Evaluation of Supraventricular Tachyarrythmias

24/11/2014

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

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.

• 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)

ATRIOVENTRICULAR NODE REENTRANT TACHYCARDIA (AVNRT)

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.

• 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).

• 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.

ATRIOVENTRICULAR REENTRANT TACHYCARDIA MEDIATED BY

ACCESSORY PATHWAYS(AVRT)

• 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.

• 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.

Orthodromic AVRT

Antidromic AVRT

• 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.

PJRT

Localization of AP

ATRIAL TACHYCARDIA

• 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.

• 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.

• 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.

• 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.

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

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.

• 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.

TACHYCARDIAS ARISING FROM THE SINUS NODE REGION

• 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.

• 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.

CLINICAL PRESENTATION

• 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.

• 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.

Approach

THERAPY

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.

• 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.

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.

• 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.

• 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.

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%.

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.