SVTs can be categorized as paroxysmal supraventricular tachycardia (PSVT), focal atrial tachycardia, atrial flutter, and AF. This classifica- tion scheme, which addresses the underlying arrhythmic mechanism, clinical presentation, and prognosis, guides evaluation and therapy.
PSVT typically manifests in young patients without structural heart disease. The PSVT syndrome is characterized by recurrent tachypalpi- tations with abrupt onset and offset. Focal atrial tachycardia is more
109 CHAPTER 9 Cardiac Arrhythmias
often observed in patients with underlying atrial enlargement and val- vular heart disease. AF and atrial flutter are associated with advancing age, hypertension, structural heart disease, diabetes, obstructive sleep apnea, and pulmonary disease. Unlike PSVT, AF carries an increased risk of stroke, heart failure, and death.
Paroxysmal Supraventricular Tachycardia
The incidence of PSVT is 35 cases per 100,000 person-years, with a prevalence of 2.25 per 1000 person-years. Patients report recurrent tachypalpitations. Associated symptoms may include shortness of breath, lightheadedness, chest pain, and syncope. Anginal chest pain and ischemic ST-segment depression are common and related to increased myocardial oxygen demand coupled with the loss of normal diastolic coronary perfusion time. These findings do not necessarily indicate underlying coronary artery disease and typically resolve with tachycardia termination.
PSVT typically occurs independent of structural heart disease and may manifest at any point from infancy to advanced age. PSVT relies on reentry, which is localized in the AV node in approximately 60% of cases and uses a concealed or manifest accessory pathway in 40%. Unless a delta wave indicative of WPW is identified, the under- lying mechanism of PSVT may not be apparent on initial clinical presentation.
An ECG obtained during PSVT can provide useful clues to establish the diagnosis and guide management. The AV relationship should be assessed during tachycardia. By ascertaining the relationship of the P wave to the preceding QRS complex, it is possible to classify PSVT as a short RP tachycardia or a long RP tachycardia. Short RP tachycar- dias demonstrate a short RP pattern with P waves embedded within or occurring closely after the preceding QRS complex. Short RP tachy- cardias occur with reentrant SVT when the retrograde VA conduction time is shorter than the antegrade AV conduction time. This pattern is observed in the two most common forms of PSVT: typical AV nodal reentry tachycardia and reciprocating AV tachycardia related to an accessory pathway.
Long RP tachycardias are characterized by an RP interval that is lon- ger than the next PR interval during tachycardia. This pattern occurs when the retrograde VA conduction time in reentrant arrhythmias is long due to a slowly conducting retrograde pathway during tachycar- dia. Atypical AV node reentry, in which retrograde conduction occurs over the slow AV nodal pathway, is the most common example of a long RP reentrant tachycardia.
Atrioventricular nodal reentry tachycardia. AVNRT is the most common form of PSVT. The arrhythmic mechanism depends on two distinct pathways in the AV node: a slowly conducting pathway with a short effective refractory period (i.e., slow pathway) and a rapidly conducting pathway with a longer refractory period (i.e., fast pathway).
The fast pathway is located anteriorly near the bundle of His, and the slow pathway posteriorly near the coronary sinus ostium. Although dual pathways are a common feature of the AV node, patients with clinical tachycardia have more robust slow pathway conduction.
Tachycardia is most commonly triggered by a premature atrial contraction that blocks in the fast pathway due to its prolonged refrac- tory period and conducts slowly antegrade down the slow pathway, producing a long PR interval on the ECG. On reaching the distal com- mon pathway where the fast and slow AV nodal inputs meet, if the fast pathway is no longer refractory, the impulse may penetrate the fast pathway in a retrograde direction and rapidly activate the atrium, producing a short RP interval and reinitiating reentry down the slow pathway and up the fast pathway. In typical slow-fast AVNRT, the RP interval is so short that the P wave is often buried in the preceding QRS complex (Fig. 9.5A).
Atypical fast-slow AVNRT may occur with antegrade conduction over the fast pathway and retrograde conduction over the slow path- way. This form of AVNRT is uncommon and produces a long RP pat- tern on the ECG with characteristically deeply inverted retrograde P waves in leads II, III, and aVF.
