Abstract

Spontaneous baroreflex sensitivity (BRS) is a widely used tool for the quantification of the cardiovascular regulation. Numerous groups use the xBRS method, which calculates the cross-correlation between the systolic beat-to-beat blood pressure and the R-R interval (resampled at 1 Hz) in a 10 s sliding window, with 0–5 s delays for the interval. The delay with the highest correlation is selected and, if significant, the quotient of the standard deviations of the R-R intervals and the systolic blood pressures is recorded as the corresponding xBRS value. In this paper we test the hypothesis that the xBRS method quantifies the causal interactions of spontaneous BRS from non-invasive measurements at rest. We use the term spontaneous BRS in the sense of the sensitivity curve is calculated from non-interventional, i.e., spontaneous, baroreceptor activity. This study includes retrospective analysis of 1828 measurements containing ECG as well as continues blood pressure under resting conditions. Our results show a high correlation between the heart rate – systolic blood pressure variability (HRV/BPV) quotient and the xBRS (r = 0.94, p < 0.001). For a deeper understanding we conducted two surrogate analyses by substituting the systolic blood pressure by its reversed time series. These showed that the xBRS method was not able to quantify causal relationships between the two signals. It was not possible to distinguish between random and baroreflex controlled sequences. It appears xBRS rather determines the HRV/BPV quotient. We conclude that the xBRS method has a potentially large bias in characterizing the capacity of the arterial baroreflex under resting conditions. During slow breathing, estimates for xBRS are significantly increased, which clearly shows that measurements at rest only involve limited baroreflex activity, but does neither challenge, nor show the full range of the arterial baroreflex regulatory capacity. We show that xBRS is exclusively dominated by the heart rate to systolic blood pressure ratio (r = 0.965, p < 0.001). Further investigations should focus on additional autonomous testing procedures such as slow breathing or orthostatic testing to provide a basis for a non-invasive evaluation of baroreflex sensitivity.

Highlights

  • The baroreflex is an important component of cardiovascular regulation to maintain homeostasis

  • Surrogate analysis (a) between xBRSS1 and RMSSDHRV showed high correlation coefficient (r = 0.84, p < 0.001), i.e., reversing one time series does not affect the results of xBRS

  • In this paper we test the hypothesis that the xBRS method quantifies the causal interactions of spontaneous baroreflex sensitivity (BRS) from non-invasive, non-interventional measurements at rest

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Summary

Introduction

The baroreflex is an important component of cardiovascular regulation to maintain homeostasis. The idea of spontaneous baroreflex sensitivity is to estimate the concomitant effect of respiration on heart period and blood pressure based on non-invasive and non-pharmacological driven measurements. BRS has been assessed by the Oxford method, based on analysis of heart rate response to drug-induced blood pressure variations (Smyth et al, 1969). This method is still the gold standard for assessing baroreflex control. Undesirable effects of medications on the state of the ANS cannot be excluded To overcome these drawbacks, numerous methods for noninvasive assessment of BRS have been developed, based on the analysis of spontaneous fluctuations in systolic blood pressure (SAP) and the RR interval (RR). The origin of RSA is known to have various mechanisms (Blaber and Hughson, 1996), including arterial baroreflex and cardiopulmonary baroreceptor responses due to fluctuations of cardiac stroke volume, a direct influence of medullary respiratory neurons on the vagal motor nucleus, and pulmonary stretch receptor response to lung inflation

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