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Procainamide effects

If a rapid procainamide effect is needed, an intravenous loading dose of up to 12 mg/kg can be given at a rate of 0.3 mg/kg/min or less rapidly. This dose is followed by a maintenance dosage of 2-5 mg/min, with careful monitoring of plasma levels. The risk of gastrointestinal or cardiac toxicity rises at plasma concentrations greater than 8 mcg/mL or NAPA concentrations greater than 20 mcg/mL. [Pg.285]

If a rapid procainamide effect is needed, an intravenous loading dose of up to 12 mg/kg can be... [Pg.329]

Procainamide. Procainamide hydrochloride is a ben2amide, synthesized to prolong the therapeutic effects of the local anesthetic procaine [59-46-1] (13) (see Anesthetics). The dmg is effective in a wide range of supraventricular and ventricular arrhythmias (14). [Pg.113]

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). [Pg.114]

Further class IA drugs include the open state blockers procainamide and disopyramide with electrophysiolog-ical effects similar to those of quinidine procainamide lacks the antimuscarinic and antiadrenergic effects. Characteristic side effects of procainamide are hypotension and immunological disorders. [Pg.99]

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). [Pg.93]

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... [Pg.373]

When two antiarrhythmic dragp are administered concurrently the patient may experience additive effects and is at increased risk for drug toxicity. When quinidine and procainamide are administered with digitalis, tiie risk of digitalis toxicity is increased. Hiarmacologic effects of procainamide may be increased when procainamide is administered with quinidine When quinidine is administered with the barbiturates or cimetidine, quinidine serum levels may be increased. When quinidine is administered with verapamil, there is an increased risk of hypotensive effects. When quinidine is administered with disopyramide, there is an increased risk of increased disopyramide blood levels and/or decreased serum quinidine levels. [Pg.373]

Propranolol may increase procainamide plasma levels. Additive cholinergic effects may occur when procainamide is administered with other drugp with anticholinergic effects. There is the potential of additive cardiodepressant effects when procainamide is administered with lidocaine. When a beta blocker, such as Inderal, is administered with lidocaine, there is an increased risk of lidocaine toxicity. [Pg.373]

ADMINISTERING PROCAINAMIDE Adverse reactions with procainamide therapy include nausea, loss of appetite, and vomiting. Small meals eaten frequently may be better tolerated than three full meals. Administering the drug with meals may decrease gastrointestinal effects. [Pg.376]

Dantrolene is the mainstay of MH treatment. It has long been available for the treatment of muscle spasm in cerebral palsy and similar diseases. It is a hydantoin derivative that was first synthesized in 1967, and reported to be effective in the treatment of porcine MH in 1975. Also in 1975, dantrolene was shown to be more effective than procainamide in the treatment of human MH, which until that time was the drug of choice. However, the intravenous preparation was not made available until November 1979. It significantly lowered mortality. The half-life of dantrolene is estimated to be 6-8 hr. Dantrolene s primary mode of action is the reduction in calcium release by the sarcoplasmic reticulum. Dantrolene also exerts a primary antiarrhythmic effect by increasing atrial and ventricular refractory periods. Side effects of dentrolene include hepatotoxicity, muscle weakness, ataxia, blurred vision, slurred speech, nausea, and vomiting. Dantrolene is not contraindicated in pregnancy, but it does cross into breast milk and its effect on the neonate is unknown. [Pg.406]

Podrid PJ, Kowey PR, Frishman WF[, et al. Comparative cost-effectiveness analysis of quinidine, procainamide and mexiletine. Am J Cardiol 1991 68 1662-7. [Pg.589]

Procainamide (Class IA antiarrhythmic drug) is an effective agent for ventricular tachycardia. Its mechanism of action involves blockade of the fast Na+ channels responsible for phase 0 in the fast response tissue of the ventricles. Therefore, its effect is most pronounced in the Purkinje fibers. The effects of this drug s activity include a decrease in excitability of myocardial cells and in conduction velocity. Therefore, a decrease in the rate of the phase 0 upstroke and a prolonged repolarization are observed. As a result, duration of the action potential and the associated refractory period is prolonged and the heart rate is reduced. These effects are illustrated by an increase in the duration of the QRS complex. [Pg.176]

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. [Pg.121]

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. [Pg.125]

In symptomatic patients, medical therapy can be tailored either to control ventricular response or to restore sinus rhythm. Nondihydropyridine calcium antagonists (e.g., verapamil) are considered first-line drug therapy for decreasing ventricular response. Type I agents (e.g., procainamide, quinidine) are only occasionally effective in restoring sinus rhythm. DCC is ineffective, and /3-blockers are usually contraindicated because of coexisting severe pulmonary disease or uncompensated HF. [Pg.84]

Some xenobiotics may have divergent mechanisms of autoimmune responses. For example, hydralazine demonstrates adduct reactivity as well as inhibition of DNA methylation [68,73], while procainamide inhibits DNA methylation, forms immunogenic NPA, and disrupts clonal selection in the thymus [68, 72, 74], It is this complicated pattern of effects that makes assessment of autoimmune potential in the laboratory for new xenobiotics almost impossible. Animal models can sometimes be recreated to resemble human disease [74], and thus may be useful for therapy considerations, but are difficult to utilize for screening chemicals for hazard potential due to the diverse nature of autoimmunity mechanisms and physiological presentation. While evidence supports many different mechanisms for xenobiotic-induced autoimmune reactions, none have conclusively demonstrated the critical events necessary to lead to the development of autoimmune disease. Therefore, it is difficult to predict or identify xenobiotics that might possess the potential to elicit autoimmune disorders. [Pg.57]

Woosley, R.L. et al., Effect of acetylator phenotype on the rate at which procainamide induces antinuclear antibodies and the lupus syndrome, New Engl. J. Med., 298, 1157, 1978. [Pg.464]

The dog is a species that is frequently used in toxicity studies. However, there are few reports in the open literature on dog studies with respect to chemical- or drug-induced hypersensitivity reactions or autoimmune effects, and those that are available lack consistency. For instance, procainamide has been shown to induce lupus-like symptoms (mainly an increase of ANA) in one study [63], but not in another study with younger dogs [64], Similar discrepancies have been observed for hydralazine-induced effects in dogs [5],... [Pg.477]

The place of the dmg in dentistry [153 4] and in electro-convulsive therapy [ 154] (with a description of a technique to surmount difficulties arising from the concurrent use ot suxamethonium) has been evaluated. A refined radio telemetric technique has enabled a detailed study [155] of the cardiovascular effects of propanidid to be made, resulting in strong evidence for a transient procainamide- or quinidine-like depression of myocardial conductive tissue. The above publications [150-5] quote a large number of relevant references. [Pg.22]

Kll. Koch-Weser, J., and Klein, S. W., Procainamide dosage schedules, plasma concentrations, and clinical effects. J. Amer. Med. Ass. 215, 1464-1460 (1971). [Pg.100]

The chemical difference between procainamide and procaine lies in the replacement of the ester group with an amide gronp. The action of procainamide is qualitatively similar to the action of procaine. Its effect on the heart is identical to that of quinidine. As an antiar-rhythmic, procainamide is preferred over procaine because unlike procaine, it is better absorbed when taken orally and it is more difficult for the esterases of the plasma to hydrolyze it, which results in long-lasting action. [Pg.247]

Pharmacology Procainamide, a class lA antiarrhythmic, increases the effective refractory period of the atria, and to a lesser extent the bundle of His-Purkinje system and ventricles of the heart. [Pg.431]

Renai insufficiency Renal insufficiency may lead to accumulation of high plasma levels from conventional oral doses of procainamide, with effects similar to those of overdosage unless dosage is adjusted for the individual patient. [Pg.434]


See other pages where Procainamide effects is mentioned: [Pg.14]    [Pg.403]    [Pg.1422]    [Pg.478]    [Pg.121]    [Pg.121]    [Pg.66]    [Pg.77]    [Pg.109]    [Pg.134]    [Pg.33]    [Pg.84]    [Pg.246]    [Pg.433]    [Pg.433]    [Pg.435]    [Pg.9]    [Pg.10]    [Pg.11]    [Pg.22]    [Pg.28]    [Pg.29]    [Pg.32]    [Pg.62]    [Pg.67]    [Pg.73]   
See also in sourсe #XX -- [ Pg.167 ]




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