Supraventricular Arrhythmia Evaluation

1. Evaluation of Supraventricular
Tachyarrythmias
24/11/2014

2. • Introduction
• Classification
• Specific Tachyarrythmias
• Clinical Presentations
• Approach for diagnosis
• Treatment
• Conclusions

3. Introduction
• Supraventricular tachycardias (SVTs) affect more than 1% of
the population, making them a relatively common clinical
problem.
• SVTs encompass a large group of arrhythmias that originate
above the bifurcation of the bundle of His.
• Most SVTs have normal narrow complex morphology, but they
also may have wide QRS complexes resulting from aberrant
conduction or, less commonly, preexcitation.

4. • The first major differentiator in correctly diagnosing
tachycardia is the width of the QRS complex.
• Narrow (<120 ms) QRS complex tachycardias (NCTs) in adults
are almost always supraventricular in origin (involving tissue
at or above the bundle of His), whereas wide (120 ms) QRS
complex tachycardias (WCTs) are often, but not always,
ventricular in origin.
• The major categories of NCTs include
– those that are primarily atrial in origin (atrial tachycardia, flutter,
fibrillation)
– those that are based in the atrioventricular (AV) junction
– those that incorporate atrium and ventricle in a large circuit (accessory
pathway medicated AV reentry)

6. ATRIOVENTRICULAR NODE
REENTRANT TACHYCARDIA (AVNRT)

7. Atrioventricular Node Reentrant Tachycardia (AVNRT)
• Accounts for greater than 60% of cases referred to an EPS
laboratory.
• Patients typically present in their 30s or 40s, with greater than
70% being women.
• Although the mechanism for AVNRT is reentry involving the
AV node, the precise location of the reentrant circuit is
uncertain but includes atrial tissue surrounding the AV node.
• The reentrant circuit consists of an anterograde limb and a
retrograde limb.

8. • Typical AVNRT usually is initiated with a premature atrial
impulse, which blocks in the fast pathway and conducts over
the slow pathway.
• Then the impulse returns up the fast pathway, which did not
conduct antegradely.
• Activation of the ventricle by way of the slow pathway occurs
almost simultaneously with atrial activation by way of the fast
pathway.
• This activity produces P waves on the surface ECG, which
either are hidden within the QRS complex or are apparent in
the initial or terminal portion of the QRS complex as a pseudo
R wave (in lead V1) or a pseudo S wave (in inferior leads).

12. • The less common, atypical AVNRTs (10%) may have various
forms, including fast-slow, slow-slow, and fast-fast.
• In atypical AVNRT (fast-slow), atrial activation is delayed
relative to ventricular activation because the retrograde limb
conducts slowly.
• Retrograde P waves are distinguishable more easily from the
QRS complex, and the R-P interval usually is longer than the P-
R interval.
• Lockwood et al, experienced with 734 patients referred for
catheter ablation of AVNRT, 515 patients (77%) had Slow/ Fast
AVNRT, 80 patients (11%) had Slow/Slow AVNRT, and 89
patients (12%) had Fast/Slow AVNRT.

14. ATRIOVENTRICULAR REENTRANT
TACHYCARDIA MEDIATED BY
ACCESSORY PATHWAYS(AVRT)

15. • Accessory pathways are discrete bundles of myocardial tissue
bridging the atrium and ventricle along the tricuspid or mitral
valve annulus.
• More than half of accessory pathways are situated in the left
free wall, 20% to 30% occur in the posteroseptal location, 10%
to 20% occur in the right free wall, and 5% to 10% occur in the
anteroseptal location near the AV node.
• These pathways can conduct anterogradely from the atrium
to the ventricle, retrogradely from the ventricle to the atrium,
or, most commonly, bidirectionally.
• About 25% of accessory pathways conduct only retrogradely
and are not manifest on the ECG during sinus rhythm. These
are called as Concealed pathways.

16. • AV reentrant circuits are relatively large involving an anterograde
and retrograde limb between the atria and ventricles.
• Reentry typically is initiated with a premature atrial or ventricular
impulse that blocks in one limb while conducting over the other.
• Orthodromic AVRT - anterograde pathway is the AV node, whereas
the retrograde limb is the accessory pathway. It commonly uses
bidirectionally conducting accessory pathways.
• Antidromic AVRT – less common, anterograde limb is the accessory
pathway, resulting in preexcitation on the surface ECG. The
retrograde limb usually is the AV node but may be another
accessory pathway capable of retrograde conduction.

