Journal article
Impact of low pulmonary vascular pressure on ventilator-induced lung injury.
- Broccard AF Division of Intensive Care, Department of Medicine, University Hospital, Lausanne, Switzerland.
- Vannay C
- Feihl F
- Schaller MD
- 2002-10-24
Published in:
- Critical care medicine. - 2002
Animals
Atrial Function, Left
Blood Pressure
Capillary Permeability
Hemodynamics
Hypertension, Pulmonary
In Vitro Techniques
Pressure
Pulmonary Circulation
Pulmonary Edema
Rabbits
Respiration, Artificial
Respiratory Distress Syndrome, Adult
Respiratory Mechanics
Weight Gain
English
OBJECTIVE
To study the impact of low pulmonary vascular pressure on ventilator-induced lung injury.
DESIGN
Randomized prospective animal study.
SUBJECTS
Isolated perfused rabbit heart-lung preparation.
SETTINGS
Animal research laboratory in a university hospital.
INTERVENTIONS
Twenty isolated sets of normal lungs were perfused (constant flow, 0.3 L/min; left atrial pressure, 6 mm Hg), ventilated for 20 min (pressure control ventilation, 15 cm H2O; baseline period), and then randomized into three groups. Group A (control, n = 7) was perfused and ventilated as previously described during three consecutive 20-min periods. In group B (high airway pressure/normal left atrial pressure, n = 7), pressure control ventilation was 20, 25, and 30 cm H2O during each period. Group C (high airway pressure/low left atrial pressure, n = 6) was ventilated as group B but, in contrast to groups A and B, left atrial pressure was reduced to 1 mm Hg.
MEASUREMENTS AND MAIN RESULTS
The rate of edema formation (WGR, weight gain per minute normalized for initial lung weight) and the ultrafiltration coefficient (Kf) were measured during and after each period and their changes from baseline [DeltaWGR (edema formation index) and DeltaKf (vascular permeability index)] calculated to compare groups. The incidence and timing of vascular failure were compared. Vascular failure was considered to be present if all the following conditions were met: pulmonary hypertension, accelerated weight gain, and occurrence of fluid leak from the lungs. At the end of the study, DeltaWGR (g.g.min(-1)) was higher in group C (0.54 +/- 0.17) than in groups B (0.08 +/- 0.04) and A (0.00 +/- 0.01; p<.05), as well as in group B compared with A (p <.05). Similar differences between groups (p <.05) were found for DeltaK (g x min(-1) x cm H2O(-1) x 100 g(-1)): C, 7.24 +/- 2.36; B, 1.40 +/- 0.49; A, 0.01 +/- 0.03. Vascular failure was not observed in groups A and B but occurred in all but one preparation in group C (p <.05; C vs. A and B).
CONCLUSION
Reducing left atrial pressure results in more severe ventilator-induced lung injury. These results suggest that lung blood volume modulates cyclic tidal lung stress.
To study the impact of low pulmonary vascular pressure on ventilator-induced lung injury.
DESIGN
Randomized prospective animal study.
SUBJECTS
Isolated perfused rabbit heart-lung preparation.
SETTINGS
Animal research laboratory in a university hospital.
INTERVENTIONS
Twenty isolated sets of normal lungs were perfused (constant flow, 0.3 L/min; left atrial pressure, 6 mm Hg), ventilated for 20 min (pressure control ventilation, 15 cm H2O; baseline period), and then randomized into three groups. Group A (control, n = 7) was perfused and ventilated as previously described during three consecutive 20-min periods. In group B (high airway pressure/normal left atrial pressure, n = 7), pressure control ventilation was 20, 25, and 30 cm H2O during each period. Group C (high airway pressure/low left atrial pressure, n = 6) was ventilated as group B but, in contrast to groups A and B, left atrial pressure was reduced to 1 mm Hg.
MEASUREMENTS AND MAIN RESULTS
The rate of edema formation (WGR, weight gain per minute normalized for initial lung weight) and the ultrafiltration coefficient (Kf) were measured during and after each period and their changes from baseline [DeltaWGR (edema formation index) and DeltaKf (vascular permeability index)] calculated to compare groups. The incidence and timing of vascular failure were compared. Vascular failure was considered to be present if all the following conditions were met: pulmonary hypertension, accelerated weight gain, and occurrence of fluid leak from the lungs. At the end of the study, DeltaWGR (g.g.min(-1)) was higher in group C (0.54 +/- 0.17) than in groups B (0.08 +/- 0.04) and A (0.00 +/- 0.01; p<.05), as well as in group B compared with A (p <.05). Similar differences between groups (p <.05) were found for DeltaK (g x min(-1) x cm H2O(-1) x 100 g(-1)): C, 7.24 +/- 2.36; B, 1.40 +/- 0.49; A, 0.01 +/- 0.03. Vascular failure was not observed in groups A and B but occurred in all but one preparation in group C (p <.05; C vs. A and B).
CONCLUSION
Reducing left atrial pressure results in more severe ventilator-induced lung injury. These results suggest that lung blood volume modulates cyclic tidal lung stress.
- Language
-
- English
- Open access status
- closed
- Identifiers
-
- DOI 10.1097/00003246-200210000-00002
- PMID 12394942
- Persistent URL
- https://sonar.ch/global/documents/277886
Statistics
Document views: 38
File downloads: