scholarly journals The Influence of Respiration on Blood Flow in the Fontan Circulation: Insights for Imaging-Based Clinical Evaluation of the Total Cavopulmonary Connection

2021 ◽  
Vol 8 ◽  
Author(s):  
Séline F. S. van der Woude ◽  
Friso M. Rijnberg ◽  
Mark G. Hazekamp ◽  
Monique R. M. Jongbloed ◽  
Sasa Kenjeres ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Fluid Dynamic ◽  
Heart Defects ◽  
Venous Pressure ◽  
Pulmonary Arteries ◽  
Fontan Circulation ◽  
Univentricular Heart ◽  
The Impact ◽  
Fontan Patients

Congenital heart disease is the most common birth defect and functionally univentricular heart defects represent the most severe end of this spectrum. The Fontan circulation provides an unique solution for single ventricle patients, by connecting both caval veins directly to the pulmonary arteries. As a result, the pulmonary circulation in Fontan palliated patients is characterized by a passive, low-energy circulation that depends on increased systemic venous pressure to drive blood toward the lungs. The absence of a subpulmonary ventricle led to the widely believed concept that respiration, by sucking blood to the pulmonary circulation during inspiration, is of great importance as a driving force for antegrade blood flow in Fontan patients. However, recent studies show that respiration influences pulsatility, but has a limited effect on net forward flow in the Fontan circulation. Importantly, since MRI examination is recommended every 2 years in Fontan patients, clinicians should be aware that most conventional MRI flow sequences do not capture the pulsatility of the blood flow as a result of the respiration. In this review, the unique flow dynamics influenced by the cardiac and respiratory cycle at multiple locations within the Fontan circulation is discussed. The impact of (not) incorporating respiration in different MRI flow sequences on the interpretation of clinical flow parameters will be covered. Finally, the influence of incorporating respiration in advanced computational fluid dynamic modeling will be outlined.

scholarly journals Elevated Low-Shear Blood Viscosity is Associated with Decreased Pulmonary Blood Flow in Children with Univentricular Heart Defects

2016 ◽  
Vol 37 (4) ◽  
pp. 789-801 ◽  
Author(s):  
Andrew L. Cheng ◽  
Cheryl M. Takao ◽  
Rosalinda B. Wenby ◽  
Herbert J. Meiselman ◽  
John C. Wood ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Viscosity ◽  
Pulmonary Blood Flow ◽  
Heart Defects ◽  
Univentricular Heart ◽  
Low Shear

scholarly journals Rarefaction and blood pressure in systemic and pulmonary arteries

2012 ◽  
Vol 705 ◽  
pp. 280-305 ◽  
Author(s):  
Mette S. Olufsen ◽  
N. A. Hill ◽  
Gareth D. A. Vaughan ◽  
Christopher Sainsbury ◽  
Martin Johnson
Keyword(s):  
Blood Flow ◽  
Theoretical Calculations ◽  
Pulmonary Arteries ◽  
Cross Sectional ◽  
Small Arteries ◽  
Large Arteries ◽  
Vascular Bed ◽  
Vascular Beds ◽  
The Impact ◽  
Averaged Model

