Mastering Antiarrhythmic Drug Therapy

Which ions are of primary importance in the action of antiarrhythmic drugs?

What is the pharmacological goal of antiarrhythmic drug therapy?

What is the ideal characteristic of an antiarrhythmic drug in terms of its effect on different tissues?

How does the Singh-Vaughn Williams system classify antiarrhythmic drugs?

What is the effect of many of the drugs presently available for treating arrhythmias?

What leads to differential sensitivity to antiarrhythmic drugs?

What is the mechanism of action of antiarrhythmic drugs?

What is the ideal characteristic of an antiarrhythmic drug in terms of side effects?

Which subclass of Class I drugs has the highest potency as sodium channel blockers and prolongs repolarization?

Which subclass of Class I drugs has the lowest potency as sodium channel blockers and may shorten repolarization (decrease QT interval)?

Which subclass of Class I drugs is the most potent sodium channel blocking agents (prolong QRS interval) and has little effect on repolarization (no effect on QT interval)?

Which class of antiarrhythmic drugs act indirectly on electrophysiological parameters by blocking beta-adrenergic receptors?

Which class of antiarrhythmic drugs prolongs repolarization, increases refractoriness, and has no effect on QRS interval?

Which class of antiarrhythmic drugs are relatively selective AV nodal L-type calcium-channel blockers and slow sinus rhythm?

Which of the antiarrhythmic drugs have minimal effects on AV node depolarization?

Which class of antiarrhythmic drugs is not included in the standard classes?

Which class of antiarrhythmic drugs binds most strongly when the Na+ channels are open and is termed 'use dependent'?

Which class of antiarrhythmic drugs is involved in blocking some of the K+ channels involved in repolarisation?

Which class of antiarrhythmic drugs acts by blocking the fast inward sodium channel?

Which class of antiarrhythmic drugs acts indirectly on electrophysiological parameters by blocking beta-adrenergic receptors?

Which class of antiarrhythmic drugs blocks the fast outward potassium current?

Which of the antiarrhythmic drugs blocks the slow inward sodium current?

Which class of antiarrhythmic drugs blocks the sodium channels preferentially in refractory phase?

Which class of antiarrhythmic drugs associate and dissociate very slowly from the sodium channels?

Which class of antiarrhythmic drugs extends the duration of the action potential?

Which class of antiarrhythmic drugs blocks voltage dependent calcium channels?

Which class of antiarrhythmic drugs inhibits conduction through the Bundles of His and Purkinje fibers, thus prolonging QRS complex?

Which class of antiarrhythmic drugs impairs impulse propagation in nodal and damaged areas?

Which class of antiarrhythmic drugs blocks the slow inward sodium current?

Which class of antiarrhythmic drugs prolongs repolarization and increases refractoriness?

Which class of antiarrhythmic drugs has little preference for refractory channels?

Which class of antiarrhythmic drugs reduces the force of contraction?

Which adverse effect of chronic amiodarone use is fatal in 10% of patients?

What is the incidence of hyperthyroidism and hypothyroidism in patients on chronic amiodarone?

What adverse effect of chronic amiodarone use can result in blue-gray skin color?

What adverse effect of chronic amiodarone use can interfere with vision?

How often are clinical assessments and chest x-rays required in patients on chronic amiodarone?

What is the mean elimination half-life of amiodarone?

What percentage of patients on chronic amiodarone develop hepatotoxicity, (looking for the percent of patients that have elevated serum liver enzyme?

What adverse effect of chronic amiodarone use has an incidence of 20-40% but is reversible by lowering dose?

Which drug, although formally classified as class III antiarrhythmic, it has multiple actions and is more appropriately considered a 'broad spectrum' antiarrhythmic?

What is the approved use of amiodarone?

What makes amiodarone a good drug when compared to other class III agents?

Which antiarrhythmic drug is superior to lidocaine for the treatment of ventricular fibrillation?

What is a potential risk of using amiodarone for chronic therapy?

Which patients should not use Flecainide (class IC) as an antiarrhythmic drug?

What is the effect of Flecainide on ventricular function?

Which antiarrhythmic drug has consistently decreased mortality in many clinical trials?

Which patients should Flecainide be used with caution in?

How long does it take to achieve steady-state plasma levels of amiodarone without loading doses?

What is the primary use of flecainide?

Which class of antiarrhythmic drugs is flecainide classified under?

What is the primary mechanism of action of flecainide?

Which antiarrhythmic drug is specifically used for symptomatic supraventricular arrhythmias?

Which class of antiarrhythmic drugs does procainamide belong to?

What is the major metabolite of procainamide?

What percentage of the population are fast acetylators of procainamide?

What is the recommended initial dosing of procainamide when given orally?

What percentage of patients discontinue procainamide therapy within 6 months due to side effects?

What percentage of patients develop a lupus-like syndrome with procainamide therapy?

What are the early warning symptoms of the lupus-like syndrome associated with procainamide therapy?

What is the major metabolite of procainamide and what class of antiarrhythmic actions does it have?

What types of arrhythmias is procainamide effective against?

Which class of antiarrhythmic drugs is lidocaine and mexiletine classified under?

What is the primary route of administration for lidocaine for arrhythmias?

Which drug is recommended before lidocaine for the treatment of ventricular fibrillation or pulseless ventricular tachycardia according to ECC/AHA 2000 guidelines?

Which antiarrhythmic drug can be used in patients with a history of torsades or DILQTs?

What is the primary use of lidocaine and mexiletine?

What are the most frequent side effects of lidocaine and mexiletine?

Which drug can cause severe interactions when co-administered with lidocaine or mexiletine?

Which class of antiarrhythmic drugs is more effective than digoxin in controlling ventricular rate in patients with atrial fibrillation?

What is the most common side effect of verapamil?

Which combination of drugs can cause AV block or suppression of SA node when used with high doses of verapamil or diltiazem?

Which patients should be cautious when using verapamil or diltiazem?

What can happen if verapamil or diltiazem are administered to patients with atrial tachycardias resulting from WPW?

What is a contraindication for using verapamil or diltiazem?

Which drug is known to increase the plasma concentrations of verapamil?

Which of the antiarrhythmic drugs is ineffective for prophylaxis of arrhythmias in post-MI patients?

What can high doses of verapamil or diltiazem cause in terms of AV and SA node function?

Which class of antiarrhythmic drugs is indicated for premature atrial, nodal or ventricular depolarization?

What is the drug therapy indicated for atrial fibrillation, flutter, and PSVT?

Which arrhythmia should AV nodal blockers be avoided in?

Which class of antiarrhythmic drugs is indicated for ventricular tachycardia with remote myocardial infarction?

Which drugs are indicated for ventricular fibrillation?

What is the acute treatment for Torsades de pointes?

What is the chronic treatment for Torsades de pointes?

What are the therapeutic considerations for antiarrhythmic drug therapy?

Which patients are most likely to benefit from antiarrhythmic drug therapy?

What should be eliminated before starting antiarrhythmic drug therapy?

Which statement about currently available antiarrhythmic drugs is most accurate?

What should be considered when choosing an antiarrhythmic drug?

What is the therapeutic index of most antiarrhythmic drugs?