Department of Internal Medicine, Thun General Hospital, Thun, Switzerland.
Department of Emergency Medicine, Inselspital, University Hospital, University of Bern, Bern, Switzerland.
Eur J Med Res. 2022 Aug 13;27(1):150. doi: 10.1186/s40001-022-00780-2.
A complex interrelation between lung and brain in patients with acute lung injury (ALI) has been established by experimental and clinical studies during the last decades. Although, acute brain injury represents one of the most common insufficiencies in patients with ALI and acute respiratory distress syndrome (ARDS), the underlying pathophysiology of the observed crosstalk remains poorly understood due to its complexity. Specifically, it involves numerous pathophysiological parameters such as hypoxemia, neurological adverse events of lung protective ventilation, hypotension, disruption of the BBB, and neuroinflammation in such a manner that the brain of ARDS patients-especially hippocampus-becomes very vulnerable to develop secondary lung-mediated acute brain injury. A protective ventilator strategy could reduce or even minimize further systemic release of inflammatory mediators and thus maintain brain homeostasis. On the other hand, mechanical ventilation with low tidal volumes may lead to self-inflicted lung injury, hypercapnia and subsequent cerebral vasodilatation, increased cerebral blood flow, and intracranial hypertension. Therefore, by describing the pathophysiology of ARDS-associated acute brain injury we aim to highlight and discuss the possible influence of mechanical ventilation on ALI-associated acute brain injury.
在过去几十年的实验和临床研究中，已经证实急性肺损伤（ALI）患者的肺部和脑部之间存在复杂的相互关系。尽管急性脑损伤是 ALI 和急性呼吸窘迫综合征（ARDS）患者最常见的并发症之一，但由于其复杂性，观察到的这种相互作用的潜在病理生理学仍了解甚少。具体来说，它涉及许多病理生理参数，如低氧血症、肺保护性通气的神经不良事件、低血压、血脑屏障破坏和神经炎症，以至于 ARDS 患者的大脑 - 尤其是海马体 - 变得非常容易发生继发性肺部介导的急性脑损伤。保护性通气策略可以减少甚至最小化炎症介质的进一步全身释放，从而维持脑内环境稳定。另一方面，低潮气量机械通气可能导致自伤性肺损伤、高碳酸血症和随后的脑血管扩张、脑血流量增加和颅内压升高。因此，通过描述 ARDS 相关急性脑损伤的病理生理学，我们旨在强调和讨论机械通气对 ALI 相关急性脑损伤的可能影响。
