Accessory Pathway

Preexcited Diagnosis

Fig. 11. Serial ECGs in a patient with WPW. (A) This initial ECG reveals AF. Although not all of the complexes are pre-excited, pre-excited R-R intervals shorter than 240 ms are evident to the right side of the tracing, suggesting the possibility of high risk. (B) After approx 500 mg iv procainamide, AF persists. There is no evidence of pre-excitation because the accessory pathway blocked by procainamide. (C) After approx 1000 mg iv procainamide, the patient has converted to sinus rhythm, with no evidence of pre-excitation. The patient underwent a successful ablation of a left posteroseptal pathway the next day.

Fig. 11. Serial ECGs in a patient with WPW. (A) This initial ECG reveals AF. Although not all of the complexes are pre-excited, pre-excited R-R intervals shorter than 240 ms are evident to the right side of the tracing, suggesting the possibility of high risk. (B) After approx 500 mg iv procainamide, AF persists. There is no evidence of pre-excitation because the accessory pathway blocked by procainamide. (C) After approx 1000 mg iv procainamide, the patient has converted to sinus rhythm, with no evidence of pre-excitation. The patient underwent a successful ablation of a left posteroseptal pathway the next day.

should undergo catheter ablation prior to hospital discharge unless there is a contraindication to the procedure. Following successful ablation, implantable cardiovascular defi-brillator (ICD) therapy is not necessary in patients with WPW and aborted sudden death. For patients with PSVT in the setting of WPW, catheter ablation is generally recommended as initial therapy because of the risk of sudden death associated with this condition. There is also the theoretic risk that long-term therapy with AV nodal-blocking agents could be detrimental if AF or atrial flutter occurs. Few long-term safety data exists regarding chronic beta-blocker, calcium-channel blocker, or digoxin therapy in patients with PSVT caused by WPW. In patients for whom catheter ablation is not undertaken, the best option may be combination therapy with an AV-nodal blocker and class I antiarrhythmic drug, to slow accessory pathway conduction.

Although some recommend catheter ablation to all patients with symptomatic PSVT in the absence of WPW, a reasonable, more conservative stance is to individualize therapy for each patient (see Fig. 16). Patients presenting with a first episode, or rare recurrences, of well-tolerated PSVT can frequently be observed without chronic therapy. These patients can be taught vagal maneuvers, which are often effective in terminating PSVT. If episodes are frequent and/or cause severe symptoms, however, chronic therapy with an AV-nodal blocking agent is reasonable. Few data are available regarding the relative efficacy of beta-blockers, calcium-channel blockers, and digoxin in patients with PSVT. If an AV-nodal blocker is unsuccessful or not tolerated, a different agent may be tried. We find that about a third of PSVT patients will find an AV-nodal blocking agent that is both effective and well-tolerated. Alternatively, catheter ablation may be employed as initial therapy in patients with severely symptomatic PSVT or a reluctance to take long-term medical therapy. In the case of PSVT refractory to multiple AV-nodal blocking agents, we generally recommend catheter ablation rather than class I or III antiarrhythmic therapy, because of the cumulative risk of toxicity and pro-arrhythmia of these agents. Success rates for catheter ablation of atrial tachycardias are not quite as high as for AVNRT and AVRT, yet these tachycardias are frequently extremely refractory to medical therapy, and the same treatment algorithm may be recommended. An important exception is inappropriate sinus tachycardia. Because the SA nodal complex constitutes an extensive area of right atrial tissue, catheter ablation is extremely difficult, and poses a higher risk. For these reasons, aggressive attempts at pharmacologic suppression with beta-blockers and/or calcium-channel blockers are usually recommended, with catheter ablation reserved for extremely refractory cases.

In patients who present with incessant tachycardia and nonischemic cardiomyopathy, the mechanism of myopathy may be tachycardia-induced. In these patients, we typically recommend catheter ablation as initial therapy, because of the higher likelihood of cure compared with medical therapy, and the possibility of recovery of ventricular function following successful treatment.

The cost-effectiveness of catheter ablation for PSVT depends on the frequency and severity of symptoms, as well as refractoriness to medical therapy. For patients with frequent emergency-room visits and hospital admissions, radiofrequency ablation results in relatively rapid cost savings (43,44). Costs are reduced further when ablations are performed on an outpatient basis, which has proven to be feasible and safe when performed by experienced operators (45). In addition, as initial therapy in patients with symptomatic SVT, radiofrequency ablation results in more complete resolution of symptoms and health-related quality of life compared with medical therapy (46). Combined

Ekg Strips Large Svt

Fig. 12. ECG in patient with nearly incessant PSVT. Note the deeply inverted P waves relatively close to the next QRS complex, a so-called "long RP" tachycardia. EPS confirmed the diagnosis of permanent junctional reciprocating tachycardia (PJRT), caused by a slowly conducting concealed right posteroseptal accessory pathway. This ECG is also consistent with atypical AVNRT, and even a low septal ectopic atrial tachycardia.

