Secondary Public Safety Answering Points Delay the Response to out of Hospital Cardiac Arrest.

Background: National guidelines recommend that high-performing systems process 9-1-1 calls within 60 s and deliver the first telecommunicator cardiopulmonary resuscitation compression within 90 s. The inability of systems employing secondary public safety answering points (PSAPs) to capture the call arrival timestamp at the primary PSAP is a challenge in out-of-hospital cardiac arrest response time research.Objective: We sought to measure the interval from call receipt at primary PSAPs to call answer at secondary PSAPs in metropolitan areas.Methods: This was a retrospective observational study evaluating 9-1-1 call transfers between PSAPs serving large urban populations. Call transfer records were extracted from the 9-1-1 telephony systems at the primary and secondary PSAPs covering seven metropolitan EMS systems. For each transferred call, we obtained the call arrival timestamp at both the primary and secondary PSAPs. The primary outcome was the interval between these two times. Results were compared to a national standard of 90% of calls forwarded within 30 s of receipt.Results: Data collected at seven metropolitan EMS agencies from January 1, 2021, through June 30, 2021, yielded 299,679 records for evaluation. The median interval required to transfer a 9-1-1 caller from primary to secondary PSAPs was 41 s (IQR 31, 59), and 86 s at the 90th percentile. The 90th percentile performance level at individual agencies ranged from 63 s to 117 s.Conclusions: The primary to secondary PSAP transfer interval lengths observed in this study preclude these EMS agencies from meeting out-of-hospital cardiac arrest performance recommendations at the 90% percentile performance level.

Determination of Endovaginal Ultrasound Proficiency and Learning Curve Among Emergency Medicine Trainees.

OBJECTIVES: Performing and interpreting endovaginal ultrasound is an important skill used during the evaluation of obstetric and gynecologic emergencies. This study aims to describe the level of proficiency and confidence achieved after performing 25 endovaginal examinations. METHODS: This is a prospective study at a single urban academic emergency department. Participants performed a minimum of 25 endovaginal ultrasounds under the supervision of a point-of-care ultrasound expert. Anatomical structures were identified by the expert under ultrasound prior to each session. Each examination was scored for agreement of findings between the participant and expert. The data were used to develop a performance curve identifying when proficiency was achieved, where experiential benefit diminished, and when participants felt confident. RESULTS: A total of 1117 endovaginal ultrasound examinations were performed by 50 participants. Agreement after 25 examinations was highest (>95%) for probe insertion and preparation, bladder and uterus identification, and directionality. Agreement was lowest for identification of the ovaries (76%). Experiential benefit plateaus occurred earliest (10 exams) for preparation and insertion followed by bladder identification and directionality. Surprisingly, ovarian experiential benefit plateaued at 16 exams. Participant confidence improved overall and was lowest for the identification of ovaries and abnormal pelvic anatomy. CONCLUSIONS: There is a significant learning curve when performing endovaginal ultrasound. Our data do not support the use of 25 examinations as a minimum standard for identification of the ovaries or abnormal ovarian pathology.

Immune complexes containing malondialdehyde (MDA) LDL induce apoptosis in human macrophages.

Immune complexes (IC) containing predominantly malondialdehyde-LDL and the corresponding autoantibodies (MDA-LDL IC) predict acute cardiovascular events, while IC rich in oxidized LDL (oxLDL IC) predict cardiovascular disease progression. Our objective was to determine mechanisms that could explain these prognostic differences. We compared the effects of the interaction of oxLDL, MDA-LDL and the corresponding IC with human macrophages focusing on apoptosis, metalloproteinases, and proinflammatory cytokines. MDA-LDL IC induced higher degrees of apoptosis, higher levels of caspase-3 expression, and increased expression and release of MMP-1 and TNF compared to MDA-LDL, oxLDL, and oxLDL IC. The pro-apoptotic effects of MDA-LDL IC were inhibited by blocking TNFR 1 or FcγRI. Blocking FcγRI abrogated the induction and expression of MMPs and proinflammatory cytokines by MDA-LDL IC. In conclusion, the interaction of MDA-LDL IC with FcγRI triggers macrophage apoptosis and increased expression and release of TNF and MMP-1, which can lead to the rupture of unstable plaques.

Pseudouridine synthase 1 deficient mice, a model for Mitochondrial Myopathy with Sideroblastic Anemia, exhibit muscle morphology and physiology alterations.

Mitochondrial myopathy with lactic acidosis and sideroblastic anemia (MLASA) is an oxidative phosphorylation disorder, with primary clinical manifestations of myopathic exercise intolerance and a macrocytic sideroblastic anemia. One cause of MLASA is recessive mutations in PUS1, which encodes pseudouridine (Ψ) synthase 1 (Pus1p). Here we describe a mouse model of MLASA due to mutations in PUS1. As expected, certain Ψ modifications were missing in cytoplasmic and mitochondrial tRNAs from Pus1(-/-) animals. Pus1(-/-) mice were born at the expected Mendelian frequency and were non-dysmorphic. At 14 weeks the mutants displayed reduced exercise capacity. Examination of tibialis anterior (TA) muscle morphology and histochemistry demonstrated an increase in the cross sectional area and proportion of myosin heavy chain (MHC) IIB and low succinate dehydrogenase (SDH) expressing myofibers, without a change in the size of MHC IIA positive or high SDH myofibers. Cytochrome c oxidase activity was significantly reduced in extracts from red gastrocnemius muscle from Pus1(-/-) mice. Transmission electron microscopy on red gastrocnemius muscle demonstrated that Pus1(-/-) mice also had lower intermyofibrillar mitochondrial density and smaller mitochondria. Collectively, these results suggest that alterations in muscle metabolism related to mitochondrial content and oxidative capacity may account for the reduced exercise capacity in Pus1(-/-) mice.