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Flecainide adverse effects

Administration with amiodarone When flecainide is given in the presence of amiodarone, reduce the usual flecainide dose by 50% and monitor the patient closely for adverse effects. Plasma level monitoring is strongly recommended to guide dosage with such combination therapy. [Pg.458]

Cardiac conduction Flecainide slows cardiac conduction in most patients to produce dose-related increases in PR, QRS, and QT intervals. The degree of lengthening of PR and QRS intervals does not predict either efficacy or the development of cardiac adverse effects. Patients may develop new first-degree AV heart block. Use caution and consider dose reductions. The JT interval (QT minus QRS) only widens approximately 4% on the average. Rare cases of torsade de pointes-type arrhythmias have occurred. [Pg.460]

These are class IC drugs with similar pharmacological profiles and with the same indication range and adverse effects. They are mainly used for the treatment of severe, lifethreatening ventricular tachyarrhythmias, and non-sustained ventricular tachycardia or high-frequency premature ventricular beats. The main adverse effects are cardiovascular, including proarrhythmic actions and severe negative inotropic effects, especially in patients with impaired cardiac function. Both flecainide and encainide increase the risk of sudden death in patients with myocardial infarction and asymptomatic unsustained ventricular arrhythmias. [Pg.160]

Propafenone has some structural similarities to propranolol and possesses weak 3-blocking activity. Its spectrum of action is very similar to that of quinidine, but it does not prolong the action potential. Its sodium channel-blocking kinetics are similar to that of flecainide. Propafenone is metabolized in the liver, with an average half-life of 5-7 hours. The usual daily dosage of propafenone is 450-900 mg in three divided doses. The drug is used primarily for supraventricular arrhythmias. The most common adverse effects are a metallic taste and constipation arrhythmia exacerbation can also occur. [Pg.289]

T effects OF amiodarone, astemizole, atorvastadn, barbiturates, bepridil, bupropion, cerivastatin, cisapride, clorazepate, clozapine, clarithromycin, desipramine, diazepam, encainide, ergot alkaloids, estazolam, flecainide, flurazepam, indinavir, ketoconazole, lovastatin, meperidine, midazolam, nelfinavir, phenytoin, pimozide, piroxicam, propafenone, propoxyphene, quinidine, rifabutin, saquinavir, sildenafil, simvastatin, SSRIs, TCAs, terfenadine, triazolam, troleandomycin, zolpidem X effects W/ barbiturates, carbamazepine, phenytoin, rifabutin, rifampin, St. John s wort, tobacco X effects OF didanosine, hypnotics, methadone, OCPs, sedatives, theophylline, warfarin EMS T Effects of amiodarone, diazepam, midazolam and BBs, may need X- doses concurrent use of Viagra-type drugs can lead to hypotension X- effects of warfarin concurrent EtOH use can T adverse effects T glucose ODs May cause an extension of adverse SEs symptomatic and supportive Rivasrigmine (Exelon) [Cholinesterase Inhibitor/Anri ... [Pg.277]

Adverse effects Flecainide can cause dizziness, blurred vision, headache, and nausea. Like other Class IC drugs, flecainide can aggravate preexisting arrhythmias or induce life-threatening ventricular tachycardia that is resistant to treatment (see p. 166). [Pg.181]

CIMETIDINE, RANITIDINE ANTIARRHYTHMICS-AMIODARONE, FLECAINIDE, MEXILETINE, PROCAINAMIDE, PROPAFENONE Likely t plasma concentrations of these antiarrhythmics and risk of adverse effects Cimetidine inhibits CYP2D6-mediated metabolism of flecainide, mexiletine, procainamide and propafenone. Ranitidine is a much weaker CYP2D6 inhibitor. Cimetidine is a potent inhibitor of organic cation transport in the kidney, and the elimination of procainamide is impaired Monitor PR and BP at least weekly until stable. Warn patients to report symptoms of hypotension (lightheadedness, dizziness on standing, etc.). Consider alternative acid suppression therapy... [Pg.638]

Antidysrhythmic dmgs can themselves cause cardiac dysrhythmias, their major adverse effect. The risk of antidysrhythmic-induced cardiac dysrhythmias (prodys-rhythmic effects) has been estimated at about 11-13% in non-invasive studies (18,19) and at up to 20% in invasive electrophysiological studies. However, the risk varies from dmg to drug and is particularly low with class III drugs. In one study the quoted risks of dysrhythmias were flecainide 30%, quinidine 18%, propafenone 7%, sotalol 6%, and amiodar-one 0% (20). However, amiodarone does cause dysrhythmias, especially when the QT interval is over 600 ms. [Pg.269]

Flecainide is a class Ic antidysrhythmic drug. Its clinical pharmacology, clinical use, and adverse effects have been reviewed (1-3). [Pg.1370]

