• T W Scheeren, L A Schwarte, and J O Arndt.
• Department of Experimental Anaesthesiology, Heinrich-Heine-Universität, Düsseldorf, Germany.
• Acta Anaesthesiol Scand. 1999 Apr 1;43(4):421-30.

BackgroundThe 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).MethodsSeven 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).ResultsIn 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.ConclusionsInhalation 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.

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