Xenon is used:
1. in the induction and maintenance of general anaesthesia and
2. for estimation of organ blood flow using a radioactive isotope.
As a colourless, odourless gas contained in 2, 5, and 10 l aluminium cylinders as a liquid. These correspond to a removable volume of 233, 555, and 1000 l, respectively, at 15°C and 1.013 bar. It has a molecular weight of 131, a specific gravity of 4.56, a critical temperature of 16.59°C, a critical pressure of 58.42 bar, and a boiling point of −108.1°C. The MAC of xenon is 60 ± 5, the oil:gas partition coefficient 1.9, and the blood:gas partition coefficient 0.115.
Mode of action
The mechanism of general anaesthesia remains to be fully elucidated. Xenon non-competitively inhibits NMDA receptors by approximately 60%. Inhibition of glutamate-gated NMDA receptors by xenon provides a mechanism for its predominant analgesic profile. It also inhibits nicotinic acetylcholine receptors. In an animal model, it competitively inhibits 5HT3A receptors. Xenon has no effect on GABAA receptors.
Routes of administration/doses
Xenon is administered by inhalation, using a compatible anaesthetic machine. Maintenance of general anaesthesia is achieved at inhalational concentrations of between 51 and 69%.
Xenon exhibits cardiovascular stability. No changes in the ventricular function occur during general anaesthesia, as measured by transoesophageal echocardiography. A reduction in the heart rate may be seen during use of the gas.
Xenon acts as a respiratory depressant, causing a reduction in the minute ventilation. The gas may improve the laminar flow and aeration of non-aerated alveoli, leading to recruitment and improved oxygenation.
The principal effect of xenon is general anaesthesia, the mechanism of which remains to be fully elucidated. The analgesic effect of xenon may possibly be mediated by inhibition of NMDA receptors and effects on the spinal cord. Xenon may also confer an element of neuroprotection at sub-anaesthetic doses. However, the gas may also cause changes in cerebral blood flow, and its use can be associated with an increase in intracranial pressure in patients with traumatic brain injury.
As with other inhalational anaesthetic agents, the uptake of xenon is affected by its solubility, cardiac output, and the concentration gradient between the alveoli and venous blood. Due to the very low blood:gas partition coefficient of xenon, the alveolar concentration reaches inspired concentration rapidly (fast wash-in), resulting in a rapid induction (and emergence from) anaesthesia.