Gattarello Simone, Pozzi Tommaso, Galizia Mauro, Busana Mattia, Ghidoni Valentina, Catozzi Giulia, Donati Beatrice, Nocera Domenico, Giovanazzi Stefano, D'Albo Rosanna, Fioccola Antonio, Velati Mara, Nicolardi Rosmery, Fratti Isabella, Romitti Federica, Gatta Alessandro, Collino Francesca, Herrmann Peter, Quintel Michael, Meissner Konrad, Sonzogni Aurelio, Marini John J, Camporota Luigi, Moerer Onnen, Gattinoni Luciano
Department of Anesthesia and Intensive Care Medicine, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Department of Anesthesiology, University Medical Center Göttingen, Göttingen, Germany.
Am J Respir Crit Care Med. 2025 Mar;211(3):331-338. doi: 10.1164/rccm.202406-1240OC.
The pathophysiological relationship among fluid administration, fluid balance, and mechanical ventilation in the development of lung injury is unclear. To quantify the relative contributions of mechanical power and fluid balance in the development of lung injury. Thirty-nine healthy female pigs, divided into four groups, were ventilated for 48 hours with high (∼18 J/min) or low (∼6 J/min) mechanical power and high (∼4 L) or low (∼1 L) targeted fluid balance. We measured physiological variables (e.g., end-expiratory lung gas volume, respiratory system mechanics, gas exchange, hemodynamics) and pathological variables (i.e., lung weight, wet-to-dry ratio, and histology score of lung injury). End-expiratory lung gas volume, respiratory system elastance, strain, and oxygenation significantly worsened in the two groups assigned to receive high fluid balance, irrespective of the mechanical power received. All four groups had similar lung weights (i.e., lung edema), lung wet-to-dry ratios, and pathological variables. Animals with higher fluid balance developed more ascites, which was associated with a decrease in end-expiratory lung gas volume. Our study did not detect a significant difference in lung injury between high and low mechanical power. Some damage is directly attributable to mechanical power, while additional injury appears to result indirectly from high fluid balance, which reduces end-expiratory lung gas volume, with ascites playing an important role in this process.
液体输注、液体平衡和机械通气在肺损伤发生发展过程中的病理生理关系尚不清楚。为了量化机械功率和液体平衡在肺损伤发生发展中的相对作用。将39只健康雌性猪分为四组,分别以高机械功率(约18焦耳/分钟)或低机械功率(约6焦耳/分钟)以及高目标液体平衡(约4升)或低目标液体平衡(约1升)进行48小时的通气。我们测量了生理变量(如呼气末肺气体容积、呼吸系统力学、气体交换、血流动力学)和病理变量(即肺重量、湿干比和肺损伤组织学评分)。无论接受何种机械功率,接受高液体平衡的两组呼气末肺气体容积、呼吸系统弹性、应变和氧合均显著恶化。所有四组的肺重量(即肺水肿)、肺湿干比和病理变量相似。液体平衡较高的动物出现更多腹水,这与呼气末肺气体容积减少有关。我们的研究未发现高机械功率和低机械功率在肺损伤方面有显著差异。一些损伤直接归因于机械功率,而额外的损伤似乎间接源于高液体平衡,高液体平衡会减少呼气末肺气体容积,腹水在此过程中起重要作用。