AV nodal reentry

PSVT arising by reentrant mechanisms includes arrhythmias caused by AV nodal reentry, AV reentry incorporating an anomalous AV pathway, sinoatrial (SA) nodal reentry, and intraatrial reentry. 

Patients frequently complain of intermittent episodes of rapid heart rate/palpitations that start and stop abruptly, usually without provocation (but occasionally during exercise). Severe symptoms include syncope. Often (in particular, those with AV nodal reentry) patients complain of a chest pressure or a fullness in the neck sensation. This is due to simultaneous AV contraction with the right atrium contracting against a closed tricuspid valve. Life-threatening symptoms (syncope, hemodynamic collapse) are associated with extremely rapid rate (e.g., >200 beats per minute) and atrial fibrillation associated with an accessory AV pathway. 

The underlying substrate of AV nodal reentry is the functional division of the AV node into two (or more) longitudinal conduction pathways, or dual AV nodal pathways." Most practitioners now believe that there are not two distinct anatomic pathways inside the AV node itself. Rather, it is likely that a fanlike network of perinodal fibers inserts into the AV node and represents the second pathway. The two... 

FIGURE 17-7. Reentry mechanism of dual-AV-nodal- pathway PSVT. A. Sinus rhythm. The impulse travels from the atrium through the fast pathway (F) and then to the His-Purkinje system. The impulse also travels through the slow pathway (S) but is stopped when refractory tissue is encountered. B. Dual-AV-nodal reentry. A critically timed premature impulse ) is stopped in the fast pathway (because of prolonged refractoriness) but is able to travel antegrade down the slow pathway and retrograde through the fast pathway. 

PSVT due to AV nodal reentry may occur by the following sequence of events The occurrence of an appropriately timed premature impulse penetrates the AV node but is blocked in the fast pathway that is still refractory from the previous beat. However, the slow pathway, which has a shorter refractory period, permits antegrade conduction of the premature impulse. By the time the impulse has reached the distal common pathway, the fast pathway has recovered its excitability and now will permit retrograde conduction. The impulse reaches the common proximal pathway, preceded by an excitable gap of tis-... 

AV reentry (PSVT) Reentry Same as AV nodal reentry channel block Na channel block with > 1 second Ablation ... 

O Paroxysmal supraventricular tachycardia is caused by reentry that includes the AV node as a part of the reentrant circuit. Typically, electrical impulses travel forward (antegrade) down the AV node and then travel back up the AV node (retrograde) in a repetitive circuit. In some patients, the retrograde conduction pathway of the reentrant circuit may exist in extra-AV nodal tissue adjacent to the AV node. One of these pathways usually conducts impulses rapidly, while the other usually conducts impulses slowly. Most commonly, during PSVT the impulse conducts antegrade through the slow... 

FIGURE 6-2. Algorithm for the treatment of acute (top portion) paroxysmal supraventricular tachycardia and chronic prevention of recurrences (bottom portion). Note For empiric bridge therapy prior to radiofrequency ablation procedures, calcium channel blockers (or other atrioventricular [AV] nodal blockers) should not be used if the patient has AV reentry with an accessory pathway. (AAD, antiarrhythmic drugs AF, atrial fibrillation AP, accessory pathway AVN, atrioventricular nodal AVNRT, atrioventricular nodal reentrant tachycardia AVRT, atrioventricular reentrant tachycardia DCC, direct-current cardioversion ECG, electrocardiographic monitoring EPS, electrophysiologic studies PRN, as needed VT, ventricular tachycardia.)... 

Paroxysmal supraventricular tachycardia is usually due to reentry in or proximal to the atrioventricular (AV) node or AV reentry incorporating an extra nodal pathway common tachycardias can be terminated acutely with AV nodal... 

Patients with Wolff-Parkinson-White (WPW) syndrome may have several different tachycardias that are treated acutely by different strategies orthodromic reentry (adenosine), antidromic reentry (adenosine or procainamide), and atrial fibrillation (procainamide or amiodarone). AV nodal blocking drugs are contraindicated with WPW syndrome and atrial fibrillation. 

Sinus node reentry or intraatrial reentry occur less commonly, and neither is as well described as AV nodal or AV reentry. Aside from a characteristic abrupt onset and termination, coupled with subtle changes in P-wave morphology, these tachycardias can be difficult to diagnose. Electrophysiologic studies may be necessary to determine the ultimate mechanism of the PSVT. 

Atrial fibrillation Disorganized functional reentry 1. Control ventricular response AV nodal block 1. Control ventricular response AV nodal block ... 

C. Clinical Use and Toxicities Calcium channel blockers are effective for converting atrioventricular nodal reentry (also known as nodal tachycardia) to normal sinus rhythm. Their major use is in the prevention of these nodal arrhythmias in patients prone to recurrence. These drugs are orally active verapamil is also available for parenteral use (Table 14—2). The most important toxicity of verapamil is excessive pharmacologic effect, since cardiac contractility, AV conduction, and blood pressure can be significantly depressed. See Chapter 12 for additional discussion of toxicity. Amiodarone has moderate calcium channel-blocking activity. 

AV nodal tissue, blocks conduction for 10-15 seconds. Used for nodal reentry arrh3fthmias. Tox hypotension, flushing. 

Nodal tachycardia A common reentrant arrhythmia that travels through the AV node it may also be conducted through atrial and ventricular tissue as part of the reentry circuit... 

---