Open lung approach ventilation abolishes the negative effects of respiratory rate in experimental lung injury

2016 ◽  
Vol 60 (8) ◽  
pp. 1131-1141 ◽  
Author(s):  
J. Retamal ◽  
J. B. Borges ◽  
A. Bruhn ◽  
R. Feinstein ◽  
G. Hedenstierna ◽  
...  
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Negative Effects ◽  
Open Lung ◽  
Open Lung Approach

scholarly journals Open lung approach vs acute respiratory distress syndrome network ventilation in experimental acute lung injury

2011 ◽  
Vol 107 (3) ◽  
pp. 388-397 ◽  
Author(s):  
P.M. Spieth ◽  
A. Güldner ◽  
A.R. Carvalho ◽  
M. Kasper ◽  
P. Pelosi ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Open Lung ◽  
Open Lung Approach

Chaotic variation of tidal volumes adds further benefit to the open lung approach in experimental acute lung injury

2007 ◽  
Vol 24 (Supplement 39) ◽  
pp. 146 ◽  
Author(s):  
P. M. Spieth ◽  
C. Meissner ◽  
M. Kasper ◽  
T. Koch ◽  
Gama M. de Abreu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Open Lung ◽  
Open Lung Approach

scholarly journals Open lung approach with low tidal volume mechanical ventilation attenuates lung injury in rats with massive brain damage

Critical Care ◽  
2014 ◽  
Vol 18 (2) ◽  
pp. R59 ◽  
Author(s):  
Joerg Krebs ◽  
Charalambos Tsagogiorgas ◽  
Paolo Pelosi ◽  
Patricia RM Rocco ◽  
Maximilia Hottenrott ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Tidal Volume ◽  
Brain Damage ◽  
Open Lung ◽  
Low Tidal Volume ◽  
Open Lung Approach

scholarly journals Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

2007 ◽  
Vol 102 (1) ◽  
pp. 331-339 ◽  
Author(s):  
Rebecca S. Syring ◽  
Cynthia M. Otto ◽  
Rebecca E. Spivack ◽  
Klaus Markstaller ◽  
James E. Baumgardner
Keyword(s):  
Cardiac Output ◽  
Lung Injury ◽  
Respiratory Rate ◽  
Pressure Control ◽  
Plateau Pressure ◽  
Control Mode ◽  
Intrinsic Peep ◽  
Mixed Venous Saturation ◽  
Mixed Venous ◽  
Saline Lavage

Cyclical recruitment of atelectasis with each breath is thought to contribute to ventilator-associated lung injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitment at end exhalation, but PEEPe depresses cardiac output and increases overdistension. Short exhalation times can also maintain end-expiratory recruitment, but if the mechanism of this recruitment is generation of intrinsic PEEP (PEEPi), there would be little advantage compared with PEEPe. In seven New Zealand White rabbits, we compared recruitment from increased respiratory rate (RR) to recruitment from increased PEEPe after saline lavage. Rabbits were ventilated in pressure control mode with a fraction of inspired O2 (FiO2) of 1.0, inspiratory-to-expiratory ratio of 2:1, and plateau pressure of 28 cmH2O, and either 1) high RR ( 24 ) and low PEEPe (3.5) or 2) low RR ( 7 ) and high PEEPe ( 14 ). We assessed cyclical lung recruitment with a fast arterial Po2 probe, and we assessed average recruitment with blood gas data. We measured PEEPi, cardiac output, and mixed venous saturation at each ventilator setting. Recruitment achieved by increased RR and short exhalation time was nearly equivalent to recruitment achieved by increased PEEPe. The short exhalation time at increased RR, however, did not generate PEEPi. Cardiac output was increased on average 13% in the high RR group compared with the high PEEPe group ( P < 0.001), and mixed venous saturation was consistently greater in the high RR group ( P < 0.001). Prevention of end-expiratory derecruitment without increased end-expiratory pressure suggests that another mechanism, distinct from intrinsic PEEP, plays a role in the dynamic behavior of atelectasis.

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