Isoflurane anaesthesia (0.6 MAC) and hypoxic ventilatory responses in humans

Abstract

In order to evaluate the difference between poikilo-capnic (no CO2 added to inspired gas) and iso-capnic (CO2 added to keep end-tidal CO2 constant) hypoxic ventilatory responses (HVR) awake and during 0.6 MAC isoflurane anaesthesia, seven cardio-pulmonary healthy patients were investigated. Pneumotachography and capnography were used before and during hypoxia (end-tidal O2 tension approx. 7 kPa). In the awake state, poikilo-capnic hypoxic challenges resulted in an increased HVR as indicated by a VE that on average increased by 1.4 +/- 1.0 (mean +/- s.d.) l.min-1, whereas the iso-capnic hypoxic challenges resulted in a VE increase that was 4.7 +/- 2.3 l.min-1 on average. In the anaesthetized state, the corresponding value during poikilocapnia was 1.3 +/- 0.8 l.min-1 (88% of the awake responses, n.s.) and during iso-capnia 2.3 +/- 1.4 l.min-1 (49% of the awake, P < 0.02). Awake HVR was achieved by greater tidal volumes during poikilocapnia as well as during isocapnic challenges, while respiratory rates were unchanged. In the anaesthetized state, during poikilocapnia, however, HVR was mediated by an increased respiratory rate, (from 17.5 +/- 1.7 breath.min-1 to 20.2 +/- 2.2) and during isocapnia by a combination of increased rate (from 17.1 +/- 1.9 breath.min-1 to 19.1 +/- 1.8) and tidal volume (from 496 +/- 80 to 560 +/- 83 ml). It is concluded that poikilocapnic HVR is maintained at 0.6 MAC isoflurane whereas iso-capnic HVR is depressed by 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

The acute hypoxic ventilatory response under halothane, isoflurane, and sevoflurane anaesthesia in rats*

“…Breathing is precisely controlled by the brain and its sensory inputs to maintain arterial blood gases and acid‐base balance within narrow limits at rest and during exercise, to counteract threats to body homeostasis. Volatile anaesthetics change the pattern (rhythm, rate, and depth) of breathing at clinically relevant concentrations [1–5]. The influence of volatile anaesthetics on resting ventilation is dose dependent and depression becomes clinically relevant at high doses > 1.0 MAC [6].…”

Emergence from isoflurane/N2O or isoflurane anaesthesia

“…The isocapnic hypoxic ventilatory response, i.e. when the end-tidal CO, is kept constant by CO, added to inspired gas, is depressed by 50% at 0.6 MAC isoflurane (17). There are some methodological limitations which should be mentioned.…”

Effects of Anesthetics, Sedatives, and Opioids on Ventilatory Control

“…Maintenance of isohypercapnia to characterize the acute hypoxic response is important, since there is a synergistic, multiplicative interaction between hypoxemia and PaCO 2 at the level of the peripheral chemoreceptors. Clinically, of course, any hyperventilation in spontaneously breathing persons subjected to hypoxic gas mixtures will immediately result in hypocapnic hypoxia, which will blunt the effect of acute hypoxia at the peripheral chemoreceptors (149,638,644). On the other hand, if the hypoxic hyperventilatory response is blunted or even abolished by anesthetics, hypercapnic hypoxia may result.…”