Relevant bibliographies by topics / Vascular resistance Measurement

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Vascular resistance Measurement'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 January 2023

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Journal articles on the topic "Vascular resistance Measurement"

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O'DWYER, J. P., J. E. KING, C. E. WOOD, B. L. TAYLOR, and G. B. SMITH. "Continuous measurement of systemic vascular resistance." Anaesthesia 49, no. 7 (February 22, 2007): 587–90. http://dx.doi.org/10.1111/j.1365-2044.1994.tb14225.x.

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Abbas, Amr E., F. David Fortuin, Bhavesh Patel, Carlos A. Moreno, Nelson B. Schiller, and Steven J. Lester. "Noninvasive measurement of systemic vascular resistance using Doppler echocardiography." Journal of the American Society of Echocardiography 17, no. 8 (August 2004): 834–38. http://dx.doi.org/10.1016/j.echo.2004.04.008.

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Schrijen, F., C. Saunier, and F. Chabot. "Peripheral pulmonary vascular resistance." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 613–16. http://dx.doi.org/10.1152/jappl.1993.74.2.613.

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The pressure-flow relationship has been studied in a peripheral portion of the lung vasculature in anesthetized dogs with use of a double-lumen catheter wedged in a distal pulmonary artery. One lumen was used to infuse mixed venous blood in the wedged area and the other to measure the corresponding perfusion pressure. Flow ranged from 0 to 9.2 ml/min, and the mean volume of the wedged area (n = 59) was 0.75 +/- 0.05 (SE) ml. In the areas where the distal pulmonary artery was in the same direction as the catheter ("coaxial"), the mean pressure-flow curve showed a negligible gamma-intercept and no significant difference between ascending and descending flow. The slope of the initial part of the ascending limb (peripheral pulmonary vascular resistance) varied from site to site and did not show a significant correlation with the overall pulmonary vascular resistance; it was inversely correlated with the volume of the wedged area (r = -0.35, P < 0.05) and directly, as expected, correlated with the y-intercept (r = 0.78, P < 0.001) and hysteresis (r = 0.48, P < 0.001). The results of two consecutive pressure-flow runs in the same site showed similar results, with no difference exceeding the error of measurement. In contrast, the slope increased by 71% during hypoxia (fraction of inspired O2 was 0.10, n = 5). This procedure seems suitable to determine the effects of physiological or pharmacological interventions on the pulmonary vessels, without interference of the systemic circulation.
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Moriyasu, Fuminori, Osamu Nishida, Nobuyuki Ban, Takefumi Nakamura, Kensuke Miura, Masahiko Sakai, Takeo Miyake, and Haruto Uchino. "Measurement of Portal Vascular Resistance in Patients With Portal Hypertension." Gastroenterology 90, no. 3 (March 1986): 710–17. http://dx.doi.org/10.1016/0016-5085(86)91127-3.

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Lautt, W. W., C. V. Greenway, D. J. Legare, and H. Weisman. "Localization of intrahepatic portal vascular resistance." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 3 (September 1, 1986): G375—G381. http://dx.doi.org/10.1152/ajpgi.1986.251.3.g375.

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The pressure drop from the portal vein to the vena cava occurs primarily across a postsinusoidal site localized to a narrow segment (less than 0.5 cm) of hepatic veins (roughly 1.5 mm diam) in the anesthetized cat. Portal venous pressure (PVP = 8.9 +/- 0.3 mmHg) and lobar hepatic venous pressure (LVP = 8.7 +/- 0.4 mmHg) are insignificantly different, and pressure changes imposed from the presinusoidal or postsinusoidal side are equally transmitted to both pressure sites. Several types of experiments were done to validate the LVP measurement. The portal vein, hepatic sinusoids, and hepatic veins proximal to the resistance site are all under a similar pressure. Previously reported calculations of hepatic vascular resistance are in error because of incorrect assumptions of sinusoidal pressure and localization of the portal resistance site as presinusoidal. Stimulation of hepatic sympathetic nerves for 3 min caused LVP and PVP to increase equally, showing that the increased "portal" resistance is postsinusoidal across the same region of the hepatic veins that was previously localized as the site of resistance in the basal state.
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Allison, R. C., B. Rippe, V. R. Prasad, J. C. Parker, and A. E. Taylor. "Pulmonary vascular permeability and resistance measurements in control and ANTU-injured dog lungs." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 6 (June 1, 1989): H1711—H1718. http://dx.doi.org/10.1152/ajpheart.1989.256.6.h1711.

