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Audience: This simulated automated chest compression device was designed for use in simulation cardiacarrest cases involving emergency medicine residents, but it would be applicable to other learners such asnurses, pharmacists, and medical students.Background: Automated chest compression devices (ACCD) are commonly utilized in cardiac arrest in theemergency department and by emergency medical services (EMS) as patients arrive in the ED.1 Prolongedsimulated cardiac arrest can be challenging to maintain proper chest compression depth and technique.2Resident learning may be enhanced during cardiac arrest in the simulation environment by implementing theuse of a simulated ACCD.Educational Objectives: By the end of this educational session using a resuscitation trainer or high-fidelitymanikin, learners should be able to:1. Recognize appropriate application of simulated ACCD to an ongoing resuscitation case2. Demonstrate proper positioning of simulated ACCD in manikin model3. Integrate simulated ACCD to provide compressions appropriately throughout cardiac arrest scenarioEducational Methods: We developed a cost-effective simulated ACCD for use in resuscitation simulationcases. An initial pilot session identified components of fidelity that were used to model the simulated ACCDafter those utilized in clinical situations. Three simulated devices were created and then tested for efficacyduring high-fidelity simulation with 25 emergency medicine residents.Research Methods: Visual analog scales were used to explore how the simulated ACCD affected perceivedrealism and stress level during the cardiac arrest simulation. Qualitative data were collected through open-ended learner feedback comments. The institutional review board at our institution reviewed this projectand determined that it was exempt.Results: With inclusion of the simulated ACCD device, learners rated the simulation "more realistic" with anaverage rating of 74/100 and "less stressful" with an average rating of 69/100 on the visual analog scales.Learner comments noted that the use of the ACCD in simulation resulted in better resource availability andaccurate environmental noise.Discussion: The simulated ACCD presented here was found to be effective, realistic, and practical for use bylearners in a resuscitation curriculum. Our results suggest that implementating a cost-effective simulatedACCD ($98 for supplies) in high-fidelity simulation cardiac arrest cases enhances the perceived realism of theenvironment and offers physician learners a low-stress opportunity to practice the clinical application ofACCD in cardiac arrest resuscitation. Additionally, the use of the simulated ACCD, specifically in a prolongedresuscitation, eliminated the need for physically demanding manual chest compressions. Anecdotally, insimulated environments we have observed poor-quality manual chest compressions due to an understandingthat the manikin is “not real,” leading to decreased psychological fidelity from the shared acceptance of thepoor-quality compressions. Thus, the presence of a simulated clinical device providing chest compressionscould have increased the feel of realism through improved psychological fidelity. Additionally, we note thatthe physical and psychological fidelity of this simulated device was sufficient for physicians to perceive clinicalimplementation, but may be suboptimal for assistive staff, who are focused on the specific functionality andmay benefit from training on the physical device in clinical use. Finally, our simulated ACCD resembles theclinical device our department uses; we advise modifications as appropriate to allow a simulated ACCDcreated for other learners to also resemble their clinically used ACCD.

Song sparrows do not need exposure to within-type variation to produce such variation. Birds trained with totally invariant song types produce songs with just as much within-type variability as birds trained with variable song types. Exposure to a few conspecific song types assists the development of a normal repertoire. Beyond this, the number of song types heard during learning has only a limited impact on the numbers of song types developed by an individual.

Because carbon monoxide (CO) has been proposed to have anti-inflammatory properties, we sought protective effects of CO in pulmonary [O.sub.2] toxicity, which leads rapidly to lung inflammation and respiratory failure. Based on published studies, we hypothesized that CO protects the lung against [O.sub.2] by selectively increasing expression of antioxidant enzymes, thereby decreasing oxidative injury and inflammation. Rats exposed to [O.sub.2] with or without CO [50-500 parts/ million (ppm)] for 60 h were compared for lung wet-to-dry weight ratio (W/D), pleural fluid volume, myeloperoxidase (MPO) activity, histology, expression of heme oxygenase-1 (HO-1), and manganese superoxide dismutase (Mn SOD) proteins. The brains were evaluated for histological evidence of damage from CO. In [O.sub.2]-exposed animals, lung W/D increased from 4.8 in normal rats to 6.3; however, only CO at 200 and 500 ppm decreased W/D significantly (to 5.9) during [O.sub.2] exposure. Large volumes of pleural fluid accumulated in all rats, with no significant CO treatment effect. Lung MPO values increased after [O.sub.2] and were not attenuated by CO treatment. CO did not enhance lung expression of oxidant-responsive proteins Mn SOD and HO-1. Animals receiving [O.sub.2] and CO at 200 or 500 ppm showed significant apoptotic cell death in the cortex and hippocampus by immunochemical staining. Thus significant protection by CO against [O.sub.2]-induced lung injury could not be confirmed in rats, even at CO concentrations associated with apoptosis in the brain. oxidative stress; reactive oxygen species; oxygen toxicity; heme oxygenase