Please welcome Dr. Ann Dougherty back to Cyberounds^®! They have put together an excellent and concise diagnosis and treatment algorithm for this relatively common and now treatable problem. I'm sure we all will benefit from it and use it as a handy reference for the future.

-- Richard W. Smalling, M.D., Ph.D., Cardiovascular Moderator

Narrow QRS tachycardias comprise a heterogeneous group of arrhythmias that are rarely life-threatening but can cause significant symptoms and morbidity if not properly diagnosed and treated. Although each of the narrow QRS complex tachycardias is a distinct entity with unique mechanisms, they share some features in common. They all have narrow QRS complexes on the 12-lead electrocardiogram with a QRS duration less than 0.12 seconds. They are called supraventricular tachycardias because the arrhythmias originate in and involve structures above the ventricles (the atria and atrio-ventricular node), although the ventricles may participate in the tachycardia.

There are a number of distinguishing features of each tachycardia. The regularity of the rhythm, the relationship of the P and R waves on the 12-lead EKG, and the initiation and termination of the rhythms can all be used to help distinguish the narrow QRS tachycardias. The mechanisms, features, diagnostic techniques and treatments of the narrow QRS complex tachycardias are discussed below.

Mechanisms

If we exclude atrial fibrillation and sinus tachycardia, reentry is the most common mechanism that causes narrow complex QRS tachycardias.(1) Reentry describes a propagating electrical wavefront that exits one conducting pathway, enters a second conducting pathway and, subsequently, reenters the first pathway, as shown in Figure 1.

For this self-propagating pattern to occur, three conditions must be met:

1. the two pathways must be connected proximally and distally by conducting tissue forming a potential circuit,
2. one pathway must have a long refractory period relative to the other pathway, and
3. the pathway with the shorter refractory period must conduct slower than the other pathway.

A typical reentry conduction pattern occurs when a premature beat arrives at the two pathways and finds the rapidly conducting pathway refractory and the slowly conducting pathway still excitable (Figure 1B). The depolarizing wavefront conducts down and exits the slowly conducting pathway. After the wavefront exits the slow pathway, the fast pathway's refractory period has lapsed and it is now capable of conduction. The wavefront then enters the fast pathway distally, exits the fast pathway proximally and reenters the slow pathway proximally, which perpetuates the arrhythmia (Figure 1C).

Abnormal automaticity is another common cause of narrow complex tachycardias. Automatic narrow QRS tachycardias involve the spontaneous repetitive discharge of an ectopic focus in the atrium. Often the automaticity of an atrial focus has been enhanced by certain disease processes or drugs. Infection, chronic obstructive pulmonary disease and myocardial infarction are some of the disease processes that may contribute to automaticity.(1) Digitalis overdose is a common drug related cause of triggered automaticity.(2) Detailed descriptions of automaticity and triggered activity are beyond the scope of this article, and the interested reader is referred to the references.

Diagnostic Criteria

There are eight narrow QRS tachycardias that can be differentiated using various electrocardiographic features: atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), atrial tachycardia, sinus tachycardia, sinus nodal reentrant tachycardia, permanent junctional reciprocating tachycardia (PJRT), atrial fibrillation and atrial flutter. The first feature of the electrocardiogram (ECG) that will help formulate a differential diagnosis of a narrow QRS tachycardia is the regularity of the QRS complexes. If the QRS complexes occur regularly (the interval between different QRS complexes is equal for all complexes), then atrial fibrillation can usually be excluded.

The P wave's location relative to the QRS complex is the most helpful tool to differentiate the regular narrow complex tachycardias.(4) The location of the P wave on the ECG is best described by the RP and PR intervals. A short RP interval is defined as an RP interval less than the PR interval, and a long RP interval is defined as an RP interval greater than the PR interval. The tachycardias with short RP intervals have a reentrant mechanism that utilizes the fast pathway of the circuit for retrograde conduction. This causes the P wave on the ECG to appear closer to the terminal portion of the preceding QRS than to the beginning of the following QRS (Figure 2A), or the P wave is masked within the preceding QRS complex. The long RP tachycardias have either a reentrant mechanism that utilizes a slow pathway of the circuit for retrograde conduction (Figure 2B), or they have an automatic mechanism.

