Alveolar edema dispersion and alveolar protein permeability during high volume ventilation: effect of positive end-expiratory pressure

2007 ◽  
Vol 33 (4) ◽  
pp. 711-717 ◽  
Author(s):  
Nicolas de Prost ◽  
Damien Roux ◽  
Didier Dreyfuss ◽  
Jean-Damien Ricard ◽  
Dominique Le Guludec ◽  
...  
1992 ◽  
Vol 73 (5) ◽  
pp. 2089-2096 ◽  
Author(s):  
E. D. Rider ◽  
A. H. Jobe ◽  
M. Ikegami ◽  
B. Sun

The effect of ventilation strategy on in vivo function of different surfactants was evaluated in preterm rabbits delivered at 27 days gestational age and ventilated with either 0 cmH2O positive end-expiratory pressure (PEEP) at tidal volumes of 10–11 ml/kg or 3 cmH2O PEEP at tidal volumes of 7–8 ml/kg after treatment with one of four different surfactants: sheep surfactant, the lipids of sheep surfactant stripped of protein (LH-20 lipid), Exosurf, and Survanta. The use of 3 cmH2O PEEP decreased pneumothoraces in all groups except for the sheep surfactant group where pneumothoraces increased (P < 0.01). Ventilatory pressures (peak pressures - PEEP) decreased more with the 3 cmH2O PEEP, low-tidal-volume ventilation strategy for Exosurf-, Survanta-, and sheep surfactant-treated rabbits (P < 0.05), whereas ventilation efficiency indexes (VEI) improved only for Survanta- and sheep surfactant-treated rabbits with 3 cmH2O PEEP (P < 0.01). Pressure-volume curves for sheep surfactant-treated rabbits were better than for all other treated groups (P < 0.01), although Exosurf and Survanta increased lung volumes above those in control rabbits (P < 0.05). The recovery of intravascular radiolabeled albumin in the lungs and alveolar washes was used as an indicator of pulmonary edema. Only Survanta and sheep surfactant decreased protein leaks in the absence of PEEP, whereas all treatments decreased labeled albumin recoveries when 3 cmH2O PEEP was used (P < 0.05). These experiments demonstrate that ventilation style will alter a number of measurements of surfactant function, and the effects differ for different surfactants.


2020 ◽  

Objective: Clinical studies have shown that eliminating performer errors is important to ensure high quality cardiopulmonary resuscitation (CPR). Literature on the effects of metronome use on the quality of CPR is scarce. This study aimed to investigate the effect of metronome use on the quality of cardiopulmonary resuscitation. Methods: Thirty volunteer emergency physicians who were divided into 15 groups participated in this prospective, observational, multi-center, manikin study. Firstly, each participant performed conventional CPR on a manikin, and then performed metronome-guided CPR after a short break. Parameters affecting CPR quality were evaluated based on the recommendations of the 2015 American Heart Association CPR and Emergency Cardiovascular Care Guideline. In addition, the fatigue levels of participants were evaluated using the Borg Fatigue Index. Results: Metronome-guided CPR significantly improved the chest compression rate (median (Interquartile Range-IQR); 128 (22) compressions/min vs. 110 (2) compressions/min; 95%CI, p < 0.001), deep compression rate (median (IQR); 95.25 (80) compressions/min vs. 72.63 (105) compressions/min; 95%CI, p < 0.001), compression depth (median (IQR); 62.50 (11) mm vs. 60.25 (14) mm; 95%CI, p = 0.016), ventilation number (median (IQR); 11.25 (6) ventilations/min vs. 9.50 (1) ventilations/min; 95%CI, p = 0.001), high-volume ventilation count (median (IQR); 10.13 (6) ventilations/min vs. 9.50 (1) ventilations/min; 95%CI, p = 0.026), minute ventilation volume (median (IQR); 11.75 (10) L/min vs. 8.03 (3) L/min; 95%CI, p < 0.05), and fatigue levels (median (IQR); 3 (2) vs. 2 (2); in 95%CI, p < 0.05). Conclusions: Our study showed that metronome is a useful device for reaching effective CPR. Metronome guidance may change the CPR parameters positively. This study is in accordance with previous studies which have investigated the effect of metronome-guided CPR on survival.


