A medication that acts as a class I antiarrhythmic agent in the heart.



It is a stereoisomer of quinine, originally derived from the bark of the cinchona tree. 



It causes increased action potential duration, as well as a prolonged QT interval.



Pregnancy category US: C (Risk not ruled out).



Routes of administration-oral , intramuscular injection, intravenous.



Bioavailability 70–85%



Metabolism 50–90% by liver.



Elimination half-life 6–8 hours



Excretion by the liver.



20% as unchanged in the urine



It is occasionally used as a class I antiarrhythmic agent to prevent ventricular arrhythmias, particularly in Brugada Syndrome, although its safety in this indication is uncertain.



Quinidine reduces the recurrence of atrial fibrillation after patients undergo cardioversion, but has proarrhythmic effects suggest that it may lead to an overall increased mortality in these patients.



Quinidine is also used to treat short QT syndrome.



Manufacture of parenteral quinidine gluconate in the US has been discontinued.



A study  that has shown that a combination of dextromethorphan and quinidine alleviates symptoms of easy laughing and crying  in pseudobulbar affect in patients with amyotrophic lateral sclerosis and multiple sclerosis.



Quinidine is also an inhibitor of the cytochrome P450 enzyme 2D6.



It  can lead to increased blood levels of lidocaine, beta blockers, opioids, and some antidepressants. 



It also inhibits the transport protein P-glycoprotein and can cause peripherally acting drugs such as loperamide to have central nervous system side effects, such as respiratory depression.



It can cause thrombocytopenia, granulomatous hepatitis, myasthenia gravis, and torsades de pointes.



Thrombocytopenia  induced by quinidine is mediated by the immune system, and may lead to thrombocytic purpura.



Quinidine intoxication can lead to cinchonism, with tinnitus being among the most characteristic and common symptoms.



It acts as a blocker of voltage-gated sodium channels: Inhibition of the Nav1.5 channel is involved in its antiarrhythmic effects as a class I antiarrhythmic agent.



Quinidine blocks voltage-gated potassium channels acts as an antimuscarinic and alpha-1 blocker,and is an antimalarial.



As a class I antiarrhythmic agent, it primarily works by blocking the fast inward sodium current.



At higher heart rates, its block increases, while at lower heart rates, the block decreases. 



By blocking the fast inward sodium current the fast inward sodium current causes the phase 0 depolarization of the cardiac action potential to decrease.



As an electrolyte dependent agent it also increases action potentials and prolongs the QT interval. 



At micromolar concentrations, quinidine inhibits Na+/K+-ATPase by binding to the same receptor sites as the digitalis glycosides.



ECG additional effects include: a wide notched P wave, wide QRS complex, depressed ST segment, and U waves due to of both slowed depolarization and repolarization.



The elimination half-life of oral quinidine is 6 to 8 hours.



It is metabolized by the cytochrome P450 system in the liver. 



About 20% of quarantine is excreted unchanged by the kidneys.






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