Tachycardia reentry

Reentry mechanism Intranodal (AV node) reentry Extranodal reentry Reentrant tachyarrhythmia Atrial flutter Atrial fibrillation Ventricular tachycardia Ventricular fibrillation Conduction B/ocks ... 

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... 

O Ventricular tachycardia is usually initiated by a precisely timed VPD, occurring during the relative refractory period, which provokes reentry within ventricular tissue. 

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.)... 

Amiodarone is effective in maintaining sinus rhythm in most patients with paroxysmal atrial hbrillation and in many patients with persistent atrial hbrillation. It is also effective in preventing recurrences of A-V nodal reentry and atrial tachyarrhythmias and in the prevention of reentrant rhythms and atrial hbrillation in patients with Wohf-Parkinson-White syndrome. Also, it is the most efficacious therapy for postoperative junctional ectopic tachycardia. 

Drugs that markedly slow conduction, such as flecainide, or high concentrations of quinidine, can result in an increased frequency of reentry arrhythmias, notably ventricular tachycardia in patients with prior myocardial infarction in whom a potential reentry circuit may be present. Treatment here consists of recognition, withdrawal of the offending agent, and intravenous sodium. 

Verapamil and diltiazem are prototypic calcium channel blockers. As indicated previously, these drugs influence cardiac function by blocking inward calcium movement through L channels. In so doing they block conduction velocity in SA and AV node cells. They are used therapeutically to treat reentry arrhythmias through the AV node as well as paroxysmal supraventricular tachycardias. In fact, verapamil has been reported to terminate 60-80 percent of paroxysmal supraventricular tachycardias within several minutes. However, because of their potent effect on AV conduction, these drugs are contraindicated in patients with preexisting conduction problems since they may produce complete AV block. 

Verapamil s major effect is on the slow Ca channel. The result is a slowing of AV conduction and the sinus rate. This inhibition of the action potential inhibits one limb of the reentry circuit believed to underlie most paroxysmal. supraventricular tachycardias that use the A V node as a reentry point. It is categorized as a class IV antiarrhythmie drug (see Classes of Antiarrhythmie Drugs" below). Hemodynami-cally. verapamil causes a change in the preload, afterload, contractility, heart rate, and coronary blood flow. The drug reduces systemic vascular resistance and mean blood pressure, with minor effects on eardiae output. 

Arrhythmias are observed during the ischemic phase as well as at reperfusion in most of the animal models. In the first 2-10 min of ischemia, a burst of irregular ventricular tachycardia occurs but evolution to ventricular flbrillation is rare. These arrhythmias are mainly of a reentry nature. A second phase of arrhythmias is evident after 20-30 min of ischemia. The percentage of animals that show this delayed phase of arrhythmias is small and the evolution to ventricular flbrillation is more frequent and the animals can die. This phase is associated with a massive release of catecholamines, changes in calcium overload and an increase in extracellular potassium, reviewed by Carmeliet.55... 

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. 

Paroxysmal supraventricular tachycardia (PSVT) arising by reentrant mechanisms includes arrhythmias caused by AV nodal reentry, AV reentry incorporating an anomalous AV pathway, SA nodal reentry, and intraatrial reentry. AV nodal reentry and AV reentry are by far the most common of these tachycardias. 

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. 

Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by... 

De Bakker JM, van Capelle FJ, Janse MJ, et al. Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease electrophysiologic and anatomic correlation. Circulation 1988 77(3) 589-606. 

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