Critical care medicine
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Critical care medicine · Nov 2008
Multicenter StudyFrom laboratory science to six emergency medical services systems: New understanding of the physiology of cardiopulmonary resuscitation increases survival rates after cardiac arrest.
The purpose of this study is to: 1) describe a newly mechanism of blood flow to the brain during cardiopulmonary resuscitation using the impedance threshold device in a piglet model of cardiac arrest, and 2) describe the survival benefits in humans of applying all of the highly recommended changes in the 2005 guidelines related to increasing circulation during cardiopulmonary resuscitation, including use of the impedance threshold device, from six emergency medical services systems in the United States. ⋯ Use of the impedance threshold device in piglets increased carotid blood flow and coronary and cerebral perfusion pressures and reduced intracranial pressure during the decompression phase of cardiopulmonary resuscitation at a faster rate than controls, resulting in a longer duration of time when intracranial pressures are at their nadir. Patients in six emergency medical services systems treated with the impedance threshold device together with the renewed emphasis on more compressions, fewer ventilations, and complete chest wall recoil had a nearly 50% increase in survival rates after out-of-hospital cardiac arrest compared with historical controls.
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Critical care medicine · Nov 2008
Comparative StudyEffects of elevating the head of bed on interface pressure in volunteers.
Intensive care unit patients are at particular risk for pressure ulcers and ventilator-associated pneumonia. Current guidelines recommend that mechanically ventilated patients be kept in a semirecumbent position with the head of bed elevated 30 degrees -45 degrees to prevent aspiration and ventilator-associated pneumonia. We tested the effects of elevating the head of bed on the interface pressure between the skin of the sacral area and the bed with healthy volunteers. ⋯ Raising the head of bed to 30 degrees or higher on a intensive care unit bed increases the peak interface pressure between the skin at the sacral area and support surface in healthy volunteers. At 45 degrees head of bed elevation or higher, the affected area attributed to a skin-intensive care unit bed interface pressure >or=32 mm Hg increased as well. Further study is needed to determine whether the increased peak interface pressures and affected areas that result from raising the head of bed actually increase the incidence of pressure ulcer formation.
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Critical care medicine · Nov 2008
Excessive tidal volume from breath stacking during lung-protective ventilation for acute lung injury.
Low tidal volume ventilation strategies for patients with respiratory failure from acute lung injury may lead to breath stacking and higher volumes than intended. ⋯ Stacked breaths occur frequently in low tidal volume ventilation despite deep sedation and result in volumes substantially above the set tidal volume. Set tidal volume has a strong influence on frequency of stacked breaths.
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Critical care medicine · Nov 2008
Impaired baroreflex sensitivity predicts outcome of acute intracerebral hemorrhage.
Impaired blood pressure regulation in the acute phase of stroke has been associated with less favorable outcome. Mechanisms and effects of blood pressure dysregulation in stroke are not well understood; however, central autonomic impairment with sympathetic overactivity and baroreflex involvement are discussed. Baroreflex sensitivity (BRS) in spontaneous intracerebral hemorrhage has not been investigated. We sought to examine BRS in patients with intracerebral hemorrhage and evaluate the relationship between BRS and short-term outcome measures. ⋯ We found that BRS was decreased in patients with acute intracerebral hemorrhage and correlated with increased beat-to-beat blood pressure variability. BRS independently predicted outcome at 10 days. Modulation of baroreceptor reflex sensitivity may represent a new therapeutic target in acute stroke and warrants future studies.
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Critical care medicine · Nov 2008
ReviewTargeting mitochondria for resuscitation from cardiac arrest.
Reversal of cardiac arrest requires reestablishment of aerobic metabolism by reperfusion with oxygenated blood of tissues that have been ischemic for variable periods of time. However, reperfusion concomitantly activates a myriad of pathogenic mechanisms causing what is known as reperfusion injury. At the center of reperfusion injury are mitochondria, playing a critical role as effectors and targets of injury. ⋯ Additional studies in similar animal models of ventricular fibrillation have shown that mitochondrial injury leads to activation of the mitochondrial apoptotic pathway, characterized by the release of cytochrome c to the cytosol, reduction of caspase-9 levels, and activation of caspase-3 coincident with marked reduction in left ventricular function. Cytochrome c also "leaks" into the bloodstream attaining levels that are inversely proportional to survival. These data indicate that mitochondria play a key role during cardiac resuscitation by modulating energy metabolism and signaling apoptotic cascades and that targeting mitochondria could represent a promising strategy for cardiac resuscitation.