Amin D V, Antaki J F, Litwak P, Thomas D, Wu Z J, Watach M
University of Pittsburgh McGowan Center for Artificial Organ Development, Pennsylvania, USA.
ASAIO J. 1998 Sep-Oct;44(5):M685-90. doi: 10.1097/00002480-199809000-00077.
An important consideration for clinical application of rotary blood pump based ventricular assist is the avoidance of ventricular collapse due to excessive operating speed. Because healthy animals do not typically demonstrate this phenomenon, it is difficult to evaluate control algorithms for avoiding suction in vivo. An acute hemodynamic study was thus conducted to determine the conditions under which suction could be induced. A 70 kg calf was implanted with an axial flow assist device (Nimbus/UoP IVAS; Nimbus Inc., Rancho Cordova, CA) cannulated from the left ventricular apex to ascending aorta. On initiation of pump operation, several vasoactive interventions were performed to alter preload, afterload, and contractility of the left ventricle. Initially, dobutamine increased contractility and heart rate ([HR] = 139; baseline = 70), but ventricular collapse was not achievable, even at the maximal pump speed of 15,000 rpm. Norepinephrine decreased HR (HR = 60), increased contractility, and increased systemic vascular resistance ([SVR] = 24; baseline = 15), resulting in ventricular collapse at a pump speed of 14,000 rpm. Isoproterenol (beta agonist) increased HR (HR = 103) and decreased SVR (SVR = 12), but ventricular collapse was not achieved. Inferior vena cava occlusion reduced preload, and ventricular collapse was achieved at speeds as low as 11,000 rpm. Esmolol (beta1 antagonist) decreased HR (HR = 55) and contractility, and ventricular collapse was achieved at 11,500 rpm. Episodes of ventricular collapse were characterized initially by the pump output exceeding the venous return and the aortic valve remaining closed throughout the cardiac cycle. If continued, the mitral valve would remain open throughout the cardiac cycle. Using these unique states of the mitral and aortic valves, the onset of ventricular collapse could reliably be identified. It is hoped that the ability to detect the onset of ventricular collapse, rather than the event itself, will assist in the development and the evaluation of control algorithms for rotary ventricular assist devices.
基于旋转血泵的心室辅助装置在临床应用中的一个重要考虑因素是避免因运行速度过快导致心室塌陷。由于健康动物通常不会出现这种现象，因此很难在体内评估避免抽吸的控制算法。因此进行了一项急性血流动力学研究，以确定可诱发抽吸的条件。将一台轴流辅助装置（Nimbus/UoP IVAS；Nimbus公司，加利福尼亚州兰乔科尔多瓦）植入一头70公斤重的小牛体内，该装置从左心室尖部插管至升主动脉。在启动泵操作时，进行了几种血管活性干预措施，以改变左心室的前负荷、后负荷和收缩力。最初，多巴酚丁胺增加了收缩力和心率（[心率]=139；基线=70），但即使在15000转/分钟的最大泵速下，也无法实现心室塌陷。去甲肾上腺素降低了心率（心率=60），增加了收缩力，并增加了全身血管阻力（[体循环血管阻力]=24；基线=15），导致在14000转/分钟的泵速下心室塌陷。异丙肾上腺素（β激动剂）增加了心率（心率=103）并降低了体循环血管阻力（体循环血管阻力=12），但未实现心室塌陷。下腔静脉闭塞降低了前负荷，在低至11000转/分钟的速度下实现了心室塌陷。艾司洛尔（β1拮抗剂）降低了心率（心率=55）和收缩力，在11500转/分钟时实现了心室塌陷。心室塌陷发作最初的特征是泵输出超过静脉回流，并且在整个心动周期中主动脉瓣保持关闭。如果持续下去，二尖瓣将在整个心动周期中保持开放。利用二尖瓣和主动脉瓣的这些独特状态，可以可靠地识别心室塌陷的开始。希望能够检测到心室塌陷的开始，而不是事件本身，将有助于旋转心室辅助装置控制算法的开发和评估。
