The purpose of this study was to determine whether physiologic doses of
epinephrine reverse the electrophysiologic effects of
quinidine in patients with an accessory atrioventricular (AV) connection. Eighteen patients with an accessory AV connection who had inducible sustained orthodromic
tachycardia underwent an electrophysiologic study in the baseline state and after at least 2 days of treatment with 1.4 to 1.9 g/day of
quinidine gluconate. The effects of
epinephrine were then determined.
Epinephrine infusion rates of 25 and 50 ng/kg/min were used in 9 patients each because these doses of
epinephrine previously have been demonstrated to result in elevated plasma
epinephrine concentrations in the range that occurs during a variety of stresses in humans.
Quinidine prolonged refractoriness in the atrium and accessory AV connection and slowed conduction through the accessory AV connection. These effects were partially or completely reversed by
epinephrine. Among 8 patients in whom
quinidine resulted in orthodromic
tachycardia becoming noninducible or nonsustained, sustained
tachycardia became inducible again in 5 patients after infusion of
epinephrine. After
quinidine,
atrial fibrillation was either noninducible or nonsustained in 8 patients; however, sustained
atrial fibrillation could be induced in 4 of these patients after infusion of
epinephrine. The results of this study demonstrate that the
therapeutic effect of
quinidine in patients who have an accessory AV connection are often reversed by physiologic increases in circulating
epinephrine.