Table 1, below, shows differential diagnoses based on the PR and RP intervals.

Further differentiation of a tachycardia may be made by examining the onset and termination of the tachycardia. If there is abrupt onset and termination of the tachycardia, then a reentrant tachycardia, such as AVNRT (AV nodal re-entrant tachycardia), AVRT (Atrio-Ventricular re-entrant tachycardia) or SNRT (Sinus node re-entrant tachycardia), is the likely diagnosis. If the tachycardia begins with a slow acceleration, or "warm up" phase, then an automatic tachycardia, such as ectopic atrial tachycardia or sinus tachycardia, is the likely diagnosis.(1) Overviews of the specific narrow complex tachycardias are discussed below.

Short RP Tachycardias

The short RP tachycardias include typical AVNRT and the common form of AVRT. For patients presenting to the emergency room with a regular narrow QRS tachycardia that do not show preexcitation on an ECG in normal sinus rhythm, 60% will have AVNRT and 30% will have AVRT.(10) Typical AVNRT and AVRT are both reentrant tachycardias that utilize the AV node as the slowly conducting portion of the circuit. The fast pathway for AVNRT is also in the AV node, whereas the fast pathway for AVRT is an accessory pathway (Kent bundle) that connects the ventricle and atrium.

Ninety to 95% of patients with AVNRT experience the typical form with antegrade conduction down the slow pathway and retrograde conduction up the fast pathway.(11) However, the P wave is not visible in 50% of typical AVNRTs because retrograde conduction in the fast pathway can cause the P wave to be masked by the QRS complex.(11) When the P wave is visible, it may be seen as a pseudo S wave in leads II, III and AVF or a pseudo r' wave in V1 (Figure 3).

The pseudo S and r' waves are P waves closely following the QRS complexes, and they are highly specific for AVNRT with specificities in one study of 91 and 100 percent respectively.(3) Five to 10% of patients with AVNRT have conduction antegradely over the fast pathway and retrogradely over the slow pathway. This atypical form of AVNRT shows a long RP interval on the ECG (Figure 4).

Most patients with AVRT experience orthodromic conduction, which is antegrade conduction down the AV node and retrograde conduction up the accessory pathway.(1) The P wave for most patients with AVRT is found in the ST segment, later than in AVNRT (Figure 5).

The axis of the P wave is variable, depending on the location of the accessory pathway.(4) An uncommon form of orthodromic AVRT utilizes an accessory pathway with slow conduction, and it will have a long RP interval on the ECG.(10)

Patients with AVRT that exhibit overt preexcitation with a delta wave in sinus rhythm on the 12-lead ECG have the Wolfe-Parkinson-White syndrome (Figure 6).

The preexcitation occurs because of the fusion of antegrade conduction over both the accessory pathway and AV node. However, some patients with AVRT have concealed accessory pathways that only conduct retrogradely; their sinus rhythm 12-lead ECGs are normal. The presence of concealed accessory pathways is evidenced by the occurrence of orthodromic tachycardia.(11)

Long RP Tachycardias

Atrial Tachycardia

Atrial tachycardia is the most common long RP tachycardia other than sinus tachycardia.(2) In atrial tachycardia, depolarization of the atria begins from a location other than the sinus node, and it can have a reentrant, automatic or triggered mechanism. The ECG for atrial tachycardia shows a long RP interval and, usually, P wave morphologies that are different from sinus P waves.(1) Initiation and termination of atrial tachycardia are abrupt if it has a reentrant mechanism, or it may exhibit a "warm up" period with gradual acceleration after initiation if it has an automatic mechanism.(1) A one- to-one relationship between the P waves and QRS complexes is not required.

