• 2018-07
  • 2019-04
  • br Conflict of interest br Case presentation A year


    Conflict of interest
    Case presentation A 64-year-old female presented to the emergency room with persistent dizziness that began early that morning. She had a 30-year history of palpitations and known electrocardiogram (ECG) abnormalities. Her pulse was irregular at 130–270min−1 and blood pressure was 90/40mmHg. There were no other abnormalities on physical examination. A chest X-ray was normal and without cardiomegaly. Echocardiography revealed normal left ventricular contraction without structural abnormalities. Blood chemistry evaluation, including electrolytes and cardiac enzymes, was within normal limits. Twelve-lead ECG showed irregular wide QRS tachycardia of various configurations (Fig. 1).
    Commentary The patient\'s ECG shows wide QRS tachycardia with a rate from 150 to 300beats/min. The RR intervals are irregularly irregular and no P wave preceding QRS was confirmed. The QRS complex has beat–beat variations in morphology. At this point, some of the arrhythmias that should be considered are: (1) irregular ventricular tachycardia (such as torsades des pointes or polymorphic ventricular tachycardia); (2) atrial fibrillation (AF) with bundle branch block; (3) AF in Wolff–Parkinson–White (WPW) syndrome (pseudo-ventricular tachycardia). The QRS complex shows right axis deviation during tachycardia with no progressive change in cardiac axis, thus polymorphic ventricular tachycardia and torsades des pointes associated with QT prolongation are excluded. Polymorphic ventricular tachycardia associated electrolyte abnormality and myocardial ischemia could not be totally excluded by this ECG, however laboratory examination did not indicate myocardial ischemia or an electrolyte abnormality. The representative arrhythmia of the patient\'s irregular Prostaglandin E2 manufacturer rate is AF, which is the most common cardiac arrhythmia. When the ventricular rate is slow, AF can be easily diagnosed. However if the ventricular rate is rapid, AF is difficult to appreciate because QRS complexes are clustered together and fibrillatory waves become more difficult to evaluate. The QRS complexes during AF with bundle branch block usually do not have beat–beat variation, and both an Rr′ pattern in lead V1 and Ratrioventricular (AV) node and accessory pathways. To terminate AF and block the accessory pathway, procainamide was given intravenously at a dose of 400mg over 30min. It is important to note that AV nodal blocking agents are contraindicated in treatment of AF in patients with WPW syndrome. AV nodal blocking agents, for example verapamil and digoxin, decrease the number of impulses conducted through the His–Purkinje system and enhance conduction across accessory pathways, thus increasing the ventricular rate during AF. If the patient is hemodynamically unstable, electrical cardioversion should be performed. After infusion of procainamide, this patient\'s AF converted to normal sinus rhythm (Fig. 2) that included a short PR interval and a delta wave. A positive delta wave and QRS in V1 indicated a left sided accessory pathway.
    Explanations of the arrhythmia AF is the most serious arrhythmia associated with WPW syndrome. This arrhythmia has the possibility of degenerating into ventricular fibrillation, which can cause sudden cardiac death. Although the occurrence of ventricular fibrillation is rare, even among symptomatic patients with WPW syndrome, AF carries the potential for sudden cardiac death. The risk of sudden cardiac death in patients with WPW syndrome is related to the short effective refractory period of the anterograde accessory pathway. Electrophysiological studies are performed to measure the refractory period of the accessory pathway. Patients with an accessory pathway with an effective refractory period of less than 250ms, as measured by an R–R interval between 2 preexcited complexes of <250ms during AF, are defined as high risk.