Table 1 Numbers %) of cardiac and non-cardiac adverse effects of flecainide in a meta-analysis of 4375 treatment courses compared with 1818 treatment courses in controls... Table 1 Numbers %) of cardiac and non-cardiac adverse effects of flecainide in a meta-analysis of 4375 treatment courses compared with 1818 treatment courses in controls...
In a review of 60 original articles detailing 1835 courses of intravenous and/or oral flecainide in both placebo-controlled and comparative studies as well as a large number of uncontrolled studies, unwanted cardiac events occurred in 8% of patients (7). The cardiac events were hypotension (1.3%), heart failure (0.4%), sinus node dysfunction (1.6%), bundle branch block (1.0%), atrial dysrhythmias (1.6%), and ventricular dysrhythmias (1.3%). However, in 8505 patients, 5507 of whom were administered flecainide for more than 4 weeks and most of whom took dosages of 100-300 mg/day, cardiac adverse effects occurred in only about 2% and non-cardiac effects in... [Pg.1371]

In the wake of the preliminary and final reports of the Cardiac Arrhjflhmia Suppression Trial (CAST) (9,10), which showed that there was an increased risk of death among patients who took encainide and flecainide after myocardial infarction, there have been many publications in which the implications of these findings have been thoroughly discussed (11-15). The relative risk of death or cardiac arrest due to dysrhjflhmias in the treated patients was 2.6 and the relative risk due to aU causes was 2.4. The risk of non-fatal cardiac adverse effects was no different in treated patients from that in those taking placebo and there was no difference between the groups in the use of other drugs. [Pg.1371]

The most common non-cardiac adverse effects of flecainide are on the central nervous system and include dizziness, drowsiness, visual disturbances, headache, nausea, paresthesia, nervousness, and tremor. The incidence of these adverse effects has varied widely (38,39). [Pg.1372]

Flecainide is occasionally used to treat fetal cardiac dysrhythmias by administration to the mother (50,51), although occasionally it can cause adverse effects in the child (SEDA-25,184) and in the mother (52). [Pg.1373]

Reports of the use of flecainide in children suggest that the risk of adverse effects is low, although these studies have been very small (54-56). [Pg.1373]

Flecainide half-life is prolonged in poor hydroxylators (59) and poor metabolizers may be at an increased risk of adverse effects. [Pg.1373]

Gentzkow GD, Sullivan JY. Extracardiac adverse effects of flecainide. Am J Cardiol 1984 53(5) B101-5. [Pg.1375]

Adverse effects of flecainide are nausea, vomiting and precipitation of arrythmias. [Pg.67]

Flecainide produces few subjective complaints in most patients dose-related blurred vision is the most common noncardiac adverse effect. It can exacerbate CHF in patients with depressed left-ventricular performance. The most serious adverse effects are provocation or exacerbation of potentially lethal arrhythmias. These include acceleration of ventricular rate in patients with atrial flutter, increased frequency of episodes of reentrant ventricular tachycardia, and increased mortality in patients convalescing from myocardial infarction. [Pg.273]

An established interaction, but the documentation is limited. Reduce the flecainide dosage by one-fhird to one-half if amiodarone is added. The manufacturers of flecainide recommend a 50% reduction in dose if amiodarone is given, and advise that adverse effects and plasma flecainide levels should be monitored. There seems to be no need to treat extensive metabolisers differently from poor metabolisers. Remember that the interaction may take 2 weeks or more to develop fully, and also that amiodarone is cleared from the body exceptionally slowly so that this interaction may persist for some weeks after it has been withdrawn. [Pg.258]

Alboni P, Botto GL, Boriani G, Russo G, Pacchioni F, lori M, Pasanisi G, Mancini M, Mariconti B, Capucci A. Intravenous administration of flecainide or propafenone in patients with recent-onset atrial fibrillation does not predict adverse effects during pill-in-the-pocket treatment. Heart 2010 96(7) 546-9. [Pg.302]

Skin There have been several reports of various cutaneous adverse effects of flecainide, such as urticaria, flushing, pruritus, and psoriasis. There has now been a report of a fixed drug eruption [65... [Pg.387]

Once the arrhythmia is controlled, it may be possible to reduce the dose, as necessary, to minimize side effects or effects on conduction. PSVT and PAF The recommended starting dose is 50 mg every 12 hours. Doses may be increased in increments of 50 mg twice daily every 4 days until efficacy is achieved. For PAF patients, a substantial increase in efficacy without a substantial increase in discontinuation for adverse experiences may be achieved by increasing the flecainide dose from 50 to 100 mg twice/day. The maximum recommended dose for patients with paroxysmal supraventricular arrhythmias is 300 mg/day. [Pg.457]


See other pages where Flecainide adverse effects is mentioned: [Pg.109]    [Pg.277]    [Pg.604]    [Pg.304]    [Pg.192]    [Pg.281]    [Pg.149]    [Pg.740]    [Pg.1370]    [Pg.1371]    [Pg.1371]    [Pg.1372]    [Pg.2941]    [Pg.347]    [Pg.597]    [Pg.600]    [Pg.304]    [Pg.358]    [Pg.1090]    [Pg.143]    [Pg.305]    [Pg.608]    [Pg.275]   
See also in sourсe #XX -- [ Pg.40 , Pg.119 ]

See also in sourсe #XX -- [ Pg.328 , Pg.328 ]

See also in sourсe #XX -- [ Pg.598 ]




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