Pressure Support Ventilation versus Pressure Controlled Ventilation with the proseal laryngeal mask airway: a randomised comparative and prospective study of anesthetized adult patients

2004 ◽  
Vol 21 (Supplement 32) ◽  
pp. 68
Author(s):  
N. Bernard ◽  
S. Bringuier-Branchereau ◽  
X. Capdevila
2020 ◽  
Vol 132 (2) ◽  
pp. 307-320 ◽  
Author(s):  
Eliete F. Pinto ◽  
Raquel S. Santos ◽  
Mariana A. Antunes ◽  
Ligia A. Maia ◽  
Gisele A. Padilha ◽  
...  

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Pressure-support ventilation may worsen lung damage due to increased dynamic transpulmonary driving pressure. The authors hypothesized that, at the same tidal volume (VT) and dynamic transpulmonary driving pressure, pressure-support and pressure-controlled ventilation would yield comparable lung damage in mild lung injury. Methods Male Wistar rats received endotoxin intratracheally and, after 24 h, were ventilated in pressure-support mode. Rats were then randomized to 2 h of pressure-controlled ventilation with VT, dynamic transpulmonary driving pressure, dynamic transpulmonary driving pressure, and inspiratory time similar to those of pressure-support ventilation. The primary outcome was the difference in dynamic transpulmonary driving pressure between pressure-support and pressure-controlled ventilation at similar VT; secondary outcomes were lung and diaphragm damage. Results At VT = 6 ml/kg, dynamic transpulmonary driving pressure was higher in pressure-support than pressure-controlled ventilation (12.0 ± 2.2 vs. 8.0 ± 1.8 cm H2O), whereas static transpulmonary driving pressure did not differ (6.7 ± 0.6 vs. 7.0 ± 0.3 cm H2O). Diffuse alveolar damage score and gene expression of markers associated with lung inflammation (interleukin-6), alveolar-stretch (amphiregulin), epithelial cell damage (club cell protein 16), and fibrogenesis (metalloproteinase-9 and type III procollagen), as well as diaphragm inflammation (tumor necrosis factor-α) and proteolysis (muscle RING-finger-1) were comparable between groups. At similar dynamic transpulmonary driving pressure, as well as dynamic transpulmonary driving pressure and inspiratory time, pressure-controlled ventilation increased VT, static transpulmonary driving pressure, diffuse alveolar damage score, and gene expression of markers of lung inflammation, alveolar stretch, fibrogenesis, diaphragm inflammation, and proteolysis compared to pressure-support ventilation. Conclusions In the mild lung injury model use herein, at the same VT, pressure-support compared to pressure-controlled ventilation did not affect biologic markers. However, pressure-support ventilation was associated with a major difference between static and dynamic transpulmonary driving pressure; when the same dynamic transpulmonary driving pressure and inspiratory time were used for pressure-controlled ventilation, greater lung and diaphragm injury occurred compared to pressure-support ventilation.


2012 ◽  
Vol 116 (6) ◽  
pp. 1227-1234 ◽  
Author(s):  
Oliver C. Radke ◽  
Thomas Schneider ◽  
Axel R. Heller ◽  
Thea Koch

Background Positive-pressure ventilation causes a ventral redistribution of ventilation. Spontaneous breathing during general anesthesia with a laryngeal mask airway could prevent this redistribution of ventilation. We hypothesize that, compared with pressure-controlled ventilation, spontaneous breathing and pressure support ventilation reduce the extent of the redistribution of ventilation as detected by electrical impedance tomography. Methods The study was a randomized, three-armed, observational, clinical trial without blinding. With approval from the local ethics committee, we enrolled 30 nonobese patients without severe cardiac or pulmonary comorbidities who were scheduled for elective orthopedic surgery. All of the procedures were performed under general anesthesia with a laryngeal mask airway and a standardized anesthetic regimen. The center of ventilation (primary outcome) was calculated before the induction of anesthesia (AWAKE), after the placement of the laryngeal mask airway (BEGIN), before the end of anesthesia (END), and after arrival in the postanesthesia care unit (PACU). Results The center of ventilation during anesthesia (BEGIN) was higher than baseline (AWAKE) in both the pressure-controlled and pressure support ventilation groups (pressure control: 55.0 vs. 48.3, pressure support: 54.7 vs. 48.8, respectively; multivariate analysis of covariance, P < 0.01), whereas the values in the spontaneous breathing group remained at baseline levels (47.9 vs. 48.5). In the postanesthesia care unit, the center of ventilation had returned to the baseline values in all groups. No adverse events were recorded. Conclusions Both pressure-controlled ventilation and pressure support ventilation induce a redistribution of ventilation toward the ventral region, as detected by electrical impedance tomography. Spontaneous breathing prevents this redistribution.


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