Saika Yuka, Wakabayashi Ryo, Ichiyanagi Hiroki, Suzuki Aki, Sato Nobukazu
Clinical Training Center, Tokyo Saiseikai Central Hospital, Tokyo, JPN.
Department of Anesthesiology, Tokyo Saiseikai Central Hospital, Tokyo, JPN.
Cureus. 2024 Feb 27;16(2):e55026. doi: 10.7759/cureus.55026. eCollection 2024 Feb.
Systolic anterior motion of the mitral valve and left ventricular outflow tract obstruction are complications following transcatheter aortic valve implantation and can lead to hemodynamic collapse. Medical management for those complications is usually centered on a reduction in left ventricular contractility with negative inotropes. An 88-year-old woman underwent transcatheter aortic valve implantation for severe aortic stenosis. Hemodynamic collapse and exacerbation of mitral regurgitation occurred immediately after valve implantation. For suspected left ventricular outflow tract obstruction, medical management centered on negative inotropes was performed. Hemodynamics and left ventricular outflow tract obstruction improved over time; however, the oxygen supply-demand imbalance progressed. On postoperative day 5, the patient suddenly went into pulseless electrical activity. Cardiopulmonary resuscitation was performed for three minutes, resulting in the return of spontaneous circulation. Subsequent refractory hypotension and oxygen supply-demand imbalance improved with continuous infusion of adrenaline, dobutamine, and phenylephrine. Her hemodynamics remained stable after she was weaned off the pressor infusions, and negative inotropes were not required again. In summary, the cause of cardiac arrest was possibly due to excessive negative inotropic effects even though the effects contributed to improvement of left ventricular outflow tract obstruction. Anesthesiologists and intensivists should recognize the risk of cardiac arrest induced by negative inotropic effects and use negative inotropes with rigorous hemodynamic monitoring, even when left ventricular outflow tract obstruction is treated effectively.
二尖瓣收缩期前向运动和左心室流出道梗阻是经导管主动脉瓣植入术后的并发症，可导致血流动力学崩溃。这些并发症的药物治疗通常以使用负性肌力药物降低左心室收缩力为中心。一名88岁女性因严重主动脉瓣狭窄接受经导管主动脉瓣植入术。瓣膜植入后立即出现血流动力学崩溃和二尖瓣反流加重。对于疑似左心室流出道梗阻，采取了以负性肌力药物为中心的药物治疗。随着时间的推移，血流动力学和左心室流出道梗阻情况有所改善；然而，氧供需失衡却进一步发展。术后第5天，患者突然出现无脉电活动。进行了3分钟的心肺复苏，恢复了自主循环。随后，通过持续输注肾上腺素、多巴酚丁胺和去氧肾上腺素，难治性低血压和氧供需失衡情况得到改善。停用升压药输注后，她的血流动力学保持稳定，不再需要使用负性肌力药物。总之，心脏骤停的原因可能是负性肌力作用过度，尽管这些作用有助于改善左心室流出道梗阻。麻醉医生和重症监护医生应认识到负性肌力作用诱发心脏骤停的风险，并在严格的血流动力学监测下使用负性肌力药物，即使左心室流出道梗阻得到有效治疗时也应如此。
