3-5 min then 2.5-10 mg/h ) therapy should be considered as second-line treatment. If hemodynamic compromise is present, R-wave synchronous DC cardioversion using 100–200 J can terminate the tachyarrhythmia. Prevention Prevention may be achieved with drugs that slow conduction in the antegrade slow pathway, such as digitalis , beta blockers , and calcium channel blockers . In patients who have a history of exercise-precipitated AVNRT, the use of beta blockers frequently eliminates symptoms. In patients who do not respond to drug therapy Catheter ablation is very effective in permanently eliminating AVNRT. Patients with recurrent AVNRT that produces significant symptoms or heart rates >200 beats/min and patients reluctant to take chronic drug therapy should be considered for ablative therapy. Catheter ablation can cure AV nodal reentry in >95% of patients with a single procedure. The risk of AV block requiring a permanent pacemaker is ~ 1% with the ablation procedure.

15. a Summary of AVNRT subtypes

16. What are “Pre-excitation syndromes” ? Term coined by Ohnell First described in 1930 by Louis Wolff, John  Parkinson  and Paul Dudley White. A group of ECG and Electrophysiological abnormalities in which The atrial impulses are conducted partly or completely, PREMATURELY , to the ventricles via a mechanism other than the normal AV-node Associated with a wide array of tachycardias with both normal QRS and prolonged QRS durations

17. Atrioventricular Reentry Tachycardias (AVRT) AVRT is a form of paroxysmal supraventricular tachycardia. A reentry circuit is formed by the normal conduction system and the accessory pathway resulting in circus movement. During tachyarrythmias the features of pre-excitation are lost as the accessory pathway forms part of the reentry circuit. AVRT often triggered by premature atrial or premature ventricular beats .

18. Bundle of KentThe classic accessory pathway is the AV bypass tract or in WPW that directly connects atrial and ventricular myocardium, bypassing the AVnode /His-Purkinje system James fibers , atrionodal tracts , connect atrium to distal or compact AV node (  " Lown - Ganong -Levin e syndrome and enhanced atrioventricular nodal conduction") Brechenmacher fibers ( atrio-Hisian tracts) connect the atrium to His bundle Mahaim fibers - Hisian -fascicular tracts , connect the atrium ( atriofascicular pathways), AV node ( nodofascicular pathways) or His bundle ( fasciculoventricular ) to distal Purkinje fibers or ventricular myocardium.

19. Bundle of KentThe classic accessory pathway is the AV bypass tract or in WPW that directly connects atrial and ventricular myocardium, bypassing the AVnode /His-Purkinje system James fibers , atrionodal tracts , connect atrium to distal or compact AV node (  " Lown - Ganong -Levin e syndrome and enhanced atrioventricular nodal conduction") Brechenmacher fibers ( atrio-Hisian tracts) connect the atrium to His bundle Mahaim fibers - Hisian -fascicular tracts , connect the atrium ( atriofascicular pathways), AV node ( nodofascicular pathways) or His bundle ( fasciculoventricular ) to distal Purkinje fibers or ventricular myocardium.

20. Understanding the variations in “Pathway – electrophysiology – Direction of Propagation & Propagation velocities

21. ORT - URAP

22. “Manifest Pathways” Per se, WPW refers to patients with pre-excitation in ECG + symptomatic episodes of tachyca “Concealed Pathways” - Patients with Accessory Pathways, but no pre-excitation . Pathways may become manifest during episodes of tachycardia

