Resuscitation
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Epinephrine is the drug of choice during advanced cardiac life support. The cumulative dose of epinephrine applied during resuscitation was shown to be independently associated with unfavourable outcome after ventricular fibrillation cardiac arrest in humans. Our objective was to investigate the association between the cumulative dose of epinephrine applied during resuscitation and unfavourable functional outcome and in-hospital mortality, in patients with asystole and pulseless electric activity. ⋯ Our results show that an increasing cumulative dose of epinephrine during resuscitation of patients with asystole and pulseless electric activity is an independent risk factor for unfavourable functional outcome and in-hospital mortality.
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Standard practice within the neonatal unit is to use heated humidified gas as it decreases respiratory complications in neonates requiring respiratory support. Using cold unhumidified gases during resuscitation could potentially cool the baby as well as exacerbate potential lung injury. We aimed to study the temperature and humidity aspects of using heated, humidified gas for neonatal resuscitation. ⋯ This in vitro test showed that heated, humidified gas is possible during neonatal resuscitation. Adequate time must be allowed for the humidifier chamber to warm to near optimal temperature. The patient circuit is initially heated faster than the humidifier chamber. The displayed T1 temperature correlates to the temperature at T3 at ≥28°C.
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The early warning score derived from 198,755 vital sign sets in the Vitalpac™ database (ViEWS) has an area under the receiver operator characteristic curve (AUROC) for death of acute unselected medical patients within 24h of 88%. ⋯ The abbreviated ViEWS score has comparable discrimination to the original score and has reasonable "goodness of fit" for most patients except for those requiring intensive care.
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Ultrastructural evidence of mitochondrial abnormalities in postresuscitation myocardial dysfunction.
Though there is evidence to implicate that the mitochondrion may play an important role in the development of postresuscitation myocardial dysfunction, limited data are available regarding the ultrastructural alterations of the mitochondria, mitochondrial energy-producing ability, and their relationship to postresuscitation myocardial dysfunction. This study was designed to determine whether mitochondrial abnormalities contribute to the development of postresuscitation myocardial dysfunction. ⋯ In this model of cardiac arrest and CPR, the presence of ultrastructural mitochondrial abnormalities, further evidenced by the incapability of utilizing energy substrates and impairment of energy-production, might, in part, contribute to the development of postresuscitation myocardial dysfunction.