AbstractThe effects of vascular rarefaction (the loss of small arteries) on the circulation of blood are studied using a multiscale mathematical model that can predict blood flow and pressure in the systemic and pulmonary arteries. We augmented a model originally developed for the systemic arteries by Olufsen and coworkers and Ottesen et al. (2004) to (a) predict flow and pressure in the pulmonary arteries, and (b) predict pressure propagation along the small arteries in the vascular beds. The systemic and pulmonary arteries are modelled as separate bifurcating trees of compliant and tapering vessels. Each tree is divided into two parts representing the ‘large’ and ‘small’ arteries. Blood flow and pressure in the large arteries are predicted using a nonlinear cross-sectional-area-averaged model for a Newtonian fluid in an elastic tube with inflow obtained from magnetic resonance measurements. Each terminal vessel within the network of the large arteries is coupled to a vascular bed of small ‘resistance’ arteries, which are modelled as asymmetric structured trees with specified area and asymmetry ratios between the parent and daughter arteries. For the systemic circulation, each structured tree represents a specific vascular bed corresponding to major organs and limbs. For the pulmonary circulation, there are four vascular beds supplied by the interlobar arteries. This paper presents the first theoretical calculations of the propagation of the pressure and flow waves along systemic and pulmonary large and small arteries. Results for all networks are in agreement with published observations. Two studies were done with this model. First, we showed how rarefaction can be modelled by pruning the tree of arteries in the microvascular system. This was done by modulating parameters used for designing the structured trees. Results showed that rarefaction leads to increased mean and decreased pulse pressure in the large arteries. Second, we investigated the impact of decreasing vessel compliance in both large and small arteries. Results showed that the effects of decreased compliance in the large arteries far outweigh the effects observed when decreasing the compliance of the small arteries. We further showed that a decrease of compliance in the large arteries results in pressure increases consistent with observations of isolated systolic hypertension, as occurs in ageing.

Altered hemodynamics controls matrix metalloproteinase activity and tenascin-C expression in neonatal pig lung

2002 ◽  
Vol 282 (1) ◽  
pp. L26-L35 ◽  
Author(s):  
Peter Lloyd Jones ◽  
Rene Chapados ◽  
H. Scott Baldwin ◽  
Gary W. Raff ◽  
Eugene V. Vitvitsky ◽  
...  
Keyword(s):  
Blood Flow ◽  
Matrix Metalloproteinase ◽  
Pulmonary Blood Flow ◽  
Type I Collagen ◽  
Heart Defects ◽  
Pulmonary Arteries ◽  
Pulmonary Vascular Disease ◽  
Type I ◽  
Pulmonary Hemodynamics ◽  
Tenascin C

Tenascin-C (TN-C) expression and matrix metalloproteinase (MMP) activity are induced within remodeling pulmonary arteries (PAs), where they promote cell growth. Because pulmonary vascular disease in children with congenital heart defects is commonly associated with changes in pulmonary hemodynamics, we hypothesized that changes in pulmonary blood flow regulate TN-C and MMPs. To test this, we ligated the left PAs of neonatal pigs. After 12 wk, we evaluated the levels of TN-C and MMPs in control and ligated lung tissue. Modifying pulmonary hemodynamics increased TN-C mRNA and protein expression, MMP activity, and the DNA-binding activity of Egr-1, a transcription factor that has been shown to activate TN-C expression. To link MMP-mediated remodeling of the extracellular matrix to increased TN-C expression and Egr-1 activity, porcine PA smooth muscle cells were cultivated either on denatured type I collagen, which supported TN-C expression and Egr-1 activity, or on native collagen, which had the opposite effect. These data provide a framework for understanding how changes in pulmonary blood flow in the neonate modify the tissue microenvironment and cell behavior.

Vascular Impedance Analysis in Human Pulmonary Circulation

2002 ◽  
Author(s):  
Qinlian Zhou ◽  
Jian Gao ◽  
Wei Huang ◽  
R. T. Yen
Keyword(s):  
Pulmonary Circulation ◽  
Fluid Dynamic ◽  
Main Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Impedance Analysis ◽  
Impedance Matrix ◽  
Dynamic Approach ◽  
Vascular Impedance ◽  
Elastic Tubes ◽  
Arteries And Veins

Vascular impedance in human pulmonary circulation is analyzed by the fluid dynamic approach. A model representing the entire system of pulmonary circulation is constructed based on experimentally measured morphometric and elasticity data of the vessels. The pulmonary arteries and veins are considered as elastic tubes. Their impedance follows Womersley’s theory and electric analogue. The “sheet-flow” theory is employed to describe the flow in capillaries and thus a microvascular impedance matrix is derived. The input impedance at the main pulmonary artery is calculated under both zone 3 and zone 2 conditions. The results are compared with available experimental data in the literature.

