Evidence map›Paper›PMID 29686625›Full record

ArticleFrontiers in physiology2018

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

Björn J P van Der Ster, Nicolaas H Sperna Weiland, Berend E Westerhof, Wim J Stok, Johannes J van Lieshout

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Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Björn J P van Der SterDepartment of Internal Medicine, Academic Medical Center, Amsterdam, Netherlands.
Nicolaas H Sperna WeilandLaboratory for Clinical Cardiovascular Physiology, Academic Medical Center, Amsterdam, Netherlands.
Berend E WesterhofLaboratory for Clinical Cardiovascular Physiology, Academic Medical Center, Amsterdam, Netherlands.
Wim J StokDepartment of Medical Biology, Academic Medical Center, Amsterdam, Netherlands.
Johannes J van LieshoutDepartment of Internal Medicine, Academic Medical Center, Amsterdam, Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

heart ratelinear mixed effect modelslower body negative pressurepulse pressuresympathetic stimulation

Identifiers

PMID29686625
PMCPMC5900383

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