Eshel Gideon M, Safar Peter
Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine, PA, USA.
Aviat Space Environ Med. 2002 Apr;73(4):327-32; discussion 333-4.
The neurological manifestations of heatstroke victims vary. The exact sequence of the central nervous system (CNS) changes during lethal hyperthermia has only been partially explored, and the data covering the post-resuscitation CNS changes, which in most cases lead to secondary cardiac arrest, are insufficient.
Following heating of the organism to cardiopulmonary arrest, successful resuscitation may be achieved by standard cardiopulmonary resuscitation (CPR), plus glucose and surface cooling. There is a characteristic sequence of neurological responses to hyperthermia preceding cardiopulmonary arrest, and questionable reversibility following successful resuscitation.
We exposed 12 pigtail monkeys under light anesthesia to total body hyperthermia (cerebral T = 42 degrees C) until cardiac arrest. We monitored EEG, mean arterial pressure (MAP), intracranial pressure (ICP), epidural temperatures, PaO2, PaCO2, serum sodium, osmolality, blood glucose, pupillary diameter, light response, corneal reflex, extremity movement, and seizures.
During hyperthermia EEG frequency decreased and amplitude increased, followed by burst suppression pattern of the EEG. Then during severe hypoglycemia, EEG seizure activity and isoelectric EEG occurred when MAP and cerebral perfusion pressure (CPP) decreased while ICP was almost unchanged. Pupils were first responsive to light and became gradually unresponsive with maximal dilation, correlating with low CPP. After temporarily successful cardiopulmonary resuscitation (restoration of spontaneous circulation), normal EEG tracing and reversibility of the unresponsive pupils were observed. As shock led to secondary rearrest, deterioration with depression of all cerebral functions was documented. Some 147 min after restoration of spontaneous circulation, brains were macroscopically (and microscopically) normal in six of the eight monkeys.
The acute cerebral derangements during and after lethal hyperthermia are reversible. The cause of death is probably not CNS damage, but systemic hemodynamic deterioration.
中暑患者的神经学表现各不相同。致死性体温过高期间中枢神经系统（CNS）变化的确切顺序仅得到部分研究，且关于复苏后CNS变化的数据不足，而在大多数情况下，复苏后CNS变化会导致继发性心脏骤停。
在机体受热至心肺骤停后，通过标准心肺复苏（CPR）、补充葡萄糖及体表降温可能实现成功复苏。在心肺骤停前，对体温过高存在特征性的神经学反应序列，且成功复苏后其可逆性存疑。
我们在浅麻醉状态下使12只猪尾猴全身受热（脑温=42摄氏度）直至心脏骤停。我们监测脑电图（EEG）、平均动脉压（MAP）、颅内压（ICP）、硬膜外温度、动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）、血清钠、渗透压、血糖、瞳孔直径、光反应、角膜反射、肢体活动及癫痫发作情况。
在体温过高期间，EEG频率降低而波幅增加，随后出现EEG爆发抑制模式。接着在严重低血糖期间，当MAP和脑灌注压（CPP）降低而ICP几乎未变时，出现EEG癫痫样活动及EEG等电位线。瞳孔最初对光有反应，随后逐渐无反应且极度散大，这与低CPP相关。在心肺复苏暂时成功（恢复自主循环）后，观察到EEG描记恢复正常且无反应的瞳孔具有可逆性。随着休克导致继发性再次骤停，记录到所有脑功能均出现恶化。在恢复自主循环约147分钟后，8只猴子中有6只的大脑在宏观（及微观）上正常。
致死性体温过高期间及之后的急性脑功能紊乱是可逆的。死亡原因可能并非CNS损伤，而是全身血流动力学恶化。