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Because questions have arisen regarding pulmonary vascular permeability and resistance measurements in isolated, perfused lungs, we sought to determine the 1) stability of repeated measurements of permeability and resistance in control lungs; and 2) magnitude of change in these measurements when permeability was greatly increased. Using blood-perfused dog lungs, we measured filtration coefficient (Kf) and isogravimetric capillary pressure (Pci) as indexes of vascular permeability, and we also determined total vascular resistance (Rt) as well as the segmental resistances using the double-occlusion pressure (Pdo). In a control group (n = 8), the base-line measurement of Kf (0.21 +/- 0.02 ml.min-1.cmH2O-1.100 g-1) and Pci (10.2 +/- 0.9 cmH2O) did not change over 4 h, indicating no changes in endothelial barrier function. Base-line Rt (13.9 +/- 2.6 cmH2O.l-1.min.100 g) also did not significantly increase. In a second group (n = 5), alpha-naphthylthiourea (ANTU) increased the initial Kf more than eight times (from 0.17 +/- 0.03 to 1.40 +/- 0.32 ml.min-1.cmH2O-1.100 g-1) and decreased Pci by 56% (from 9.4 +/- 0.6 to 4.1 +/- 0.4 cmH2O) at 1 h, indicating severely damaged endothelium. In addition, the Pdo determined during isogravimetric conditions correlated very well with Pci not only in control lungs (observed previously) but also in very permeable lungs (not previously reported). We conclude that this experimental model provides an excellent means of assessing changes in pulmonary microvascular permeability, with a spectrum ranging from no changes in hourly measurements for 4 h to obvious changes in permeability by 1 h.
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Parker, James C., Mark N. Gillespie, Aubrey E. Taylor, and Sherri L. Martin. "Capillary filtration coefficient, vascular resistance, and compliance in isolated mouse lungs." Journal of Applied Physiology 87, no. 4 (October 1, 1999): 1421–27. http://dx.doi.org/10.1152/jappl.1999.87.4.1421.

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Although many recently produced transgenic mice possess gene alterations affecting pulmonary vascular function, there are few baseline measurements of vascular resistance and permeability. Therefore, we excised the lungs of C57/BL6 mice and perfused them with 5% bovine serum albumin in RPMI-1640 culture medium at a nominal flow of 0.5 ml/min and ventilated them with 20% O2-5% CO2-75% N2. The capillary filtration coefficient, a sensitive measurement of hydraulic conductivity, was unchanged over 2 h (0.33 ± 0.03 ml ⋅ min−1 ⋅ cmH2O−1 ⋅ 100 g−1) in a control group ventilated with low peak inflation pressures (PIP) but increased 4.3-fold after high PIP injury. Baseline pulmonary vascular resistance was 6.1 ± 0.4 cmH2O ⋅ ml−1 ⋅ min ⋅ 100 g−1 and was distributed 34% in large arteries, 18% in small arteries, 14% in small veins, and 34% in large veins on the basis of vascular occlusion pressures. Baseline vascular compliance was 5.4 ± 0.3 ml ⋅ cmH2O−1 ⋅ 100 g−1 and decreased significantly with increased vascular pressures. Baseline pulmonary vascular resistance was inversely related to both perfusate flow and microvascular pressure and increased to 202% of baseline after infusion of 10−4 M phenylephrine due to constriction of large arterial and venous segments. Thus isolated mouse lung vascular permeability, vascular resistance, and the longitudinal distribution of vascular resistance are similar to those in other species and respond in a predictable manner to microvascular injury and a vasoconstrictor agent.
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Giesen, Leonie A., Michelle White, and Robert M. R. Tulloh. "Comparison of the effect of inhaled anaesthetic with intravenous anaesthetic on pulmonary vascular resistance measurement during cardiac catheterisation." Cardiology in the Young 25, no. 2 (February 19, 2014): 368–72. http://dx.doi.org/10.1017/s1047951114000195.

