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A 29-year-old man comes to the emergency department with tachycardia and palpitations. He has been experiencing episodes of racing heartbeat, accompanied by dizziness, lightheadedness, chest palpitations, and, sometimes, fainting for the past several months. The man states that the palpitations can occur at any time and that he manages to control them by holding his breath for a long time. He has no family history of heart disease. Previous ECG examination showed a shortened PR interval, a widened QRS complex, and a delta wave. His blood pressure is 100/70 mm Hg, and his pulse is 180/min. Cardiac monitoring shows atrial fibrillation. He is given an antiarrhythmic, reverts to sinus rhythm, but then develops ventricular fibrillation. Which of the following drugs would be most appropriate to prevent ventricular fibrillation in this patient?
A. Adenosine
B. Digoxin
C. Flecainide
D. Lidocaine
E. Verapamil
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????????? flecainide
its a case of WPW SYNDROME
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its verapamil...sorry....
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sammy u r right its a case of WPWS
The correct answer is C.
The basic treatment principle in Wolff-Parkinson-White syndrome (WPW)-associated atrial fibrillation is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. If atrial fibrillation is treated in a conventional manner by drugs that prolong the refractory period of the AV node (beta-blockers, calcium channel blockers, digoxin), the rate of transmission through the accessory pathway likely will increase, with a corresponding increase in ventricular rate. This could cause the arrhythmia to deteriorate into ventricular fibrillation. The drugs that increase refractoriness of the AV accessory pathways are the drugs of choice. Class IC (flecainide, propafenone) and class III (amiodarone, sotalol) antiarrhythmics are indicated for the treatment of tachyarrhythmias in WPW. Flecainide has local anesthetic activity and belongs to the membrane-stabilizing class IC antiarrhythmic agents. It blocks sodium channels, producing a dose-related decrease in intracardiac conduction, particularly H-V conduction. Flecainide shortens phase 2 and phase 3 repolarization, resulting in decreased action potential duration. AV nodal conduction time and intraatrial conduction time are less affected by flecainide. Besides WPW syndrome, it is indicated for the prevention of paroxysmal supraventricular tachycardias, including atrioventricular nodal reentrant tachycardia and paroxysmal atrial fibrillation/flutter. It is also indicated in the prevention of sustained ventricular tachycardia and other documented ventricular arrhythmias.
Adenosine (choice A) slows conduction time through the AV node, can interrupt nodal reentrant pathways, and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia. It is not blocked by atropine, but is antagonized competitively with methylxanthines such as caffeine and theophylline. Adenosine is not effective in terminating atrial fibrillation/flutter in the presence of WPW. Moreover, by accelerating accessory conduction rate, it can cause degeneration of atrial fibrillation into ventricular fibrillation.
Digoxin (choice B) is a cardiac glycoside that inhibits the sodium-potassium ATPase, with the subsequent activation of Na/Ca exchange transport and increased intracellular calcium. It also slows heart rate and decreases conduction velocity through the AV node (vagomimetic effect). Digoxin is used as an antiarrhythmic for the control of ventricular response in patients with chronic atrial fibrillation. In patients with WPW syndrome, it may increase anterograde conduction across the accessory pathways, bypassing the AV node, and leading to a very rapid ventricular response or ventricular fibrillation. Most deaths from WPW syndrome have been associated with digoxin use. It is also contraindicated in patients with ventricular fibrillation.
Lidocaine (choice D) has applications as local anesthetic and antiarrhythmic. The drug suppresses automaticity of the His-Purkinje system and elevates the electrical stimulation threshold of the ventricles during diastole. Indications for its use are ventricular fibrillation and tachycardia. In patients with WPW, lidocaine shortens the refractory period of the accessory pathway, and therefore may cause an accelerated ventricular rate and the appearance of ventricular fibrillation.
Verapamil (choice E), a calcium channel blocker, is a class IV antiarrhythmic agent. It may facilitate conduction down the accessory pathways and increase risk of ventricular fibrillation. Therefore, it is contraindicated in the treatment of atrial fibrillation/flutter with WPW syndrome.
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you are really good i mean what an explanation
i am new to this forum
you guys are really very good
