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Safety-net hospitals (SNHs) may gain little financial benefit from the rapidly spreading adoption of public reporting and pay-for-performance, but may feel compelled to participate (and bear the costs of data collection) to meet public expectations of transparency and accountability. To better understand the concerns that SNH administrators have regarding public reporting and pay-for-performance, we interviewed 37 executives at randomly selected California SNHs. The main concerns noted by SNH executives were that human and financial resource constraints made it difficult for SNHs to accurately measure their performance. Additionally, some executives felt that market-driven public reporting and pay-for-performance may focus on clinical areas and incentive structures that may not be high-priority clinical areas for SNHs. Executives at SNHs suggested several policy responses to these concerns-such as offering training programs for SNH data collectors-that could be relatively inexpensive and might improve the cost-benefit ratio of public reporting and pay-for-performance programs.

Background We have used a computational model of the thalamocortical system to investigate the effects of a GABAergic anesthetic (etomidate) on cerebral cortical and thalamic neuronal function. We examined the effects of phasic and tonic inhibition, as well as the relative importance of anesthetic action in the thalamus and cortex. Methods The amount of phasic GABAergic inhibition was adjusted in the model to simulate etomidate concentrations of between 0.25 and 2 μM, with the concentration range producing unconsciousness assumed to be between 0.25-0.5 μM. In addition, we modeled tonic inhibition separately, and then phasic and tonic inhibition together. We also introduced phasic and tonic inhibition into the cerebral cortex and thalamus separately to determine the relative importance of each of these structures to anesthetic-induced depression of the thalamocortical system. Results Phasic inhibition decreased cortical neuronal firing by 11-18% in the 0.25-0.5 μM range and by 38% at 2 μM. Tonic inhibition produced similar depression (11-21%) in the 0.25-0.5 μM range but 65% depression at 2 μM; phasic and tonic inhibition combined produced the most inhibition (76% depression at 2 μM). When the thalamus and cortex were separately subjected to phasic and tonic inhibition, cortical firing rates decreased less compared to when both structures were targeted. In the 0.25-0.5 μM range, cortical firing rate was minimally affected when etomidate action was simulated in the thalamus only. Conclusions This computational model of the thalamocortical system indicated that tonic GABAergic inhibition appears to be more important than phasic GABAergic inhibition (especially at larger etomidate concentrations), although both combined had the most effect on cerebral cortical firing rates. Furthermore, etomidate action in the thalamus, by itself, does not likely explain etomidate-induced unconsciousness.

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