ABSTRACT
AIM: Emergency medicine (EM) trainees often work nightshifts. We sought to measure how this circadian disruption affects EM resident performance during simulated resuscitations. METHODS: This retrospective cohort study enrolled EM residents at a single Canadian academic centre over a six-year period. Residents completed twice-annual simulation-based resuscitation-focused objective structured clinical examinations (OSCEs) with assessment in four domains (primary assessment, diagnostic actions, therapeutic actions and communication), and a global assessment score (GAS). Primary and secondary exposures of interest were the presence of a nightshift (late-evening shifts ending between midnight and 03h00 or overnight shifts ending after 06h00) the day before or within three days before an OSCE. A random effects linear regression model was used to quantify the association between nightshifts and OSCE scores. RESULTS: From 57 residents, 136 OSCE scores were collected. Working a nightshift the day before an OSCE did not affect male trainee scores but was associated with a significant absolute decrease in mean total scores (-6% [95% CI -12% to 0%]), GAS (-7% [-13% to 0%]), and communication (-9% [-16% to -2%]) scores among women. Working any nightshift within three days before an OSCE lowered absolute mean total scores by 4% [-7% to 0%] and communication scores by 5% [-5% to 0%] irrespective of gender. CONCLUSION: Our results suggest that shift work may impact EM resident resuscitation performance, particularly in the communication domain. This impact may be more significant in women than men, suggesting a need for further investigation.
Subject(s)
Cardiopulmonary Resuscitation/education , Clinical Competence , Emergency Medicine/education , Internship and Residency , Shift Work Schedule/adverse effects , Adult , Female , Humans , Interprofessional Relations , Male , Retrospective Studies , Sex Factors , Simulation TrainingABSTRACT
Apoptosis of polymorphonuclear cells (PMNs) is a fundamental mechanism to halt inflammation. It limits the lifespan of PMNs and thereby decreases tissue injury. In PMNs, unlike in other cells, hypoxia profoundly inhibits apoptosis. However, most studies investigating hypoxic effects on the functioning of PMN focus on acute or chronic sustained hypoxia. Thus, the mechanisms by which intermittent hypoxia (IH) affects PMN apoptosis are not known. Flow cytometry and Western blotting were used to evaluate mechanisms of constitutive and TNF-α-mediated PMN apoptosis in IH. The levels of NF-κB, p38 mitogen-activated protein kinase (MAPK), TNF receptor-2 (TNFR-2), intracellular IL-8 and its surface receptor CXCR2, were determined. Specific NF-κB (gliotoxin and parthenolide) and p38MAPK (SB202190) inhibitors were also used. TNF-α-mediated PMN apoptosis was concentration-dependent; low concentration increased PMN survival, whereas higher concentrations accelerated apoptosis. However, at all TNF-α concentrations, PMN survival was higher after four IH cycles than in normoxia. However, increasing the IH cycles to six abolished the pro-apoptotic/anti-apoptotic effects of TNF-α. Also, IH increased TNRF2 expression, nuclear NF-κB translocation, p38MAPK phosphorylation, and expression of IL-8 and CXCR2. The NF-κB inhibitors gliotoxin and parthenolide increased apoptosis and decreased IL-8 and CXCR2 expression. Also, the p38MAPK inhibitor SB202190 increased apoptosis and decreased IL-8 expression but had no effect on CXCR2 expression. Collectively, these findings provide insights into the mechanisms that prolong PMN survival after IH exposure and demonstrate the essential role played by NF-κB, the p38MAPK signaling pathway, and downstream genes in this process.
Subject(s)
Apoptosis , Neutrophils/metabolism , Tumor Necrosis Factor-alpha/metabolism , Adult , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Cell Hypoxia/drug effects , Cell Survival/drug effects , Cells, Cultured , Enzyme Inhibitors/pharmacology , Female , Gene Expression Regulation/drug effects , Gliotoxin/pharmacology , Humans , Imidazoles/pharmacology , Immunosuppressive Agents/pharmacology , Interleukin-8/biosynthesis , Male , NF-kappa B/antagonists & inhibitors , NF-kappa B/metabolism , Neutrophils/pathology , Phosphorylation/drug effects , Pyridines/pharmacology , Receptors, Interleukin-8B/biosynthesis , Receptors, Tumor Necrosis Factor, Type II/biosynthesis , Sesquiterpenes/pharmacology , p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors , p38 Mitogen-Activated Protein Kinases/metabolismABSTRACT
Nocturnal asthma (NA) is increasing in prevalence, affecting millions of people worldwide. In addition to being associated with increased mortality, NA is associated with a decreased quality of life. NA associated sleep disturbances and increased daytime sleepiness are especially important in children due to the accompanying behavioral and developmental difficulties. As diurnal spirometry is not a practical tool for the diagnosis and monitoring of NA, self or parental reports are used. Children underreport and underestimate their NA symptoms and parents are not fully aware of their child's NA indicators. In addition, there is the lack of physician familiarity regarding the assessment and treatment of NA. Therefore, NA is chronically underreported. The development of a non-invasive, objective, home-based diagnostic tool is crucial in diagnosing and monitoring children with NA. The presence of wheeze during sleep has been successfully employed as a tool to measure NA in children. This review discusses the increasing prevalence of NA, current diagnostic tools and the consequences of undiagnosed NA in children. In conclusion, this paper suggests that an automated wheeze detective device is an objective and practical tool to aid the diagnosis and monitoring of NA.
