Department of Intensive Care, Hôpital Universitaire de Bruxelles, Université Libre de Bruxelles, Route de Lennik, 808, Brussels, Belgium.
Department of Intensive Care, Azienda Ospedaliera Univesitaria Integrata Di Verona, Verona, Italy.
Neurocrit Care. 2024 Apr;40(2):750-758. doi: 10.1007/s12028-023-01833-y. Epub 2023 Sep 11.
Cerebral hypoxia is a frequent cause of secondary brain damage in patients with acute brain injury. Although hypercapnia can increase intracranial pressure, it may have beneficial effects on tissue oxygenation. We aimed to assess the effects of hypercapnia on brain tissue oxygenation (PbtO).
This single-center retrospective study (November 2014 to June 2022) included all patients admitted to the intensive care unit after acute brain injury who required multimodal monitoring, including PbtO monitoring, and who underwent induced moderate hypoventilation and hypercapnia according to the decision of the treating physician. Patients with imminent brain death were excluded. Responders to hypercapnia were defined as those with an increase of at least 20% in PbtO values when compared to their baseline levels.
On a total of 163 eligible patients, we identified 23 (14%) patients who underwent moderate hypoventilation (arterial partial pressure of carbon dioxide [PaCO] from 44 [42-45] to 50 [49-53] mm Hg; p < 0.001) during the study period at a median of 6 (4-10) days following intensive care unit admission; six patients had traumatic brain injury, and 17 had subarachnoid hemorrhage. A significant overall increase in median PbtO values from baseline (21 [19-26] to 24 [22-26] mm Hg; p = 0.02) was observed. Eight (35%) patients were considered as responders, with a median increase of 7 (from 4 to 11) mm Hg of PbtO, whereas nonresponders showed no changes (from - 1 to 2 mm Hg of PbtO). Because of the small sample size, no variable independently associated with PbtO response was identified. No correlation between changes in PaCO and in PbtO was observed.
In this study, a heterogeneous response of PbtO to induced hypercapnia was observed but without any deleterious elevations of intracranial pressure.
脑缺氧是急性颅脑损伤患者继发性脑损伤的常见原因。虽然高碳酸血症会增加颅内压，但它可能对组织氧合有有益影响。我们旨在评估高碳酸血症对脑组织氧合（PbtO）的影响。
这是一项单中心回顾性研究（2014 年 11 月至 2022 年 6 月），纳入了所有因急性颅脑损伤入住重症监护病房且需要多模态监测（包括 PbtO 监测）的患者，这些患者根据治疗医生的决定接受了诱导性中度低通气和高碳酸血症。排除即将发生脑死亡的患者。高碳酸血症反应者定义为 PbtO 值与基线相比至少增加 20%的患者。
在总共 163 名符合条件的患者中，我们确定了 23 名（14%）患者在研究期间接受了中度低通气（动脉血二氧化碳分压[PaCO]从 44[42-45]至 50[49-53]mmHg；p<0.001），在入住重症监护病房后中位数为 6（4-10）天；6 名患者患有创伤性脑损伤，17 名患者患有蛛网膜下腔出血。与基线相比，PbtO 值的中位数总体显著增加（从 21[19-26]至 24[22-26]mmHg；p=0.02）。8 名（35%）患者被认为是反应者，PbtO 中位数增加 7（从 4 至 11）mmHg，而非反应者 PbtO 无变化（从-1 至 2mmHg）。由于样本量小，未发现与 PbtO 反应独立相关的变量。未观察到 PaCO 和 PbtO 变化之间的相关性。
在这项研究中，观察到 PbtO 对诱导性高碳酸血症的反应存在异质性，但没有导致颅内压升高。
