Objective: To determine end-expiratory lung volumes (EELVs) and the distribution of gas and perflubron during low- and high-dose partial liquid ventilation (PLV) in healthy and oleic-acid-injured lungs.
Design: A prospective, randomized study.
Setting: A university medical school laboratory approved for animal research.
Subjects: Adult sheep.
Interventions: A total of 18 sheep were randomly divided into two groups (healthy and oleic acid lung injury) and received PLV with perflubron at incremental doses.
Measurements and main results: Animals were ventilated in a volume-control mode with a positive end-expiratory pressure of 5 cm H2O. Baseline computed tomographic scans of the entire lung were obtained during end-expiratory hold. Thereafter, the animals were randomized to undergo either PLV alone (healthy group) or after oleic acid lung injury was introduced (injury group). In both groups, PLV was induced by instilling 10 mL/kg perflubron into the endotracheal tube over 5 mins (low-dose PLV). At 60 mins after dosing, another set of computed tomographic scans during end-expiratory hold was obtained. Thereafter, another 20 mL/kg perflubron was instilled in both groups (cumulative dose, 30 mL/kg perflubron, high-dose PLV), and computed tomographic scanning was repeated 60 mins later. EELVs were calculated. To study density distribution patterns, the lungs were divided into nine segments, and the mean Hounsfield attenuation number was calculated for each segment. In healthy animals, low-dose PLV did not change EELV (47.5 +/- 8.1 mL/kg vs. 44.5 +/- 6.1 mL/kg at 10 mL/kg perflubron), whereas high-dose PLV significantly increased EELV (58.1 +/- 3.3 mL/kg, p <.01). Oleic acid lung injury significantly reduced EELV (53.9 +/- 7.5 mL/kg vs. 43.9 +/- 8.7 mL/kg, p <.01). Low-dose PLV reestablished baseline EELV (59.8 +/- 10.5 mL/kg), and high-dose PLV resulted in a significant increase in EELV (89.2 +/- 12 mL/kg, p =.003). PLV increased the mean Hounsfield attenuation number along the ventrodorsal axis in the three coronal blocks in a dose-dependent manner. In the oleic acid lung injury group, PLV produced a more homogeneous pattern of density distribution, with the highest Hounsfield attenuation numbers observed in the medial segments.
Conclusion: High-dose PLV significantly increased EELV in both states, indicating lung distention. Healthy lungs were filled in a dose-dependent, gravity-governed fashion, showing steep craniocaudal and ventrodorsal gradients. In the oleic acid lung injury model studied, perflubron tended to accumulate on top of the most severely injured dorsal and diaphragmatic parts, rendering effective recruitment by liquid positive end-expiratory pressure in these regions questionable.