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Assessing and adjusting dosage for optimal therapeutic
level
Assessing toxicity
Quinidine is indicated in the treatment of premature atrial and ventricular
contractions, paroxysmal atrial tachycardia, paroxysmal atrioventricular
(A-V) junctional rhythm, and atrial flutter. Quinidine is contraindicated in
A-V block and in digitalis-induced A-V conduction disorders.
The dose of quinidine required to achieve optimally effective serum
concentrations is highly variable (in the range of 2.0-5.0 ug/mL).
Quinidine is 70% protein bound in plasma with a volume of
distribution of 2.7 L/kg. It undergoes renal clearance at a rate of
5 mL/min/kg with an elimination half-life of 6 to 8 hours.
There are no significant active metabolites, and toxicity is invariably
observed when concentrations are > or =7.0 ug/mL. Symptoms of toxicity
include cinchonism, tinnitus, light-headedness, premature ventricular
contractions, and A-V node block. Gastrointestinal distress is a
frequent side effect. It becomes more severe and is associated with
nausea and vomiting at higher blood concentrations.
Physiologic processes that generally reduce metabolism and
clearance increase the blood concentration of quinidine.
Co-administration of drugs that activate the cytochrome oxidase
enzymes enhance clearance resulting in lower blood concentrations.
While digoxin co-administration does not affect quinidine
concentration, quinidine does reduce digoxin clearance.
Therapeutic concentration: 2.0-5.0 ug/mL
Toxic concentration: > or =7.0 ug/mL
Optimal response to quinidine occurs when the serum level is between
2.0 ug/mL to 5.0 ug/mL.
No significant cautionary statements
Ochs HR, Greenblatt DJ, Woo E: Clinical Pharmacokinetics of quinidine.
Clin Pharmacokinet 1980;5:150-168