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AbstractBackground: Children with pulmonary hypertension routinely undergo pulmonary vascular resistance studies to assess the disease severity and vasodilator responsiveness. It is vital that results are accurate and reliable and are not influenced by the choice of anaesthetic agent. However, there are anecdotal data to suggest that propofol and inhalational agents have different effects on pulmonary vascular resistance. Methods: A total of 10 children with pulmonary hypertension were selected sequentially to be included in the study. To avoid confounding because of baseline anatomic or demographic details, a crossover protocol was implemented, using propofol or isoflurane, with time for washout in between each agent and blinding of the interventionalist. Results: Pulmonary and systemic vascular resistance were not significantly different when using propofol or isoflurane. However, the calculated resistance fraction – ratio of pulmonary resistance to systemic resistance – was significantly lower when using propofol than when using isoflurane. Conclusions: Although no difference in pulmonary vascular resistance was demonstrated, this pilot study suggests that the choice of anaesthetic agent may affect the calculation of relative pulmonary and systemic vascular resistance, and provides some preliminary evidence to favour propofol over isoflurane. These findings require replication in a larger study, and thus they should be considered in future calculations to make informed decisions about the management of children with pulmonary hypertension.
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Parvin, S. D., D. H. Evans, and P. R. F. Bell. "Peripheral resistance measurement in the assessment of severe peripheral vascular disease." British Journal of Surgery 72, no. 9 (September 1985): 751–53. http://dx.doi.org/10.1002/bjs.1800720928.

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Rothe, C. F., and R. Maass-Moreno. "Gastrointestinal hemodynamics during compensation for hemorrhage and measurement of Pmcf." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 3 (March 1, 1994): H1242—H1250. http://dx.doi.org/10.1152/ajpheart.1994.266.3.h1242.

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To quantify the degree of autonomic reflex control of the gastrointestinal vasculature, we studied the responses to a 10-ml/kg hemorrhage or transfusion and autonomic blockade in fentanyl- and pentobarbital-anesthetized dogs. The active total blood volume was estimated by indocyanine green dilution. Transfusion and hemorrhage did not significantly change gastrointestinal vascular compliance [1.82 +/- 0.68 (SD) ml/mmHg], but autonomic blockade with hexamethonium and atropine increased it by 0.57 +/- 0.37 ml/mmHg. Neither hemorrhage nor autonomic blockade significantly changed gastrointestinal vascular resistance from its control value of 10.8 +/- 4 mmHg.ml-1.min.kg body wt, but transfusion reduced it by 3.0 +/- 1.2 mmHg.ml-1.min.kg body wt. The ratio of gastrointestinal vascular resistance to total peripheral resistance was not significantly changed, however. We conclude that vascular compliance and resistance of the gastrointestinal bed are minimally influenced by the autonomic nervous system under the conditions studied. Portal pressure and flow measurements (transit-time ultrasound) during the above maneuvers were also combined with estimations of mean circulatory filling pressure (Pmcf) to test the hypothesis that, when the heart is stopped to measure Pmcf, portal pressure equals central venous pressure (Pcv) and hence that portal flow is zero. Seven seconds after the heart was stopped, portal venous pressure (Ppv) remained 0.83 +/- 0.78 mmHg higher than Pcv and portal flow decreased to only 25% of its control value. However, gastrointestinal compliance times (Ppv-Pcv), an estimate of the extra distending volume, was only 0.07 +/- 0.07 ml/kg body wt. Thus we conclude that the error in estimating Pmcf, given this (Ppv-Pcv) difference, is physiologically insignificant.
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Dissertations / Theses on the topic "Vascular resistance Measurement"

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Duncan, Henry J. (Henry John). "An isotope washout technique to study skin perfusion pressure and vascular resistance in diabetes, hypertension and peripheral vascular disease." 1986. http://web4.library.adelaide.edu.au/theses/09MD/09mdd911.pdf.

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Duncan, Henry J. (Henry John). "An isotope washout technique to study skin perfusion pressure and vascular resistance in diabetes, hypertension and peripheral vascular disease / by Henry J. Duncan." Thesis, 1986. http://hdl.handle.net/2440/38294.

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Books on the topic "Vascular resistance Measurement"

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Comparison of total peripheral resistance and blood velocity as obtained from Doppler ultrasound waveforms during rest, exercise and recovery. 1991.

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Comparison of total peripheral resistance and blood velocity as obtained from Doppler ultrasound waveforms during rest, exercise and recovery. 1991.

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Comparison of total peripheral resistance and blood velocity as obtained from Doppler ultrasound waveforms during rest, exercise and recovery. 1992.

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Prout, Jeremy, Tanya Jones, and Daniel Martin. Respiratory system. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0002.

