杉本 晃一

Background Patients with single ventricle often undergo the Fontan operation to alleviate cyanosis and reduce ventricle volume load. However, long-term outcomes are limited by complications and hemodynamic issues, including collateral vessels, leading to cyanosis and heart failure. Studies have demonstrated considerable blood flow through these collateral vessels; however, their hemodynamic impact on Fontan circulation remains inadequately explained from a theoretical perspective. This study aims to clarify the effects of dobutamine and vasodilators on Fontan circulation in the presence of aortopulmonary collaterals (APCs) and venovenous collaterals (VVCs). Methods A Fontan hemodynamic model incorporating VVC and APC was created. Scenarios were simulated by adjusting dobutamine dosage and oxygen delivery/consumption, predicting arterial and central venous oxygen saturations. Cardiac function was evaluated based on cardiac output, arterial elastance, ejection fraction, and stroke work to pressure-volume ratio. Results Fontan circulations with VVC and APC had lower arterial and venous oxygen saturations (92% and 54%, respectively) compared with those without collaterals (96% and 62%, respectively). Decreased arterial elastance and increased stroke work to pressure-volume ratio indicated poor tissue perfusion. High pulmonary resistance decreased oxygen saturations and systemic blood flow, regardless of collaterals. Dobutamine (10 μg/kg/min) raised venous oxygen from 53% to 58%, respectively, in the presence of VVC and APC, but decreased arterial oxygen from 92% to 88%, respectively. Conclusions The results align with clinical findings, suggesting pulmonary vasodilators may improve oxygenation and perfusion in Fontan patients with collaterals. However, dobutamine effects are limited. Validation with actual patient data is needed to enhance model accuracy.

Abstract Objective. This study aims to accurately identify the effects of respiration on the hemodynamics of the human cardiovascular system, especially the cerebral circulation. Approach: we have developed a machine learning (ML)-integrated zero–one-dimensional (0–1D) multiscale hemodynamic model combining a lumped-parameter 0D model for the peripheral vascular bed and a one-dimensional (1D) hemodynamic model for the vascular network. In vivo measurement data of 21 patients were retrieved and partitioned into 8000 data samples in which respiratory fluctuation (RF) of intrathoracic pressure (ITP) was fitted by the Fourier series. ML-based classification and regression algorithms were used to examine the influencing factors and variation trends of the key parameters in the ITP equations and the mean arterial pressure. These parameters were employed as the initial conditions of the 0–1D model to calculate the radial artery blood pressure and the vertebral artery blood flow volume (VAFV). Main results: during stable spontaneous respiration, the VAFV can be augmented at the inhalation endpoints by approximately 0.1 ml s⁻¹ for infants and 0.5 ml s⁻¹ for adolescents or adults, compared to those without RF effects. It is verified that deep respiration can further increase the ranges up to 0.25 ml s⁻¹ and 1 ml s⁻¹, respectively. Significance. This study reveals that reasonable adjustment of respiratory patterns, i.e. in deep breathing, enhances the VAFV and promotes cerebral circulation.