scholarly journals Circulatory Response to Rapid Volume Expansion and Cardiorespiratory Fitness in Fontan Circulation

2021 ◽  
Author(s):  
Thomas Möller ◽  
Vibeke Klungerbo ◽  
Simone Diab ◽  
Henrik Holmstrøm ◽  
Elisabeth Edvardsen ◽  
...  
Keyword(s):  
Steady State ◽  
Right Ventricular ◽  
Cardiorespiratory Fitness ◽  
Volume Expansion ◽  
Fontan Operation ◽  
Venous Pressure ◽  
Systolic Pressure ◽  
Fontan Circulation ◽  
Peak Oxygen Consumption ◽  
The Impact

AbstractThe role of dysfunction of the single ventricle in Fontan failure is incompletely understood. We aimed to evaluate hemodynamic responses to preload increase in Fontan circulation, to determine whether circulatory limitations in different locations identified by experimental preload increase are associated with cardiorespiratory fitness (CRF), and to assess the impact of left versus right ventricular morphology. In 38 consecutive patients (median age = 16.6 years, 16 females), heart catheterization was supplemented with a rapid 5-mL/kg body weight volume expansion. Central venous pressure (CVP), ventricular end-diastolic pressure (VEDP), and peak systolic pressure were averaged for 15‒30 s, 45‒120 s, and 4‒6 min (steady state), respectively. CRF was assessed by peak oxygen consumption (VO2peak) and ventilatory threshold (VT). Median CVP increased from 13 mmHg at baseline to 14.5 mmHg (p < 0.001) at steady state. CVP increased by more than 20% in eight patients. Median VEDP increased from 10 mmHg at baseline to 11.5 mmHg (p < 0.001). Ten patients had elevated VEDP at steady state, and in 21, VEDP increased more than 20%. The transpulmonary pressure difference (CVP‒VEDP) and CVP were consistently higher in patients with right ventricular morphology across repeated measurements. CVP at any stage was associated with VO2peak and VT. VEDP after volume expansion was associated with VT. Preload challenge demonstrates the limitations beyond baseline measurements. Elevation of both CVP and VEDP are associated with impaired CRF. Transpulmonary flow limitation was more pronounced in right ventricular morphology. Ventricular dysfunction may contribute to functional impairment after Fontan operation in young adulthood.ClinicalTrials.govidentifier NCT02378857

Features of the course and diagnosis of heart failure in non-coronary myocardial lesions

1982 ◽  
Vol 63 (5) ◽  
pp. 67-71
Author(s):  
V. E. Anisimov
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Coronary Arteries ◽  
Functional Capacity ◽  
Pulmonary Circulation ◽  
Heart Defects ◽  
Heart Damage ◽  
Valve Insufficiency ◽  
Myocardial Lesions

Heart failure occurs as a result of various diseases, both caused by damage to the coronary arteries (in most cases, atherosclerosis), and not associated with the involvement of the coronary arteries in the process. A decrease in the functional capacity of the myocardium with heart damage is either a consequence of its excessive overload with an increased volume of blood entering the chambers of the heart during diastole, or the result of increased resistance to blood outflow during systole. The first occurs with heart defects with valve insufficiency, and the second occurs in case of obstruction of the blood flow in patients with stenosis of the holes or with hypertension of the large and pulmonary circulation.

In Vitro Study of Pulmonary Vascular Resistance in Fontan Circulation With Respiration Effects

2012 ◽  
Author(s):  
Marija Vukicevic ◽  
Timothy A. Conover ◽  
Jian Zhou ◽  
Tain-Yen Hsia ◽  
Richard S. Figliola
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Heart Defects ◽  
Superior Vena ◽  
Fontan Procedure ◽  
Fontan Operation ◽  
Venous Pressure ◽  
Pulmonary Arteries ◽  
Pulmonary Regurgitation ◽  
Vena Cava

