Adult: As quinidine gluconate: 800 mg via slow infusion at an initial rate of up to 0.25 mg/kg/min. Discontinue treatment if conversion to sinus rhythm has not occurred after reaching max dose. Max: 10 mg/kg.
Adult: As quinidine gluconate: Loading: 24 mg/kg via infusion over 4 hr. Maintenance: 12 mg/kg via intermittent infusion over 4 hr 8 hrly (starting 8 hr after the beginning of loading dose) until 3 maintenance doses, until parasitaemia is reduced to ≤1%, and oral therapy can be used. Alternatively, a loading dose of 10 mg/kg via infusion over 1-2 hr. Maintenance: 0.02 mg/kg/min via continuous infusion for at least 24 hr, until parasitaemia is reduced to ≤1%, and oral therapy can be used.
Oral Conversion of atrial fibrillation
Adult: As conventional quinidine sulfate: Initially, 400 mg 6 hrly, may cautiously increase if conversion is not achieved after 4 or 5 doses. As extended-release quinidine sulfate: Initially, 300 mg 8-12 hrly, may cautiously increase to desired effect. As extended-release quinidine gluconate: Initially, 648 mg 8 hrly, may cautiously increase if conversion is not achieved after 3 or 4 doses.
Oral Uncomplicated falciparum malaria
Adult: As quinidine sulfate: 300-600 mg or 10 mg/kg 8 hrly for 5-7 days.
Oral Atrial fibrillation relapse reduction
Adult: As conventional quinidine sulfate: Initially, 200 mg 6 hrly. As extended-release quinidine sulfate: Initially, 300 mg 8-12 hrly. As extended-release quinidine gluconate: Initially, 324 mg 8-12 hrly. Doses may be cautiously increased to desired effect.
Reduce dose by 25%.
Should be taken with food. Best taken at meal times.
Atrial fibrillation and flutter: Dilute a vial labelled as containing 80 mg/mL in 40 mL of dextrose 5% to provide a soln containing 16 mg/mL. Malaria: Dilute loading dose in 250 mL (intermittent) or approx 5 mL/kg (continuous) of NaCl 0.9% inj.
Y-site: Incompatible w/ furosemide.
Complete AV block (w/o functional pacemaker), myasthenia gravis, history of quinidine/quinine-associated thrombocytopenic purpura.
Patient w/ 2nd degree AV block (w/o functional pacemaker), digitalis intoxication, severe intraventricular conduction defect, prolonged QT interval or history of torsades de pointes, myocarditis, uncompensated heart failure, severe myocardial damage, pre-existing asthma, muscle weakness, infection w/ fever. Renal and hepatic impairment. Pregnancy and lactation.
Monitor cardiac function including BP and ECG (during IV admin), CBC, liver and renal function tests regularly during long-term admin.
Symptoms: Resp depression or distress, ataxia, apnoea, severe hypotension, syncope, diarrhoea, vomiting, anuria, absence of P waves, PR and QT interval, and QRS complex broadening, extrasystoles, ventricular arrhythmias, heart block, heart failure, coma, irritability, lethargy, thrashing, hallucinations, twitching, paraesthesia, generalised seizures, signs of cinchonism. Management: Symptomatic treatment. Monitor ECG and BP. Perform gastric lavage, induce emesis, or administer activated charcoal for recent ingestion. May require artificial resp or other supportive measures.
Reduced renal clearance w/ drugs that alkalinise the urine (e.g. carbonic-anhydrase inhibitors, Na bicarbonate, thiazide diuretics). Increased plasma levels w/ cimetidine, amiodarone, ketoconazole, verapamil. Decreased plasma levels w/ nifedipine. Increased hepatic elimination w/ rifampicin, phenytoin, phenobarbital. Potentiates the action of depolarising (e.g. suxamethonium) and nondepolarising (e.g. pancuronium) neuromuscular blocking agents, and warfarin. May increase plasma levels of digoxin, haloperidol, procainamide.
Grapefruit juice may delay absorption and inhibit metabolism of quinidine.
Description: Quinidine is a class Ia antiarrhythmic w/ antimuscarinic and α-adrenoceptor blocking activities. It depresses phase O of the action potential, and reduces Na influx during depolarisation and K efflux in repolarisation, thereby decreasing myocardial excitability and conduction velocity, and myocardial contractility. It also decreases Ca transport across cell membrane. Pharmacokinetics: Absorption: Rapidly absorbed from the GI tract. Bioavailability: 45-100% (as sulfate); 70-80% (as gluconate). Time to peak plasma concentration: 2 hr (as sulfate); 3-6 hr (as gluconate). Distribution: Widely distributed throughout the body; crosses the placenta and enters breast milk. Volume of distribution: 2-3 L/kg. Plasma protein binding: 80-90% mainly to α1-acid glycoprotein. Metabolism: Extensively metabolised hepatically via CYP3A4 enzyme to inactive metabolites; undergoes first-pass metabolism. Excretion: Via urine (15-25% as unchanged drug). Elimination half-life: Approx 6-8 hr.
Anon. Quinidine. Lexicomp Online. Hudson, Ohio. Wolters Kluwer Clinical Drug Information, Inc. https://online.lexi.com. Accessed 09/02/2016.Buckingham R (ed). Quinidine. Martindale: The Complete Drug Reference [online]. London. Pharmaceutical Press. https://www.medicinescomplete.com. Accessed 09/02/2016.McEvoy GK, Snow EK, Miller J et al (eds). Quinidine Gluconate, Quinidine Sulfate. AHFS Drug Information (AHFS DI) [online]. American Society of Health-System Pharmacists (ASHP). https://www.medicinescomplete.com. Accessed 09/02/2016.Quinidine Gluconate Solution (Eli Lilly and Company). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed/. Accessed 09/02/2016.Quinidine Gluconate Tablet, Extended Release (Watson Laboratories, Inc.). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed/. Accessed 09/02/2016.Quinidine Sulfate Tablet (Watson Laboratories, Inc.). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed/. Accessed 09/02/2016.