Sinus Node Reentrant Tachycardia

Sinus node reentry tachycardia is a reentrant tachycardia that utilizes tissue in and around the sinus complex with variable conduction properties. It comprises approximately 3% of all atrial arrhythmias induced in the electrophysiology laboratory.(10) Because sinus node reentry tachycardia originates in or near the sinus node, its P wave morphology on the 12-lead electrocardiogram looks identical to that of sinus tachycardia. However, the initiation and termination of sinus node reentrant tachycardia are abrupt, and this observation may be the only way to differentiate this tachycardia from sinus tachycardia.(2)

Permanent Junctional Recriprocating Tachycardia

Permanent junctional recriprocating tachycardia is a reentrant tachycardia that utilizes an accessory pathway with properties similar to those of the AV node. Such accessory pathways are located in the posteroseptal region and, typically, have slow retrograde conduction and no antegrade conduction. The ECG shows retrograde P waves with a superior axis. The RP interval is long because of the slow conduction of the accessory pathway. PJRT is frequently incessant and may cause a tachycardia-induced cardiomyopathy.(11)

Atrial Fibrillation

Atrial fibrillation is the most common clinical arrhythmia in the general population with a prevalence of 0.4%.(10) It is identified on the ECG by an irregular baseline, the lack of discrete P waves and the irregularly irregular occurring QRS complexes. The mechanism of atrial fibrillation has been debated for many years. Traditionally, various reentrant mechanisms have been used to explain the propagation of atrial fibrillation wavelets, but recent studies have shown that some cases of atrial fibrillation may be initiated by a rapidly firing automatic focus, usually associated with the pulmonary veins.(10)

Atrial Flutter

The prevalence of atrial flutter is unclear but it is commonly associated with atrial fibrillation. Atrial flutter rarely persists because it frequently degenerates into atrial fibrillation if it lasts for any significant length of time. Typical atrial flutter is a reentrant arrhythmia contained within the right atrium, and it propagates in a counterclockwise direction up the septum and down the right atrial free wall. Atrial flutter can also propagate in a clockwise direction in the right atrium or it can occur in the left atrium. Typical atrial flutter can be identified on the ECG by negative "saw tooth" flutter waves in leads II, III and AVF. The atrial rate ranges from 240 to 340 beats per minute and the ventricular rate varies depending on the degree of AV block.(10)

Treatment

Acute Treatment

If the AV node is an obligate part of a reentry circuit, as in AVNRT or AVRT, drugs that depress AV nodal conduction may be useful in terminating the tachycardia. These drugs include beta-blockers, non-dihydropyridine calcium channel blockers, digoxin and adenosine. Adenosine terminates 90% of narrow complex tachycardias that utilize the AV node.(2) Atrial tachycardias may respond to Class I or Class III antiarrhythmic drugs such as flecanide or ibutilide, which slow conduction in the atrium and prolong refractoriness respectively.

Long-Term Treatment

Catheter ablation is 90-95% successful in curing AVRT and AVNRT with an incidence of major complications of 1% or less;(2) it is the treatment of choice for most patients with these arrhythmias. Atrial tachycardias and atrial flutter can also be treated with catheter ablation. Recently, catheter ablation in the pulmonary veins has shown promise to be an effective treatment of paroxysmal atrial fibrillation in selected patients.(10)

Atrial tachycardia, atrial flutter and atrial fibrillation may also be treated chronically with antiarrhythmic agents, such as Class IA, IC or Class III drugs, in selected patients. In general, Class IC drugs, such as flecanide, are better tolerated than Class IA drugs like quinidine.(2) However, these drug classes should be avoided in patients with structural heart disease, as they have been shown to increase mortality in this subset of patients.(9) Class III agents, such as amiodarone, dofetilide or sotalol, are preferred in the high risk groups. Amiodarone is a class III antiarrhythmic drug that also has class I, II, and IV effects.(12) Amiodarone is approved for the treatment of life threatening ventricular arrhythmias. Dofetilide is also an oral class III antiarrhythmic drug recently approved for the treatment of nonparoxysmal atrial fibrillation and flutter.(5) It selectively blocks the rapidly inactivating component of the delayed rectifier current (I^kr) of the cardiac action potential which prolongs the cardiac action potential duration.(6) Dofetilide has been shown in clinical trials to be efficacious in converting atrial fibrillation to sinus rhythm, maintaining sinus rhythm and preventing new-onset atrial fibrillation.(7),(8) Sotalol is another Class III oral antiarrhythmic agent, but it also has beta-adrenergic receptor blocking actions. Sotalol has been shown to be efficacious in treating both supraventricular and ventricular tachycardias.(12)

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