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Quinidine dosing

Quinidine is 70-80% bioavailable following oral administration. It is 80% bound to albumin and a i-acid glycoprotein. It is eliminated primarily by hepatic metabolism. The principal metabolite, 3-hydroxy quinidine is biologically active with half the activity of the parent compound. Twenty percent of the quinidine dose appears in the unchanged form in the urine. The elimination half-life is 6-8 hours. Quinidine is usually administered in a slow release formulation, eg, that of the gluconate salt. [Pg.328]

Quinidine Therapeutic drug monitoring recommended may require quinidine dose increase. [Pg.2029]

A man with sustained ventricular tachycardia taking high-dose intravenous procainamide 2 g every 8 hours had a 70% increase in his steady-state plasma procainamide levels, from 9.1 to 15.4 nanograms/mL, when he also took quinidine gluconate 324 mg every 8 hours. The procainamide half-life increased from 3.7 to 7.2 hours and its clearance fell from 27 to 16 L/hour. His QTc interval increased from 648 to 678 milliseconds. In another study in patients with ventricular arrhythmias, quinidine was combined with procainamide. The doses were adjusted based in part on the QT interval. The QTc interval was longer with the combination (499 milliseconds) than each drug alone (quinidine 470 milliseconds, procainamide 460 milliseconds) despite using reduced doses in the combination (mean quinidine dose reduced by 28% mean procainamide dose reduced by 32%) ... [Pg.273]

As found in commerce, the cinchona alkaloids are not necessarily pure quinidine, for example, may contain up to 30 per cent, of dihydroquinidine. Working with carefully pmdfied specimens of the four chief cinchona alkaloids and their dihydro-derivatives, Buttle, Henry and Trevan found the results recorded in the table (p. 471) in tests with malaria in canaries. The figures in brackets represent the dose of quinine necessary to produce the same degree of protection as unit dose of the alkaloid named. To the results are also added the data found later by the same authors, with Solomon and Gibbs, for some of the transformation products (p. 449) of quinine and quinidine. The Roman numeral at the head of each column refers to the type formula on p. 470. [Pg.472]

ADM INI STERI NG DISOPYRAMID E Disopyramide is administered to tiie patient with a full glass of water either 1 hour before or 2 hours after meals. If patients are receiving procainamide or quinidine tiie manufacturer suggests that disopyramide therapy not be started for 6 to 12 hours after tiie last dose of quinidine and 3 to 6 hours after tiie last dose of procainamide When tiie patient is to switch from taking tiie regular capsules to taking extended-release capsules, 6 hours should lapse after tiie last capsule before therapy is begun with tiie extended-release capsules. [Pg.375]

Decrease loading dose in end stage renal disease uncontrolled hypothyroidism, or patients on quinidine by 30-50%... [Pg.13]

Propranolol (at high doses) has been noted to have quinidine-like activity. [Pg.39]

Antacids also have clinically significant drug interactions with tetracycline, ferrous sulfate, isoniazid, quinidine, sul-fonylureas, and quinolone antibiotics. Antacid-drug interactions are influenced by antacid composition, dose, dosage schedule, and formulation. [Pg.263]

The loading dose of quinidine should be omitted in those patients who have received quinine or mefloquine. [Pg.1148]

Maintenance dose 0.125-0.25 mg PO/IV qd low potassium or magnesium levels potentiate toxicity reduce dose in renal failure toxicity indicated by nausea, headache, visual disturbances (yellow-green halos), ventricular arrhythmias. Quinidine, verapamil, and amiodarone elevate digoxin level. [Pg.19]

Preliminary studies [241, 249, 250] of the cardiovascular and sympatholytic properties of prenylamine demonstrated that coronary blood flow and oxygenation could be increased under experimental conditions (in dogs) and that the drug interacted in complex fashion with sympathetically innervated organs, but the picture presented was someudiat confused because of the many uncontrolled variables and limitations of the actual techniques used. Anti-arrhythmic activity of potency comparable with that of quinidine, plus local anaesthetic properties, were also demonstrated [251] but the same worker was notable to reproduce these effects in intact live animals with any consistency. Large doses of the drug actually provoked cardiac fibrillation in some cases. [Pg.32]

Test dose Administer a single 200 mg tablet of quinidine sulfate or 200 mg IM quinidine gluconate to determine whether the patient has an idiosyncratic reaction. Adjust the dosage to maintain plasma concentration between 2 to 6 mcg/mL. [Pg.422]

IM- n the treatment of acute tachycardia, the initial dose is 600 mg quinidine gluconate. Subsequently, 400 mg quinidine gluconate can be repeated as often as every 2 hours. [Pg.422]

IV (quinidine gluconate) - 2 to 10 mg/kg/dose every 3 to 6 hours as needed however, this route is not recommended. [Pg.423]

Metabolism/Excretion - From 60% to 80% of a dose is metabolized via the liver into several metabolites. Quinidine is excreted unchanged (10% to 50%) in the urine within 24 hours. The elimination half-life ranges from 4 to 10 hours in healthy patients, with a mean of 6 to 7 hours. Urinary acidification facilitates quinidine elimination, and alkalinization retards it. In patients with cirrhosis, the elimination half-life may be prolonged and the volume of distribution increased. [Pg.424]

Transfer to disopyramide Use the regular maintenance schedule, without a loading dose, 6 to 12 hours after the last dose of quinidine or 3 to 6 hours after the last dose of procainamide. Where withdrawal of quinidine or procainamide is likely to produce life-threatening arrhythmias, consider hospitalization. [Pg.438]

Concomitant use with potential CYP2D6 inhibitors - During coadministration of potential CYP2D6 inhibitors such as quinidine, fluoxetine, or paroxetine with aripiprazole, reduce the aripiprazole dose to at least one-half of its normal dose. [Pg.1129]

Uses HTN, stable or unstable angina Action CCB relaxes coronary vascular smooth muscle Dose 2.5-10 mg/d PO -1- w/ h atic impair Caution [C, ] Disp Tabs SE Peripheral edema, HA, palpitations, flushing Interactions t Effect of hypotension M7 antih5rpCTtensives, fentanyl, nitrates, quinidine, EtOH, grapefruit juice t risk of neurotox W/Li -1- effects W/ NSAIDs EMS Concurrent EtOH and... [Pg.73]


See other pages where Quinidine dosing is mentioned: [Pg.664]    [Pg.276]    [Pg.283]    [Pg.936]    [Pg.664]    [Pg.276]    [Pg.283]    [Pg.936]    [Pg.112]    [Pg.196]    [Pg.176]    [Pg.371]    [Pg.376]    [Pg.574]    [Pg.1148]    [Pg.1148]    [Pg.1148]    [Pg.154]    [Pg.334]    [Pg.197]    [Pg.423]    [Pg.764]    [Pg.9]    [Pg.11]    [Pg.12]    [Pg.12]    [Pg.19]    [Pg.22]    [Pg.29]    [Pg.29]    [Pg.32]    [Pg.33]    [Pg.62]    [Pg.73]    [Pg.74]    [Pg.81]   
See also in sourсe #XX -- [ Pg.330 ]




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Quinidin

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