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  • Title: [Buprenorphine as a postoperative analgesic following halothane anesthesia. Hemodynamic and respiratory effects].
    Author: Piepenbrock S, Zenz M, Reichelt W, Wölfel D, Reinhart K.
    Journal: Anaesthesist; 1983 Feb; 32(2):67-74. PubMed ID: 6846782.
    Abstract:
    In 10 healthy patients, buprenorphine was given as the postoperative analgesic (dosage: peripheral venous injection of 5 microgram/kg BW) after traumatological interventions in the lower extremities, which had been performed under barbiturate-induced halothane anaesthesia. The haemodynamic investigations revealed that buprenorphine has only a minor effect on the high pressure system. In the area of the pulmonary circulation, there was a significant increase in mean pulmonary artery pressure from 15.9 mm Hg to 17.8 mm Hg (+12%), as well as an increase in pulmonary vascular resistance by 16.5%. These changes were most marked 30 to 60 min after the administration of buprenorphine. When 2-3 1 O2/min were administered, none of the patients had PaO2 values of less than 100 mm Hg. 60 min after the injection, the PaCO2 value increased from 33.7 mm Hg to a maximum of 43.9 mm Hg. In 3 patients, PaCO2 increased to more than 45 mm Hg. All patients with greater increases of PaCO2 also evidenced greater increases in the pulmonary vascular resistance. Altogether the haemodynamic changes after buprenorphine administration following halothane anesthesia were not very distinct. In individual cases, however, there were greater increases in PaCO2. The cause of this could involve the additive effects of premedication and anaesthesia medication, and possibly the pain level as well. Both the increase in pulmonary artery pressure and the increase in total pulmonary vascular resistance in these patients were due to hypercapnia (von Euler-Liljestrand mechanism).
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