18. Orthodromic AVRT

19. Antidromic AVRT

20. • Most orthodromic AVRTs use a rapidly conducting accessory
pathway, giving rise to a P wave shortly after the QRS complex in
the ST segment.
• In contrast, a few orthodromic AVRTs involve a slowly conducting
retrograde accessory pathway, which delays atrial activation relative
to the QRS complex; this is manifest on the ECG as an R-P interval
longer than the P-R interval.
• These accessory pathways also display decremental conduction,
resulting in further conduction slowing as a function of more rapid
rates.
• These AVRTs frequently are incessant, beginning spontaneously
during sinus rhythm without a premature atrial or ventricular
impulse.
• It was initially referred to as permanent form of junctional
reciprocating tachycardia (PJRT) because AV nodal reentry
originally was thought to be the mechanism of the tachycardia.

21. PJRT

22. Localization of AP

23. ATRIAL TACHYCARDIA

24. • Atrial tachycardia is less common than AVNRT or AVRT,
accounting for fewer than 15% of patients referred for
electrophysiology study.
• Atrial tachycardia usually arises from a single localized atrial
focus.
• The tachycardia mechanism is variable and may depend on
the presence of underlying atrial disease.
• Localized reentry is more likely with diseased, dilated atrial
muscle, which creates the electric milieu of slowed
conduction velocity and prolonged refractoriness necessary
for a reentrant.

25. • In children, reentrant forms of atrial tachycardia frequently
are associated with prior surgery for congenital heart disease.
• Reentrant atrial tachycardias typically are initiated with a
spontaneous atrial premature beat and tend to be
paroxysmal.
• In healthy atrial muscle, enhanced automaticity or triggered
activity may play a role.
• The AV relationship can be 1:1, or varying degrees of AV block
may be present.

26. • P wave morphology during atrial tachycardia depends on the
location of the focus.
• Analysis of leads aVL and V1 provides a reasonable guide to
the right-sided or left-sided origin of the atrial tachycardia.
• A positive P wave in V1,has a sensitivity of 93% and a
specificity of 88% in predicting a left atrial focus.
• A positive or biphasic P wave in lead aVL has a sensitivity of
88% and specificity of 79% for predicting a right atrial focus.
• Examination of P wave polarity in the inferior leads is helpful
in distinguishing a superior focus (positive P wave) from an
inferior focus (negative P wave) in right and left atria.

27. • The P-R interval often is shorter than the R-P interval in atrial
tachycardia.
• Although the rate of atrial tachycardia generally is 140 to 200
beats/ min, it may exceed 250 beats/&, which can be similar
to the rate of atrial flutter.

29. Multifocal Atrial Tachycardia
• It involves more than one atrial focus and requires at least
three distinct P wave morphologies to be diagnosed on the
surface ECG.
• Because the foci fire independently of one another, the atrial
rate is irregular and typically averages 100 beats/min.
• The P-R interval also may vary depending on the location of
the foci relative to the AV node.
• Isoelectric periods between adjacent P waves help distinguish
multifocal atrial tachycardia from atrial fibrillation.
• The mechanism for multifocal atrial tachycardia has not been
defined clearly but may be due to enhanced automaticity or
triggered activity

31. Junctional Tachycardia
• Junctional tachycardias arise from a discrete focus within the
AV node or the His bundle.
• Junctional ectopic tachycardia presenting before 6 months of
age usually is associated with underlying heart disease that
carries a high mortality.
• In contrast, adult junctional tachycardia has a more benign
prognosis and typically develops after the acute phase of
myocardial infarction, digitalis intoxication, and acute
myocarditis.
• Junctional tachycardia also is seen immediately after cardiac
surgery in children and adults and may be due to perinodal AV
node trauma.

32. • It is likely due to enhanced impulse initiation in the region of
the AV node by automaticity or triggered activity rather than
reentry.
• The junctional rate often is irregular, which can mimic atrial
fibrillation if the P waves are not obvious.
• Retrograde atrial activation may follow each junctional
impulse, giving 1:1 ventriculoatrial activation, with P waves
often concealed within the QRS complex.

33. TACHYCARDIAS ARISING FROM THE
SINUS NODE REGION

34. • Sinus node reentry and inappropriate sinus tachycardia are
less common SVTs.
• Sinus node reentry tachycardia arises from a reentrant circuit
involving the sinus node, producing P waves that are fairly
similar if not identical to those during sinus rhythm.
• In contrast to sinus rhythm and inappropriate sinus
tachycardia, sinus node reentry can be initiated and
terminated abruptly by a premature atrial stimulus, which is
consistent with its reentrant mechanism.
• It is usually nonsustained and associated with slower rates
than inappropriate sinus tachycardia, making it clinically
insignificant.

35. • Inappropriate sinus tachycardia is a clinical syndrome characterized
by sinus tachycardia without an identifiable physiologic stimulus.
• Secondary causes for resting sinus tachycardia must be ruled out.
• At least two clinical variants have been described:
– resting heart rate of 100 beats/min or greater
– increased heart rate response to minimal exertion.
• These patients have preserved left ventricular function with no
underlying heart disease.
• Sinus rates greater than 200 beats/min are not characteristic of
inappropriate sinus tachycardia, and paroxysmal increases in heart
rate are not seen.
• Because atrial depolarization is through the sinus node, P waves
have typical sinus morphology.

