TY - JOUR
T1 - Cardiovascular mechanics in the early stages of pulmonary hypertension
T2 - a computational study
AU - Acosta, Sebastián
AU - Puelz, Charles
AU - Rivière, Béatrice
AU - Penny, Daniel J.
AU - Brady, Kenneth Martin
AU - Rusin, Craig G.
N1 - Publisher Copyright:
© 2017, Springer-Verlag GmbH Germany.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - We formulate and study a new mathematical model of pulmonary hypertension. Based on principles of fluid and elastic dynamics, we introduce a model that quantifies the stiffening of pulmonary vasculature (arteries and arterioles) to reproduce the hemodynamics of the pulmonary system, including physiologically consistent dependence between compliance and resistance. This pulmonary model is embedded in a closed-loop network of the major vessels in the body, approximated as one-dimensional elastic tubes, and zero-dimensional models for the heart and other organs. Increasingly severe pulmonary hypertension is modeled in the context of two extreme scenarios: (1) no cardiac compensation and (2) compensation to achieve constant cardiac output. Simulations from the computational model are used to estimate cardiac workload, as well as pressure and flow traces at several locations. We also quantify the sensitivity of several diagnostic indicators to the progression of pulmonary arterial stiffening. Simulation results indicate that pulmonary pulse pressure, pulmonary vascular compliance, pulmonary RC time, luminal distensibility of the pulmonary artery, and pulmonary vascular impedance are much better suited to detect the early stages of pulmonary hypertension than mean pulmonary arterial pressure and pulmonary vascular resistance, which are conventionally employed as diagnostic indicators for this disease.
AB - We formulate and study a new mathematical model of pulmonary hypertension. Based on principles of fluid and elastic dynamics, we introduce a model that quantifies the stiffening of pulmonary vasculature (arteries and arterioles) to reproduce the hemodynamics of the pulmonary system, including physiologically consistent dependence between compliance and resistance. This pulmonary model is embedded in a closed-loop network of the major vessels in the body, approximated as one-dimensional elastic tubes, and zero-dimensional models for the heart and other organs. Increasingly severe pulmonary hypertension is modeled in the context of two extreme scenarios: (1) no cardiac compensation and (2) compensation to achieve constant cardiac output. Simulations from the computational model are used to estimate cardiac workload, as well as pressure and flow traces at several locations. We also quantify the sensitivity of several diagnostic indicators to the progression of pulmonary arterial stiffening. Simulation results indicate that pulmonary pulse pressure, pulmonary vascular compliance, pulmonary RC time, luminal distensibility of the pulmonary artery, and pulmonary vascular impedance are much better suited to detect the early stages of pulmonary hypertension than mean pulmonary arterial pressure and pulmonary vascular resistance, which are conventionally employed as diagnostic indicators for this disease.
KW - Blood flow
KW - Cardiovascular mechanics
KW - Computational hemodynamics
KW - Pulmonary arterial hypertension
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U2 - 10.1007/s10237-017-0940-4
DO - 10.1007/s10237-017-0940-4
M3 - Article
C2 - 28733923
AN - SCOPUS:85025461253
SN - 1617-7959
VL - 16
SP - 2093
EP - 2112
JO - Biomechanics and Modeling in Mechanobiology
JF - Biomechanics and Modeling in Mechanobiology
IS - 6
ER -