Vagal maneuvers cause temporary AV nodal blockade and may terminate sustained AVNRT. Alternatively, intravenous adenosine is a highly effective acute therapy. The need for chronic or defin- itive therapy is determined by symptoms, arrhythmia frequency, and patient preference. Catheter ablation of the slow pathway at the posterior AV node is highly successful, eliminating AVNRT with a greater than 95% success rate and a low risk of complications. Drug therapy with β-blockers and calcium-channel blockers directed at the AV node may be helpful for chronic suppression. Occasionally, class IC and III antiarrhythmics may be required. AVNRT should be easily distinguished from automatic junctional tachycardia, with a narrow complex and rapid, irregular rhythm typically demonstrating AV dis- sociation (see Fig. 9.5B).
Reciprocating atrioventricular tachycardia and preexcitation syndromes. Congenital anomalous extranodal AV muscle fibers or accessory pathways may arise as a consequence of incomplete development of the AV annulus. These pathways are usually observed in patients with otherwise anatomically normal hearts, although right- sided accessory pathways are infrequently associated with Ebstein’s anomaly and left-sided accessory pathways with hypertrophic cardiomyopathy.
Accessory pathways, or bypass tracts, may conduct antegrade, retro- grade, or bidirectionally. They typically fail to demonstrate decremental conduction or the slowed conduction with increasingly frequent stim- ulation that characterizes the AV node. Accessory pathways capable of antegrade conduction produce early activation of the ventricle in sinus rhythm because conduction over the accessory pathway surpasses con- duction over the AV node. The relatively rapid AV conduction produces a shortened PR interval, and eccentric ventricular activation over the pathway slurs the QRS onset, resulting in a delta wave (see Fig. 9.5C).
If the accessory pathway is capable only of retrograde conduction, the baseline ECG in sinus rhythm does not show evidence of an accessory pathway, and the extranodal AV connection is called concealed.
Short PR intervals during sinus rhythm are also observed in patients with Lown-Ganong-Levine syndrome. These patients have a normal-appearing QRS complex without a delta wave because ventric- ular activation occurs through the His-Purkinje system (see Fig. 9.5D).
Whether accessory pathways are concealed or manifest, the most common associated arrhythmia is orthodromic AV reentrant tachycardia (AVRT). Tachycardia is mediated by antegrade conduction down the AV node to the ventricle and subsequent retrograde conduction up the acces- sory pathway to activate the atrium, then antegrade again down the AV node. Because the ventricles are activated during tachycardia exclusively over the AV node, the resulting tachycardia is typically a narrow complex unless aberrancy occurs (see Fig. 9.5E). A short RP pattern is observed on the ECG, although the RP is slightly longer than commonly observed in a typical AVNRT. Because the atria and ventricles constitute portions of the reentrant circuit, tachycardia depends on 1:1 AV conduction.
Less frequently, antidromic AV reentrant tachycardia is seen in patients with accessory pathways capable of antegrade conduction.
The accessory pathway provides the antegrade limb of the reentrant circuit, and the AV node serves as the retrograde pathway, resulting in a wide QRS tachycardia due to complete preexcitation of the ventricles, or activation of the ventricles entirely over the accessory pathway.
Special considerations for patients with supraventricular tachy- cardia and delta waves in sinus rhythm. Asymptomatic patients may have delta waves on the ECG, which is called a WPW pattern. Prevalence
of the WPW pattern in the general population is approximately 1 case per 1000 people. Accessory pathways may be poorly conducting and less likely to promote tachycardia, accounting for the absence of symptoms.
These patients have a favorable prognosis, particularly if spontaneous and abrupt cessation of ECG preexcitation (delta wave) occurs with exercise or during ambulatory monitoring. In many cases, no specific therapy is required for asymptomatic patients.
Asymptomatic young patients participating in high-risk activities with WPW pattern may be subjected to invasive electrophysiologic testing for risk stratification. Patients with delta waves demonstrating clinical SVT or suggestive arrhythmic symptoms are said to have WPW syndrome, and invasive electrophysiologic testing is ordinarily recom- mended in these patients. Invasive testing helps to stratify the risk of sudden cardiac death.
Curative ablation is highly effective, with a success rate of 95%, and poses a low risk of procedural complications. Chronic therapy with
antiarrhythmic drugs that prolong the accessory pathway refractory period (i.e., class IA, IC, or III agents) may be effective, but the poten- tial for adverse drug effects has made accessory pathway ablation the treatment of choice for symptomatic and high-risk patients.
