Quinidine

• Class IA antidysrhythmic agent

• Blocks cardiac sodium channels
• Decreases conduction velocity in atria and ventricles
• Depresses myocardial excitability and contractility (negative inotropic effect)
• Delays myocardial repolarization by blocking potassium channels
• Strong anticholinergic actions block vagal stimulation of AV node
• Widening of QRS and prolonged QT interval

Antidysrhythmic medication for:

• PAC's, PJC's, PVC's

• Paroxysmal atrial tachycardia
• Chronic ventricular tachycardia not associated with heart block

• Maintenance therapy post cardioversion for atrial fibrillation or atrial flutter

Long term suppression of supraventricular and ventricular dysrhythmias

• Onset: 1-3 hours (oral)
• Peak: (oral) 1 hour
• Half-Life: 6-8 hours
• Metabolism:  Metabolized in liver and excreted by kidneys

• Diarrhea, nausea, vomiting, abdominal pain
• Hypotension, widened QRS, bradycardia, heart blocks, torsades de pointes
• Cinchonism (nausea, vomiting, headache, dizziness, vertigo, tinnitis)
• Acute hemolytic anemia
• Anticholinergic effects (tachycardia, mydriasis, constipation, urinary retention)

• Cardiotoxicity:  widening of QRS (> 50%) and prolonged QT interval

• Hypersensitivity to quinine or cinchona derivatives
• Thrombocytopenic purpura 2ndary to previous quinidine exposure
• 2nd or 3rd degree AV block
• Thyrotoxicosis.
• Acute rheumatic fever
• Subacute bacterial endocarditis
• Extensive myocardial damage
• Severe left sided heart failure
• Hypotensive states
• Myasthenia gravis
• Digoxin toxicity
• Cautious use in impaired liver or kidney function
• Safety not established in pregnancy or lactation (Category C).

• Oral:  200-300 mg t.i.d. or q.i.d.
• Intravenous: 16 mg/min slow IV bolus until: 1) dysrhythmia is suppressed, 2) hypotension develops, 3) QRS widens > 50%
• IV Drip:  ≤ 16 mg/min diluted in D₅W or NS

• Drug Interactions:  1) Quinidine will increase digoxin serum levels; 2) Amiodarone and diltiazem will increase quinidine serum levels; 3) Anticholinergic drugs may enhance anticholinergic symptoms; 4) Reserpine and phenothiazines increase cardiac depressant effect; 5) Cholinergic agents may antagonize cardiac effects; 6) Anticonvulsants, barbiturates, and refampin will increase metabolism of quinidine; Antacids decrease renal elimination of quinidine; 7) Verapamil will potentiate the hypotensive effect of quinidine.
• Incompatibilities with intravenous infusion include amiodarone, atracurium, furosemide, and heparin.
• Check apical pulse, BP, and cardiac monitor prior to administration of quinidine.
• Monitor blood pressure, QRS duration, and QT interval frequently for patients receiving quinidine.  If QRS widens > 50%, notify physician.
• Serum quinidine levels should be between 2 – 5 mcg/ml.
• Take oral quinidine with a full glass of water on an empty stomach to enhance absorption.
• If GI symptoms occur, take quinidine with food.
• Quinidine is preferred over procainamide for long term suppression of dysrhythmias due to probability of SLE syndrome and blood dyscrasias.
• Obtain baseline cardiac rhythm strip, CBC, lab tests for liver and renal functions, and blood pressure.
• Quinidine will double digoxin serum levels, so digoxin doses will have to be reduced.  Monitor patient for digoxin toxicity.
• During conversion of atrial fibrillation, patient may develop thromboembolism (sudden chest pain, dyspnea, or CVA).