The Fontan operation is the final stage of palliative surgery for children born with single ventricle heart defects. The most common configuration is called total cavopulmonary connection (TCPC), wherein the inferior vena cava and superior vena cava are anastomosed directly to the pulmonary arteries; therefore the pulmonary circulation is driven by venous pressure only. The Fontan procedure, although successful in the early postoperative period, with time can decrease in efficiency or even fail within several years after the operation. The reasons of different clinical outcomes for some of the Fontan patients are not clear enough, even though it is commonly accepted that certain factors such as low pulmonary vascular resistance and proper shape and size of the TCPC construction are crucial for the succesful long term outcomes. Accordingly, one of the major problems is the increase in pulmonary vascular resistance due to altered hemodynamics after the surgery, causing venous hypertension and respiratory-dependent pulmonary regurgitation [1]. The main pulmonary arteries may also see increased resistance due to congenital malformations, surgical scarring, or deliberate surgical banding. Thus, the consequence of the increased pulmonary vascular resistance at both proximal and distal locations with respect to the TCPC junction, and its effect on the systemic pressures and flow rates, is the main objective of this study.

scholarly journals Augmentation of pulmonary blood flow and cardiac output by non-invasive external ventilation late after Fontan palliation

Heart ◽  
2020 ◽  
Vol 107 (2) ◽  
pp. 142-149
Author(s):  
Pradeepkumar Charla ◽  
Gauri Rani Karur ◽  
Kenichiro Yamamura ◽  
Shi-Joon Yoo ◽  
John T Granton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arteries ◽  
Primary Objective ◽  
Non Invasive ◽  
Lateral Tunnel ◽  
The Impact ◽  
Fontan Palliation ◽  
Cmr Imaging

ObjectivesAlthough a life-preserving surgery for children with single ventricle physiology, the Fontan palliation is associated with striking morbidity and mortality with advancing age. Our primary objective was to evaluate the impact of non-invasive, external, thoraco-abdominal ventilation on pulmonary blood flow (PBF) and cardiac output (CO) as measured by cardiovascular magnetic resonance (CMR) imaging in adult Fontan subjects.MethodsAdults with a dominant left ventricle post-Fontan palliation (lateral tunnel or extracardiac connections) and healthy controls matched by sex and age were studied. We evaluated vascular flows using phase-contrast CMR imaging during unassisted breathing, negative pressure ventilation (NPV) and biphasic ventilation (BPV). Measurements were made within target vessels (aorta, pulmonary arteries, vena cavae and Fontan circuit) at baseline and during each ventilation mode.ResultsTen Fontan subjects (50% male, 24.5 years (IQR 20.8–34.0)) and 10 matched controls were studied. Changes in PBF and CO, respectively, were greater following BPV as compared with NPV. In subjects during NPV, PBF increased by 8% (Δ0.20 L/min/m2 (0.10–0.53), p=0.011) while CO did not change significantly (Δ0.17 L/min/m2 (−0.11–0.23), p=0.432); during BPV, PBF increased by 25% (Δ0.61 L/min/m2 (0.20–0.84), p=0.002) and CO increased by 16% (Δ0.47 L/min/m2 (0.21–0.71), p=0.010). Following BPV, change in PBF and CO were both significantly higher in subjects versus controls (0.61 L/min/m2 (0.2–0.84) vs −0.27 L/min/m2 (−0.55–0.13), p=0.001; and 0.47 L/min/m2 (0.21–0.71) vs 0.07 L/min/m2 (−0.47–0.33), p=0.034, respectively).ConclusionExternal ventilation acutely augments PBF and CO in adult Fontan subjects. Confirmation of these findings in larger populations with longer duration of ventilation and extended follow-up will be required to determine sustainability of haemodynamic effects.

