ABSTRACT
AIMS: Most out-of-hospital cardiac arrests occur at home with dismal bystander defibrillation rates. We investigated automated external defibrillator coverage of home arrests, and the proportion potentially reachable with an automated external defibrillator before emergency medical service arrival according to different bystander activation strategies. METHODS AND RESULTS: Cardiac arrests in homes (private/nursing/senior homes) in Copenhagen, Denmark (2008-2016) and registered automated external defibrillators (2007-2016), were identified. Automated external defibrillator coverage (distance from arrest to automated external defibrillator) and accessibility at the time of arrest were examined according to route distance to nearest automated external defibrillator and emergency medical service response time. The proportion of arrests reachable with an automated external defibrillator by bystander was calculated using two-way (from patient to automated external defibrillator and back) and one-way (from automated external defibrillator to patient) potential activation strategies. Of 1879 home arrests, automated external defibrillator coverage ≤100 m was low (6.3%) and a two-way bystander could potentially only retrieve an accessible automated external defibrillator before emergency medical service in 31.1% (n=37) of cases. If a bystander only needed to travel one-way to bring an automated external defibrillator (≤100 m, ≤250 m and ≤500 m), 45.4% (n=54/119), 37.1% (n=196/529) and 29.8% (n=350/1174) could potentially be reached before the emergency medical service based on current automated external defibrillator accessibility. CONCLUSIONS: Few home arrests were reachable with an automated external defibrillator before emergency medical service if bystanders needed to travel from patient to automated external defibrillator and back. However, nearly one-third of arrests ≤500 m of an automated external defibrillator could be reached before emergency medical service arrival if the bystander only needed to travel one-way from the automated external defibrillator to the patient.
Subject(s)
Cardiopulmonary Resuscitation/methods , Defibrillators , Emergency Medical Services/methods , Out-of-Hospital Cardiac Arrest/therapy , Registries , Aged , Aged, 80 and over , Female , Follow-Up Studies , Humans , Male , Middle Aged , Retrospective StudiesABSTRACT
Neonatal hypoxic-ischemic encephalopathy causes neurodegeneration and brain injury, leading to sensorimotor dysfunction. Xyloketal B is a novel marine compound isolated from a mangrove fungus Xylaria species (no. 2508) with unique antioxidant effects. In this study, we investigated the effects and mechanism of xyloketal B on oxygen-glucose deprivation-induced neuronal cell death in mouse primary cortical culture and on hypoxic-ischemic brain injury in neonatal mice in vivo. We found that xyloketal B reduced anoxia-induced neuronal cell death in vitro, as well as infarct volume in neonatal hypoxic-ischemic brain injury model in vivo. Furthermore, xyloketal B improved functional behavioral recovery of the animals following hypoxic-ischemic insult. In addition, xyloketal B significantly decreased calcium entry, reduced the number of TUNEL-positive cells, reduced the levels of cleaved caspase-3 and Bax proteins, and increased the level of Bcl-2 protein after the hypoxic-ischemic injury. Our findings indicate that xyloketal B is effective in models of hypoxia-ischemia and thus has potential as a treatment for hypoxic-ischemic brain injury.
