Effects of Spontaneous Breathing During Airway Pressure Release Ventilation on Cerebral and Spinal Cord Perfusion in Experimental Acute Lung Injury

2010 ◽  
Vol 22 (4) ◽  
pp. 323-329 ◽  
Author(s):  
Stefan Kreyer ◽  
Christian Putensen ◽  
Andreas Berg ◽  
Martin Soehle ◽  
Thomas Muders ◽  
...  
1990 ◽  
Vol 18 (Supplement) ◽  
pp. S231 ◽  
Author(s):  
Lynn D. Martin ◽  
Anthony L. Bilenki ◽  
James F. Rafferty ◽  
Randall C. Wetzel

2003 ◽  
Vol 99 (5) ◽  
pp. 1137-1144 ◽  
Author(s):  
Rudolf Hering ◽  
Andreas Viehöfer ◽  
Jörg Zinserling ◽  
Hermann Wrigge ◽  
Stefan Kreyer ◽  
...  

Background In critical illness, the gut is susceptible to hypoperfusion and hypoxia. Positive-pressure ventilation can affect systemic hemodynamics and regional blood flow distribution, with potentially deleterious effects on the intestinal circulation. The authors hypothesized that spontaneous breathing (SB) with airway pressure release ventilation (APRV) provides better systemic and intestinal blood flow than APRV without SB. Methods Twelve pigs with oleic acid-induced lung injury received APRV with and without SB. When SB was abolished, either the tidal volume or the ventilator rate was increased to maintain pH and arterial carbon dioxide tension constant as compared to APRV with SB. Systemic hemodynamics were determined by double indicator dilution. Blood flow to the intestinal mucosa-submucosa and muscularis-serosa was measured using colored microspheres. Results Systemic blood flow increased during APRV with SB. During APRV with SB, mucosal-submucosal blood flow (ml. g-1. min-1) was 0.39 +/- 0.21 in the stomach, 0.76 +/- 0.35 in the duodenum, 0.71 +/- 0.35 in the jejunum, 0.71 +/- 0.59 in the ileum, and 0.63 +/- 0.21 in the colon. During APRV without SB and high tidal volumes, it decreased to 0.19 +/- 0.03 in the stomach, 0.42 +/- 0.21 in the duodenum, 0.37 +/- 0.10 in the jejunum, 0.3 +/- 0.14 in the ileum, and 0.41 +/- 0.14 in the colon (P < 0.001, respectively). During APRV without SB and low tidal volumes, the respective mucosal-submucosal blood flows decreased to 0.24 +/- 0.10 (P < 0.01), 0.54 +/- 0.21 (P < 0.05), 0.48 +/- 0.17 (P < 0.01), 0.43 +/- 0.21 (P < 0.01), and 0.50 +/- 0.17 (P < 0.001) as compared to APRV with SB. Muscularis-serosal perfusion decreased during full ventilatory support with high tidal volumes in comparison with APRV with SB. Conclusion Maintaining SB during APRV was associated with better systemic and intestinal blood flows. Improvements were more pronounced in the mucosal-submucosal layer.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Gary F. Nieman ◽  
Louis A. Gatto ◽  
Penny Andrews ◽  
Joshua Satalin ◽  
Luigi Camporota ◽  
...  

AbstractMortality in acute respiratory distress syndrome (ARDS) remains unacceptably high at approximately 39%. One of the only treatments is supportive: mechanical ventilation. However, improperly set mechanical ventilation can further increase the risk of death in patients with ARDS. Recent studies suggest that ventilation-induced lung injury (VILI) is caused by exaggerated regional lung strain, particularly in areas of alveolar instability subject to tidal recruitment/derecruitment and stress-multiplication. Thus, it is reasonable to expect that if a ventilation strategy can maintain stable lung inflation and homogeneity, regional dynamic strain would be reduced and VILI attenuated. A time-controlled adaptive ventilation (TCAV) method was developed to minimize dynamic alveolar strain by adjusting the delivered breath according to the mechanical characteristics of the lung. The goal of this review is to describe how the TCAV method impacts pathophysiology and protects lungs with, or at high risk of, acute lung injury. We present work from our group and others that identifies novel mechanisms of VILI in the alveolar microenvironment and demonstrates that the TCAV method can reduce VILI in translational animal ARDS models and mortality in surgical/trauma patients. Our TCAV method utilizes the airway pressure release ventilation (APRV) mode and is based on opening and collapsing time constants, which reflect the viscoelastic properties of the terminal airspaces. Time-controlled adaptive ventilation uses inspiratory and expiratory time to (1) gradually “nudge” alveoli and alveolar ducts open with an extended inspiratory duration and (2) prevent alveolar collapse using a brief (sub-second) expiratory duration that does not allow time for alveolar collapse. The new paradigm in TCAV is configuring each breath guided by the previous one, which achieves real-time titration of ventilator settings and minimizes instability induced tissue damage. This novel methodology changes the current approach to mechanical ventilation, from arbitrary to personalized and adaptive. The outcome of this approach is an open and stable lung with reduced regional strain and greater lung protection.


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