Yamagishi Toshinobu, Tanabe Takahiro, Fujita Hiroshi, Miyazaki Kazuki, Yukawa Takahiro, Sugiyama Kazuhiro, Hamabe Yuichi
Tertiary Emergency Medical Center, Tokyo Metropolitan Bokutoh Hospital, 4-23-15 Kotobashi, Sumida-ku, Tokyo, 130-8575, Japan.
Department of Transfusion Medicine, Tokyo Metropolitan Bokutoh Hospital, Tokyo, Japan.
J Med Case Rep. 2018 Aug 20;12(1):229. doi: 10.1186/s13256-018-1767-z.
Patients with left ventricular outflow tract obstruction who do not exhibit a dynamic pressure gradient at rest, experience pressure gradient increases of ≥ 30 mmHg only during specific situations; this is called latent left ventricular outflow tract obstruction. It is provoked by increased cardiac contraction and preload and afterload depletion. There are a few reports of patients with it developing cardiac arrest. We present a case of latent left ventricular outflow tract obstruction in which the patient with a sigmoid septum experienced refractory pulseless electrical activity due to conventional advanced cardiac life support.
A 73-year-old Asian woman on escitalopram and lorazepam was transported to our hospital for chest and back pain with altered consciousness. On arrival, she was in shock and developed pulseless electrical activity. After initiation of conventional cardiopulmonary resuscitation according to adult advanced cardiovascular life support guidelines, she could not regain spontaneous circulation. She was ultimately resuscitated via venoarterial extracorporeal membrane oxygenation initiation. The only abnormal laboratory result at admission was anemia. Her hemodynamic status stabilized after red blood cell transfusion, and venoarterial extracorporeal membrane oxygenation was subsequently terminated. Transthoracic echocardiography showed a sigmoid septum; dobutamine-infused Doppler echocardiography revealed a significant outflow gradient, and continuous monitoring showed Brockenbrough-Braunwald sign, which confirmed a diagnosis of latent left ventricular outflow tract obstruction due to a sigmoid septum. As a result, carvedilol and verapamil were initiated. A follow-up dobutamine-infused Doppler echocardiography showed a reduction of outflow gradient, and she was discharged without any sequelae. Latent left ventricular outflow tract obstruction worsened due to increasing cardiac contraction and the depletion of preload and afterload. Depleted preload occurred due to dehydration and anemia, whereas depleted afterload occurred due to the prescribed drugs, which subsequently caused pulseless electrical activity. Moreover, β-stimulation from the adrenaline probably enhanced the hypercontractile state and caused refractory pulseless electrical activity in our case.
Patients with latent left ventricular outflow tract obstruction can progress to cardiogenic shock and pulseless electrical activity due to increased cardiac contraction and depletion of preload and afterload. We should consider the patient's underlying conditions that induced pulseless electrical activity.
左心室流出道梗阻患者在静息状态下未表现出动态压力阶差，仅在特定情况下压力阶差增加≥30 mmHg；这被称为隐匿性左心室流出道梗阻。它由心脏收缩增强以及前负荷和后负荷降低所诱发。有少数关于此类患者发生心脏骤停的报道。我们报告一例隐匿性左心室流出道梗阻病例，该患者因乙状结肠样间隔出现难治性无脉性电活动，常规高级心脏生命支持措施无效。
一名73岁亚洲女性，正在服用艾司西酞普兰和劳拉西泮，因胸痛、背痛伴意识改变被送至我院。入院时，她处于休克状态并出现无脉性电活动。按照成人高级心血管生命支持指南开始常规心肺复苏后，她未能恢复自主循环。最终通过启动静脉 - 动脉体外膜肺氧合使其复苏。入院时唯一异常的实验室检查结果是贫血。输注红细胞后她的血流动力学状态稳定，随后静脉 - 动脉体外膜肺氧合被终止。经胸超声心动图显示乙状结肠样间隔；多巴酚丁胺激发的多普勒超声心动图显示明显的流出道梯度，连续监测显示布罗肯布罗夫 - 布劳恩瓦尔德征，确诊为由乙状结肠样间隔导致的隐匿性左心室流出道梗阻。因此，开始使用卡维地洛和维拉帕米。后续多巴酚丁胺激发的多普勒超声心动图显示流出道梯度降低，她出院时无任何后遗症。隐匿性左心室流出道梗阻因心脏收缩增强以及前负荷和后负荷降低而加重。前负荷降低是由于脱水和贫血，而后负荷降低是由于所使用的药物，随后导致了无脉性电活动。此外，肾上腺素的β刺激可能增强了高收缩状态，在我们的病例中导致了难治性无脉性电活动。
隐匿性左心室流出道梗阻患者可能因心脏收缩增强以及前负荷和后负荷降低而进展为心源性休克和无脉性电活动。我们应考虑导致无脉性电活动的患者基础状况。
