Modelling the economic constraints and consequences of anaesthesia associate expansion in the UK National Health Service: a narrative review.

Shortages in the physician anaesthesia workforce have led to proposals to introduce new staff groups, notably in the UK National Health Service (NHS) Anaesthesia Associates (AAs) who have shorter training periods than doctors and could potentially contribute to workflow efficiencies in several ways. We analysed the economic viability of the most efficient staffing model, previously endorsed by both the UK Royal College of Anaesthetists and the Association of Anaesthetists, wherein one physician supervises two AAs across two operating lists (1:2 model). For this model to be economically rational (something which neither national organisation considered), the employment cost of the two AAs should be equal to or less than that of a single supervisor physician (i.e. AAs should be paid <50% of the supervisor's salary). As the supervisor can be an autonomous specialty and specialist (SAS) doctor, this sets the economically viable AA salary envelope at less than £40,000 per year. However, we report that actual advertised AA salaries greatly exceed this, with even student AAs paid up to £48,472. Economically, one way to justify such salaries is for AAs to become autonomous such that they eventually replace SAS doctors at a lower cost. We discuss some other options that might increase AA productivity to justify these salaries (e.g. ≥1:3 staffing ratios), but the medico-political consequences of each of them are also profound. Alternatively, the AA programme should be terminated as economically nonviable. These results have implications for any country seeking to introduce new models of working in anaesthesia.

Enzyme-linked oxygen sensing by potassium channels.

The ability of ion channels to respond to an acute perturbation in oxygen tension is a widespread phenomenon, which encompasses many of the major ion channel families. Integral to the ability of several ion channels to respond to acute hypoxic challenge is modulation by upstream enzymatic reactions, suggesting that many ion channels sense oxygen via enzyme-linked processes. Several enzyme-linked oxygen sensing systems have been proposed, including nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent production of hydrogen peroxide, hemoxygenase-dependent generation of carbon monoxide, adenosine monophosphate (AMP) kinase-dependent channel phosphorylation, and src-Lck protein tyrosine kinase, via a currently undetermined mechanism. Each of these enzymes has been shown to endow specific ion channels with the ability to respond to changes in oxygen, with hypoxia exclusively evoking channel inhibition. This article reviews these proposed mechanisms and presents new insights into how one system, hemeoxygenase-2, confers oxygen sensitivity to large conductance, voltage- and calcium-activated potassium channels.