Woehlck H J, Vicenzi M N, Bajic J, Sokolyk S M, Bosnjak Z J, Atlee J L
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Anesthesiology. 1995 Jun;82(6):1447-55. doi: 10.1097/00000542-199506000-00016.
Subsidiary atrial pacemakers assume control after sinoatrial (SA) node excision, and anesthetic-catecholamine interactions can produce severe bradycardia during isoflurane anesthesia. We hypothesized that epinephrine enhances atrial, atrioventricular junctional, and ventricular dysrhythmias after SA node excisions in dogs and that inhalation anesthetics would facilitate such dysrhythmias.
In eight dogs, SA nodes were excised and epicardial electrodes implanted at the atrial appendages, at the His bundle, and along the sulcus terminalis. Site of the earliest atrial activation and incidences of nonatrial beats were determined in the conscious state, with methylatropine, with epinephrine, and during halothane, isoflurane, or enflurane anesthesia.
After SA node excision, a stable, regular subsidiary atrial pacemaker rhythm resulted. Epinephrine and halothane shifted the site of earliest activation to more remote atrial sites. Epinephrine-induced ventricular escape was increased by all anesthetics tested, but atropine prevented ventricular escape. Epinephrine-induced His bundle (atrioventricular junctional) and premature ventricular beats were increased by halothane and enflurane. After SA node excision, ventricular escape occurred as a result of epinephrine-anesthetic interactions, especially during anesthesia with isoflurane.
In dogs with excised SA nodes, anesthetic-catecholamine interaction facilitates ventricular escape, His bundle dysrhythmias, and premature ventricular beats. In addition, halothane and enflurane, more than isoflurane, facilitate ectopic ventricular tachydysrhythmias with epinephrine. Compared to intact dogs, dogs with excised SA nodes may be more susceptible to epinephrine anesthetic dysrhythmias. If findings can be extrapolated to humans, intrinsic SA node dysfunction may facilitate severe cardiac dysrhythmias with inhalation anesthetics and catecholamines.
窦房结切除术后，次级心房起搏器开始发挥控制作用，并且在异氟烷麻醉期间，麻醉药与儿茶酚胺的相互作用可导致严重心动过缓。我们假设肾上腺素会增强犬类窦房结切除术后心房、房室交界区和心室的心律失常，并且吸入麻醉药会促使此类心律失常的发生。
对8只犬切除窦房结，并在心房附件、希氏束和终沟沿线植入心外膜电极。在清醒状态下、使用甲基阿托品时、使用肾上腺素时以及在氟烷、异氟烷或恩氟烷麻醉期间，确定最早心房激动的部位和非心房搏动的发生率。
窦房结切除术后，出现了稳定、规则的次级心房起搏器节律。肾上腺素和氟烷将最早激动的部位转移至更远端的心房部位。所有受试麻醉药均增加了肾上腺素诱发的心室逸搏，但阿托品可防止心室逸搏。氟烷和恩氟烷增加了肾上腺素诱发的希氏束（房室交界区）和室性早搏。窦房结切除术后，由于肾上腺素与麻醉药的相互作用出现了心室逸搏，尤其是在异氟烷麻醉期间。
在窦房结切除的犬类中，麻醉药与儿茶酚胺的相互作用促使心室逸搏、希氏束心律失常和室性早搏的发生。此外，与异氟烷相比，氟烷和恩氟烷更易促使肾上腺素诱发异位室性快速心律失常。与完整犬类相比，窦房结切除的犬类可能对肾上腺素麻醉性心律失常更敏感。如果研究结果能够外推至人类，那么内在的窦房结功能障碍可能会促使吸入麻醉药和儿茶酚胺诱发严重的心脏心律失常。