23. ACCESSORY PATHWAYS AND THE WOLFF-PARKINSON-WHITE SYNDROME Accessory pathways (APs) occur in 1 in 1500–2000 people and are associated with a variety of arrhythmias including narrow-complex PSVT , wide-complex tachycardias , and , rarely, sudden death . Most patients have structurally normal hearts, but APs are associated with Ebstein’s anomaly of the tricuspid valve. APs are abnormal connections that allow conduction between the atrium and ventricles across the AV ring. They are present from birth and are due to failure of complete partitioning of atrium and ventricle by the fibrous AV rings. They occur across either an AV valve annulus or the septum, most frequently between the left atrium and free wal l of the left ventricle, followed by posteroseptal , right free wall , and anteroseptal locations. If the AP conducts from atrium to ventricle ( antegrade ) with a shorter conduction time than the AV node and His bundle , then the ventricles are preexcited during sinus rhythm, and the ECG shows a short P-R interval (<0.12 s ), slurred initial portion of the QRS ( delta wave ), and prolonged QRS duration produced by slow conduction through direct activation of ventricular myocardium over the AP. The morphology of the QRS and delta wave is determined by the AP location and the degree of fusion between the excitation wavefronts from conduction over the AV node and conduction over the AP. Right-sided pathways preexcite the right ventricle , producing a left bundle branch block–like configuration in lead V1, and often show marked preexcitation because of relatively close proximity of the AP to the sinus node.

24. Left-sided pathways preexcite the left ventricle and may produce a right bundle branch–like configuration in lead V1 and a negative delta wave in aVL , indicating initial depolarization of the lateral portion of the left ventricle that can mimic q waves of lateral wall infarction. Preexcitation due to an AP at the diaphragmatic surface of the heart, typically in the paraseptal region , produces delta waves that are negative in leads III and aVF , mimicking the q waves of inferior wall infarction . Wolff-Parkinson-White (WPW) syndrome is defined as a preexcited QRS during sinus rhythm and episodes of PSVT. There are a number of variations of APs, which may not cause preexcitation and/ or arrhythmias. Concealed APs allow only retrograde conduction, from ventricle to atrium, so no preexcitation is present during sinus rhythm , but SVT can occur. Fasciculoventricular connections between the His bundle and ventricular septum produce preexcitation but do not cause arrhythmia, nor do fibers such as atrio-Hisian connections, probably because the circuit is too short to promote reentry. Atriofascicular pathways, also known as Mahaim fibers, probably represent a duplicate AV node and His-Purkinje system that connect the right atrium to fascicles of the right bundle branch and conduct slowly only in the anterograde direction.

25. WPW PR interval <120ms Delta wave  – slurring slow rise of initial portion of the QRS QRS prolongation > 120ms ST Segment and T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex Pseudo-infarction pattern can be seen in up to 70% of patients – due to negatively deflected delta waves in the inferior / anterior leads (“pseudo-Q waves ”), or as a prominent R wave in V1-3 (mimicking posterior infarction ). WPW in sinus rhythm

26. NARROW QRS TACHYCARDIA

27. WPW – ORT (ORTHODROMIC AVRT) The most common PSVT. The circulating reentry wavefront propagates from the atrium anterogradely over the AV node and His-Purkinje system to the ventricles and then reenters the atria via retrograde conduction over the AP. The QRS is narrow or may have typical right or left bundle branch block. W ithout preexcitation . Most commonly, during tachycardia the R-P interval is shorter than the P-R interval and can resemble AVNRT. P-wave timing is never simultaneous with a narrow QRS complex because the ventricles must be activated before the reentry wavefront reaches the AP and conducts back to the atrium. The morphology of the P wave is determined by the pathway location. The p wave in posteroseptal APs is negative in leads II, III , and aVF , similar to that of AVNRT.

28. ATYPICAL ORT Occasionally, an AP conducts extremely slowly in the retrograde direction, which results in tachycardia with a long R-P interval. NARROW QRS TACHYCARDIA

29. WPW - ORT

30. NARROW QRS TACHYCARDIA

31. Orthodromic AVRT using a rapidly conducting accessory pathway: Most common type of AVRT Initiated by either an APB or VPB AV conduction is over the AV node & VA conduction over accessory pathway Activation of ventricle & atrium follow sequentially  P waves are separated from the QRS complex. Retrograde conduction is rapid  P wave closer to the preceding QRS  RP < PR.

