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Left ventricular assist device (LVAD) saves lives in patients with severe left ventricular (LV) failure. However, predicting how much LVAD boosts total cardiac output (CO) remains difficult. This study aimed to develop a framework to quantitatively predict the impact of LVAD on hemodynamics. We adopted the circulatory equilibrium framework and incorporated LVAD into the integrated CO curve to derive the circulatory equilibrium. In anesthetized dogs, we ligated left coronary arteries to create LV failure and inserted a centrifugal pump as LVAD. Using CO and right (PRA) and left atrial pressure (PLA) measured before LVAD support, we predetermined the stressed volume (V) and logarithmic slope of right heart CO curve (SR). Next, we initiated LVAD at maximum level and then decreased LVAD flow stepwise while monitoring hemodynamic changes. We predicted LVAD-induced CO and PRA for given PLA from the predetermined SR and V and compared with those measured experimentally. The predicted CO [r² = 0.907, SE of estimate (SEE) = 5.59 ml·min-1·kg-1, P < 0.001] and PRA (r² = 0.967, SEE = 0.307 mmHg, P < 0.001) matched well with measured values indicating the validity of the proposed framework. We further conducted simulation using the validated framework to analyze the impact of LVAD on PRA under various right ventricular (RV) functions. It indicated that PRA is relatively insensitive to changes in RV end-systolic elastance or pulmonary arterial resistance, but sensitive to changes in V. In conclusion, the circulatory equilibrium framework predicts quantitatively the hemodynamic impact of LVAD. This knowledge would contribute to safe management of patients with LV failure undergoing LVAD implantation. [ABSTRACT FROM AUTHOR]

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·minâ'1·kgâ'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·minâ'1·kgâ'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. [ABSTRACT FROM AUTHOR]

Baroreflex modulates both the ventricular and vascular properties and stabilizes arterial pressure (AP). However, how changes in those mechanical properties quantitatively impact the dynamic AP regulation remains unknown. We developed a framework of circulatory equilibrium, in which both venous return and cardiac output are expressed as functions of left ventricular (LV) end-systolic elastance (Ees), heart rate (HR), systemic vascular resistance (R), and stressed blood volume (V). We investigated the contribution of each mechanical property using the framework of circulatory equilibrium. In six anesthetized dogs, we vascularly isolated carotid sinuses and randomly changed carotid sinus pressure (CSP), while measuring the LV Ees, aortic flow, right and left atrial pressure, and AP for at least 60 min. We estimated transfer functions from CSP to Ees, HR, R, and V in each dog. We then predicted these parameters in response to changes in CSP from the transfer functions using a data set not used for identifying transfer functions and predicted changes in AP using the equilibrium framework. Predicted APs matched reasonably well with those measured (r² = 0.85-0.96, P < 0.001). Sensitivity analyses indicated that Ees and HR (ventricular properties) accounted for 14 ± 4 and 4 ± 2%, respectively, whereas R and V (vascular properties) accounted for 32 ± 4 and 39 ± 4%, respectively, of baroreflex-induced AP regulation. We concluded that baroreflex-induced dynamic AP changes can be accurately predicted by the transfer functions from CSP to mechanical properties using our framework of circulatory equilibrium. Changes in the vascular properties, not the ventricular properties, predominantly determine baroreflex-induced AP regulation. [ABSTRACT FROM AUTHOR]