Resuscitation
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The incidence and timing of electrographic seizures and epileptiform activity in comatose, adult, post-cardiac arrest syndrome (PCAS) patients treated with therapeutic hypothermia (TH) have not been extensively investigated. We hypothesized that onset most frequently occurs within the first 24 h post-arrest and is associated with poor neurologic outcome. ⋯ Electrographic seizures and epileptiform activity are common cEEG findings in comatose, PCAS patients treated with TH. In this preliminary study, most seizures were status epilepticus, had onset prior to rewarming, evolved from prior interictal epileptiform activity, and were associated with short-term mortality and poor neurologic outcome. Larger, prospective studies are needed to further characterize seizure activity in comatose post-arrest patients.
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Randomized Controlled Trial
BML-111, a lipoxin receptor agonist, protects haemorrhagic shock-induced acute lung injury in rats.
The main pathogenesis of acute lung injury induced by haemorrhagic shock is inflammation. BML-111, a lipoxinA(4)-receptor agonist, promotes acute inflammatory resolution. We sought to elucidate whether BML-111 protects haemorrhagic shock-induced acute lung injury in rats. ⋯ BML-111 protects haemorrhagic shock-induced acute lung injury in rats.
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Mild therapeutic hypothermia (TH) has been shown to improve neurologic outcome in patients experiencing cardiac arrest after return of spontaneous circulation (ROSC). The best timing to initiate TH is currently not known. The aim of this study by the ICE (Italian Cooling Experience) group was to investigate the relationship between the timing of initiation of therapeutic hypothermia (TH) and both patient survival and neurologic outcome. ⋯ Despite similar neurologic outcomes at every time point, mortality was significantly higher when therapeutic hypothermia was started within 2h of cardiac arrest than when it was started later. Due to the lack of possibility to control several putative confounding factors, such results should be considered as preliminary observations warranting further research.
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To explore the molecular mechanisms by which mild hypothermia following resuscitation improves neurological function in a porcine model of cardiac arrest. ⋯ Brain protection induced by hypothermia involves inhibition of inflammatory and brain edema pathways.
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The amount of myocardial perfusion required for successful defibrillation after cardiac arrest is unknown. Coronary perfusion pressure (CPP) is a surrogate for myocardial perfusion. One limited clinical study identifies a threshold of 15 mmHg required for return of spontaneous circulation (ROSC). Our exploration of threshold and dose models of CPP during the initial bout of CPR indicates higher levels than previously demonstrated are required. CPP required for shock success throughout on-going resuscitation is unknown and other conceptual models of CPP have not been explored. ⋯ Threshold, delta, cumulative delta, dose, and cumulative dose CPP predict individual defibrillation success throughout resuscitation.