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Ventilator-induced lung injury
No full textThe purpose of mechanical ventilation is to rest the respiratory muscles while providing adequate gas exchange. Ventilatory support proved to be indispensable during the 1952 polio epidemic in Copenhagen, decreasing mortality among patients with paralytic polio from more than 80% to approximately 40%.1 Despite the clear benefits of this therapy, many patients eventually die after the initiation of mechanical ventilation, even though their arterial blood gases may have normalized.
This mortality has been ascribed to multiple factors, including complications of ventilation such as barotrauma (i.e., gross air leaks), oxygen toxicity, and hemodynamic compromise.2,3 During the polio epidemic, investigators noted that mechanical ventilation could cause structural damage to the lung.4 In 1967, the term “respirator lung” was coined to describe the diffuse alveolar infiltrates and hyaline membranes that were found on postmortem examination of patients who had undergone mechanical ventilation.5 More recently, there has been a renewed focus on the worsening injury that mechanical ventilation can cause in previously damaged lungs and the damage it can initiate in normal lungs. This damage is characterized pathologically by inflammatory-cell infiltrates, hyaline membranes, increased vascular permeability, and pulmonary edema. The constellation of pulmonary consequences of mechanical ventilation has been termed ventilator-induced lung injury.
The concept of ventilator-induced lung injury is not new. In 1744, John Fothergill discussed a case of a patient who was “dead in appearance” after exposure to coal fumes and who was successfully treated by mouth-to-mouth resuscitation.6 Fothergill noted that mouth-to-mouth resuscitation was preferable to using bellows because “the lungs of one man may bear, without injury, as great a force as those of another man can exert; which by the bellows cannot always be determin'd.” Fothergill clearly understood the concept that mechanical forces generated by bellows (i.e., a ventilator) could lead to injury.
However, it was not until early in this century that the clinical importance of ventilator-induced lung injury in adults was confirmed by a study showing that a ventilator strategy designed to minimize such injury decreased mortality among patients with the acute respiratory distress syndrome (ARDS).7 Given the clinical importance of ventilator-induced lung injury, this article will review mechanisms underlying the condition, its biologic and physiological consequences, and clinical strategies to prevent it and mitigate its effects
Mechanical ventilation as a mediator of multisistem organ failure in acute respiratory distress syndrome
No full textIschemia and reperfusion increases susceptibility to ventilator-induced lung injury in rats
No full textOBJECTIVES: Hemorrhagic shock followed by resuscitation (HSR) commonly triggers an inflammatory response that leads to acute respiratory distress syndrome. Hypothesis: HSR exacerbates mechanical stress-induced lung injury by rendering the lung more susceptible to ventilator-induced lung injury. METHODS: Rats were subjected to HSR, and were randomized into an HSR + high tidal volume and zero positive end-expiratory pressure (PEEP) or a HSR + low tidal volume with 5 cm H(2)O PEEP. A sham-operated rat + high tidal volume and zero PEEP served as a control. RESULTS: HSR increased susceptibility to ventilator-induced lung injury as evidenced by an increase in lung elastance and the wet/dry ratio and a reduction in Pa(O(2)) as compared with the other groups. The lung injury observed in the HSR + high tidal volume group was associated with a higher level of interleukin 6 in the lung and blood, increased epithelial cell apoptosis in the kidney and small intestine villi, and a tendency toward high levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and creatinine in plasma. CONCLUSIONS: HSR priming renders the lung and kidney more susceptible to mechanical ventilation-induced organ injury
Mechanical ventilation activates renal endothelial cells in a rat model of acute respiratory distress syndrome
No full textAdaptive support ventilation versus conventional ventilation for total ventilatory support in acute respiratory failure
No full textAbstract
OBJECTIVE: To compare the short-term effects of adaptive support ventilation (ASV), an advanced closed-loop mode, with conventional volume or pressure-control ventilation in patients passively ventilated for acute respiratory failure.
DESIGN: Prospective crossover interventional multicenter trial.
SETTING: Six European academic intensive care units.
PATIENTS: Eighty-eight patients in three groups: patients with no obvious lung disease (n = 22), restrictive lung disease (n = 36) or obstructive lung disease (n = 30).
INTERVENTIONS: After measurements on conventional ventilation (CV) as set by the patients' clinicians, each patient was switched to ASV set to obtain the same minute ventilation as during CV (isoMV condition). If this resulted in a change in PaCO(2), the minute ventilation setting of ASV was readjusted to achieve the same PaCO(2) as in CV (isoCO(2) condition).
MEASUREMENTS AND RESULTS: Compared with CV, PaCO(2) during ASV in isoMV condition and minute ventilation during ASV in isoCO(2) condition were slightly lower, with lower inspiratory work/minute performed by the ventilator (p < 0.01). Oxygenation and hemodynamics were unchanged. During ASV, respiratory rate was slightly lower and tidal volume (Vt) slightly greater (p < 0.01), especially in obstructed patients. During ASV there were different ventilatory patterns in the three groups, with lower Vt in patients with restrictive disease and prolonged expiratory time in obstructed patients, thus mimicking the clinicians' choices for setting CV. In three chronic obstructive pulmonary disease patients the resulting Vt was unacceptably high.
CONCLUSIONS: Comparison between ASV and CV resulted either in similarities or in minor differences. Except for excessive Vt in a few obstructed patients, all differences were in favor of ASV
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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