Procainamide arrhythmia with

D. Treatment. Perform CPR if necessary, and follow standard guidelines for management of arrhythmias, with the exception that procainamide and bretylium should not be used, especially if tricyclic antidepressant or sodium channel-blocking drug overdose is suspected. 

Fleca.inide, Elecainide acetate, a fluorobenzamide, is a derivative of procainamide, and has been reported to be efficacious in suppressing both supraventricular and ventricular arrhythmias (26—29). The dmg is generally reserved for patients with serious and life-threatening ventricular arrhythmias. Elecainide depresses phase 0 depolarization of the action potential, slows conduction throughout the heart, and significantly prolongs repolarization (30). The latter effect indicates flecainide may possess some Class III antiarrhythmic-type properties (31). 

Concurrent use of the fluoroquinolones with theophylline causes an increase in serum theophylline levels. When used concurrently with cimetidine, the cimetidine may interfere with the elimination of the fluoroquinolones. Use of the fluoroquinolones with an oral anticoagulant may cause an increase in the effects of the oral coagulant. Administration of the fluoroquinolones with antacids, iron salts, or zinc will decrease absorption of the fluoroquinolones. There is a risk of seizures if fluoroquinolones are given with the NSAIDs. There is a risk of severe cardiac arrhythmias when the fluoroquinolones gatifloxacin and moxifloxacin are administered with drains that increase the QT interval (eg, quini-dine, procainamide, amiodarone, and sotalol). 

All antiarrhythmic dra are used cautiously in patients with renal or hepatic disease. When renal or hepatic dysfunction is present, a dosage reduction may be necessary. All patients should be observed for renal and hepatic dysfunction. Quinidine and procainamide are used cautiously in patients with CHF. Disopyramide is used cautiously in patients with CHF, myasthenia gravis, or glaucoma, and in men with prostate enlargement. Bretylium is used cautiously in patients with digitalis toxicity because the initial release of norepinephrine with digitalis toxicity may exacerbate arrhythmias and symptoms of toxicity. Verapamil is used cautiously in patients with a history of serious ventricular arrhythmias or CHF. Electrolyte disturbances such as hypokalemia, hyperkalemia, or hypomagnesemia may alter the effects of the antiarrhythmic dru . Electrolytes are monitored frequently and imbalances corrected as soon as possible... 

The answer is e. (Hardman, pp 858-874.) Because verapamil, a Ca channel blocker, has a selective depressing action on AV nodal tissue, it is an ideal drug for both immediate and prophylactic therapy of supraventricular tachycardia (SVT). Nifedipine, another Ca channel blocker, has little effect on SAT Lidocaine and adenosine are parenteral drugs with short ha If-lives and, thus, are not suitable for prophylactic therapy. Procainamide is more suitable for ventricular arrhythmias and has the potential for serious adverse reactions with long-term use. 

The answer is b. (Hardman, pp 868 869.) Persons with low hepatic iY-acetyltransferase activity are known as slow acetylators. A major pathway of metabolism of procainamide, which is used to treat arrhythmias, is iV-acetylation. Slow acetylators receiving this drug are more susceptible than normal persons to side effects, because slow acetylators will have higher-than-normal blood levels of these drugs N-acetylprocainamide, the metabolite of procainamide, is also active. 

Like procainamide, lidocaine is an amide with local anesthetizing action. Lidocaine is usually administered intravenously for short-term therapy of ventricular extrasystole, tachycardia, especially in the severe phase of myocardial infarction, arrhythmia of natural cause, and for arrhythmia that can originate in the heart during surgical manipulations. Synonyms of this drug are lidopen, xylocaine, xylocard, and others. 

The applicability of these results to other populations (eg, those without recent Mis) is uncertain. Considering the known proarrhythmic properties of procainamide and the lack of evidence of improved survival for any antiarrhythmic drug in patients without life-threatening arrhythmias, the use of procainamide and other antiarrhythmic agents should be reserved for patients with life-threatening ventricular arrhythmias. 

IM administration - IM administration may be used as an alternative to the oral route for patients with less threatening arrhythmias but who are nauseated or vomiting, who are ordered to receive nothing by mouth preoperatively, or who may have malabsorptive problems. An initial daily dose of 50 mg/kg may be estimated. Divide this amount into fractional doses of 1/8 to % to be injected IM every 3 to 6 hours until oral therapy is possible. If more than 3 injections are given, assess patient factors such as age and renal function, clinical response and, if available, blood levels of procainamide and NAPA in adjusting further doses for that individual. For treatment of arrhythmias associated with... 

Digitalis intoxication Exercise caution in the use of procainamide in arrhythmias associated with digitalis intoxication. Procainamide can suppress digitalis-induced arrhythmias however, if there is concomitant marked disturbance of AV conduction, additional depression of conduction and ventricular asystole or fibrillation may result. Consider use of procainamide only if discontinuation of digitalis, and therapy with potassium, lidocaine, or phenytoin are ineffective. 

