Ebata T, Watanabe Y, Amaha K, Hosaka Y, Takagi S
Department of Anesthesiology and Critical Care Medicine, School of Medicine, Tokyo Medical and Dental University, Japan.
Can J Anaesth. 1991 May;38(4 Pt 1):436-40. doi: 10.1007/BF03007579.
Haemodynamic responses to the apnoea test for the diagnosis of brain death were investigated in nine patients with severe head injury or cerebrovascular disease. To prove apnoea, the ventilator was disconnected for ten minutes and oxygen was insufflated to avoid hypoxaemia. No respiratory movement was seen in any patient. Ten minutes after disconnecting the ventilator, PaCO2 was increased to 78 +/- 3 mmHg and pH was reduced to 7.17 +/- 0.02. Adequate oxygenation was maintained in all patients. Cardiac output increased from 4.8 +/- 0.7 to 5.7 +/- 0.8 L.min-1 (P less than 0.05), and mean pulmonary artery pressure increased from 11 +/- 1 to 17 +/- 2 mmHg (P less than 0.01). However, mean arterial pressure, heart rate, pulmonary artery wedge pressure and right atrial pressure did not change. Plasma catecholamines were measured in three patients. Plasma norepinephrine concentrations increased in all three patients but the changes in plasma epinephrine were minimal. These circulatory responses to acute hypercapnia were less than those reported in awake volunteers and in patients during general anaesthesia. However, since plasma norepinephrine concentration increased during the test, some sympathoadrenal response, probably of spinal origin, was present, and may have prevented the direct depressant circulatory effects of acute hypercapnia. In conclusion, the apnoea test did not produce haemodynamic disturbances when respiratory acidosis was limited to a pH 7.17 +/- 0.02 and PaCO2 60-80 mmHg.
对9例重度颅脑损伤或脑血管疾病患者进行了用于诊断脑死亡的窒息试验的血流动力学反应研究。为证实窒息,将呼吸机断开10分钟,并吹入氧气以避免低氧血症。所有患者均未见呼吸运动。断开呼吸机10分钟后,动脉血二氧化碳分压(PaCO2)升至78±3 mmHg,pH降至7.17±0.02。所有患者均维持了充分的氧合。心输出量从4.8±0.7升/分钟增至5.7±0.8升/分钟(P<0.05),平均肺动脉压从11±1 mmHg升至17±2 mmHg(P<0.01)。然而,平均动脉压、心率、肺动脉楔压和右心房压未发生变化。对3例患者测定了血浆儿茶酚胺。所有3例患者血浆去甲肾上腺素浓度均升高,但血浆肾上腺素变化极小。这些对急性高碳酸血症的循环反应低于清醒志愿者和全身麻醉患者的报道。然而,由于试验期间血浆去甲肾上腺素浓度升高,存在一些可能起源于脊髓的交感肾上腺反应,并可能预防了急性高碳酸血症直接的循环抑制作用。总之,当呼吸性酸中毒限于pH 7.17±0.02和PaCO2 60 - 80 mmHg时,窒息试验未产生血流动力学紊乱。