Increased endothelial NOS in lambs with increased pulmonary blood flow and pulmonary hypertension

1998 ◽  
Vol 275 (5) ◽  
pp. H1643-H1651 ◽  
Author(s):  
Stephen M. Black ◽  
Jeffrey R. Fineman ◽  
Robin H. Steinhorn ◽  
James Bristow ◽  
Scott J. Soifer
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Vascular Graft ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Vascular Reactivity ◽  
Heart Defects ◽  
Pulmonary Arteries ◽  
Enos Gene ◽  
Rnase Protection

Altered pulmonary vascular reactivity is a source of morbidity and mortality for children with congenital heart defects and increased pulmonary blood flow. Nitric oxide (NO) is an important mediator of pulmonary vascular reactivity. The objective of this study was to characterize potential early alterations in expression, localization, and activity of endothelial NO synthase (eNOS) induced by increased pulmonary blood flow and pulmonary hypertension. Utilizing aortopulmonary vascular graft placement in the fetal lamb, we have established a unique animal model of pulmonary hypertension that mimics congenital heart disease with increased pulmonary blood flow. Ten fetal lambs underwent in utero placement of an aortopulmonary vascular graft (shunt). RNase protection assays and Western blotting were performed on lung tissue prepared from 4-wk-old shunt lambs and age-matched controls. eNOS mRNA (2.4:1, P < 0.05) and protein (2.08:1, P < 0.05) were increased in lungs of shunt lambs. In situ hybridization and immunohistochemistry revealed that the increase was confined to the endothelium of pulmonary arteries. eNOS protein (1.55:1, P < 0.05) and tissue cGMP concentrations (2.1:1, P < 0.05) were also increased in isolated fifth-generation pulmonary arteries of shunt lambs. In addition, total lung eNOS activity was increased (2.9:1, P < 0.05). Thus we report a previously undescribed, early upregulation of eNOS gene expression and activity in lambs with increased pulmonary blood flow and pulmonary hypertension.

scholarly journals Circulatory Response to Rapid Volume Expansion and Cardiorespiratory Fitness in Fontan Circulation

2021 ◽  
Author(s):  
Thomas Möller ◽  
Vibeke Klungerbo ◽  
Simone Diab ◽  
Henrik Holmstrøm ◽  
Elisabeth Edvardsen ◽  
...  
Keyword(s):  
Steady State ◽  
Right Ventricular ◽  
Cardiorespiratory Fitness ◽  
Volume Expansion ◽  
Fontan Operation ◽  
Venous Pressure ◽  
Systolic Pressure ◽  
Fontan Circulation ◽  
Peak Oxygen Consumption ◽  
The Impact

Abstract BackgroundThe role of dysfunction of the single ventricle in Fontan failure is incompletely understood.ObjectivesWe aimed to evaluate haemodynamic responses to preload increase in Fontan circulation, to determine whether circulatory limitations in different locations identified by experimental preload increase are associated with cardiorespiratory fitness (CRF), and to assess the impact of left versus right ventricular morphology.MethodsIn 38 consecutive patients (median age=16.6 years, 16 females), heart catheterisation was supplemented with a rapid 5-mL/kg body weight volume expansion. Central venous pressure (CVP), ventricular end-diastolic pressure (VEDP), and peak systolic pressure were averaged for 15‒30 s, 45‒120 s, and 4‒6 min (steady state), respectively. CRF was assessed by peak oxygen consumption (VO2peak) and ventilatory threshold (VT).ResultsMedian CVP increased from 13 mmHg at baseline to 14.5 mmHg (p<0.001) at steady state. CVP increased by more than 20% in eight patients. Median VEDP increased from 10 mmHg at baseline to 11.5 mmHg (p<0.001). Ten patients had elevated VEDP at steady state, and in 21, VEDP increased more than 20%. The transpulmonary pressure difference (CVP‒VEDP) and CVP were consistently higher in patients with right ventricular morphology across repeated measurements. CVP at any stage was associated with VO2peak and VT. VEDP after volume expansion was associated with VT.ConclusionsPreload challenge demonstrates the limitations beyond baseline measurements. Elevation of both CVP and VEDP are associated with impaired CRF. Transpulmonary flow limitation was more pronounced in right ventricular morphology. Ventricular dysfunction may contribute to functional impairment after Fontan operation in young adulthood.ClinicalTrials.govidentifier: NCT02378857

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