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Arterial pressure and flow wave analysis using time-domain 1-D hemodynamics.

Willemet M, Alastruey J - Ann Biomed Eng (2014)

Bottom Line: We reviewed existing methods for analyzing, in the time domain, physical mechanisms underlying the patterns of blood pressure and flow waveforms in the arterial system.We assessed the physical information provided by each method and showed how to combine existing methods in order to quantify contributions to numerically generated waveforms from previous cardiac cycles and from specific regions and properties of the numerical domain: the aortic root, arterial bifurcations and tapered vessels, peripheral reflection sites, and the Windkessel function of the aorta.We illustrated our results with numerical examples involving generalized arterial stiffening in a distributed one-dimensional model or localized changes in the model parameters due to a femoral stenosis, carotid stent or abdominal aortic aneurysm.

View Article: PubMed Central - PubMed

Affiliation: Division of Imaging Sciences and Biomedical Engineering, St. Thomas' Hospital, King's College London, London, UK, marie.willemet@kcl.ac.uk.

ABSTRACT
We reviewed existing methods for analyzing, in the time domain, physical mechanisms underlying the patterns of blood pressure and flow waveforms in the arterial system. These are wave intensity analysis and separations into several types of waveforms: (i) forward- and backward-traveling, (ii) peripheral and conduit, or (iii) reservoir and excess. We assessed the physical information provided by each method and showed how to combine existing methods in order to quantify contributions to numerically generated waveforms from previous cardiac cycles and from specific regions and properties of the numerical domain: the aortic root, arterial bifurcations and tapered vessels, peripheral reflection sites, and the Windkessel function of the aorta. We illustrated our results with numerical examples involving generalized arterial stiffening in a distributed one-dimensional model or localized changes in the model parameters due to a femoral stenosis, carotid stent or abdominal aortic aneurysm.

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Pressure and flow waveforms in the midpoint of the thoracic aorta, left carotid, left brachial, and right external iliac of the 55-artery model sketched in Fig. 1a. (a) Pressure (P) and (b) flow (Q) waveforms separated into their peripheral (P Q) and conduit components (P Q). Cardiac conduit pressure (P) is plotted in red in (a). (c) Reservoir and excess pressures computed using the two-element () or three-element () Windkessel models
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Fig3: Pressure and flow waveforms in the midpoint of the thoracic aorta, left carotid, left brachial, and right external iliac of the 55-artery model sketched in Fig. 1a. (a) Pressure (P) and (b) flow (Q) waveforms separated into their peripheral (P Q) and conduit components (P Q). Cardiac conduit pressure (P) is plotted in red in (a). (c) Reservoir and excess pressures computed using the two-element () or three-element () Windkessel models

Mentions: Figure 3a shows that peripheral pressure waveforms dominate over conduit waveforms throughout the cardiac cycle. Conduit pressures have a greater magnitude in systole than in diastole. They make up the main features of the pressure waveform in systole, such as most of the amplitude of the pressure pulse and the dicrotic notch or point of inflection at the end of systole; the notch completely disappears from peripheral pressure waveforms calculated using the linearized 1-D equations (1a), (1b), and (2) (data not shown). Figure 3b shows that conduit flows dominate over peripheral flows in systole and produce the main features of the flow waveform. Conduit flows vanish in diastole so that the flow is mainly peripheral towards the end of diastole.Figure 3


Arterial pressure and flow wave analysis using time-domain 1-D hemodynamics.

Willemet M, Alastruey J - Ann Biomed Eng (2014)

Pressure and flow waveforms in the midpoint of the thoracic aorta, left carotid, left brachial, and right external iliac of the 55-artery model sketched in Fig. 1a. (a) Pressure (P) and (b) flow (Q) waveforms separated into their peripheral (P Q) and conduit components (P Q). Cardiac conduit pressure (P) is plotted in red in (a). (c) Reservoir and excess pressures computed using the two-element () or three-element () Windkessel models
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4286649&req=5

Fig3: Pressure and flow waveforms in the midpoint of the thoracic aorta, left carotid, left brachial, and right external iliac of the 55-artery model sketched in Fig. 1a. (a) Pressure (P) and (b) flow (Q) waveforms separated into their peripheral (P Q) and conduit components (P Q). Cardiac conduit pressure (P) is plotted in red in (a). (c) Reservoir and excess pressures computed using the two-element () or three-element () Windkessel models
Mentions: Figure 3a shows that peripheral pressure waveforms dominate over conduit waveforms throughout the cardiac cycle. Conduit pressures have a greater magnitude in systole than in diastole. They make up the main features of the pressure waveform in systole, such as most of the amplitude of the pressure pulse and the dicrotic notch or point of inflection at the end of systole; the notch completely disappears from peripheral pressure waveforms calculated using the linearized 1-D equations (1a), (1b), and (2) (data not shown). Figure 3b shows that conduit flows dominate over peripheral flows in systole and produce the main features of the flow waveform. Conduit flows vanish in diastole so that the flow is mainly peripheral towards the end of diastole.Figure 3

Bottom Line: We reviewed existing methods for analyzing, in the time domain, physical mechanisms underlying the patterns of blood pressure and flow waveforms in the arterial system.We assessed the physical information provided by each method and showed how to combine existing methods in order to quantify contributions to numerically generated waveforms from previous cardiac cycles and from specific regions and properties of the numerical domain: the aortic root, arterial bifurcations and tapered vessels, peripheral reflection sites, and the Windkessel function of the aorta.We illustrated our results with numerical examples involving generalized arterial stiffening in a distributed one-dimensional model or localized changes in the model parameters due to a femoral stenosis, carotid stent or abdominal aortic aneurysm.

View Article: PubMed Central - PubMed

Affiliation: Division of Imaging Sciences and Biomedical Engineering, St. Thomas' Hospital, King's College London, London, UK, marie.willemet@kcl.ac.uk.

ABSTRACT
We reviewed existing methods for analyzing, in the time domain, physical mechanisms underlying the patterns of blood pressure and flow waveforms in the arterial system. These are wave intensity analysis and separations into several types of waveforms: (i) forward- and backward-traveling, (ii) peripheral and conduit, or (iii) reservoir and excess. We assessed the physical information provided by each method and showed how to combine existing methods in order to quantify contributions to numerically generated waveforms from previous cardiac cycles and from specific regions and properties of the numerical domain: the aortic root, arterial bifurcations and tapered vessels, peripheral reflection sites, and the Windkessel function of the aorta. We illustrated our results with numerical examples involving generalized arterial stiffening in a distributed one-dimensional model or localized changes in the model parameters due to a femoral stenosis, carotid stent or abdominal aortic aneurysm.

Show MeSH
Related in: MedlinePlus