Figure 82.1. Wolf-Parkinson-White (WPW) Pattern. Note the short PR interval and delta waves (arrows).
Regular tachycardia that utilizes an accessory pathway is referred to as atrioventricular reentrant tachycardia(AVRT). Except in the rare instances of multiple accessory pathways, the circuit involves the atria, ventricles, AV node, and the accessory pathway. When the impulse travels anterograde down the AV node and back up the accessory pathway, it is referred to as orthodromic reentrant tachycardia (ORT), whereas when the impulse travels anterograde down the accessory pathway and back up the AV node it is referred to as antidromic reentrant tachycardia (ART). ORT is manifested by a narrow complex tachycardia whereas ART, which is maximally preexcited, is a wide complex tachycardia. Of note, given that the atria and ventricles are integral parts of the tachycardia circuit, there is an obligatory 1:1 AV relationship in any form of AVRT. Tachycardia that persists in spite of evident variable conduction to the atria or ventricles effectively rules out AVRT.
Diagnosis and Treatment
The presence of a WPW pattern on a surface EKG reveals the presence of an accessory pathway, although the mere presence of an accessory pathway does not imply that AVRT has or will occur, and furthermore, it may be an innocent bystander in the context of another underlying tachycardia mechanism. The absence of a delta wave does not rule AVRT, as the accessory pathway may be far from the sinus node and/or may only conduct in the retrograde direction, that is, a concealed accessory pathway.
The primary concern with WPW is the possibility of developing atrial fibrillation rapidly conducting over the accessory pathway leading to a rapid ventricular response and possibly ventricular fibrillation (VF). Risk factors for sudden death in WPW include a younger age at time of diagnosis, prior atrial fibrillation or AVRT, rapidly conducting pathways or multiple pathways, and a history of syncope. An electrophysiological (EP) study can risk stratify the conduction characteristics of an accessory pathway and thereby determine the suitability of catheter ablation of the accessory pathway. In the case of a high-risk pathway, the patient may be placed on a sodium-channel-blocking drug to stabilize him or her until an EP study can be performed. Furthermore, as in the case of AVNRT, nodal-blocking agents can be used as first-line therapy in AVRT with concealed accessory pathways, but more definitive treatment is achieved with catheter ablation of accessory pathways.
JUNCTIONAL TACHYCARDIA
The normal AV junctional escape rate is 40–60 bpm but an accelerated junctional rhythm with rates between 70 and 130 bpm may occur, most often in the context of irritability of the AV junction. Junctional ectopic tachycardia may be due to conditions such as recent cardiac valvular surgery, myocardial ischemia, digitalis toxicity, or myocarditis. Rarely primary junctional automaticity can occur in isolation.
It is important to recognize that the entity paroxysmal junctional reciprocating tachycardia (PJRT), a slow long RP tachycardia, is a bit of a misnomer, actually resulting from a slowly conducting posteroseptal accessory pathway. This entity is an important cause of a tachycardia-induced cardiomyopathy in pediatric patients and is responsive to catheter ablation.
Diagnosis and Treatment
The diagnosis of junctional tachycardia is made by the observation of QRS morphology identical to that seen during sinus rhythm but with AV dissociation or evidence of retrograde P waves. True junctional ectopic tachycardia typically resolves as the inciting condition improves.
VENTRICULAR ARRHYTHMIAS
There are several features of ventricular tachycardia (VT) that should be considered during evaluation. It is of course important to initially look for clues that the wide complex tachycardia is not supraventricular in origin (see Figure 82.2). The occurrence of three or more ventricular beats is termed nonsustained VT (NSVT) unless it lasts for >30 seconds, in which case it is referred to as sustained VT. The rates of VT are generally >120 bpm. A ventricular rate <110 bpm is referred to as an accelerated idioventricular rhythm (AIVR). VT with a single QRS morphology is referred to as monomorphic VT, whereas polymorphic VT is characterized by a constantly changing QRS morphology. Following the acute stabilization of the patient, it is critically important to ascertain the cardiac history and cardiac function of a patient with VT as this information alone can point to the underlying etiology of the arrhythmia.
Figure 82.2. Algorithm to Differentiate VT from SVT with Aberrancy. A-V dissociation refers to independent atrial and ventricular activity. Capture beats refer to regularly conducted supraventricular beats during ventricular tachycardia while fusion beats refer to a QRS morphology that is a combination of the ventricular tachycardia and a supraventricular beat conducted down the conduction system.
SYNDROMES ASSOCIATED WITH VENTRICULAR ARRHYTHMIAS AND SUDDEN CARDIAC DEATH
Brugada Syndrome: This syndrome is an autosomal dominant syndrome characterized by EKG abnormalities and predisposition to ventricular arrhythmias. The primary mode of diagnosis is the EKG, which shows complete- or incomplete right bundle branch block pattern along with ST elevations in leads V1 and V2, in the context of a structurally normal heart. Occasionally these findings may be concealed and can be elicited with a class IC agent such as flecainide. Risk factors for sudden cardiac death (SCD) include an abnormal EKG pattern and a history of syncope. Given the lack of effective medications for this syndrome, the treatment is often prophylactic implantable cardioverter-defibrillator (ICD) placement.
Long QT Syndrome: The long QT syndrome is characterized by a prolonged QT interval and T wave abnormalities
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