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

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

doi:10.3389/fphys.2018.00353

Björn J P Van Der Ster, Wim J Stok + Show 3 more

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https://doi.org/10.3389/fphys.2018.00353

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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.

Highlights

In the resting condition an elevated arterial pulse pressure (PP), the pulsatile component of blood pressure (BP), usually reflects decreased arterial compliance in the elderly and is associated with multiple adverse cardiovascular outcomes
lower body negative pressure (LBNP) induced a rapid decline in Stroke volume (SV) (∼25%) and PP (∼15%) accompanied by an immediate ∼30% increase in heart rate (HR) (Figure 3)
The novel finding of this study is that in a setting of a sustained increase in sympathetic outflow by LBNP PP can be estimated from a linear mixed effect (LME) model based on HR

Summary

Introduction

In the resting condition an elevated arterial pulse pressure (PP), the pulsatile component of blood pressure (BP), usually reflects decreased arterial compliance in the elderly and is associated with multiple adverse cardiovascular outcomes. When healthy subjects exercise PP increases by the combined effects of an increase in systolic pressure concomitant to the elevated cardiac output (CO) and a reduction in diastolic pressure related to the vasodilatation. The duration of the cardiac cycle determines the length of diastole and influences the shape of the arterial pressure waveform (Wilkinson et al, 2000; Lantelme et al, 2002; Albaladejo et al, 2004; Haesler et al, 2004; Westerhof et al, 2008; Mackenzie et al, 2009; Benetos et al, 2010; Westerhof and Westerhof, 2013; Rimoldi et al, 2016) Studies in both animals and humans using pacing or a selective negative chronotropic agent alleged evidence for an inverse relationship between PP and heart rate (HR) (Lantelme et al, 2002; Albaladejo et al, 2004; Haesler et al, 2004; Rimoldi et al, 2016). A lower HR prolongates diastole more than systole, widening PP (Figure 1; Folkow and Ely, 1998)

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