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
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
7. AVNRT has been traditionally classified as:
Slow–fast ( Typical AVNRT),
Fast–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.
14. 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
15. 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)
16.
17.
18. 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.
19. 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.
21. 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
22. 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.
23. 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-Levine 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.
24. 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-Levine 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.
26. Propagation
Direction
Antegrade Retrograde Unidirectional Bidirectional
Propagation
Velocity
Non-
Decremental
Decremental
10%
Understanding the variations in “Pathway – electrophysiology –
Direction of Propagation & Propagation velocities
27. “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
28. 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 wall 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.
29. 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.
30. 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
33. 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.
Without 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.
34. ATYPICAL ORT
Occasionally, an AP conducts extremely slowly in the retrograde
direction, which results in tachycardia with a long R-P interval.
37. 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
38. 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.
39. 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.
41. 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.
43. 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
45. 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