32. Electrophysiological Study for confirmation of ORT Premature ventricular beat placed when the His Bundle is refractory results in blocking-off of the Accessory Pathway resulting in termination of the tachycardia without atrial activation Ventriculo-Atrial (VA) interval is prolonged by introduction of a premature VPB when the His is refractoy Retrograde atrial activation pattern demonstrating eccentric atrial conduction, identically matching that during ventricular pacing BBB during tachycardia results in persistent lengthening of the tachycardia cycle-length VA prolongation occurs with BBB aberration when AP is ipsilateral to the BBB

33. Termination of tachycardia Spontaneous OR drug-induced block in either the AVN OR AP OR placement of a critically timed APC that encounters AVN or AP when they are refractory Spontaneous termination occurs more frequently with AVN due to increases in the vagal tone When the last beat of the tachycardia is manifest as an atrial stimulus without the following ventricular stimulus = Termination in the AVN When the last beat of the tachycardia is manifest as a ventricular stimulus without the following atrial stimulus = Termination in the AP

34. Electrophysiological features for differentiating ORT from AVNRT Atrial recording ( INTRACARDIAC or ESOPHAGEAL ) ORT : VA interval > 95 milliseconds ( intracardiac recording) or > 70 milliseconds ( esophageal recording) in ORT Typical AVNRT : VA interval < 70 milliseconds.

35. Electrophysiological features for differentiating ORT from AVNRT ORT via ‘ Septal pathways’ Vs AVNRT - Para- Hissian pacing Comparison of the VA intervals with high-output & low-output pacing { Hight output captures both His and the ventricle ; low output only captures the ventricle } Unchanged VA makes Septal pathway more likely Premature VPB when His is refractory confirms presence of Acc Pathway

36. Antidromic WPW (ANTIDROMIC AVRT) AVRT With Antidromic Conduction In antidromic AVRT antegrade conduction occurs via the accessory pathway with retrograde conduction via the AV node.  Much less common than orthodromic AVRT occuring in ~5% of patients with WPW. ECG features of AVRT with antidromic conduction are: Rate usually 200 – 300 bpm . Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway.

37. Antidromic WPW

38. Preexcitated tachycardia also occurs if an AP allows antegrade conduction to the ventricles during AT, atrial flutter, atrial fibrillation or AV nodal reentry. Atrial fibrillation and atrial flutter are potentially life threatening if the AP allows very rapid repetitive conduction . Approximately 25% of APs causing preexcitation allow minimum R-to-R intervals of less than 250 ms during atrial fibrillation are therefore associated with a risk of inducing ventricular fibrillation and sudden death . Administration of AV nodal–blocking agents including oral or intravenous verapamil, diltiazem , beta blockers, intravenous adenosine , and intravenous amiodarone are contraindicated. Preexcited tachycardias should be treated with electrical cardioversion or intravenous procainamide or ibutilide , which may terminate or slow the ventricular rate.

39. ANTIDROMIC AVRT-REGULAR BROAD COMPLEX TACHYCARDIA

40. Other Pre-Excitation Syndromes / Accessory Pathways Lown - Ganong -Levine (LGL) Syndrome Proposed pre-excitation syndrome Accessory pathway composed of  James fibres ECG features: PR interval <120ms Normal QRS morphology The term should not be used in the absence of paroxysmal tachycardia Existence is disputed and may not exist

41. Lown - Ganong -Levine Syndrome

42. s AVNRT AVRT Incidence Most common Less than AVNRT sex female males Pathway Slow-fast, Ventricles not required for activation Accesory Ventricles required for activation Activation Simultaneous activation Sequential activation Rate <200 >200 P-wave Burried in QRS Will be seen after QRS Pseudo- r,pseudo - s,pseudo -q present absent RP-interval <70msec >70msec ST-T changes Less common more ST elevation in aVR lesss more Notch in aVL more less QRS alternans Rare common Abberancy Rare common BBB Doesnot alter rate Alters rate( coumel’s law) AV block Possible Not possible in its presence

43. THANK YOU NARROW QRS TACHYCARDIA