The effectiveness of an intensive care quick reference checklist manual--a randomized simulation-based trial.

PURPOSE: We aimed to test the effectiveness of checklists for emergency procedures on medical staff performance in intensive care crises. MATERIALS AND METHODS: This is a prospective single-center randomized trial in a high-fidelity simulation center modeling an intensive care unit (ICU) in a tertiary care hospital in Germany. Teams consisted of 1 ICU resident and 2 ICU nurses (in total, n = 48). All completed 4 crisis scenarios, in which they were randomized to use checklists or to perform without any aid. In 2 of the scenarios, checklists could be used immediately (type 1 scenarios); and for the remaining, some further steps, for example, confirming diagnosis, were required first (type 2 scenarios). Outcome measurements were number of predefined items and time to completion of more than 50% and more than 75% of steps, respectively. RESULTS: When using checklists, participants initiated items faster and more completely according to appropriate treatment guidelines (9 vs 7 items with and without checklists, P < .05). Benefit of checklists was better in type 2 scenarios than in type 1 scenarios (2 vs 1 additional item, P < .05). In type 2 scenarios, time to complete 50% and 75% of items was faster with the use of checklists (P < .005). CONCLUSIONS: Use of checklists in ICU crises has a benefit on the completion of critical treatment steps. Within the type 2 scenarios, items were fulfilled faster with checklists. The implementation of checklists for intensive care crises is a promising approach that may improve patients' care.

Syndecan-4 signalling inhibits apoptosis and controls NFAT activity during myocardial damage and remodelling.

AIMS: Myocardial infarction (MI) results in acute impairment of left ventricular (LV) function through the initial development of cardiomyocyte death and subsequent progression of LV remodelling. The expression of syndecan-4 (Sdc4), a transmembrane proteoglycan, is up-regulated after MI, but its function in the heart remains unknown. Here, we characterize the effects of Sdc4 deficiency in murine myocardial ischaemia and permanent infarction. METHODS AND RESULTS: Targeted deletion of Sdc4 (Sdc4(-/-)) leads to increased myocardial damage after ischaemic-reperfusion injury due to enhanced cardiomyocyte apoptosis associated with reduced activation of extracellular signal-regulated kinase in cardiomyocytes in vitro and in vivo. After ischaemic-reperfusion injury and permanent infarction, we observed an increase in cardiomyocyte area, nuclear translocation of nuclear factor of activated T cells (NFAT), and transcription of the NFAT target rcan1.4 in wild-type mice. NFAT pathway activation was enhanced in Sdc4(-/-) mice. In line with the in vivo data, NFAT activation and hypertrophy occurs in isolated cardiomyocytes with reduced Sdc4 expression during phenylephrine stimulation in vitro. Despite the initially increased myocardial damage, echocardiography revealed improved LV geometry and function in Sdc4(-/-) mice 7 days after MI. CONCLUSION: Interception of the Sdc4 pathway enhances infarct expansion and hypertrophic remodelling during early infarct healing in ischaemic-reperfusion injury and permanent infarction mouse models and exerts net beneficial effects on LV function.