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PubMed · 3661954

[Pindolol in intraoperatively developing isorhythmic AV dissociation].

D Knüttgen·M Doehn
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Abstract

The pathogenetic mechanism of isorhythmic AV dissociation (ID)--the often so-called nodal rhythm--developing during anesthesia is unclear. It has been proposed that stimulation of the AV node is caused by elevated sympathetic tone and a simultaneous blockade of the sinus node. In our prospective, randomized study the effect of the beta-blocking agent pindolol in converting ID into normal sinus rhythm has been investigated. Methods. Fourty patients (27 men, 13 women) aged 17 to 81 years, ASA class I and II, who developed ID during an elective surgical procedure were divided into four equal, randomized groups. The biometric data, type of operation, and anesthesia technique were comparable: induction of anesthesia with thiopental, intubation, and continuation with N2O/O2 combined with halothane or enflurane. The patients in group A formed the control group. The other patients received pindolol in a dose of 0.5 (group B), 1.0 (group C), and 2.0 (group D) micrograms/kg over a period of 30 s intravenously. The frequency of restoration of sinus rhythm during a testing period of 15 min in the pindolol-treated patients was compared with the frequency of the spontaneous converting rate in the control group. Results. A spontaneous return to sinus rhythm occurred in 2 of 10 (20%) patients of the control group, whereas with pindolol the restoration of sinus rhythm was effected in 25 of 30 (83.3%) patients during the observation period of 15 min (p less than 0.001). The dose of 2.0 micrograms/kg pindolol (group D) was most effective.(ABSTRACT TRUNCATED AT 250 WORDS)

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AdultArrhythmias, CardiacAtrioventricular NodeElectrocardiographyFemaleHeart Conduction SystemHeart RateHumansIntraoperative ComplicationsMalePindololClinical TrialEnglish AbstractJournal ArticleRandomized Controlled Trial

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BibTeXRIS

D Knüttgen, M Doehn. 1987. [Pindolol in intraoperatively developing isorhythmic AV dissociation].. https://pubmed.ncbi.nlm.nih.gov/3661954/

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