TY - JOUR
T1 - Prediction of the impact of venoarterial extracorporeal membrane oxygenation on hemodynamics
AU - Sakamoto, Kazuo
AU - Saku, Keita
AU - Kishi, Takuya
AU - Kakino, Takamori
AU - Tanaka, Atsushi
AU - Sakamoto, Takafumi
AU - Ide, Tomomi
AU - Sunagawa, Kenji
N1 - Publisher Copyright:
© 2015 the American Physiological Society.
Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 2015
Y1 - 2015
N2 - 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 (r2) = 0.99, standard error of estimate (SEE) = 5.8 ml•min−1•kg−1, PRA: r2 = 0.95, SEE = 0.23 mmHg, PLA: r2 = 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 (r2 = 0.93, SEE = 0.5 ml•min−1•kg−1), PRA (r2 = 0.99, SEE = 0.54 mmHg), and PLA (r2 = 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.
AB - 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 (r2) = 0.99, standard error of estimate (SEE) = 5.8 ml•min−1•kg−1, PRA: r2 = 0.95, SEE = 0.23 mmHg, PLA: r2 = 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 (r2 = 0.93, SEE = 0.5 ml•min−1•kg−1), PRA (r2 = 0.99, SEE = 0.54 mmHg), and PLA (r2 = 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.
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U2 - 10.1152/ajpheart.00603.2014
DO - 10.1152/ajpheart.00603.2014
M3 - Article
C2 - 25659486
AN - SCOPUS:84927928486
VL - 308
SP - H921-H930
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6135
IS - 8
ER -