Paramedic and EMT Program Performance on Certification Examinations Varies by Program Size and Geographic Location.

Introduction: The quality of an Emergency Medical Technician (EMT) or paramedic training program is likely one factor that contributes to a candidate's success on the National Registry Cognitive Examination. However, program pass rates and their associated geographic location have not previously been evaluated. Our objective was to evaluate the performance of EMT and paramedic programs in the United States, pass rates on the National Registry Cognitive Examinations, and relationship to geography.Methods: We conducted a cross-sectional evaluation of EMT and paramedic programs' first and cumulative third attempt pass rates on the National Registry Cognitive Examination in 2015. Included were civilian EMT and paramedic programs with >5 graduates testing for certification. Descriptive statistics were calculated for program pass rates, total graduates testing, and pass rates by National Association of State EMS Officials (NASEMSO) regions.Results: We included 1,939 EMT programs (6-1,892 graduates testing/program) and 602 paramedic programs (6-689 graduates testing/program). We excluded 262 (11.9%) EMT and 51 (7.8%) paramedic programs with ≤5 graduates testing annually due to unstable estimates of program pass rates. EMT programs in the highest quartile for total number of graduates testing outperformed the lowest quartile in both first attempt (65.7% vs. 61.9%, p < 0.001) and cumulative third attempt pass rates (79.1% vs 72.7%, p < 0.001). This difference was also seen for paramedic programs on first attempt (77.3% vs. 62.5%, p < 0.001) and cumulative third attempt (91.9% vs. 76.9%, p < 0.001). EMT program pass rates for first and cumulative third attempts also varied by NASEMSO region (first: 62-68%; third: 74-78%) with the Great Lakes and West regions outperforming the other regions. Paramedic program pass rates differed by NASEMSO regions as well (first: 65-83%; third: 81-95%) with highest pass rates in the West region.Conclusions Program performance for both EMT and paramedic programs varies by total number of graduates testing and geographic location. Graduates from larger EMT and paramedic programs have higher first and cumulative third attempt pass rates compared to graduates from smaller programs. Additionally, there is variability in program pass rates across NASEMSO regions for both certification levels. Further evaluation is necessary to better understand the variability in program performance in the United States.

Does academic practice protect emergency physicians against burnout?

Burnout is a complex syndrome thought to result from long-term exposure to career-related stressors. Physicians are at higher risk for burnout than the general United States (US) working population, and emergency medicine has some of the highest burnout rates of any medical specialty. Burnout impacts physicians' quality of life, but it can also increase medical errors and negatively affect patient safety. Several studies have reported lower burnout rates and higher job satisfaction in academic medicine as compared with private practice. However, researchers have only begun to explore the factors that underlie this protective effect. This paper aims to review existing literature to identify specific aspects of academic practice in emergency medicine that may be associated with lower physician burnout rates and greater career satisfaction. Broadly, it appears that spending time in the area of emergency medicine one finds most meaningful has been associated with reduced physician burnout. Certain non-clinical academic work, including involvement in research, leadership, teaching, and mentorship, have been identified as specific activities that may protect against burnout and contribute to higher job satisfaction. Given the epidemic of physician burnout, hospitals and practice groups have a responsibility to address burnout, both by prevention and by early recognition and support. We discuss methods by which organizations can actively foster physician well-being and provide examples of 2 leading academic institutions that have developed comprehensive programs to promote physician wellness and prevent burnout.

Mouse ERG K(+) channel clones reveal differences in protein trafficking and function.