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This chapter includes a summary of respiratory physiology, respiratory mechanics (pressure-volume relationships and compliance, airway resistance and the work of breathing) and the pulmonary circulation (pulmonary vascular resistance, shunt and lung zones). Measurement of respiratory flow, lung volumes and diffusion capacity is summarized, as well as measurement and interpretation of arterial blood gases. The physics behind capnography and pulse oximetry are explained with abnormalities related to clinical contexts. The common clinical scenarios of respiratory failure and asthma are discussed with initial management and resuscitation.
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Dussaule, Jean-Claude, Martin Flamant, and Christos Chatziantoniou. Function of the normal glomerulus. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0044_update_001.

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Glomerular filtration, the first step leading to the formation of primitive urine, is a passive phenomenon. The composition of this primitive urine is the consequence of the ultrafiltration of plasma depending on renal blood flow, on hydrostatic pressure of glomerular capillary, and on glomerular coefficient of ultrafiltration. Glomerular filtration rate (GFR) can be precisely measured by the calculation of the clearance of freely filtrated exogenous substances that are neither metabolized nor reabsorbed nor secreted by tubules: its mean value is 125 mL/min/1.73 m² in men and 110 mL/min/1.73 m² in women, which represents 20% of renal blood flow. In clinical practice, estimates of GFR are obtained by the measurement of creatininaemia followed by the application of various equations (MDRD or CKD-EPI) and more recently by the measurement of plasmatic C-cystatin. Under physiological conditions, GFR is a stable parameter that is regulated by the intrinsic vascular and tubular autoregulation, by the balance between paracrine and endocrine agents acting as vasoconstrictors and vasodilators, and by the effects of renal sympathetic nerves. The mechanisms controlling GFR regulation are complex. This is due to the variety of vasoactive agents and their targets, and multiple interactions between them. Nevertheless, the relative stability of GFR during important variations of systemic haemodynamics and volaemia is due to three major operating mechanisms: autoregulation of the afferent arteriolar resistance, local synthesis and action of angiotensin II, and the sensitivity of renal resistance vessels to respond to NO release.
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Magder, Sheldon. Central venous pressure monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0132.

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Central venous pressure (CVP) is at the crucial intersection of the force returning blood to the heart and the force produced by cardiac function, which drives the blood back to the systemic circulation. The normal range of CVP is small so that before using it one must ensure proper measurement, specifically the reference level. A useful approach to hypotension is to first determine if arterial pressure is low because of a decrease in vascular resistance or a decrease in cardiac output. This is done by either measuring cardiac output or making a clinical assessment blood flow. If the cardiac output is decreased, next determine whether this is because of a cardiac pump problem or a return problem. It is at this stage that the CVP is most helpful for these options can be separated by considering the actual CVP or even better, how it changed with the change in cardiac output. A high CVP is indicative of a primary pump problem, and a low CVP and return problem. Understanding the factors that determine CVP magnitude, mechanisms that produce the components of the CVP wave form and changes in CVP with respiratory efforts can also provide useful clinical information. In many patients, CVP can be estimated on physical exam.
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Book chapters on the topic "Vascular resistance Measurement"

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L. Hungerford, Sara, Dhruv Nayya, Peter S. Hansen, Ravinay Bhindi, and Christopher Choong. "Perspective Chapter: Evolution of Techniques to Assess Vascular Impedance in Patients with Aortic Stenosis." In Aortic Stenosis - Recent Advances, New Perspectives and Applications [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104795.

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Aortic stenosis (AS) once was conceptualized as a mechanical problem with a fixed left ventricular (LV) afterload because of an obstructive valve. With time, there has been growing recognition that AS functions more like a series circuit, with important contributions from the ventricle through to the vasculature. Emerging evidence suggests that higher blood pressure and increased arterial stiffness, synonymous with vascular aging, increases global LV afterload in patients with AS. This in turn, has adverse consequences on quality-of-life measures and survival. Although traditional methods have emphasized measurement of the transvalvular pressure gradient, focusing on valvular hemodynamics alone may be inadequate. By definition, total vascular load of the human circulation includes both steady and pulsatile components. Steady load is best represented by the systemic vascular resistance whereas pulsatile load occurs because of wave reflections and vascular stiffness, and is often referred to as the valvulo-arterial impedance. In the following Review, we evaluate existing and upcoming methods to assess vascular load in patients with AS in order to better understand the effects of vascular aging on this insidious disease process.
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Heyndrickx, Guy, and Carlo Di Mario. "Haemodynamic data." In ESC CardioMed, 613–17. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0130.

