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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 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 6-8 hours.
There are no significant active metabolites, and toxicity is invariably
observed when concentrations are >7.0 ug/mL. Symptoms of
toxicity include cinchonism, and A-V node block. Gastrointestinal
distress is a frequent side effect, which becomes more severe and is
associated with nausea and vomiting at higher blood concentrations.
Physiologic processes that generally reduce quinidine metabolism and
clearance increase the blood concentration. Coadministration of drugs
that activate the cytochrome oxidase enzymes enhance clearance
resulting in lower blood concentrations. While digoxin coadministration
does not affect quinidine concentration, quinidine does reduce digoxin
clearance.
Therapeutic concentration: 2.0-5.0 mcg/mL
Toxic concentration: > or =7.0 mcg/mL
Optimal response to quinidine occurs when the serum level is between
2.0 and 5.0 ug/mL.
No significant cautionary statements.
1. Valdes Jr R, Jortani S, Gheordhiade M: Standards of laboratory
practice: cardiac drug monitoring. Clin Chem 1998 May;44(5):
1096-1109
2. Grace A, Camm AJ: Therapy, Quinidine. New Engl J Med
1998 Jan 1;338(1):35-45
3. Krishna S, White NJ: Pharmacokinetics of quinine, chloroquine,
and amodiaquine. Clinical Implications. Clin Pharmacokinet
1996 Apr;30(4):263-299