36. CLINICAL PRESENTATION

37. • SVTs can produce a wide spectrum of symptoms.
• Palpitations are the most common symptom, which can be of
variable frequency, severity and duration.
• Sudden-onset, regular palpitations suggest a reentrant or
triggered paroxysmal SVT, such as AVNRT, AVRT, atrial flutter,
sinus node reentry tachycardia, or junctional tachycardia.
• In contrast, gradual-onset, regular palpitations may be due to
an automatic SVT, such as an atrial or junctional tachycardia.
• Irregular palpitations of sudden onset most likely are due to
atrial fibrillation.

38. • Nonspecific symptoms, such as chest or neck discomfort,
pressure in the head, dyspnea, lightheadedness, or frank
syncope.
• In patients with coronary artery disease, impaired left
ventricular function, or stenotic valvular heart disease, SVTs
with rapid heart rates may precipitate myocardial ischemia or
congestive heart failure.
• Most regular SVTs occur in patients without organic heart
disease, however, and carry an excellent overall prognosis.

39. Approach

40. THERAPY

41. Acute Medical Therapy
• The rapid heart rates associated with SVTs typically are
hemodynamically well tolerated, unless there is concomitant
left ventricular dysfunction.
• Immediate electric cardioversion rarely is necessary.
• Valsalva maneuvers or carotid sinus massage may be helpful
in terminating AV node-dependent and sinoatrial node-
dependent SVTs.
• Alternative vagal maneuvers may include the gag reflex and
facial immersion in cold water.
• Failing these maneuvers, adenosine is firstline therapy for the
acute conversion of SVTs, most of which are AV node
dependent.

42. • In the case of AV nodei ndependent tachycardias, adenosine
and verapamil provide diagnostic information and may be
therapeutic.
• Ten percent of atrial tachycardias and most SNRTs terminate
with adenosine.
• The remaining atrial tachycardias may convert with an
antiarrhythmic drug that suppresses atrial electric activity.

43. Long-Term Medical Therapy
• SVTs are associated with an excellent long-term prognosis in
the setting of a structurally normal heart.
• Most patients can be reassured that their arrhythmia will not
be life-threatening or cause permanent myocardial injury.
• Long-term medical therapy or catheter ablation should be
considered for patients with symptoms that are intolerably
frequent, severe, or prolonged.
• In patients with AV node-dependent tachycardias, long-term
medical therapy with an AV node blocker, such as a calcium
channel blocker or a β–blocker is first-line therapy.

44. • For patients with atrial tachycardia, long-term drug therapy
generally has limited effectiveness.
• Some atrial tachycardias are catecholamine sensitive, and β-
blockers are appropriate therapy for them. Otherwise, a trial of
class IC or III agents may offer better control.
• Long-term medical therapy of junctional tachycardia and multifocal
atrial tachycardia is limited.
• Their management begins with improving the metabolic, cardiac, or
pulmonary derangements that typically precipitate these
arrhythmias.
• For patients with sinus node-dependent tachycardias, β-blockers
are appropriate therapy to suppress sinoatrial node activity.

45. • WPW syndrome is a special consideration.
• Medical therapy with class IC or III agents is required to
lengthen the accessory pathway refractory period as well as
to suppress the underlying atrial arrhythmia.
• WPW syndrome patients at highest risk for sudden death
develop ventricular rates greater than 240 beats/min during
atrial fibrillation.
• These patients should be offered catheter ablation instead of
medical therapy as a more definitive means of preventing
potentially lethal arrhythmia.

47. Catheter Ablation
• The role of long-term drug therapy has been challenged in the
present era of safe, effective catheter ablation.
• Despite the high rate of success with ablation, there is still a
small but finite risk of serious complications (1% to 2%),
including stroke, myocardial infarction, cardiac or aortic
perforation, aortic valve injury, femoral vein or artery injury,
and AV node conduction block.
• Currently, catheter ablation should be offered as first-line
therapy instead of medical therapy for symptomatic patients
with accessory pathway conduction.
• The success and ease of catheter ablation is determined by
pathway location, but overall success rates are greater than
95%.

48. Conclusions
• Patients with minimally symptomatic SVTs often can be
managed conservatively without medical or ablation therapy.
• The decision to treat should take into account the patient’s
preference, age, myocardial function, and timely access to
medical facilities.
• More symptomatic AVNRT should be treated initially with
long-term β-blockers or calcium channel blockers.
• Failing this therapy, catheter ablation should be
recommended before instituting class I or III antiarrhythmic
therapy.