Fig. 12. ECG in patient with nearly incessant PSVT. Note the deeply inverted P waves relatively close to the next QRS complex, a so-called "long RP" tachycardia. EPS confirmed the diagnosis of permanent junctional reciprocating tachycardia (PJRT), caused by a slowly conducting concealed right posteroseptal accessory pathway. This ECG is also consistent with atypical AVNRT, and even a low septal ectopic atrial tachycardia.

Concealed Septal Accessory Pathway Ecg
Fig. 13. ECG in a patient with nonparoxysmal junctional tachycardia (NPJT). The tachycardia is regular and narrow complex, though A-V dissociation is clearly present (seen best in the lead Vi rhythm strip).
Junctional Tachycardia Ecg

Fig. 14. ECG in a patient with asymptomatic, intermittent pre-excitation. Note that every other beat is pre-excited. This suggests a long anterograde refractory period and therefore low-risk accessory pathway. No further workup was recommended, and the patient remained asymptomatic during follow-up. Note that this ECG is also consistent with sinus rhythm with ventricular bigeminy. At lower rates, however, the short PR interval and delta wave were present on every beat, confirming the diagnosis of ventricular pre-excitation.

Fig. 14. ECG in a patient with asymptomatic, intermittent pre-excitation. Note that every other beat is pre-excited. This suggests a long anterograde refractory period and therefore low-risk accessory pathway. No further workup was recommended, and the patient remained asymptomatic during follow-up. Note that this ECG is also consistent with sinus rhythm with ventricular bigeminy. At lower rates, however, the short PR interval and delta wave were present on every beat, confirming the diagnosis of ventricular pre-excitation.

Atrial Fibrillation Intracardiac Ecg

Fig. 15. Response of various SVTs to adenosine infusion. In each panel, surface ECG lead II and an intracardiac right atrial electrogram are depicted. During AVRT, atrial activation clearly follows ventricular activation. During AVNRT, atrial and ventricular activation are nearly simultaneous; in this case, atrial activation precedes ventricular activation. Because AVRT and AVNRT require AV nodal conduction, both are terminated by adenosine. During atrial tachycardia and atrial flutter, adenosine transiently increases the level of AV block, but tachycardia persists in the atrium. However, in some atrial tachycardias, the atrial tachycardia mechanism itself may be susceptible to adenosine termination (not shown). (Reproduced from Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995;332:162-173. Copyright © 1995 Massachusetts Medical Society.)

Fig. 15. Response of various SVTs to adenosine infusion. In each panel, surface ECG lead II and an intracardiac right atrial electrogram are depicted. During AVRT, atrial activation clearly follows ventricular activation. During AVNRT, atrial and ventricular activation are nearly simultaneous; in this case, atrial activation precedes ventricular activation. Because AVRT and AVNRT require AV nodal conduction, both are terminated by adenosine. During atrial tachycardia and atrial flutter, adenosine transiently increases the level of AV block, but tachycardia persists in the atrium. However, in some atrial tachycardias, the atrial tachycardia mechanism itself may be susceptible to adenosine termination (not shown). (Reproduced from Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995;332:162-173. Copyright © 1995 Massachusetts Medical Society.)

Wpw Treatment

Fig. 16. Algorithm for long-term management in patients who present with PSVT. For patients with WPW, EPS and radiofrequency catheter ablation are recommended as initial therapy. In the absence of WPW, the long-term treatment strategy depends on the frequency and severity of episodes, as well as patient preference.

Fig. 16. Algorithm for long-term management in patients who present with PSVT. For patients with WPW, EPS and radiofrequency catheter ablation are recommended as initial therapy. In the absence of WPW, the long-term treatment strategy depends on the frequency and severity of episodes, as well as patient preference.

with the limited natural history data suggesting a low rate of spontaneous resolution of SVT, these studies would suggest that relatively early intervention with catheter ablation is appropriate, particularly in younger patients.

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Responses

  • thomas beich
    What causes junctional tachycardia?
    8 years ago
  • CURZIO
    How to easily determine atrial fibrillation on an EKG?
    7 years ago
  • brigida
    Where are the septal leads on a ekg?
    7 years ago
  • awate
    Can you have both Accessory Pathway and Atrial Ectopic Tachycardia?
    7 years ago

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