Concurrent antiarrhythmic agents Concurrent antiarrhythmic agents may produce enhanced prolongation of conduction or depression of contractility and hypotension, especially in patients with cardiac decompensation. Reserve concurrent use of procainamide with other Class lA antiarrhythmic agents (eg, quinidine, disopyramide) for patients with serious arrhythmias unresponsive to a single drug and use only if close observation is possible. 

This is the amide analogue of procaine hydrochloride. It has an active metabolite with significant class III activity. Procainamide is particularly effective in the treatment of lifethreatening ventricular arrhythmias unresponsive to other therapies. It is also used to maintain sinus rhythm following cardioversion. Intravenous administration can cause hypotension, mainly due to peripheral vasodilatation, and it should not be given faster than 50 mg-min-1. It should be given intravenously as a bolus of 100 mg over 2-5 min, followed by an infusion of 30-90 pg-kg-l-min-1. 

Procainamide is effective against most atrial and ventricular arrhythmias. However, many clinicians attempt to avoid long-term therapy because of the requirement for frequent dosing and the common occurrence of lupus-related effects. Procainamide is the drug of second or third choice (after lidocaine or amiodarone) in most coronary care units for the treatment of sustained ventricular arrhythmias associated with acute myocardial infarction. 

Quinidine has actions similar to those of procainamide it slows the upstroke of the action potential and conduction, and prolongs the QRS duration of the ECG, by blockade of sodium channels. The drug also prolongs the action potential duration by blockade of several potassium channels. Its toxic cardiac effects include excessive QT interval prolongation and induction of torsade de pointes arrhythmia. Toxic concentrations of quinidine also produce excessive sodium channel blockade with slowed conduction throughout the heart. 

Procainamide INa (primary) and IKr (secondary) blockade Slows conduction velocity and pacemaker rate prolongs action potential duration and dissociates from INa channel with intermediate kinetics direct depressant effects on sinoatrial (SA) and atrioventricular (AV) nodes Most atrial and ventricular arrhythmias drug of second choice for most sustained ventricular arrhythmias associated with acute myocardial infarction Oral, IV, IM eliminated by hepatic metabolism to /V-acetylprocainamide (NAPA see text) and renal elimination NAPA implicated in torsade de pointes in patients with renal failure Toxicity Hypotension long-term therapy produces reversible lupus-related symptoms... 

The cardiac arrhythmias are life-threatening, so the patient must be closely monitored, with facilities available for possible resuscitation. Drugs such as quinidine and procainamide are contraindicated, but lidocaine, propranolol, or phenytoin has been used safely and effectively. The arterial blood gas levels, pH, and electrolyte concentrations should be monitored so that metabolic acidosis or hypokalemia can be identified that would further aggravate the arrhythmias. Electrical pacing may be required if the antiarrhythmic drugs fail. Hyperpyrexia is treated by cooling. Seizures may be managed by intravenous doses of diazepam. 

Adverse effects With chronic use, procainamide causes a high incidence of side effects, including a reversible lupus erythe-matosus-like syndrome that develops in 25 to 30% of patients. Toxic concentrations of procainamide may cause asystole or induction of ventricular arrhythmias. Central nervious system (CNS) side effects include depression, hallucination and psychosis. With this drug, gastrointestinal intolerance is less frequent than with quinidine. 

Actions This Class IA drug shows actions similar to those of quinidine. Disopyramide [dye so PEER a mide] produces a negative inotropic effect that is greater than the weak effect exerted by quinidine and procainamide, and unlike the latter drugs, disopyramide causes peripheral vasoconstriction. The drug may produce a clinically important decrease in myocardial contractility in patients with preexisting impairment of left ventricular function. Disopyramide is used for treatment of ventricular arrhythmias as an alternative to procainamide or quinidine. 

PROPAFENONE I. ANTIARRHYTHMICS - disopyra-mide, procainamide 2. ANTIBIOTICS - macrolides (especially azithromycin, clarithromycin, parenteral erythromycin, telithromycin), quinolones (especially moxifloxacin), quinupristin/ dalfopristin 3. ANTICANCER AND IMMUNOMODULATING DRUGS -arsenic trioxide 4. ANTIDEPRESSANTS - TCAs, venlafaxine 5. ANTIEMETICS-dolasetron 6. ANTIFUNGALS-fluconazole, posaconazole, voriconazole 7. ANTIHISTAMINES - terfenadine, hydroxyzine, mizolastine 8. ANTI-M ALARIALS - artemether with lumefantrine, chloroquine, hydroxychloroquine, mefloquine, quinine 9. ANTIPROTOZOALS - pentamidine isetionate 10. ANTIPSYCHOTICS-atypicals, phenothiazines, pimozide II. BETA-BLOCKERS - sotalol 12. BRONCHODILATORS -parenteral bronchodilators 13. CNS STIMULANTS - atomoxetine Risk of ventricular arrhythmias, particularly torsades de pointes Additive effect these drugs prolong the Q-T interval. Also, amitriptyline, clomipramine and desipramine levels may be t by propafenone. Amitriptyline and clomipramine may t propafenone levels. Propafenone and these TCAs inhibit CYP2D6-mediated metabolism of each other Avoid co-administration... 

---