Clifton G L, Robertson C S, Grossman R G
Baylor College of Medicine, Department of Neurosurgery, Houston, Texas.
Neurosurg Rev. 1989;12 Suppl 1:465-73. doi: 10.1007/BF01790692.
The cardiovascular and metabolic responses to severe head injury were studied in the acute phase after severe head injury with the object of determining if a common response was present and, if so, its significance in the management of the patients' intracranial and systemic physiological states. The cardiovascular response to head injury was studied by measurement of cardiac output, pulmonary capillary wedge pressure, arterial blood pressure, arterial and mixed venous blood gases and arterial and mixed venous epinephrine and norepinephrine serially in 15 patients during the first three days after injury. A hyperdynamic state was found characterized by increased cardiac output and cardiac work, moderate hypertension, tachycardia, decreased or normal systemic and pulmonary vascular resistance, increased pulmonary shunting and increased oxygen delivery and utilisation. Arterial E and NE levels correlated well with the cardiac output, cardiac work, blood pressure, heart rate, oxygen delivery, and oxygen utilization but not with vascular resistance or pulmonary shunt. The magnitude of the hyperdynamic state did not correlate with intracranial pressure, Glasgow Coma Score, or findings on CT scan. The metabolic response to head injury was studied by measurement of resting metabolic expenditure (RME) in 14 comatose head-injured patients in the first nine days after injury. During this period patients were fed with a continuous parenteral infusion of a formula containing 2 Kcal/cc and 10 mg nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated, nonparalyzed patients was 138 +/- 37% of that expected for a non-injured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 109 patient-days. The mean excretion was 20.2 +/- 6.4 mg/day. The mean protein caloric contribution was 23.9 +/- 6.7% and was greater than 25% for six patients, compared to normal values of 10-15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with the parenterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20-40% of the body surface.
在重度颅脑损伤后的急性期,对心血管和代谢反应进行了研究,目的是确定是否存在共同反应,如果存在,其在患者颅内和全身生理状态管理中的意义。通过在15例患者受伤后的头三天连续测量心输出量、肺毛细血管楔压、动脉血压、动脉血和混合静脉血气体以及动脉血和混合静脉血中的肾上腺素和去甲肾上腺素,研究了颅脑损伤后的心血管反应。发现一种高动力状态,其特征为心输出量和心脏做功增加、中度高血压、心动过速、全身和肺血管阻力降低或正常、肺分流增加以及氧输送和利用增加。动脉血中的肾上腺素和去甲肾上腺素水平与心输出量、心脏做功、血压、心率、氧输送和氧利用密切相关,但与血管阻力或肺分流无关。高动力状态的程度与颅内压、格拉斯哥昏迷评分或CT扫描结果无关。通过测量14例昏迷颅脑损伤患者受伤后头九天的静息代谢消耗(RME),研究了颅脑损伤后的代谢反应。在此期间,患者通过持续肠外输注含有2千卡/立方厘米和10毫克氮/升的配方进行喂养。进行了102个患者日的间接测热法。非镇静、非麻痹患者的平均静息代谢消耗(RME)为年龄、性别和体表面积相当的非受伤静息者预期值的138±37%。测量了109个患者日的氮排泄量。平均排泄量为20.2±6.4毫克/天。平均蛋白质热量贡献为23.9±6.7%,6例患者大于25%,而正常值为10 - 15%。尽管进行了全胃肠外营养,但仅7例患者在任何3天期间实现了正氮平衡,并且需要用肠外给予的配方替代RME的161%至240%。颅脑损伤患者的代谢反应与报道的体表20 - 40%烧伤患者的代谢反应相似。