Audit of antimicrobial stewardship in medical inpatients in Waikato, New Zealand 2021.

AIMS: Given the threat of rising antimicrobial resistance (AMR), 10 audit standards were selected to audit antimicrobial stewardship (AMS) in secondary care to assess guideline adherence and establish quality improvement initiatives in antimicrobial prescribing. METHODS: Patients were included if they received intravenous (IV) antibiotics across seven medical wards in Waikato or Thames hospitals, New Zealand, in November 2021. Audit standards were defined from the regional antimicrobial prescribing policy and adult antimicrobial guidelines. RESULTS: In total, 205 patients were audited. Microbiological sampling standards were met in 87 of 126 occasions (69.0%). Antimicrobial choices adhered to guidelines in 89 of 163 patients (54.6%), where guidelines were available. Documentation of antimicrobial indications in the medical notes and antimicrobial review at 48 to 72 hours met the standards at over 90%. Only 2 of 13 patients (15.4%) receiving piperacillin/tazobactam or a carbapenem were discussed with Infectious Diseases (ID). Documentation of indications and durations on paper-based medication charts was infrequent, around 12%. Evaluating for health equity, similar results were observed for Maori and non-Maori. CONCLUSIONS: Our audit identified specific areas for AMS quality improvement initiatives. Regular audit should become an essential element of the New Zealand AMS strategy. We believe increased AMS resources are required.

Disruption of Transverse-Tubules Eliminates the Slow Force Response to Stretch in Isolated Rat Trabeculae.

Ventricular muscle has a biphasic response to stretch. There is an immediate increase in force that coincides with the stretch which is followed by a second phase that takes several minutes for force to develop to a new steady state. The initial increase in force is due to changes in myofilament properties, whereas the second, slower component of the stretch response (known as the "slow force response" or SFR) is accompanied by a steady increase in Ca2+ transient amplitude. Evidence shows stretch-dependent Ca2+ influx during the SFR occurs through some mechanism that is continuously active for several minutes following stretch. Many of the candidate ion channels are located primarily in the t-tubules, which are consequently lost in heart disease. Our aim, therefore, was to investigate the impact of t-tubule loss on the SFR in non-failing cardiac trabeculae in which expression of the different Ca2+ handling proteins was not altered by any disease process. For comparison, we also investigated the effect of formamide detubulation of trabeculae on ß-adrenergic activation (1 µM isoproterenol), since this is another key regulator of cardiac force. Measurement of intracellular calcium ([Ca2+]i) and isometric stress were made in RV trabeculae from rat hearts before, during and after formamide treatment (1.5 M for 5 min), which on washout seals the surface sarcolemmal t-tubule openings. Results showed detubulation slowed the time course of Ca2+ transients and twitch force, with time-to-peak, maximum rate-of-rise, and relaxation prolonged in trabeculae at optimal length (Lo). Formamide treatment also prevented development of the SFR following a step change in length from 90 to 100% Lo, and blunted the response to ß-adrenergic activation (1 µM isoproterenol).