Paired Spontaneous Awakening Trial and Spontaneous Breathing Trial Protocol Implementation
Other Titles
Spontaneous Awakening and Breathing TrialAbstract
Problem & Purpose: Mechanical ventilation (MV) is a commonly used life-saving modality in the intensive care unit (ICU) patients. Sedation is widely used for improved patient MV tolerance. However, evidence shows a link between sedation use and increased MV duration and risk for MV-associated complications. This quality improvement (QI) project aimed to implement a paired Spontaneous Awakening Trial (SAT) and Spontaneous Breathing Trial (SBT) protocol in the ICU to promote early extubation and endorse a practice change that includes sedation guidelines and safety screening to identify appropriate candidates for extubation with a goal to reduce MV days. Methods: The QI project was implemented over a three months period on all intubated, MV adult ICU patients aged 18 years and older. Data was collected on monthly MV days, and Standardized Utilization Ratio (SUR) obtained from the infection prevention department as reported to the National Healthcare Safety Network (NHSN), and the percentage of mean staff compliance with the protocol implementation using a manual audit. Results: During the implementation period, the SUR decreased from 0.99 to 0.89, while the MV days increased from 154 to 162, and the percentage of mean staff compliance increased from 3% to 82%. Conclusion: The staff compliance goal was met, but the MV data is inconclusive. Data from the past 24 months have shown a seasonal variance pattern in the MV days and SUR, and there is insufficient data to analyze the impact of the protocol implementation on the clinical site. Barriers that affected the project implementation includes the synchronous merging of the Neuro and the Cardiothoracic ICUs with the hospital relocation during the implementation month.Identifier to cite or link to this item
http://hdl.handle.net/10713/12945Collections
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In vivo insulin action on skeletal muscle and adipose tissue glycogen synthase and phosphorylase activities in rhesus monkeys with varying degrees of spontaneous insulin resistanceResistance to the action of insulin, particularly in the glycogen storage pathway, is one of the earliest detectable defects in the development of non-insulin-dependent diabetes mellitus (NIDDM) in humans and in monkeys, but the nature of the underlying defect and its role in the pathogenesis of diabetes are unknown. The present studies were carried out in monkeys (Macaca mulatta) who develop adult-onset obesity-associated NIDDM which is remarkably similar to human NIDDM. These experiments examined, under basal and insulin-stimulated conditions (euglycemic hyperinsulinemic clamp), the in vivo action of insulin on glycogen synthase (GS), the rate-limiting enzyme for glycogenesis, and on glycogen phosphorylase (GP), the key enzyme in glycogenolysis. To determine possible tissue specificity in the development of such defects, both muscle and adipose tissue biopsies were studied. Additional experiments addressed the possibility that in insulin resistance, a component of a putative mediator of insulin action, chiroinositol (CI), might be reduced or absent, and if restored, might improve insulin action. Urinary CI excretion rates, previously shown to be abnormally low in both monkeys and humans with NIDDM, were also determined. Twenty-seven monkeys chosen for study consisted of three groups: normal (nondiabetic), hyperinsulinemic (pre-diabetic), and impaired glucose tolerant/NIDDM. Results showed that covalent activation of muscle GS was significantly reduced in the insulin-resistant (pre-diabetic) monkeys and further reduced in the diabetic monkeys as compared to the normal monkeys. The covalent activation of adipose tissue GS was absent in both the insulin-resistant and diabetic groups. The independent activity and the percent independent to total activity (activity ratio) of muscle and adipose tissue GS in response to insulin were significantly related to whole-body insulin-mediated glucose disposal rate (M). Insulin activation of muscle GS was shown to be significantly inversely correlated with insulin activation of muscle GP. Urinary CI excretion rate was significantly inversely related to in vivo insulin resistance, and positively related to insulin activation of muscle and adipose tissue GS, and was inversely related to insulin activation of muscle GP. In addition, the intravenous administration of CI significantly increased the activity of muscle GS and inhibited the activity of muscle GP. We conclude that a reduced activation of GS by insulin is a major contributor to insulin resistance and NIDDM in monkeys, and this defect may be due to reduced amounts of chiroinositol-containing insulin mediator.
