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Cardiovascular and blood gas responses to inhaled anaesthetics in normoxic and hypoxic dogs
Author(s) -
Naeije R.,
Lambert M.,
Lejeune P.,
Leeman M.,
Deloof T.
Publication year - 1986
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1986.tb02471.x
Subject(s) - medicine , anesthesia , hypoxia (environmental) , blood gas analysis , pharmacology , oxygen , chemistry , organic chemistry
Changes in haemodynamics and blood gases were investigated before and after administration of 0.5, I and 1.5 MAC of halothane, enflurane and isoflurane in respectively 7, 7 and 9 dogs ventilated alternatively with a fraction of inspired O 2 in N 2 (FiO 2 ) of 0.4 and with brief periods (10 min) of Fio 2 of 0.1. Anaesthesia was induced with pentobarbital and the animals were paralysed with pancuronium. Acute hypoxic challcnges with Fio 2 of 0.1 consistently decreased arterial Po 2 to 3.5–4.5 kPa and increased pulmonary vascular resistances by 60–100%. At identical inspired concentrations, as expressed in MAC: units, all thrrr inhaled anaesthetics induced a broadly comparable dose‐related decrease in systemic blood pressures, due to a depression in cardiac performance as well as a reduction in systemic vascular resistances. Enfluraw was the most potent myocardial depressor and isoflurane the most potent vasodilator, halothane being intermediate. Oxygen deprivation was associated with some enhancement of the cardiovascular depressant effects of the inhaled anaesthetics but, in spite of this, matching of 02 transport to tissue O 2 demand appeared to be improved, probably in relation to a concomitant reduction in metabolic rate. Only isoflurane inhibited the hypoxic pulmonary pressor response, and this was associated with a slight deterioration in arterial oxygrnation in both normoxic and hypoxic conditions.