Benzel E C, Gross C D, Hadden T A, Kesterson L, Landreneau M D
Division of Neurosurgery, Louisiana State University Medical Center, Shreveport.
J Neurosurg. 1989 Aug;71(2):191-4. doi: 10.3171/jns.1989.71.2.0191.
By conventional criteria, an apneic patient's PaCO2 must be greater than 60 mm Hg before apnea can be attributed to brain death. The rate of a PaCO2 increase in the apneic patient traditionally has been thought to be in the range of 3 mm Hg/min. In order to assess the validity of these data and the validity of the "apnea test" for determination of brain death, the results of this test were reviewed in 20 patients. In all patients, arterial blood samples were drawn for blood gas measurements every 2 minutes following the cessation of volume ventilation (with an oxygen cannula at 6 liters O2/min passed into the tracheobronchial tree). The rate of PaCO2 increase was noted to be very erratic. The average rate of rise was 3.7 +/- 2.3 mm Hg/min (+/- standard deviation). This, however, varied from 0.5 to 10.5 mm Hg/min and was not predictable from the variables evaluated. The rate of PaCO2 increase was noted to decline throughout the duration of the test. This ranged from 3.9 +/- 1.2 mm Hg/min (for patients with baseline PaCO2 less than or equal to 30 mm Hg) and 4.5 +/- 1.9 mm Hg/min (for patients with baseline PaCO2 greater than or equal to 30 mm Hg) in the first 4 minutes of the test to an average of 0.92 mm Hg/min for patients with test lasted longer than 12 minutes. These unpredictable results might be related to CO2 washout, atelectasis, cardiac ventilations, or other yet-undefined parameters. The nonlinear relationship between rate of PaCO2 increase and time following onset of apnea resulted in the test being prolonged in several patients. In these patients, the PaCO2 approached 60 mm Hg in an asymptotic fashion. These lengthy tests could have been avoided by utilizing a standardized apnea test with a baseline PaCO2 of 40 mm Hg or greater. The observation that a high baseline PaCO2 greatly augments the efficiency and safety of the test allows criteria that have previously been based on conjecture to be documented and applied clinically. A standardized apnea test, utilizing these principles, may satisfy many of the criticisms regarding brain-death testing that have been raised by neurologists, neurosurgeons, and transplant surgeons.
按照传统标准，在将呼吸暂停归因于脑死亡之前，呼吸暂停患者的动脉血二氧化碳分压（PaCO2）必须大于60毫米汞柱。传统上认为，呼吸暂停患者的PaCO2升高速率在3毫米汞柱/分钟左右。为了评估这些数据的有效性以及“呼吸暂停试验”用于判定脑死亡的有效性，对20例患者的该试验结果进行了回顾。在所有患者中，停止容量通气后（通过将氧流量为6升/分钟的氧气管插入气管支气管树），每隔2分钟采集动脉血样本进行血气测量。结果发现，PaCO2升高速率非常不稳定。平均升高速率为3.7±2.3毫米汞柱/分钟（±标准差）。然而，其变化范围为0.5至10.5毫米汞柱/分钟，且无法根据所评估的变量进行预测。在整个试验过程中，PaCO2升高速率呈下降趋势。在试验的前4分钟，对于基线PaCO2小于或等于30毫米汞柱的患者，该速率为3.9±1.2毫米汞柱/分钟，对于基线PaCO2大于或等于30毫米汞柱的患者，为4.5±1.9毫米汞柱/分钟，而对于试验持续时间超过12分钟的患者，平均为0.92毫米汞柱/分钟。这些不可预测的结果可能与二氧化碳排出、肺不张、心脏通气或其他尚未明确的参数有关。PaCO2升高速率与呼吸暂停开始后的时间之间的非线性关系导致在一些患者中试验时间延长。在这些患者中，PaCO2以渐近方式接近60毫米汞柱。通过采用基线PaCO2为40毫米汞柱或更高的标准化呼吸暂停试验，本可避免这些冗长的试验。高基线PaCO2可极大提高试验效率和安全性这一观察结果，使得先前基于推测的标准得以记录并应用于临床。利用这些原则的标准化呼吸暂停试验，可能会满足神经科医生、神经外科医生和移植外科医生对脑死亡检测提出的许多批评。
