Aagaard Rasmus, Caap Philip, Hansson Nicolaj C, Bøtker Morten T, Granfeldt Asger, Løfgren Bo
1Research Center for Emergency Medicine, Aarhus University Hospital, Aarhus, Denmark.2Department of Anesthesiology, Randers Regional Hospital, Randers, Denmark.3Department of Cardiology, Aarhus University Hospital, Skejby, Aarhus, Denmark.4Research and Development, Prehospital Emergency Medical Services, Central Denmark Region, Denmark.5Department of Anesthesiology and Intensive Care Medicine, Aarhus University Hospital, Aarhus, Denmark.6Department of Internal Medicine, Randers Regional Hospital, Randers, Denmark.
Crit Care Med. 2017 Jul;45(7):e695-e702. doi: 10.1097/CCM.0000000000002334.
The aim of this study was to test the hypothesis that the right ventricle is more dilated during resuscitation from cardiac arrest caused by pulmonary embolism, compared with hypoxia and primary arrhythmia.
Twenty-four pigs were anesthetized and cardiac arrest was induced using three different methods. Pigs were resuscitated after 7 minutes of untreated cardiac arrest. Ultrasonographic images were obtained and the right ventricular diameter was measured.
University hospital animal laboratory.
Female crossbred Landrace/Yorkshire/Duroc pigs (27-32 kg).
Pigs were randomly assigned to cardiac arrest induced by pulmonary embolism, hypoxia, or primary arrhythmia.
There was no difference at baseline. During induction of cardiac arrest, the right ventricle dilated in all groups (p < 0.01 for all). The primary endpoint was right ventricle diameter at the third rhythm analysis: 32 mm (95% CI, 29-36) for pulmonary embolism which was significantly larger than both hypoxia: 23 mm (95% CI, 20-27) and primary arrhythmia: 25 mm (95% CI, 22-28)-the absolute difference was 7-9 mm. Physicians with basic training in focused cardiac ultrasonography were able to detect a difference in right ventricle diameter of approximately 10 mm with a sensitivity of 79% (95% CI, 64-94) and a specificity of 68% (95% CI, 56-80).
The right ventricle was more dilated during resuscitation when cardiac arrest was caused by pulmonary embolism compared with hypoxia and primary arrhythmia. However, the right ventricle was dilated, irrespective of the cause of arrest, and diagnostic accuracy by physicians with basic training in focused cardiac ultrasonography was modest. These findings challenge the paradigm that right ventricular dilatation on ultrasound during cardiopulmonary resuscitation is particularly associated with pulmonary embolism.
本研究旨在验证以下假设:与缺氧和原发性心律失常相比,在因肺栓塞导致的心搏骤停复苏过程中,右心室扩张更为明显。
对24头猪进行麻醉,并使用三种不同方法诱导心搏骤停。在未经处理的心搏骤停7分钟后对猪进行复苏。获取超声图像并测量右心室直径。
大学医院动物实验室。
雌性长白/约克夏/杜洛克杂交猪(27 - 32千克)。
将猪随机分配至因肺栓塞、缺氧或原发性心律失常诱导的心搏骤停组。
基线时无差异。在心搏骤停诱导期间,所有组的右心室均扩张(所有p < 0.01)。主要终点是第三次心律分析时的右心室直径:肺栓塞组为32毫米(95%置信区间,29 - 36),显著大于缺氧组的23毫米(95%置信区间,20 - 27)和原发性心律失常组的25毫米(95%置信区间,22 - 28)——绝对差值为7 - 9毫米。接受过心脏聚焦超声基础培训的医生能够检测出右心室直径约10毫米的差异,灵敏度为79%(95%置信区间,64 - 94),特异度为68%(95%置信区间,56 - 80)。
与缺氧和原发性心律失常相比,因肺栓塞导致的心搏骤停复苏过程中右心室扩张更为明显。然而,无论心搏骤停原因如何,右心室都会扩张,接受过心脏聚焦超声基础培训的医生的诊断准确性一般。这些发现挑战了心肺复苏期间超声检查显示右心室扩张尤其与肺栓塞相关的范例。