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Direct catheter-based measurements of right and left heart saturations and pressures allow full characterization of patient haemodynamics, including the presence of cardiac shunts, valve gradients and valve areas, and pulmonary and vascular resistances.
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Conference papers on the topic "Vascular resistance Measurement"

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Mori, Nobuhito, Yuya Morimoto, and Shoji Takeuchi. "Transendothelial electrical resistance (TEER) measurement system of 3D tubular vascular channel." In 2018 IEEE Micro Electro Mechanical Systems (MEMS). IEEE, 2018. http://dx.doi.org/10.1109/memsys.2018.8346551.

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Hunter, Kendall S., Craig J. Lanning, Joseph A. Albietz, Masahiko Oka, Karen A. Fagan, Kurt R. Stenmark, and Robin Shandas. "Measurement of In-Vivo Pulmonary Vascular Impedance in Two Animal Models of Pulmonary Hypertension." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175993.

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Pulmonary vascular input impedance has been increasingly promoted as an important diagnostic for pulmonary arterial hypertension (PAH) [1,2]. The gold-standard clinical diagnostic for the disease, pulmonary vascular resistance (PVR), quantifies only the mean resistance to flow but ignores the impact of vascular stiffness and flow pulsatility, which in PAH can represent up to 40% of the total load presented to the right ventricle. PVR has also been found to be only a moderate predictor of PAH outcomes [3]. The first of these deficiencies is not present in impedance; clinical studies have found the sum of its 1st and 2nd harmonic moduli to have good correlation (r2 = 0.812) with global pulmonary vascular stiffness (PVS) [2], a hemodynamically-measured quantifier of vascular stiffness. Additionally, the 0th harmonic modulus of impedance has excellent correlation to PVR (r2 = 0.974); thus, it also quantifies the resistive load. Moreover, because PVS has recently been found as a valuable determinant of mortality in PAH [4], we believe that impedance, as a combined measure of PVR and PVS, might be an excellent predictor of disease outcomes.
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Su, Zhenbi, Kendall Hunter, Wei Tan, and Robin Shandas. "Influence of Distal Resistance and Proximal Vascular Stiffness on Vascular Impedance and Hemodynamics in Pulmonary Hypertension: A Computational Study With Validation Using an Animal Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204759.

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Clinically, invasive measurement of pulmonary vascular flow and pressure provides the hemodynamic status of the pulmonary circulation with pulmonary arterial hypertension (PAH). Current diagnostics and therapeutics for PAH revolve around pulmonary vascular resistance (PVR), which is determined by the mean pressure divided by mean flow [1]. Though PVR correlates well with right ventricular (RV) afterload, failure of which is the primary determinant of mortality [2–4], PVR does not provide the complete measure of RV afterload since it neglects dynamic impedance effects [4, 5]. Although we have shown that impedance predicts clinical outcomes better than PVR alone, several key questions remain about the relationship between hemodynamics and impedance changes in pulmonary hypertension.
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Su, Zhenbi, Kendall Hunter, and Robin Shandas. "Effect of Vascular Stiffness on Pulmonary Flow in Normotensive and Hypertensive States: Numerical Study With Fluid Structure Interaction." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192831.

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Invasive measurement of pulmonary vascular flow and pressure provides the hemodynamic status of the pulmonary circulation for children with pulmonary arterial hypertension (PAH). Clinicians are primarily interested in pulmonary vascular resistance, which is the mean pressure of the circuit divided by the mean flow through it [1], in that it is believed to well-quantify the right ventricular (RV) afterload, the primary determinant of mortality. However, previous and current investigations on the pulmonary vascular stiffness (PVS), input impedance and RV power [2–4] have found PVS to be an important contributor to power, and thus, afterload. These previous and current investigations focus on the analysis of clinical data, which is limited by the clinical equipment and techniques.
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Lee, Qim Y., Gregory S. H. Chan, Stephen J. Redmond, Paul M. Middleton, E. Steel, P. Malouf, C. Critoph, G. Flynn, E. O'Lone, and Nigel H. Lovell. "Classification of low systemic vascular resistance using photoplethysmogram and routine cardiovascular measurements." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5628062.

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Reich, Alton, and Jason Heym. "Application of Model-Based Condition Monitoring to the Human Cardiovascular System." In ASME 2017 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/pvp2017-65500.

