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Effects of positive end-expiratory pressure on dead space and its partitions in acute lung injury

Beydon, L ; Uttman, Leif LU ; Rawal, R and Jonson, Björn LU (2002) In Intensive Care Medicine 28(9). p.1239-1245
Abstract
Objective: A large tidal volume (VT) and lung collapse and re-expansion may cause ventilator-induced lung injury (VILI) in acute lung injury (ALI). A low VT and a positive end-expiratory pressure (PEEP) can prevent VILI, but the more VT is reduced, the more dead space (VD) compromises gas exchange. We investigated how physiological, airway and alveolar VD varied with PEEP and analysed possible links to respiratory mechanics. Setting: Medical and surgical intensive care unit (ICU) in a university hospital. Design: Prospective, non-randomised comparative trial. Patients: Ten consecutive ALI patients. Intervention: Stepwise increases in PEEP from zero to 15 cmH(2)O. Measurements and results: Lung mechanics and VD were measured at each PEEP... (More)
Objective: A large tidal volume (VT) and lung collapse and re-expansion may cause ventilator-induced lung injury (VILI) in acute lung injury (ALI). A low VT and a positive end-expiratory pressure (PEEP) can prevent VILI, but the more VT is reduced, the more dead space (VD) compromises gas exchange. We investigated how physiological, airway and alveolar VD varied with PEEP and analysed possible links to respiratory mechanics. Setting: Medical and surgical intensive care unit (ICU) in a university hospital. Design: Prospective, non-randomised comparative trial. Patients: Ten consecutive ALI patients. Intervention: Stepwise increases in PEEP from zero to 15 cmH(2)O. Measurements and results: Lung mechanics and VD were measured at each PEEP level. Physiological VD was 41-64% of VT at zero PEEP and increased slightly with PEEP due to a rise in airway VD. Alveolar VD was 11-38% of VT and did not vary systematically with PEEP. However, in individual patients a decrease and increase of alveolar VD paralleled a positive or negative response to PEEP with respect to oxygenation (shunt), respectively. VD fractions were independent of respiratory resistance and compliance. Conclusions: Alveolar VD is large and does not vary systematically with PEEP in patients with various degrees of ALI. Individual measurements show a diverse response to PEEP. Respiratory mechanics were of no help in optimising PEEP with regard to gas exchange. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
acute lung injury, respiratory mechanics, respiratory dead space, artificial respiration, pulmonary gas exchange
in
Intensive Care Medicine
volume
28
issue
9
pages
1239 - 1245
publisher
Springer
external identifiers
  • pmid:12209271
  • wos:000178282400010
  • scopus:0036374145
ISSN
0342-4642
DOI
10.1007/s00134-002-1419-y
language
English
LU publication?
yes
id
c8c36d14-fe00-4f30-a62a-fc39da259e17 (old id 326600)
date added to LUP
2016-04-01 12:38:25
date last changed
2022-02-04 00:56:07
@article{c8c36d14-fe00-4f30-a62a-fc39da259e17,
  abstract     = {{Objective: A large tidal volume (VT) and lung collapse and re-expansion may cause ventilator-induced lung injury (VILI) in acute lung injury (ALI). A low VT and a positive end-expiratory pressure (PEEP) can prevent VILI, but the more VT is reduced, the more dead space (VD) compromises gas exchange. We investigated how physiological, airway and alveolar VD varied with PEEP and analysed possible links to respiratory mechanics. Setting: Medical and surgical intensive care unit (ICU) in a university hospital. Design: Prospective, non-randomised comparative trial. Patients: Ten consecutive ALI patients. Intervention: Stepwise increases in PEEP from zero to 15 cmH(2)O. Measurements and results: Lung mechanics and VD were measured at each PEEP level. Physiological VD was 41-64% of VT at zero PEEP and increased slightly with PEEP due to a rise in airway VD. Alveolar VD was 11-38% of VT and did not vary systematically with PEEP. However, in individual patients a decrease and increase of alveolar VD paralleled a positive or negative response to PEEP with respect to oxygenation (shunt), respectively. VD fractions were independent of respiratory resistance and compliance. Conclusions: Alveolar VD is large and does not vary systematically with PEEP in patients with various degrees of ALI. Individual measurements show a diverse response to PEEP. Respiratory mechanics were of no help in optimising PEEP with regard to gas exchange.}},
  author       = {{Beydon, L and Uttman, Leif and Rawal, R and Jonson, Björn}},
  issn         = {{0342-4642}},
  keywords     = {{acute lung injury; respiratory mechanics; respiratory dead space; artificial respiration; pulmonary gas exchange}},
  language     = {{eng}},
  number       = {{9}},
  pages        = {{1239--1245}},
  publisher    = {{Springer}},
  series       = {{Intensive Care Medicine}},
  title        = {{Effects of positive end-expiratory pressure on dead space and its partitions in acute lung injury}},
  url          = {{http://dx.doi.org/10.1007/s00134-002-1419-y}},
  doi          = {{10.1007/s00134-002-1419-y}},
  volume       = {{28}},
  year         = {{2002}},
}