Sakamoto Kazuo, Saku Keita, Kishi Takuya, Kakino Takamori, Tanaka Atsushi, Sakamoto Takafumi, Ide Tomomi, Sunagawa Kenji
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan; and
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan; and.
Am J Physiol Heart Circ Physiol. 2015 Apr 15;308(8):H921-30. doi: 10.1152/ajpheart.00603.2014. Epub 2015 Feb 6.
Although venoarterial extracorporeal membrane oxygenation (ECMO) was developed to rescue patients with cardiogenic shock, the impact of ECMO on hemodynamics is often unpredictable and can lead to hemodynamic collapse. In this study, we developed a framework in which we incorporated ECMO into the extended Guyton's model of circulatory equilibrium and predicted hemodynamic changes in response to ECMO. We first determined the cardiac output (CO) curves of left and right heart (to generate the integrated CO curve) without ECMO in eight normal and seven dogs with left ventricular dysfunction. Using the CO curves obtained and standard parameters for the venous return surface, we predicted the circulatory equilibrium under various levels of ECMO support. The predicted total flow (native left heart flow plus ECMO flow), right atrial pressure (PRA), and left atrial pressure (PLA) matched well with those measured [total flow: coefficient of determination (r(2)) = 0.99, standard error of estimate (SEE) = 5.8 ml·min(-1)·kg(-1), PRA: r(2) = 0.95, SEE = 0.23 mmHg, PLA: r(2) = 0.99, SEE = 0.59 mmHg]. Lastly, we estimated the CO curves under ECMO support from minute changes in hemodynamics induced by change in ECMO. From the CO curves estimated, we predicted the circulatory equilibrium. The predicted total flow (r(2) = 0.93, SEE = 0.5 ml·min(-1)·kg(-1)), PRA (r(2) = 0.99, SEE = 0.54 mmHg), and PLA (r(2) = 0.95, SEE = 0.89 mmHg) matched reasonably well with those measured. A numerical simulation indicated that ECMO support may cause pulmonary edema, if right ventricular function is compromised. We conclude that the proposed framework may enhance the benefit and reduce the risk of ECMO support in patients with critical hemodynamic conditions.
尽管静脉-动脉体外膜肺氧合（ECMO）是为抢救心源性休克患者而研发的，但ECMO对血流动力学的影响往往不可预测，且可能导致血流动力学崩溃。在本研究中，我们构建了一个框架，将ECMO纳入扩展的盖顿循环平衡模型，以预测ECMO引起的血流动力学变化。我们首先测定了8只正常犬和7只左心室功能不全犬在无ECMO情况下左、右心的心输出量（CO）曲线（以生成综合CO曲线）。利用获得的CO曲线和静脉回流表面的标准参数，我们预测了不同水平ECMO支持下的循环平衡。预测的总流量（自身左心流量加ECMO流量）、右心房压力（PRA）和左心房压力（PLA）与测量值匹配良好[总流量：决定系数（r²）=0.99，估计标准误差（SEE）=5.8 ml·min⁻¹·kg⁻¹，PRA：r² =0.95，SEE =0.23 mmHg，PLA：r² =0.99，SEE =0.59 mmHg]。最后，我们根据ECMO变化引起的血流动力学微小变化估计了ECMO支持下的CO曲线。根据估计的CO曲线，我们预测了循环平衡。预测的总流量（r² =0.93，SEE =0.5 ml·min⁻¹·kg⁻¹）、PRA（r² =0.99，SEE =0.54 mmHg）和PLA（r² =0.95，SEE =0.89 mmHg）与测量值相当吻合。数值模拟表明，如果右心室功能受损，ECMO支持可能导致肺水肿。我们得出结论，所提出的框架可能会提高ECMO支持对血流动力学危急患者的益处并降低风险。
