Abstract：
OBJECTIVE: Numerous clinical and pathological studies have confirmed that lung injury can cause cardiovascular disease, but there is no explanation for the mechanism by which the degree of lung injury affects cardiac function. We attempt to reveal this mechanism of influence by simulating a cyclic model.
METHODS: This study established a closed-loop cardiovascular model with a series of electrical parameters. Including the heart, lungs, arteries, veins, etc., each part of the cardiovascular system is modeled using centralized parameters. Adjusting these lung resistances to alter the degree of lung injury is aimed at reflecting the impact of different degrees of lung injury on cardiac function. Finally, analyze and compare the changes in blood pressure, aortic flow, atrioventricular volume, and atrioventricular pressure among different lung injuries to obtain the changes in cardiac function.
RESULTS: In this model, the peak aortic flow decreased, the earlier the trough appeared, and the total aortic flow decreased. Left atrial blood pressure decreased from 6.5 mmHg to around 5.5 mmHg, left ventricular blood pressure decreased from 100 mmHg to around 50 mmHg, and aortic blood pressure also decreased from 100 mmHg to around 50 mmHg. The blood pressure in the pulmonary artery, right atrium, and right ventricle increases. The right ventricular blood pressure decreased from 20 mmHg to around 40 mmHg, while the right atrial blood pressure slightly increased. It can be seen that the increase in impedance has a greater impact on ventricular blood pressure than on atrium. Pulmonary arterial pressure significantly increases, rising from 20 mmHg to around 50 mmHg, forming pulmonary hypertension. The left ventricular end-systolic potential energy, filling energy, stroke work, stroke output, left ventricular filling period, maximum blood pressure during ventricular ejection period, and stroke energy efficiency decrease.
CONCLUSIONS: We established a closed-loop cardiovascular model that reveals that the more severe lung injury, the higher blood pressure in the pulmonary artery, right atrium, and right ventricle, while the lower blood pressure in the left atrium, left ventricle, and aorta. The increase in pulmonary impedance leads to abnormalities in myocardial contraction, diastolic function, and cardiac reserve capacity, leading to a decrease in cardiac function. This closed-loop model provides a method for pre assessment of cardiovascular disease after lung injury.
METHODS: This study established a closed-loop cardiovascular model with a series of electrical parameters. Including the heart, lungs, arteries, veins, etc., each part of the cardiovascular system is modeled using centralized parameters. Adjusting these lung resistances to alter the degree of lung injury is aimed at reflecting the impact of different degrees of lung injury on cardiac function. Finally, analyze and compare the changes in blood pressure, aortic flow, atrioventricular volume, and atrioventricular pressure among different lung injuries to obtain the changes in cardiac function.
RESULTS: In this model, the peak aortic flow decreased, the earlier the trough appeared, and the total aortic flow decreased. Left atrial blood pressure decreased from 6.5 mmHg to around 5.5 mmHg, left ventricular blood pressure decreased from 100 mmHg to around 50 mmHg, and aortic blood pressure also decreased from 100 mmHg to around 50 mmHg. The blood pressure in the pulmonary artery, right atrium, and right ventricle increases. The right ventricular blood pressure decreased from 20 mmHg to around 40 mmHg, while the right atrial blood pressure slightly increased. It can be seen that the increase in impedance has a greater impact on ventricular blood pressure than on atrium. Pulmonary arterial pressure significantly increases, rising from 20 mmHg to around 50 mmHg, forming pulmonary hypertension. The left ventricular end-systolic potential energy, filling energy, stroke work, stroke output, left ventricular filling period, maximum blood pressure during ventricular ejection period, and stroke energy efficiency decrease.
CONCLUSIONS: We established a closed-loop cardiovascular model that reveals that the more severe lung injury, the higher blood pressure in the pulmonary artery, right atrium, and right ventricle, while the lower blood pressure in the left atrium, left ventricle, and aorta. The increase in pulmonary impedance leads to abnormalities in myocardial contraction, diastolic function, and cardiac reserve capacity, leading to a decrease in cardiac function. This closed-loop model provides a method for pre assessment of cardiovascular disease after lung injury.
摘要：
目的：大量临床和病理研究证实肺损伤可引起心血管疾病,但是对于肺损伤程度影响心脏功能的机制尚无解释。我们试图通过模拟循环模型来揭示这种影响机制。
方法：本研究建立了具有一系列电参数的闭环心血管模型。包括心脏,肺,动脉,静脉,等。,使用集中参数对心血管系统的每个部分进行建模。调整这些肺阻力以改变肺损伤的程度旨在反映不同程度的肺损伤对心脏功能的影响。最后,分析和比较血压的变化，主动脉血流,房室容积,和房室压在不同肺损伤之间，以获得心功能的变化。
结果：在此模型中，主动脉血流峰值减少,槽出现得越早，主动脉总流量减少。左心房血压从6.5mmHg降至5.5mmHg左右，左心室血压从100mmHg下降到50mmHg左右，主动脉血压也从100mmHg降至50mmHg左右。肺动脉的血压,右心房,右心室增大.右心室血压从20mmHg下降到40mmHg左右,而右心房血压略有升高。可以看出，阻抗的增加对心室血压的影响大于对心房的影响。肺动脉压显著升高,从20mmHg上升到50mmHg左右，形成肺动脉高压。左心室收缩末期电位能量,填充能量，中风工作，行程输出,左心室充盈期,心室射血期间的最大血压，和冲程能量效率降低。
结论：我们建立了一个闭环心血管模型，显示肺损伤越严重，肺动脉血压越高,右心房,和右心室,而左心房血压较低，左心室,和主动脉.肺阻抗的增加导致心肌收缩异常，舒张功能,和心脏储备能力，导致心脏功能下降。该闭环模型提供了一种用于预先评估肺损伤后心血管疾病的方法。
方法：本研究建立了具有一系列电参数的闭环心血管模型。包括心脏,肺,动脉,静脉,等。,使用集中参数对心血管系统的每个部分进行建模。调整这些肺阻力以改变肺损伤的程度旨在反映不同程度的肺损伤对心脏功能的影响。最后,分析和比较血压的变化，主动脉血流,房室容积,和房室压在不同肺损伤之间，以获得心功能的变化。
结果：在此模型中，主动脉血流峰值减少,槽出现得越早，主动脉总流量减少。左心房血压从6.5mmHg降至5.5mmHg左右，左心室血压从100mmHg下降到50mmHg左右，主动脉血压也从100mmHg降至50mmHg左右。肺动脉的血压,右心房,右心室增大.右心室血压从20mmHg下降到40mmHg左右,而右心房血压略有升高。可以看出，阻抗的增加对心室血压的影响大于对心房的影响。肺动脉压显著升高,从20mmHg上升到50mmHg左右，形成肺动脉高压。左心室收缩末期电位能量,填充能量，中风工作，行程输出,左心室充盈期,心室射血期间的最大血压，和冲程能量效率降低。
结论：我们建立了一个闭环心血管模型，显示肺损伤越严重，肺动脉血压越高,右心房,和右心室,而左心房血压较低，左心室,和主动脉.肺阻抗的增加导致心肌收缩异常，舒张功能,和心脏储备能力，导致心脏功能下降。该闭环模型提供了一种用于预先评估肺损伤后心血管疾病的方法。