BACKGROUND: The mouse ether-a-go-go-related gene 1a (mERG1a, mKCNH2) encodes mERG K(+) channels in mouse cardiomyocytes. The mERG channels and their human analogue, hERG channels, conduct IKr. Mutations in hERG channels reduce IKr to cause congenital long-QT syndrome type 2, mostly by decreasing surface membrane expression of trafficking-deficient channels. Three cDNA sequences were originally reported for mERG channels that differ by 1 to 4 amino acid residues (mERG-London, mERG-Waterston, and mERG-Nie). We characterized these mERG channels to test the postulation that they would differ in their protein trafficking and biophysical function, based on previous findings in long-QT syndrome type 2. METHODS AND RESULTS: The 3 mERG and hERG channels were expressed in HEK293 cells and neonatal mouse cardiomyocytes and were studied using Western blot and whole-cell patch clamp. We then compared our findings with the recent sequencing results in the Welcome Trust Sanger Institute Mouse Genomes Project (WTSIMGP). CONCLUSIONS: First, the mERG-London channel with amino acid substitutions in regions of highly ordered structure is trafficking deficient and undergoes temperature-dependent and pharmacological correction of its trafficking deficiency. Second, the voltage dependence of channel gating would be different for the 3 mERG channels. Third, compared with the WTSIMGP data set, the mERG-Nie clone is likely to represent the wild-type mouse sequence and physiology. Fourth, the WTSIMGP analysis suggests that substrain-specific sequence differences in mERG are a common finding in mice. These findings with mERG channels support previous findings with hERG channel structure-function analyses in long-QT syndrome type 2, in which sequence changes in regions of highly ordered structure are likely to result in abnormal protein trafficking.

Properties of WT and mutant hERG K(+) channels expressed in neonatal mouse cardiomyocytes.

Mutations in human ether-a-go-go-related gene 1 (hERG) are linked to long QT syndrome type 2 (LQT2). hERG encodes the pore-forming alpha-subunits that coassemble to form rapidly activating delayed rectifier K(+) current in the heart. LQT2-linked missense mutations have been extensively studied in noncardiac heterologous expression systems, where biogenic (protein trafficking) and biophysical (gating and permeation) abnormalities have been postulated to underlie the loss-of-function phenotype associated with LQT2 channels. Little is known about the properties of LQT2-linked hERG channel proteins in native cardiomyocyte systems. In this study, we expressed wild-type (WT) hERG and three LQT2-linked mutations in neonatal mouse cardiomyocytes and studied their electrophysiological and biochemical properties. Compared with WT hERG channels, the LQT2 missense mutations G601S and N470D hERG exhibited altered protein trafficking and underwent pharmacological correction, and N470D hERG channels gated at more negative voltages. The DeltaY475 hERG deletion mutation trafficked similar to WT hERG channels, gated at more negative voltages, and had rapid deactivation kinetics, and these properties were confirmed in both neonatal mouse cardiomyocyte and human embryonic kidney (HEK)-293 cell expression systems. Differences between the cardiomyocytes and HEK-293 cell expression systems were that hERG current densities were reduced 10-fold and deactivation kinetics were accelerated 1.5- to 2-fold in neonatal mouse cardiomyocytes. An important finding of this work is that pharmacological correction of trafficking-deficient LQT2 mutations, as a potential innovative approach to therapy, is possible in native cardiac tissue.

Small GTPase determinants for the Golgi processing and plasmalemmal expression of human ether-a-go-go related (hERG) K+ channels.

The pro-arrhythmic Long QT syndrome (LQT) is linked to 10 different genes (LQT1-10). Approximately 40% of genotype-positive LQT patients have LQT2, which is characterized by mutations in the human ether-a-go-go related gene (hERG). hERG encodes the voltage-gated K(+) channel alpha-subunits that form the pore of the rapidly activating delayed rectifier K(+) current in the heart. The purpose of this study was to elucidate the mechanisms that regulate the intracellular transport or trafficking of hERG, because trafficking is impaired for about 90% of LQT2 missense mutations. Protein trafficking is regulated by small GTPases. To identify the small GTPases that are critical for hERG trafficking, we coexpressed hERG and dominant negative (DN) GTPase mutations in HEK293 cells. The GTPases Sar1 and ARF1 regulate the endoplasmic reticulum (ER) export of proteins in COPII and COPI vesicles, respectively. Expression of DN Sar1 inhibited the Golgi processing of hERG, decreased hERG current (I(hERG)) by 85% (n > or = 8 cells per group, *, p < 0.01), and reduced the plasmalemmal staining of hERG. The coexpression of DN ARF1 had relatively small effects on hERG trafficking. Surprisingly, the coexpression of DN Rab11B, which regulates the endosomal recycling, inhibited the Golgi processing of hERG, decreased I(hERG) by 79% (n > or = 8 cells per group; *, p < 0.01), and reduced the plasmalemmal staining of hERG. These data suggest that hERG undergoes ER export in COPII vesicles and endosomal recycling prior to being processed in the Golgi. We conclude that hERG trafficking involves a pathway between the ER and endosomal compartments that influences expression in the plasmalemma.