Critical care medicine
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Critical care medicine · Nov 2008
Minimal interruption of cardiopulmonary resuscitation for a single shock as mandated by automated external defibrillations does not compromise outcomes in a porcine model of cardiac arrest and resuscitation.
Current automated external defibrillations require interruptions in chest compressions to avoid artifacts during electrocardiographic analyses and to minimize the risk of accidental delivery of an electric shock to the rescuer. The earlier three-shock algorithm, with prolonged interruptions of chest compressions, compromised outcomes and increased severity of postresuscitation myocardial dysfunction. In the present study, we investigated the effect of timing of minimal automated external defibrillation-mandated interruptions of chest compressions on cardiopulmonary resuscitation outcomes, using a single-shock algorithm. We hypothesized that an 8-sec interruption of chest compressions for a single shock, as mandated by automated external defibrillations, would not impair initial resuscitation and outcomes of cardiopulmonary resuscitation. ⋯ In this experimental model of cardiac arrest and cardiopulmonary resuscitation, minimal automated external defibrillation-mandated interruption of chest compressions for a single-shock algorithm did not have adverse effects on postresuscitation myocardial or neurologic function. All animals, whether subjected to cardiopulmonary resuscitation interruptions or not, survived.
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Critical care medicine · Nov 2008
The use of regional citrate anticoagulation for continuous venovenous hemodiafiltration in acute kidney injury.
Continuous renal replacement therapy is commonly used in the treatment of acute kidney injury. Although the optimal anticoagulation system is not well defined, citrate has emerged as the most promising method. We evaluated the data of 143 patients with acute kidney injury subjected to citrate-based continuous venovenous hemodiafiltration. ⋯ Besides a trend toward higher mortality rate observed in the group with liver failure, we found that citrate-based continuous venovenous hemodiafiltration allowed an effective dialysis dose and reasonable filter patency.
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Critical care medicine · Nov 2008
Neuroprotective effects of the inhalational anesthetics isoflurane and xenon after cardiac arrest in pigs.
Neurologic outcome after cardiopulmonary resuscitation from cardiac arrest carries a poor prognosis and treatment options to ameliorate brain damage are limited. ⋯ Although Xe conferred functional neurologic improvement even when treatment was delayed for 1 hr, the early treatment with either Xe or Iso translated to only marginal functional improvement.
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Critical care medicine · Nov 2008
Treatment-related risk factors for hospital mortality in Candida bloodstream infections.
To examine the relationship between treatment-related variables for Candida bloodstream infection and hospital mortality. ⋯ Treatment-related factors, including retention of central vein catheters and inadequate initial fluconazole dosing, were associated with increased hospital mortality in patients with Candida bloodstream infections. These data suggest that optimization of initial antifungal therapy and removal of central vein catheters may improve the outcomes of patients with Candida bloodstream infections.
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Critical care medicine · Nov 2008
Early mitochondrial dysfunction in electron transfer activity and reactive oxygen species generation after cardiac arrest.
Mitochondrial biology appears central to many conditions that progress to death but remains poorly characterized after cardiac arrest. Mitochondrial dysfunction in electron transfer and reactive oxygen species leakage during ischemia may lead to downstream events including mitochondrial protein oxidation, tyrosine nitrosylation, cytochrome c loss, and eventual death. We sought to better define early fixed alterations in these mitochondrial functions after whole animal cardiac arrest. ⋯ A relatively "orderly" process of mitochondrial dysfunction progresses during ischemia and reperfusion. Changes in mitochondrial reactive oxygen species generation and electron transfer from complex I occur along with tyrosine nitrosylation and loss of cytochrome c; these may represent important new targets for future human therapies.