A 22-year-old woman with systemic lupus erythematosus complicated by mild renal insufficiency and severe systemic hypertension inadvertently received an excessive amount of clonidine hydrochloride. In association with a presumed toxic level of clonidine in the serum, the patient developed abnormalities of cardiac conduction, including 2:1 atrioventricular block, complete heart block, 3:2 Wenckebach block, and first-degree atrioventricular block. The transient nature of these abnormalities, with the return of normal conduction upon the cessation of therapy with clonidine, implicates this drug as being capable of producing high-grade atrioventricular block at toxic levels.