CHEST Journal ◽  
1988 ◽  
Vol 93 (5) ◽  
pp. 1035-1037 ◽  
Author(s):  
Jorge Serra ◽  
Kathleen W. McNicholas ◽  
Roger Moore ◽  
Gerald M. Lemole

2007 ◽  
Vol 292 (1) ◽  
pp. L144-L153 ◽  
Author(s):  
Daisuke Okutani ◽  
Bing Han ◽  
Marco Mura ◽  
Thomas K. Waddell ◽  
Shaf Keshavjee ◽  
...  

Pentraxin 3 (PTX3) is an acute-phase protein, which can be produced by a variety of tissue cells at the site of infection or inflammation. It plays an important role in innate immunity in the lung and in mediating acute lung injury. The aim of this study was to determine the effect of mechanical ventilation on PTX3 expression in multiple lung injury models. Male Sprague-Dawley rats were challenged with intravenous injection of lipopolysaccharide (LPS) or hemorrhage followed by resuscitation (HS). The animals were then subjected to either relatively higher (12 ml/kg) or lower (6 ml/kg, positive end-expiratory pressure of 5 cmH2O) volume ventilation for 4 h. High-volume ventilation significantly enhanced PTX3 expression in the lung, either alone or in combination with LPS or hemorrhage. A significant increase of PTX3 immunohistochemistry staining in the lung was seen in all injury groups. The PTX3 expression was highly correlated with the severity of lung injury determined by blood gas, lung elastance, and wet-to-dry ratio. To determine the effects of HS, LPS, or injurious ventilation (25 ml/kg) alone on PTX3 expression, another group of rats was studied. Injurious ventilation significantly damaged the lung and increased PTX3 expression. A local expression of PTX3 induced by high-volume ventilation, either alone or in combination with other pathological conditions, suggests that it may be an important mediator in ventilator-induced lung injury.


1999 ◽  
Vol 27 (9) ◽  
pp. 1940-1945 ◽  
Author(s):  
Peter C. Rimensberger ◽  
Gorsev Pristine ◽  
J. Brendan M. Mullen ◽  
Peter N. Cox ◽  
Arthur S. Slutsky

2005 ◽  
Vol 98 (4) ◽  
pp. 1264-1271 ◽  
Author(s):  
Sawako Yoshikawa ◽  
Takashige Miyahara ◽  
Susan D. Reynolds ◽  
Barry R. Stripp ◽  
Mircea Anghelescu ◽  
...  

Lung vascular permeability is acutely increased by high-pressure and high-volume ventilation. To determine the roles of mechanically activated cytosolic PLA2 (cPLA2) and Clara cell secretory protein (CCSP), a modulator of cPLA2 activity, we compared lung injury with and without a PLA2 inhibitor in wild-type mice and CCSP-null mice (CCSP−/−) ventilated with high and low peak inflation pressures (PIP) for 2- or 4-h periods. After ventilation with high PIP, we observed significant increases in the bronchoalveolar lavage albumin concentrations, lung wet-to-dry weight ratios, and lung myeloperoxidase in both genotypes compared with unventilated controls and low-PIP ventilated mice. All injury variables except myeloperoxidase were significantly greater in the CCSP−/− mice relative to wild-type mice. Inhibition of cPLA2 in wild-type and CCSP−/− mice ventilated at high PIP for 4 h significantly reduced bronchoalveolar lavage albumin and total protein and lung wet-to-dry weight ratios compared with vehicle-treated mice of the same genotype. Membrane phospho-cPLA2 and cPLA2 activities were significantly elevated in lung homogenates of high-PIP ventilated mice of both genotypes but were significantly higher in the CCSP−/− mice relative to the wild-type mice. Inhibition of cPLA2 significantly attenuated both the phospho-cPLA2 increase and increased cPLA2 activity due to high-PIP ventilation. We propose that mechanical activation of the cPLA2 pathway contributes to acute high PIP-induced lung injury and that CCSP may reduce this injury through inhibition of the cPLA2 pathway and reduction of proinflammatory products produced by this pathway.


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