Eshel G, Safar P, Radovsky A, Stezoski S W
Safar Center for Resuscitation Research, Israel.
Aviat Space Environ Med. 1997 May;68(5):415-20.
Successful resuscitation from heatstroke cardiopulmonary arrest has been only partially explored and the data covering the post resuscitation pathophysiology leading to secondary arrest is, in most cases, insufficient.
Following heatstroke-cardiopulmonary arrest, successful resuscitation may be achieved by standard CPR with surface cooling and administration of glucose. We ponder the sequence of early circulatory responses and the pathophysiological changes following successful resuscitation.
We exposed 12 pigtail monkeys to total-body hyperthermia (cerebral T 42 degrees C) until cardiac arrest ensued. Standard external CPR with surface cooling and glucose 5% IV were administered for up to 30 min. Control group A (n = 6) was compared with experimental group B (n = 6), which received additional steroid, glucagon and hypertonic glucose during CPR attempts.
No significant differences were found between the outcome of the two groups. The 30-min CPR attempt succeeded in restoration of spontaneous circulation (ROSC) in 8/12 monkeys-5 animals from group A and 3 in group B. The animals in whom resuscitation was unsuccessful had significantly prolonged periods of rectal temperature exceeding 42.5 degrees C (p < 0.05), and significantly higher rectal temperatures at the end of 30 min of CPR and cooling (p < 0.05). All the resuscitated animals later rearrested at 158 +/- 68 (95-228) min after ROSC; pulmonary edema occurred in 6/8 animals.
We conclude that experimentally-induced heatstroke can be transiently reversed by standard resuscitative procedures, but is followed by a delayed, irreversible, secondary shock state, which could not be prevented by the treatment we employed. We were, however, able to document in detail the pathophysiologic processes involved in the resuscitation, and the irreversible shock one sees after "successful" CPR.
中暑性心肺骤停成功复苏的相关情况仅得到部分研究，且大多数情况下，有关复苏后导致二次骤停的病理生理学数据并不充分。
中暑性心肺骤停后，通过标准心肺复苏术结合体表降温及葡萄糖给药或许可实现成功复苏。我们思考成功复苏后早期循环反应的顺序以及病理生理变化。
将12只猪尾猴暴露于全身高温（脑温42摄氏度）直至发生心脏骤停。给予标准体外心肺复苏术，同时进行体表降温并静脉注射5%葡萄糖，持续30分钟。将对照组A（n = 6）与实验组B（n = 6）进行比较，实验组B在进行心肺复苏尝试期间额外给予类固醇、胰高血糖素和高渗葡萄糖。
两组结果之间未发现显著差异。30分钟的心肺复苏尝试成功使8/12只猴子恢复自主循环（ROSC）——A组5只动物，B组3只。复苏未成功的动物直肠温度超过42.5摄氏度的时间显著延长（p < 0.05），且在心肺复苏和降温30分钟结束时直肠温度显著更高（p < 0.05）。所有复苏成功的动物在恢复自主循环后158 +/- 68（95 - 228）分钟后再次骤停；6/8只动物发生肺水肿。
我们得出结论，实验性诱导的中暑可通过标准复苏程序暂时逆转，但随后会出现延迟的、不可逆的继发性休克状态，我们所采用的治疗方法无法预防这种情况。然而，我们能够详细记录复苏过程中涉及的病理生理过程，以及“成功”心肺复苏后出现的不可逆休克。
