Less invasive and inotrope-reduction approach to automated closed-loop control of hemodynamics in decompensated heart failure.

Less invasive and inotrope-reduction approach to automated closed-loop control of hemodynamics in decompensated heart failure.
复制标题

失代偿性心力衰竭的血流动力学自动闭环控制的微创和正性肌力减少方法。

DOI:
10.1109/tbme.2015.2499782
复制
发表时间:
2015
期刊:
IEEE Trans Biomed Eng
影响因子:
--
通讯作者:
Sugimachi M.
Sugimachi M.
中科院分区:
--
文献类型:
--
作者:
Uemura K;Kawada T;Zheng C;Sugimachi M.

文献摘要

相似文献

我们一直在开发一种自动心血管药物输注系统,用于同时控制失代偿性心力衰竭(HF)患者的动脉压(AP)、心输出量(CO)和左房压(PLA)。在我们的原型系统中,通过开胸对CO和LA进行了侵入性测量。此外,控制逻辑不可避免地需要使用肌力调节剂来改善血流动力学,这不符合心衰临床指南。本研究的目标是解决这些问题,并开发出一套临床上可行的系统。我们将我们最近开发的CO和肺毛细血管楔压(PCWP)的微创监测仪集成到该系统中。我们还重新设计了控制逻辑,以减少正性肌力的使用。我们将新开发的系统应用于9只患有失代偿性心衰的狗。一旦激活,我们的系统就开始控制所有动物体内血管扩张剂和利尿剂的输注。在三只动物中没有输注肌力调节剂,而在六只不能单独输注血管扩张剂的动物中以最小剂量输注。在50分钟内,我们的系统将AP、CO和PCWP精确地控制到各自的目标位置。肺动脉插管证实血流动力学得到改善(AP由98±4增至74±11 mm Hg;CO由2.2±0.5增至2.9±0.3 L·min-1·m-2;PCWP由2 7.0±6.6增至13.8±3.0 mm Hg)。在减少肌力调节剂使用的同时,在微创环境下,我们的系统成功地自动优化了犬心力衰竭模型的整体血流动力学。本研究结果为自动输液系统的临床应用奠定了基础。
We have been developing an automated cardiovascular drug infusion system for simultaneous control of arterial pressure (AP), cardiac output (CO), and left atrial pressure (PLA) in decompensated heart failure (HF). In our prototype system, CO and PLA were measured invasively through thoracotomy. Furthermore, the control logic inevitably required use of inotropes to improve hemodynamics, which was not in line with clinical HF guidelines. The goal of this study was to solve these problems and develop a clinically feasible system. We integrated to the system minimally invasive monitors of CO and pulmonary capillary wedge pressure (PCWP, surrogates for PLA) that we developed recently. We also redesigned the control logic to reduce the use of inotrope. We applied the newly developed system to nine dogs with decompensated HF. Once activated, our system started to control the infusion of vasodilator and diuretics in all the animals. Inotrope was not infused in three animals, and infused at minimal doses in six animals that were intolerant of vasodilator infusion alone. Within 50 min, our system controlled AP, CO, and PCWP to their respective targets accurately. Pulmonary artery catheterization confirmed optimization of hemodynamics (AP, from 98 ± 4 to 74 ± 11 mmHg; CO, from 2.2 ± 0.5 to 2.9 ± 0.3 L·min-1·m-2; PCWP, from 27.0 ± 6.6 to 13.8 ± 3.0 mmHg). In a minimally invasive setting while reducing the use of inotrope, our system succeeded in automatically optimizing the overall hemodynamics in canine models of HF. The present results pave the way for clinical application of our automated drug infusion system.