Hagmann Henning, Oelmann Katrin, Stangl Robert, Michels Guido
Department II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.
Department II of Internal Medicine, University Hospital Cologne, Kerpener Str. 62, 50937, Cologne, Germany.
J Med Case Rep. 2016 Dec 20;10(1):364. doi: 10.1186/s13256-016-1148-4.
The phenomenon of autoresuscitation is rare, yet it is known to most emergency physicians. However, the pathophysiology of the delayed return of spontaneous circulation remains enigmatic. Among other causes hyperinflation of the lungs and excessively high positive end-expiratory pressure have been suggested, but reports including cardiopulmonary monitoring during cardiopulmonary resuscitation are scarce to support this hypothesis.
We report a case of autoresuscitation in a 44-year-old white man after 80 minutes of advanced cardiac life support accompanied by continuous capnometry and repeated evaluation by ultrasound and echocardiography. After prolonged cardiopulmonary resuscitation, refractory electromechanical dissociation on electrocardiogram and ventricular akinesis were recorded. In addition, a precipitous drop in end-tidal partial pressure of carbon dioxide was noted and cardiopulmonary resuscitation was discontinued. Five minutes after withdrawal of all supportive measures his breathing resumed and a perfusing rhythm ensued.
Understanding the underlying pathophysiology of autoresuscitation is hampered by a lack of reports including extensive cardiopulmonary monitoring during cardiopulmonary resuscitation in a preclinical setting. In this case, continuous capnometry was combined with repetitive ultrasound evaluation, which ruled out most assumed causes of autoresuscitation. Our observation of a rapid decline in end-tidal partial pressure of carbon dioxide supports the hypothesis of increased intrathoracic pressure. Continuous capnometry can be performed easily during cardiopulmonary resuscitation, also in a preclinical setting. Knowledge of the pathophysiologic mechanisms may lead to facile interventions to be incorporated into cardiopulmonary resuscitation algorithms. A drop in end-tidal partial pressure of carbon dioxide, for example, might prompt disconnection of the ventilation to allow left ventricular filling. Further reports and research on this topic are encouraged.
自主复苏现象罕见，但大多数急诊医生都知晓。然而，自主循环延迟恢复的病理生理学仍不清楚。除其他原因外，有人提出肺过度膨胀和呼气末正压过高，但缺乏包括心肺复苏期间心肺监测的报告来支持这一假设。
我们报告一例44岁白人男性在接受80分钟高级心脏生命支持后出现自主复苏的病例，期间伴有持续二氧化碳监测以及超声和超声心动图的反复评估。长时间心肺复苏后，心电图记录到难治性电机械分离和心室运动减弱。此外，呼气末二氧化碳分压急剧下降，心肺复苏终止。撤除所有支持措施五分钟后，他恢复呼吸并出现灌注节律。
由于缺乏在临床前环境下心肺复苏期间进行广泛心肺监测的报告，对自主复苏潜在病理生理学的理解受到阻碍。在本病例中，持续二氧化碳监测与重复超声评估相结合，排除了大多数假定的自主复苏原因。我们观察到呼气末二氧化碳分压迅速下降，支持胸内压升高的假设。在心肺复苏期间，即使在临床前环境中也可轻松进行持续二氧化碳监测。了解病理生理机制可能会促使将简便的干预措施纳入心肺复苏算法。例如，呼气末二氧化碳分压下降可能提示断开通气以允许左心室充盈。鼓励对此主题进行进一步的报告和研究。