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The techniques applied by mechanical engineers to problems of machinery condition monitoring can also be applied in other fields. This paper discusses applying techniques that are regularly applied to machinery and system condition monitoring to the human cardiovascular system. Techniques such as physics-based system modeling coupled with limited measurements can be used to infer the condition of a system or specific component. In this case, a mathematical model of the flow through the cardiovascular system was implemented and can be used independently to simulate system performance. Given basic system parameters including heart rate and vascular resistances, the model generates time varying flows and pressures in different portions of the system. The model can be used to interpret a measurement performed on the system to obtain additional information about the state of the system. In this case pulse waveform information is used to make a system flow measurement. This paper will provide an overview of the technique used, the structure of the model, and the initial validation with patient data.
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Ooi, Chen Yen, and Naomi C. Chesler. "The Role of Collagen in Pulmonary Hypertension-Induced Large Artery Stiffening." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192951.

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Hypoxic pulmonary hypertension (HPH) leads to stiffening of large pulmonary arteries, which affects right ventricular afterload. We hypothesized that vascular collagen accumulation is the major cause of large pulmonary artery (PA) stiffening in HPH. We tested this hypothesis with transgenic mice that produce collagen type I resistant to degradation (Col1a1R/R) and wild type littermate controls (Col1a1+/+) exposed to hypoxia and allowed to recover. Pressure-diameter testing on left PAs demonstrated that stiffness in control mice increased with hypoxia and decreased with recovery (p < 0.05). Preliminary tests in degradation-resistant mice suggest that PA stiffness decreases less with recovery than in controls. Quantitative measurements of vascular collagen content in right PAs are planned to develop statistical correlations between structure and function.
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Burgett Graves, Shawna L., Craig Lanning, K. S. kirby, Michelle Calderbank, Jennifer Geppner, Shawn J. Nolan, Dunbar D. Ivy, Robin Shandas, and Kendall Hunter. "In-Vivo Pulmonary Vascular Stiffness Obtained From Color M-Mode Tissue Doppler Imaging And Pressure Measurements Predicts Clinical Outcomes Better Than Indexed Pulmonary Vascular Resistance In Pediatric Patients With Pulmonary Arterial Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5748.

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Kato, Mitsuaki, Kenji Hirohata, Akira Kano, Shinya Higashi, Akihiro Goryu, Takuya Hongo, Shigeo Kaminaga, and Yasuko Fujisawa. "Fast CT-FFR Analysis Method for the Coronary Artery Based on 4D-CT Image Analysis and Structural and Fluid Analysis." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-51124.

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Non invasive fractional flow reserve derived from CT coronary angiography (CT-FFR) has to date been typically performed using the principles of computational fluid analysis in which a lumped parameter coronary vascular bed model is assigned to represent the impedance of the downstream coronary vascular networks absent in the computational domain for each coronary outlet. This approach may have a number of limitations. It may not account for the impact of the myocardial contraction and relaxation during the cardiac cycle, patient-specific boundary conditions for coronary artery outlets and vessel stiffness. We have developed a novel approach based on 4D-CT image tracking (registration) and structural and fluid analysis based on one dimensional mechanical model, to address these issues. In our approach, we analyzed the deformation variation of vessels and the volume variation of vessels to better define boundary conditions and stiffness of vessels. We focused on the blood flow and vessel deformation of coronary arteries and aorta near coronary arteries in the diastolic cardiac phase from 70% to 100 %. The blood flow variation of coronary arteries relates to the deformation of vessels, such as expansion and contraction of the cross-sectional area, during this period where resistance is stable, pressure loss is approximately proportional to flow. We used a statistical estimation method based on a hierarchical Bayes model to integrate 4D-CT measurements and structural and fluid analysis data. Under these analysis conditions, we performed structural and fluid analysis to determine pressure, flow rate and CT-FFR. Furthermore, the reduced-order model based on fluid analysis was studied in order to shorten the computational time for 4D-CT-FFR analysis. The consistency of this method has been verified by a comparison of 4D-CT-FFR analysis results derived from five clinical 4D-CT datasets with invasive measurements of FFR. Additionally, phantom experiments of flexible tubes with and without stenosis using pulsating pumps, flow sensors and pressure sensors were performed. Our results show that the proposed 4D-CT-FFR analysis method has the potential to accurately estimate the effect of coronary artery stenosis on blood flow.
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