Skip to main content

Advertisement

We're creating a new version of this page. See preview

Volume 3 Supplement 1

ESICM LIVES 2015

  • Poster presentation
  • Open Access

Effects of pressure control and pressure support ventilation on ventilator induced lung injury in experimental acute respiratory distress syndrome with intra-abdominal hypertension

  • 1, 2,
  • 1,
  • 1,
  • 1,
  • 1,
  • 3, 4,
  • 1,
  • 5,
  • 6,
  • 2,
  • 1 and
  • 1
Intensive Care Medicine Experimental20153 (Suppl 1) :A806

https://doi.org/10.1186/2197-425X-3-S1-A806

  • Published:

Keywords

  • Lung Injury
  • Acute Respiratory Distress Syndrome
  • Pancuronium
  • Pressure Support Ventilation
  • Ventilator Induce Lung Injury

Introduction

In acute respiratory distress syndrome (ARDS), intra-abdominal hypertension (IAH) increases intra-thoracic pressures, leading atelectasis and deterioration of respiratory mechanics and gas-exchange. The optimal setting of mechanical ventilation (MV) and its impact on respiratory function and ventilator-induced lung injury (VILI) in ARDS associated with IAH needs to be better clarified. Lung-protective MV with low tidal volume (VT) and positive end-expiratory pressure (PEEP) has been recommended; however, assisted MV may be a favorable alternative to controlled MV at the early phase of ARDS, since it requires less sedation, no paralysis and is associated with better lung protection, reducing the risk of VILI. We hypothesized that pressure-support ventilation (PSV) improve pulmonary morphofunction and minimize lung injury in ARDS with IAH.

Objectives

To compare the effects of PSV with protective MV (PCV) on arterial blood gases, lung mechanics and histology, as well as to identify biological markers of inflammation and fibrogenesis in a model of ARDS with IAH.

Methods

24 Wistar rats (250-300 g) were submitted to the a sequence of events: 1) receive Escherichia coli lipopolysaccharide (LPS) intraperitoneally (1,000 µg); 2) waiting period of 24 hours for development of ARDS; 3) anesthesia and mechanical ventilation; 4) induction of IAH (15 mmHg) or not; 5) random assignment to PCV (VT = 6 mL/kg, respiratory rate (RR) = 80 breaths/min, fraction of inspired oxygen (FIO2) = 0.4 and PEEP = 5 cmH2O) or PSV. During PCV, animals were paralyzed with pancuronium bromide. In PCV and PSV, the driving pressure was adjusted to achieve VT = 6 ml/kg. In addition, in PCV, the RR was controlled to keep minute ventilation constant (160 ml/min). Peak (Ppeak,RS), and mean (Pmean,RS) airway pressures and arterial blood gases were analyzed at baseline and at the end of 1 h ventilation. Lungs were removed for lung histology and molecular biology analysis [mRNA expression of interleukin (IL)-6, and pro-collagen type III (PCIII)].

Results

PSV improved oxygenation regardless of IAH. In ARDS with IAH, PSV, compared to PCV group, was associated with greater reduction in Ppeak,RS (PSV: 11.4 ± 2.4 cmH2O, PCV: 16.9 ± 0.5 cmH2O, p < 0.05) and Pmean,RS (PSV: 5.8 ± 1.9 cmH2O, PCV: 9.6 ± 0.2 cmH2O, p < 0.05). Furthermore, PSV reduced the amount of alveolar collapse, and the mRNA expression of interleukin (IL)-6 and type III procollagen compared to PCV.

Conclusions

In this model of ARDS with IAH, PSV, compared to PCV, promoted functional and lung morphological benefit thus mitigating VILI.

Grant Acknowledgment

CNPq, FAPERJ, CAPES, PRONEX, INCT-INOFAR

Authors’ Affiliations

(1)
Laboratory of Pulmonary Investigation, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
(2)
Department of Surgery, Faculty of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
(3)
D'Or Institute for Research and Education, Hospital Copa D'Or, Rio de Janeiro, Brazil
(4)
D'Or Institute for Research and Education, Hospital Caxias D'Or, Duque de Caxias, Brazil
(5)
Department of Anesthesiology, Dresden University of Technology, Dresden, Germany
(6)
Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy

References

  1. Rocco PR, Pelosi P: Pulmonary and extrapulmonary acute respiratory distress syndrome: myth or reality?. Curr Opin Crit Care. 2008, 14: 50-55. 10.1097/MCC.0b013e3282f2405b.PubMedView ArticleGoogle Scholar
  2. Quintel M, Pelosi P, Caironi P, et al: An increase of abdominal pressure increases pulmonary edema in oleic acid-induced lung injury. Am J Respir Crit Care Med. 2004, 169: 534-541. 10.1164/rccm.200209-1060OC.PubMedView ArticleGoogle Scholar

Copyright

© Santos et al.; 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Advertisement