The Effect of Positive end Expiratory pressure on the Pulmonary Capillary Pressure in Acute Lung Injury Patients

2000 ◽  
Vol 49 (5) ◽  
pp. 594
Author(s):  
Byung Chun Chung ◽  
Chang Gyoo Byun ◽  
Chang Youl Lee ◽  
Hyung Jung Kim ◽  
Chul Min An ◽  
...  
2002 ◽  
Vol 30 (2) ◽  
pp. 403-409 ◽  
Author(s):  
Andrew A. Pellett ◽  
Kevin C. Lord ◽  
Michael S. Champagne ◽  
Bennett P. deBoisblanc ◽  
Royce W. Johnson ◽  
...  

1995 ◽  
Vol 83 (6) ◽  
pp. 1153-1161 ◽  
Author(s):  
A. Benzing ◽  
P. Brautigam ◽  
K. Geiger ◽  
T. Loop ◽  
U. Beyer ◽  
...  

Abstract Background In acute lung injury, when pulmonary microvascular permeability is enhanced, transvascular fluid filtration mainly depends on pulmonary capillary pressure. Inhaled nitric oxide has been shown to decrease pulmonary capillary pressure. Therefore, the effect of inhaled nitric oxide at a concentration of 40 ppm on pulmonary transvascular albumin flux was studied in nine patients with acute lung injury.


1992 ◽  
Vol 39 (6) ◽  
pp. 474-483
Author(s):  
Chul Gyu Yoo ◽  
Young Whan Kim ◽  
Sung Koo Han ◽  
Young Soo Shim ◽  
Keun Youl Kim ◽  
...  

2006 ◽  
Vol 34 (4) ◽  
pp. 1106-1112 ◽  
Author(s):  
Josefina López-Aguilar ◽  
Enrique Piacentini ◽  
Ana Villagrá ◽  
Gastón Murias ◽  
Sara Pascotto ◽  
...  

1994 ◽  
Vol 76 (3) ◽  
pp. 1324-1329 ◽  
Author(s):  
B. P. Kavanagh ◽  
A. Mouchawar ◽  
J. Goldsmith ◽  
R. G. Pearl

Inhaled nitric oxide (NO) decreases pulmonary arterial pressure (Ppa) and improves oxygenation in the adult respiratory distress syndrome. Endogenous NO can modulate the development of acute tissue injury. We investigated the effects of inhaled NO and of inhibition of endogenous NO synthase in oxidant-induced acute lung injury in the isolated buffer-perfused rabbit lung. A rapid (45 min) and a more gradual (3 h) model of oxidant-induced acute lung injury were developed using the production of superoxide free radicals from the reaction of purine with low and high doses of xanthine oxidase, respectively. The effects of rapid injury included increases in Ppa, precapillary pulmonary vascular resistance, capillary filtration coefficient (Kfc), and lung weight. In the gradual-injury model, only lung weight and Kfc increased. Pretreatment with inhaled NO (90–120 ppm) prevented the rise in Ppa and precapillary pulmonary vascular resistance in the rapid-injury model and prevented elevation of Kfc in the gradual-injury model. Pretreatment with an inhibitor of endogenous NO synthase (NG-nitro-L-arginine methyl ester) resulted in increased pulmonary capillary pressure and postcapillary pulmonary vascular resistance in the rapid-injury model and increased peak Ppa, pulmonary capillary pressure, and pulmonary vascular resistance in the gradual-injury model. These data suggest that in oxidant-induced acute lung injury 1) inhaled NO may attenuate increases in capillary permeability and 2) endogenous NO may function as a modulator of pulmonary vascular tone without affecting capillary permeability.


1968 ◽  
Vol 07 (02) ◽  
pp. 125-129
Author(s):  
J. Měštan ◽  
V. Aschenbrenner ◽  
A. Michaljanič

SummaryIn patients with acquired and congenital valvular heart disease correlations of the parameters of the radiocardiographic curve (filling time of the right heart, minimal pulmonary transit time, peak-to-peak pulmonary transit time, and the so-called filling time of the left heart) with the mean pulmonary artery pressure and the mean pulmonary “capillary” pressure were studied. Further, a regression equation was determined by means of which the mean pulmonary “capillary” pressure can be predicted.


2012 ◽  
Vol 117 (6) ◽  
pp. 1322-1334 ◽  
Author(s):  
Aline M. Ambrosio ◽  
Rubin Luo ◽  
Denise T. Fantoni ◽  
Claudia Gutierres ◽  
Qin Lu ◽  
...  

Background In acute lung injury positive end-expiratory pressure (PEEP) and recruitment maneuver are proposed to optimize arterial oxygenation. The aim of the study was to evaluate the impact of such a strategy on lung histological inflammation and hyperinflation in pigs with acid aspiration-induced lung injury. Methods Forty-seven pigs were randomly allocated in seven groups: (1) controls spontaneously breathing; (2) without lung injury, PEEP 5 cm H2O; (3) without lung injury, PEEP titration; (4) without lung injury, PEEP titration + recruitment maneuver; (5) with lung injury, PEEP 5 cm H2O; (6) with lung injury, PEEP titration; and (7) with lung injury, PEEP titration + recruitment maneuver. Acute lung injury was induced by intratracheal instillation of hydrochloric acid. PEEP titration was performed by incremental and decremental PEEP from 5 to 20 cm H2O for optimizing arterial oxygenation. Three recruitment maneuvers (pressure of 40 cm H2O maintained for 20 s) were applied to the assigned groups at each PEEP level. Proportion of lung inflammation, hemorrhage, edema, and alveolar wall disruption were recorded on each histological field. Mean alveolar area was measured in the aerated lung regions. Results Acid aspiration increased mean alveolar area and produced alveolar wall disruption, lung edema, alveolar hemorrhage, and lung inflammation. PEEP titration significantly improved arterial oxygenation but simultaneously increased lung inflammation in juxta-diaphragmatic lung regions. Recruitment maneuver during PEEP titration did not induce additional increase in lung inflammation and alveolar hyperinflation. Conclusion In a porcine model of acid aspiration-induced lung injury, PEEP titration aimed at optimizing arterial oxygenation, substantially increased lung inflammation. Recruitment maneuvers further improved arterial oxygenation without additional effects on inflammation and hyperinflation.


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