Abstract
BackgroundLung injury is often studied without consideration for pathologic changes in the chest wall. In order to reduce the incidence of lung injury using preemptive mechanical ventilation, it is important to recognize the influence of altered chest wall mechanics on disease pathogenesis. In this study, we hypothesize that airway pressure release ventilation (APRV) may be able to reduce the chest wall elastance associated with an extrapulmonary lung injury model as compared with low tidal volume (LVt) ventilation.MethodsFemale Yorkshire pigs were anesthetized and instrumented. Fecal peritonitis was established, and the superior mesenteric artery was clamped for 30 min to induce an ischemia/reperfusion injury. Immediately following injury, pigs were randomized into (1) LVt (n = 3), positive end-expiratory pressure (PEEP) 5 cmH2O, Vt 6 cc kg−1, FiO2 21 %, and guided by the ARDSnet protocol or (2) APRV (n = 3), PHigh 16–22 cmH2O, PLow 0 cmH2O, THigh 4.5 s, TLow set to terminate the peak expiratory flow at 75 %, and FiO2 21 %. Pigs were monitored continuously for 48 h. Lung samples and bronchoalveolar lavage fluid were collected at necropsy.ResultsLVt resulted in mild acute respiratory distress syndrome (ARDS) (PaO2/FiO2 = 226.2 ± 17.1 mmHg) whereas APRV prevented ARDS (PaO2/FiO2 = 465.7 ± 66.5 mmHg; p < 0.05). LVt had a reduced surfactant protein A concentration and increased histologic injury as compared with APRV. The plateau pressure in APRV (34.3 ± 0.9 cmH2O) was significantly greater than LVt (22.2 ± 2.0 cmH2O; p < 0.05) yet transpulmonary pressure between groups was similar (p > 0.05). This was because the pleural pressure was significantly lower in LVt (7.6 ± 0.5 cmH2O) as compared with APRV (17.4 ± 3.5 cmH2O; p < 0.05). Finally, the elastance of the lung, chest wall, and respiratory system were all significantly greater in LVt as compared with APRV (all p < 0.05).ConclusionsAPRV preserved surfactant and lung architecture and maintenance of oxygenation. Despite the greater plateau pressure and tidal volumes in the APRV group, the transpulmonary pressure was similar to that of LVt. Thus, the majority of the plateau pressure in the APRV group was distributed as pleural pressure in this extrapulmonary lung injury model. APRV maintained a normal lung elastance and an open, homogeneously ventilated lung without increasing lung stress.
Highlights
Lung injury is often studied without consideration for pathologic changes in the chest wall
We demonstrate that the transpulmonary pressures are similar between the two ventilation strategies, despite the increased tidal volumes and plateau pressures in the airway pressure release ventilation (APRV) group, and that APRV was able to limit increases in chest wall elastance
Pulmonary data The end-expiratory release pressure was significantly greater in APRV as compared with low tidal volume ventilation (LVt) (p < 0.05; Table 2), despite a PLow of 0 cmH2O, demonstrating the importance of setting the TLow appropriately to ensure the end-expiratory pressure never has the time to reach 0 cmH2O
Summary
Lung injury is often studied without consideration for pathologic changes in the chest wall. ARDS can be broadly sub-classified into pulmonary versus extrapulmonary ARDS, the ultimate pathology of which may be similar; the etiology and physiology of the two subtypes are distinct [1] Despite these physiologic differences, many of the randomized controlled trials evaluating the impact of ventilator strategies on the incidence and mortality of ARDS analyze patients with pulmonary and extrapulmonary ARDS combined, usually with a preponderance of pulmonary ARDS [2,3,4,5,6,7,8], and despite decades of study, the mortality associated with ARDS has not changed since 1994 [8]. Chest wall elastance represents only a small fraction of the respiratory system elastance (Ers) in patients with ARDS with normal chest wall elastance [9]; in patients with altered chest wall mechanics, the Ecw to Ers ratio ranges from 20 to 80 % [10] This great variability demonstrates the fallibility of targeting airway opening pressures without taking the Ecw and transpulmonary pressure into consideration
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