Metabolic regulation of cardiac output during inhalation anaesthesia in dogs

Background: The metabolic regulation of tissue blood flow manifests itself in a linear relation between blood flow and oxygen consumption, the latter being the independent variable. It is unknown, however, if this fundamental physiological principle operates also during inhalation anaesthesia known to be associated with decreases in both cardiac output (Q) and oxygen consumption (VO₂). Methods: Seven dogs (23-32 kg) with chronically implanted flow probes around the pulmonary artery were repeatedly anaesthetized with halothane, enflurane, isoflurane, sevoflurane, and desflurane at increasing minimum alveolar concentrations (1-3 MAC). Cardiac output (ultrasound transit-time flowmeter) and VO₂ (indirect calorimetry) were measured continuously. We also imposed selective changes in Q, and thus of O₂ supply, to see if and to what extent this would alter VO₂ during anaesthesia (1.5 MAC). Results: In awake dogs under basal metabolic conditions, VO₂ was 4.6±0.1 ml · kg^-1 · min^-1 and Q 105±3 ml · kg^{- 1} · min^-1 (mean±SEM). During inhalation anaesthesia, VO₂ and Q decreased by approximately 30% and 60%, respectively. The concentration- effect relations of both variables did not differ between anaesthetics, yielding a uniform Q/VO₂ relation, which was nearly linear in the range (0- 2 MAC) with an average slope of 39±1 (range 30-55). Above 2 MAC, Q decreased more for a given change in VO₂, and O₂ extraction increased by 50%, indicating compromised oxygen delivery (DO₂). Imposed changes in Q, both in awake and anaesthetized dogs, yielded Q/VO₂ relations which were notably steeper (slopes 114 to 187) than those observed during inhalation anaesthesia. More important, imposed increases in Q and thus DO₂ during anaesthesia (1.5 MAC) to rates comparable to that in the awake state produced a much less than proportional increase in VO₂ without restoring it to baseline. Conclusions: Inhalation anaesthesia is characterized by a uniform Q/VO₂ relation with an almost linear course at an anaesthetic concentration up to 2 MAC, regardless of the anaesthetic. Metabolic regulation of blood flow apparently operates also during inhalation anaesthesia up to 2 MAC so that the decrease in VO₂ determines Q. This implies that cardiac output alone provides little information on the function of the circulation during inhalation anaesthesia unless related to metabolic demands, i.e. to VO₂.