Introduction Despite the increasing reliance on simulation to train residents as code blue leaders, the perceived role and effectiveness of code blue simulations from the learners' perspective have not been explored. A code blue Simulation Program (CBSP), developed based on evidence-based simulation principles, was implemented at our institution. We explored the role of simulation in code blue training and the differences between real and simulated code blues from the learner perspective. Methods Using a thematic analysis approach and a purposeful sampling strategy, residents who participated in the CBSP were invited to participate in one of the three focus groups. Data were collected through small group discussions guided by semistructured interviews. The interviews were audio-recorded and transcribed. Interview transcripts were coded to assess underlying themes. Results Thematic analysis revealed that participants believed that the CBSP enhanced preparedness by capturing aspects of real codes (eg, inclusion of precode scenarios with awake patients, lack of readily available information) and facilitating automatization of code blue processes. Despite efforts to develop a high-fidelity simulation, participants noted that they experienced more anxiety, observed more chaos in the environment, and encountered different communication challenges in real codes. Conclusions The CBSP enhanced resident preparedness to serve as code blue leaders. Learners highlighted that they valued the CBSP; however, differences remain between simulated and real codes that could be addressed to enhance the fidelity of future simulations.

Previous studies have shown an association between elevated atrial NADPH-dependent oxidative stress and decreased plasma apelin in patients with atrial fibrillation (AF), though the basis for this relationship is unclear. In the current study, RT-PCR and immunofluorescence studies of human right atrial appendages (RAAs) showed expression of the apelin receptor, APJ , and reduced apelin content in the atria, but not in plasma, of patients with AF versus normal sinus rhythm. Disruption of the apelin gene in mice increased (2.4-fold) NADPH-stimulated superoxide levels and slowed atrial conduction velocities in optical mapping of a Langendorff-perfused isolated heart model, suggesting that apelin levels may influence AF vulnerability. Indeed, in mice with increased AF vulnerability (induced by chronic intense exercise), apelin administration reduced the incidence and duration of induced atrial arrhythmias in association with prolonged atrial refractory periods. Moreover, apelin decreased AF induction in isolated atria from exercised mice while accelerating conduction velocity and increasing action potential durations. At the cellular level, these changes were associated with increased atrial cardiomyocyte sodium currents. These findings support the conclusion that reduced atrial apelin is maladaptive in fibrillating human atrial myocardium and that increasing apelin bioavailability may be a worthwhile therapeutic strategy for treating and preventing AF.

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