Critical care : the official journal of the Critical Care Forum
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Consequences of lung recruitment with prolonged high positive end-expiratory pressure (PEEP) ventilation for liver function are unclear. We therefore investigated liver dysfunction during two different ventilation treatment regimens of experimental acute respiratory distress syndrome. ⋯ The PCV+R group showed a more prominent inflammatory reaction in their liver sinusoids accompanied by increased serum levels of liver enzymes and HA. Therefore, recruitment with higher PEEP levels for treatment of respiratory failure might lead to liver dysfunction.
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Clinical Trial
Efficacy of and tolerance to mild induced hypothermia after out-of-hospital cardiac arrest using an endovascular cooling system.
We evaluated the efficacy of and tolerance to mild therapeutic hypothermia achieved using an endovascular cooling system, and its ability to reach and maintain a target temperature of 33 degrees C after cardiac arrest. ⋯ The intravascular cooling system is effective, safe and allows a target temperature to be reached fairly rapidly and steadily over a period of 36 hours.
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Comparative Study
Injurious mechanical ventilation in the normal lung causes a progressive pathologic change in dynamic alveolar mechanics.
Acute respiratory distress syndrome causes a heterogeneous lung injury, and without protective mechanical ventilation a secondary ventilator-induced lung injury can occur. To ventilate noncompliant lung regions, high inflation pressures are required to 'pop open' the injured alveoli. The temporal impact, however, of these elevated pressures on normal alveolar mechanics (that is, the dynamic change in alveolar size and shape during ventilation) is unknown. In the present study we found that ventilating the normal lung with high peak pressure (45 cmH(2)0) and low positive end-expiratory pressure (PEEP of 3 cmH(2)O) did not initially result in altered alveolar mechanics, but alveolar instability developed over time. ⋯ A large change in lung volume with each breath will, in time, lead to unstable alveoli and pulmonary damage. Reducing the change in lung volume by increasing the PEEP, even with high inflation pressure, prevents alveolar instability and reduces injury. We speculate that ventilation with large changes in lung volume over time results in surfactant deactivation, which leads to alveolar instability.
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In patients with acute respiratory distress syndrome (ARDS), supportive therapy with mechanical ventilation and oxygen is often life saving. Further acute lung injury however, is an unfortunate consequence of oxygen therapy as well as mechanical injury secondary to ventilator induced/associated lung injury (VI/ALI). In this issue of Critical Care, Li et al. expand on the intra-cellular signaling pathways regulating interactions between injury cascades resulting from hyperoxia and high tidal volume ventilation. The findings, suggest that interference or cooperation of different signals may have critical consequences as evidenced by indices of increased lung inflammation, microvascular permeability, and lung epithelial apoptotic cell death.
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The origin of hyperlactataemia during critical illness is complex but its presence can provide an indicator of inadequate tissue oxygen delivery. Cardiopulmonary bypass (CPB) represents a unique situation where systemic oxygen delivery can be directly measured and controlled. In the previous issue of Critical Care, Ranucci and colleagues use this phenomenon to identify independent variables associated with the development of hyperlactataemia during CPB. In doing so they highlight the complexity of interpreting hyperlactataemia during critical illness and provide further evidence of its association with worse postoperative morbidity.