Depret J, Teboul J L, Benoit G, Mercat A, Richard C
Service de Réanimation Médicale, Hôpital de Bicêtre, Faculté de Médecine Paris-Sud, Kremlin-Bicetre, France.
Transplantation. 1995 Nov 15;60(9):966-71.
The objective of this prospective, clinical study of consecutive patients was to test the hypothesis of a global energetic failure in brain-dead patients by analyzing indices of peripheral oxygenation during brain-dead resuscitation. Subjects comprised 24 subjects with brain death criteria from a multidisciplinary intensive care unit. The causes of brain death were multiple: severe traumatic head injury, cerebrovascular event, cerebral anoxia, primary brain tumor, and gunshot wound to the head. Interventions used were radial and pulmonary artery catheterization. Hemodynamic and gasometric parameters and blood lactate levels were measured immediately after the diagnosis of brain death (T0) and 4 hr later (T4), while patients were receiving a therapeutic protocol (fluids, vasopressive drugs) adjusted to reach a mean arterial pressure of 75 mmHg. In 18 of our 24 patients, a blood lactate level > or = 2 mmol/L (mean +/- SD: 4 +/- 2 mmol/L) associated with an increased mean lactate to pyruvate ratio (14.4 +/- 3.2) was observed at T0, while oxygen delivery (DO2) was high (533 +/- 208 ml/min/m2) and mean arterial pressure was 76 +/- 21 mmHg. Patients were subdivided into two groups according to changes in DO2 from T0 to T4: group D comprised 14 patients (10 with hyperlactatemia and 4 with normal lactate) in whom DO2 and oxygen consumption (VO2) simultaneously decreased from T0 to T4 without significant change in lactate level; group I comprised 10 patients (8 with hyperlactatemia and 2 with normal lactate) in whom DO2 and VO2 simultaneously increased, while the blood lactate level decreased significantly from 3.5 +/- 2.5 mmol/L at T0 to 2.1 +/- 1.0 mmol/L at T4 (P < 0.05). Our results indicate that the brain-dead state was frequently associated with a global energetic failure probably due to a cellular oxygen deficit, despite blood pressure within the normal range. This energetic failure, because it is associated with high levels of DO2, could result from a defect in peripheral oxygen extraction. Aggressive therapy, achieved by producing a further increase in DO2, may reduce this global tissue oxygen deficit.
这项针对连续患者的前瞻性临床研究的目的是，通过分析脑死亡复苏期间外周氧合指标，来验证脑死亡患者存在全身性能量衰竭的假设。研究对象包括来自多学科重症监护病房的24例符合脑死亡标准的患者。脑死亡的原因多种多样：严重创伤性颅脑损伤、脑血管事件、脑缺氧、原发性脑肿瘤和头部枪伤。采用的干预措施是桡动脉和肺动脉插管。在诊断脑死亡后即刻（T0）和4小时后（T4）测量血流动力学和气体测量参数以及血乳酸水平，此时患者正在接受调整以达到平均动脉压75 mmHg的治疗方案（液体、血管活性药物）。在我们的24例患者中，有18例在T0时观察到血乳酸水平≥2 mmol/L（均值±标准差：4±2 mmol/L），同时平均乳酸与丙酮酸比值升高（14.4±3.2），而氧输送（DO2）较高（533±208 ml/min/m2），平均动脉压为76±21 mmHg。根据从T0到T4的DO2变化将患者分为两组：D组包括14例患者（10例高乳酸血症患者和4例乳酸正常患者），其DO2和氧消耗（VO2）从T0到T4同时下降，乳酸水平无显著变化；I组包括10例患者（8例高乳酸血症患者和2例乳酸正常患者），其DO2和VO2同时升高，而血乳酸水平从T0时的3.5±2.5 mmol/L显著降至T4时的2.1±1.0 mmol/L（P<0.05）。我们的结果表明，尽管血压在正常范围内，但脑死亡状态常与可能由于细胞性氧缺乏导致的全身性能量衰竭相关。这种能量衰竭，因为它与高水平的DO2相关，可能是由于外周氧摄取缺陷所致。通过使DO2进一步升高实现的积极治疗，可能会减少这种全身性组织氧缺乏。
