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Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia

Heart rate (HR) has an impact on the central blood pressure (BP) wave shape and is related to pulse wave velocity and therefore to timing and duration of systole and diastole. This study tested the hypothesis that in healthy subjects both in rest and during sympathetic stimulation the relation betwe...

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Autores principales: van Der Ster, Björn J. P., Sperna Weiland, Nicolaas H., Westerhof, Berend E., Stok, Wim J., van Lieshout, Johannes J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5900383/
https://www.ncbi.nlm.nih.gov/pubmed/29686625
http://dx.doi.org/10.3389/fphys.2018.00353
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author van Der Ster, Björn J. P.
Sperna Weiland, Nicolaas H.
Westerhof, Berend E.
Stok, Wim J.
van Lieshout, Johannes J.
author_facet van Der Ster, Björn J. P.
Sperna Weiland, Nicolaas H.
Westerhof, Berend E.
Stok, Wim J.
van Lieshout, Johannes J.
author_sort van Der Ster, Björn J. P.
collection PubMed
description Heart rate (HR) has an impact on the central blood pressure (BP) wave shape and is related to pulse wave velocity and therefore to timing and duration of systole and diastole. This study tested the hypothesis that in healthy subjects both in rest and during sympathetic stimulation the relation between HR and pulse pressure (PP) is described by a linear effect model. Forty-four healthy volunteers were subjected to sympathetic stimulation by continuous lower body negative pressure (LBNP) until the onset of pre-syncopal symptoms. Changes in PP and HR were tracked non-invasively and modeled by linear mixed effect (LME) models. The dataset was split into two groups: the first was used for creating a model and the second for its evaluation. Models were created on the data obtained during LBNP. Model performance was expressed as absolute median error (1st; 3rd quantiles) and bias with limits of agreement (LOA) between modeled and measured PP. From rest to sympathetic stimulation, mean BP was maintained while HR increased (~30%) and PP decreased gradually (~20%). During baseline, PP could be modeled with an absolute error of 6 (4; 10) mm Hg and geometric mean ratio of the bias was 0.97 (LOA: 0.8–1.1). During LBNP, absolute median model error was 5 (4; 8) mmHg with geometric mean ratio 1.02 (LOA: 0.8–1.3). In conclusion, both during rest and during sustained sympathetic outflow induced by progressive central hypovolemia, a LME model of HR provides for an estimate of PP in healthy young adults.
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spelling pubmed-59003832018-04-23 Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia van Der Ster, Björn J. P. Sperna Weiland, Nicolaas H. Westerhof, Berend E. Stok, Wim J. van Lieshout, Johannes J. Front Physiol Physiology Heart rate (HR) has an impact on the central blood pressure (BP) wave shape and is related to pulse wave velocity and therefore to timing and duration of systole and diastole. This study tested the hypothesis that in healthy subjects both in rest and during sympathetic stimulation the relation between HR and pulse pressure (PP) is described by a linear effect model. Forty-four healthy volunteers were subjected to sympathetic stimulation by continuous lower body negative pressure (LBNP) until the onset of pre-syncopal symptoms. Changes in PP and HR were tracked non-invasively and modeled by linear mixed effect (LME) models. The dataset was split into two groups: the first was used for creating a model and the second for its evaluation. Models were created on the data obtained during LBNP. Model performance was expressed as absolute median error (1st; 3rd quantiles) and bias with limits of agreement (LOA) between modeled and measured PP. From rest to sympathetic stimulation, mean BP was maintained while HR increased (~30%) and PP decreased gradually (~20%). During baseline, PP could be modeled with an absolute error of 6 (4; 10) mm Hg and geometric mean ratio of the bias was 0.97 (LOA: 0.8–1.1). During LBNP, absolute median model error was 5 (4; 8) mmHg with geometric mean ratio 1.02 (LOA: 0.8–1.3). In conclusion, both during rest and during sustained sympathetic outflow induced by progressive central hypovolemia, a LME model of HR provides for an estimate of PP in healthy young adults. Frontiers Media S.A. 2018-04-09 /pmc/articles/PMC5900383/ /pubmed/29686625 http://dx.doi.org/10.3389/fphys.2018.00353 Text en Copyright © 2018 van Der Ster, Sperna Weiland, Westerhof, Stok and van Lieshout. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
van Der Ster, Björn J. P.
Sperna Weiland, Nicolaas H.
Westerhof, Berend E.
Stok, Wim J.
van Lieshout, Johannes J.
Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia
title Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia
title_full Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia
title_fullStr Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia
title_full_unstemmed Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia
title_short Modeling Arterial Pulse Pressure From Heart Rate During Sympathetic Activation by Progressive Central Hypovolemia
title_sort modeling arterial pulse pressure from heart rate during sympathetic activation by progressive central hypovolemia
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5900383/
https://www.ncbi.nlm.nih.gov/pubmed/29686625
http://dx.doi.org/10.3389/fphys.2018.00353
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