Rudolf J, Haupt W F, Neveling M, Grond M
Klinik und Poliklinik für Neurologie, Universität zu Köln.
Acta Neurochir (Wien). 1998;140(7):659-63. doi: 10.1007/s007010050160.
To determine the influence of baseline paCO2 on the results of apnea testing in the diagnosis of brain death, we performed an open prospective study on 36 patients fulfilling all other criteria for the diagnosis of brain death according to the criteria proposed by the Advisory Board of the German Federal Chamber of Physicians. For testing of apnea, patients underwent hypoventilation with 100% oxygen supply until a baseline paCO2 of 40 torr (5.3 kPa, n = 24, group 1) or 60 torr (8.0 kPa, n = 12, group 2) was reached. Then, patients were disconnected from the ventilator and apneic oxygenation with insufflation of 61 O2/min into the tracheal cannula was performed for five minutes. Arterial blood gas samples were obtained every minute during the testing period. In parallel, patients were observed for signs of spontaneous breathing. All patients remained apneic during the five minute test period. No relevant hypoxia (paO2 < 80 torr [10.6 kPa]) was observed in either group. In group 1, a mean baseline paCO2 of 45 torr (6.0 kPa) was registered, mean end-paCO2 was 75 torr (10.0 kPa). In group 2, paCO2 values were 66 torr (8.8 kPa) and 90 torr (12 kPa), respectively. Baseline pH in group 1 (7.32) decreased to 7.18 at the end of testing and from 7.23 to 7.13 in group 2. Patients in group 2 were in possible danger of developing a CO2-induced narcosis mimicking apnea. Secondary organ damage due to severe respiratory acidosis could not be excluded in the patients of group 2. As no complications were observed in group 1 and apnea was evident in all these patients, we consider a baseline paCO2 of 40 torr (5.3 kPa) sufficient to establish apnea after five minutes of apneic oxygenation if an increase of baseline paCO2 of at least 20 mmHg is documented by arterial blood gas sampling. A higher baseline paCO2 may endanger patients without yielding more specific testing results.
为了确定基线动脉血二氧化碳分压（paCO₂）对用于脑死亡诊断的 apnea 测试结果的影响，我们对 36 例符合德国联邦医师公会顾问委员会提出的脑死亡诊断所有其他标准的患者进行了一项开放性前瞻性研究。为了进行 apnea 测试，患者在 100%氧气供应下进行通气不足，直到达到 40 托（5.3 千帕，n = 24，第 1 组）或 60 托（8.0 千帕，n = 12，第 2 组）的基线 paCO₂。然后，将患者与呼吸机断开连接，并通过向气管插管内以每分钟 6 升的速度吹入氧气进行无呼吸氧合 5 分钟。在测试期间每分钟采集动脉血气样本。同时，观察患者有无自主呼吸迹象。在 5 分钟的测试期内所有患者均无呼吸。两组均未观察到相关的低氧血症（动脉血氧分压[paO₂]<80 托[10.6 千帕]）。在第 1 组中，记录到平均基线 paCO₂为 45 托（6.0 千帕），平均终末动脉血二氧化碳分压为 75 托（10.0 千帕）。在第 2 组中，paCO₂值分别为 66 托（8.8 千帕）和 90 托（12 千帕）。第 1 组的基线 pH 值（7.32）在测试结束时降至 7.18，第 2 组从 7.23 降至 7.13。第 2 组患者有可能发生类似无呼吸的二氧化碳诱导性麻醉。第 2 组患者不能排除因严重呼吸性酸中毒导致的继发性器官损伤。由于第 1 组未观察到并发症且所有这些患者均明显无呼吸，如果动脉血气采样记录到基线 paCO₂至少升高 20 毫米汞柱，我们认为 40 托（5.3 千帕）的基线 paCO₂足以在无呼吸氧合 5 分钟后确定无呼吸。更高的基线 paCO₂可能会危及患者，而不会产生更具特异性的测试结果。
