Quantification of atelectatic lung volumes in two different porcine models of ARDS.
BACKGROUND
Cyclic recruitment during mechanical ventilation contributes to ventilator associated lung injury. Two different pathomechanisms in acute respiratory distress syndrome (ARDS) are currently discussed: alveolar collapse vs persistent flooding of small airways and alveoli. We compare two different ARDS animal models by computed tomography (CT) to describe different recruitment and derecruitment mechanisms at different airway pressures: (i) lavage-ARDS, favouring alveolar collapse by surfactant depletion; and (ii) oleic acid ARDS, favouring alveolar flooding by capillary leakage.


METHODS
In 12 pigs [25 (1) kg], ARDS was randomly induced, either by saline lung lavage or oleic acid (OA) injection, and 3 animals served as controls. A respiratory breathhold manoeuvre without spontaneous breathing at different continuous positive airway pressure (CPAP) was applied in random order (CPAP levels of 5, 10, 15, 30, 35 and 50 cm H(2)O) and spiral-CT scans of the total lung were acquired at each CPAP level (slice thickness=1 mm). In each spiral-CT the volume of total lung parenchyma, tissue, gas, non-aerated, well-aerated, poorly aerated, and over-aerated lung was calculated.


RESULTS
In both ARDS models non-aerated lung volume decreased significantly from CPAP 5 to CPAP 50 [oleic acid lung injury (OAI): 346.9 (80.1) to 96.4 (48.8) ml, P<0.001; lavage-ARDS: 245 17.6) to 42.7 (4.8) ml, P<0.001]. In lavage-ARDS poorly aerated lung volume decreased at higher CPAP levels [232 (45.2) at CPAP 10 to 84 (19.4) ml at CPAP 50, P<0.001] whereas in OAI poorly aerated lung volume did not vary at different airway pressures.


CONCLUSIONS
In both ARDS models well-aerated and non-aerated lung volume respond to different CPAP levels in a comparable fashion: Thus, a cyclical alveolar collapse seems to be part of the derecruitment process also in the OA-ARDS. In OA-ARDS, the increase in poorly aerated lung volume reflects the specific initial lesion, that is capillary leakage with interstitial and alveolar oedema.
Karmrodt
J
J
Department of Anaesthesiology, Johannes Gutenberg-University, Mainz, Germany. karmrodt@uni-mainz.de
Bletz
C
C
Yuan
S
S
David
M
M
Heussel
C-P
CP
Markstaller
K
K
D000818:Animals; D001794:Blood Pressure; D045422:Continuous Positive Airway Pressure / Q000379:methods; D004195:Disease Models, Animal; D007091:Image Processing, Computer-Assisted / Q000379:methods; D008176:Lung Volume Measurements; D019301:Oleic Acid; D011650:Pulmonary Alveoli / Q000503:physiopathology; D001261:Pulmonary Atelectasis / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D011659:Pulmonary Gas Exchange; D012128:Respiratory Distress Syndrome / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D012965:Sodium Chloride; D013552:Swine; D014057:Tomography, X-Ray Computed
D019301:Oleic Acid; D012965:Sodium Chloride