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Antiarrhythmic drugs side effects

The antiepileptic drug phenytoin, an orally available class DB antiarrhythmic, is mainly effective in digitalis-induced arrhythmias. This diug exhibits nonlinear pharmacokinetics and a number of side effects including neuropathy, gingival hypetplasia, hepatitis, immunological disorders and suppression of white blood cells. [Pg.99]

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]

The use of antiarrhythmic drugs in the United States is declining because of major trials that showed increased mortality with their use in several clinical situations, the realization of proarrhythmia as a significant side effect, and the advancing technology of nondrug therapies such as ablation and the implantable cardioverter-defibrillator (ICD). [Pg.76]

Central Motor restlessness, progressing to maniacal agitation, psychic disturbances, disorientation, and hallucinations. Elderly subjects are more sensitive to such central effects, in this context, the diversity of drugs producing atropine-like side effects should be borne in mind e.g., tricyclic antidepressants, neuroleptics, antihistamines, antiarrhythmics, antiparkinsonian agents. [Pg.106]

Drugs that may increase the effects or side effects of bupropion include levodopa, MAOIs, ritonavir, antidepressants, antipsychotics, beta blockers, type 1C antiarrhythmics. [Pg.1339]

Hi-receptor but also at muscarinic cholinoceptors, serotonin receptors, and adrenoceptors. This explains the atropine-like side effects of those drugs. The cationic amphophilic structure of these substances resemble that of antiarrhythmic agents which might explain the arrhythmogenic properties seen with some of these Hi-antagonists. [Pg.313]

Amiodarone may elicit life-threatening side effects in addition to presenting substantial management difh-culties associated with its use. The oral formulation of amiodarone is indicated only for the treatment of life-threatening recurrent ventricular arrhythmias (e.g., recurrent ventricular hbrillation and/or recurrent hemo-dynamicaUy unstable ventricular tachycardia) that have not responded to other potentially effective antiarrhythmic drugs or when alternative interventions could not be tolerated. Despite its efficacy as an antiarrhythmic agent, there is no evidence from clinical trials that the use of amiodarone favorably affects survival. [Pg.187]

Sparteine, lupanine, and other QA exhibit antiarrhythmic properties. Since only sparteine can be isolated easily from broom (Cytisus scoparius) it is the only lupin alkaloid that is commercially available and exploited in medicine as an antiarrhythmic drug. However, about 10% of all patients are unable to metabolize sparteine and suffer from sparteine intoxication. Because of these side effects and the availability of more reliable synthetic heart drugs, the use of sparteine in... [Pg.207]

Correct answer = A. A bidirectional block can decrease arrhythmias caused by reentry. All antiarrhythmic drugs exert some negative inotropic effect and decrease cardiac output. The i side effects of this group of drugs are serious and include arrhythmias that can lead to sudden death. Some antiarrhythmic drugs affect K+ or Ca++ channels, or p adrenoreceptors. [Pg.185]

NITRATES 1. ANALGESICS-nefopam 2. ANTIARRHYTHMICS -disopyramide, propafenone 3. ANTIDEPRESSANTS-TCAs 4. ANTI EMETICS-cydizine 5. ANTIHISTAMINES -chlorphenamine, cyproheptadine, hydroxyzine 6. ANTIMUSCARINICS -atropine, benzatropine, cydopentolate, dicydover-ine, flavoxate, homat-ropine, hyoscine, orphenadrine, oxybutynin, procyclidine, propantheline, tolterodine, trihexyphenidyl, tropicamide. 7. ANTI-PARKINSON S DRUGS-dopaminergics 8. ANTI-PSYCHOTICS - pheno-thiazines, clozapine, pimozide 9. MUSCLE RELAXANTS-baclofen 1. t risk of antimuscarinic side-effects when isosorbide dinitrate is co-administered with these drugs 2. 1 efficacy of sublingual nitrate tablets... [Pg.131]

Interestingly, the secondary effects of enantiomers may be masked by the presence of their antipodes and only surface after the therapeutic and toxicity properties of the enantiomers are compared with their respective racemate. For example, enantiomers of disopyramide illicit equal antiarrhythmic effects, but the S enantiomer possesses a greater extent of anticholinergic side-effects (12). Intuitively, a formulation composed of the R enantiomer would seem to be a safer alternative. However, it appears that the single enantiomer of disopyramide possesses additional side-effects that are minimal after administration of the racemic drug. [Pg.377]

Singh BN. Side effects of antiarrhythmic drugs. Pharmacol Ther 1977 2 151. [Pg.272]

Regardless of the method for choosing long-term therapy, chronic antiarrhythmic drug treatment in these often young, otherwise healthy patients is problematic. Besides the necessity of taking daily medication possibly for life, antiarrhythmic drugs are not weU tolerated, sometimes precipitate severe side effects, and commonly... [Pg.339]


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See also in sourсe #XX -- [ Pg.67 ]

See also in sourсe #XX -- [ Pg.67 ]




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