The use of agents that slow AV nodal conduction in patients with WPW syndrome warrants special mention. Digoxin, β-blockers, and calcium-channel blockers should not be used in patients with WPW because they slow conduction through the AV node, resulting in pref- erential excitation of the ventricles over the accessory pathway. In the setting of AF or atrial flutter, this may cause rapid ventricular rates and hemodynamic instability.
Wolff-Parkinson-White syndrome and atrial fibrillation. WPW syndrome is associated with a 0.25% per year risk of sudden cardiac death (SCD), which is related to the development of AF with rapid antegrade conduction over the accessory pathway producing VF. This risk is greatest for patients demonstrating very short preexcited RR A
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Fig. 9.5 Atrioventricular (AV) nodal (junctional) rhythm disturbances. (A) Supraventricular tachycardia. The lack of visible P waves during tachycardia suggests that they are concealed within the QRS complex, a pat- tern indicative of underlying AV nodal reentrant tachycardia. (B) Automatic junctional tachycardia. Notice the AV dissociation during tachycardia. The P waves (arrows) are dissociated from the QRS complexes. (C) Sinus rhythm with a short PR interval due to the presence of delta waves in a patient with Wolff-Parkinson-White (WPW) syndrome. The slurred QRS upstroke of the delta wave results from early activation of the ventricle by the extranodal bypass tract, followed by fusion with rapid conduction down the normal conduction system and resulting in narrowing of the terminal QRS. (D) Sinus rhythm with a short PR interval but no delta waves.
Despite the short PR, the P wave is normally vectored, excluding a junctional rhythm that appears similar but with an inverted P wave. A short PR interval in sinus rhythm without delta waves is caused by an abnormally rapid AV nodal conduction and is described as a Lown-Ganong-Levine pattern. (E) Supraventricular tachycar- dia. Unlike tracing A, there is a clear P wave (arrow) inscribed immediately after each QRS in the ST segment.
This pattern is seen most commonly with orthodromic AV reciprocating tachycardia in a patient with WPW syndrome. The early P wave in WPW is caused by retrograde conduction up the accessory pathway after ventricular activation during tachycardia. (F) Preexcited atrial fibrillation (AF) in a patient with WPW syndrome.
Notice the rapid and irregular ventricular response with widening of the QRS due to preexcitation. This pat- tern results from rapid conduction of the AF down the accessory pathway, bypassing the normal conduction system. As in this arrhythmia, occasional conduction down the AV node may occur during ongoing tachycar- dia, resulting in periods with a narrow QRS complex.
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intervals during AF. For some WPW patients, SCD may be the initial presentation. Successful catheter ablation of the accessory pathway eliminates this possibility.
Patients with WPW and rapidly conducted AF have the character- istic electrocardiographic findings of a rapid, irregularly irregular, wide QRS rhythm with various degrees of QRS widening or preexcitation from beat to beat (see Fig. 9.5F). During AF in the setting of underly- ing WPW, activation of the ventricle over the AV node produces con- cealed retrograde activation of the accessory pathway, prolonging the refractory period of the pathway and moderating the rate of antegrade accessory pathway conduction.
Treating patients with AV nodal–blocking therapy decreases con- cealed retrograde activation of the pathway, facilitating antegrade accessory pathway conduction and potentiating hemodynamic insta- bility. Appropriate acute therapy includes drugs that prolong the accessory pathway refractory period, such as intravenous procain- amide, ibutilide, or amiodarone. In the event of hemodynamic insta- bility, electrical cardioversion is preferred.
Role of catheter ablation in Wolff-Parkinson-White syndrome.
Catheter ablation is highly effective for treating WPW, with success rates of approximately 95% and recurrence rates of only 5%. Procedural complications are uncommon, with major complications occurring in 2% to 4% of cases and deaths related to ablation occurring in 0.1%.
Although antiarrhythmic drug therapy may control symptoms, the expense and risks of pharmacologic therapy along with the safety and efficacy of ablation have made radiofrequency ablation the first- line therapy for symptomatic WPW. Because older patients with
asymptomatic WPW patterns have a favorable prognosis, they should not routinely be subjected to ablation.