Abstract
IntroductionThe ideal ventilation strategy for patients with massive brain damage requires better elucidation. We hypothesized that in the presence of massive brain injury, a ventilation strategy using low (6 milliliters per kilogram ideal body weight) tidal volume (VT) ventilation with open lung positive end-expiratory pressure (LVT/OLPEEP) set according to the minimal static elastance of the respiratory system, attenuates the impact of massive brain damage on gas-exchange, respiratory mechanics, lung histology and whole genome alterations compared with high (12 milliliters per kilogram ideal body weight) VT and low positive end-expiratory pressure ventilation (HVT/LPEEP).MethodsIn total, 28 adult male Wistar rats were randomly assigned to one of four groups: 1) no brain damage (NBD) with LVT/OLPEEP; 2) NBD with HVT/LPEEP; 3) brain damage (BD) with LVT/OLPEEP; and 4) BD with HVT/LPEEP. All animals were mechanically ventilated for six hours. Brain damage was induced by an inflated balloon catheter into the epidural space. Hemodynamics was recorded and blood gas analysis was performed hourly. At the end of the experiment, respiratory system mechanics and lung histology were analyzed. Genome wide gene expression profiling and subsequent confirmatory quantitative polymerase chain reaction (qPCR) for selected genes were performed.ResultsIn NBD, both LVT/OLPEEP and HVT/LPEEP did not affect arterial blood gases, as well as whole genome expression changes and real-time qPCR. In BD, LVT/OLPEEP, compared to HVT/LPEEP, improved oxygenation, reduced lung damage according to histology, genome analysis and real-time qPCR with decreased interleukin 6 (IL-6), cytokine-induced neutrophil chemoattractant 1 (CINC)-1 and angiopoietin-4 expressions. LVT/OLPEEP compared to HVT/LPEEP improved overall survival.ConclusionsIn BD, LVT/OLPEEP minimizes lung morpho-functional changes and inflammation compared to HVT/LPEEP.
Highlights
The ideal ventilation strategy for patients with massive brain damage requires better elucidation
All animals in the No brain damage (NBD) LVT/open lung PEEP” (OLPEEP) and brain damage (BD) LVT/ OLPEEP groups survived, whereas in the NBD HVT/ LPEEP group, one animal out of seven, and in the BD HVT/LPEEP group, three out of seven animals died. Mixing both NBD and BD groups together, LVT/ OLPEEP resulted in improved survival compared to HVT/LPEEP (100% vs. 71.4%, P = 0.034)
After six hours, mean arterial pressure (MAP) was decreased in both BD groups compared to NBD groups (75.9 ± 10.6 mmHg (NBD LVT/OLPEEP End) vs. 64.6 ± 8.7 mmHg (BD LVT/OLPEEP End), P = 0.035, respectively, 72.4 + 20.3 mmHg (NBD HVT/LPEEP End) vs. 51.6 ± 14.1 (BD HVT/LPEEP End), P = 0.043) (Table 1)
Summary
The ideal ventilation strategy for patients with massive brain damage requires better elucidation. Pulmonary dysfunction is the most frequent extracerebral complication in neurological patients undergoing mechanical ventilation [2] and acute respiratory It has been clearly shown in experimental [7,8] as well as clinical settings that mechanical ventilation itself might induce [9,10] or worsen [11] existing lung damage (ventilator-associated lung injury, VALI). VALI is caused by alveolar over-distension and repetitive opening and closing of atelectatic lung regions, respectively [12] Both conditions lead to parenchymatous inflammation and, consecutively, ARDS [7], which may cause dysfunction in downstream organs, such as the small bowel, kidney [13] or the brain itself [14]. As an additional component of ventilation strategy for patients with ARDS, the use of recruitment maneuvers in addition to adequate PEEP set during a decremental PEEP trial targeting maximum compliance [15] has been suggested, albeit scientific proof is lacking [16]
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