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      Fine structure of the low-frequency spectra of heart rate and blood pressure

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      1 , , 2 , 3 , 4
      BMC Physiology
      BioMed Central

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          Abstract

          Background

          The aim of this study was to explore the principal frequency components of the heart rate and blood pressure variability in the low frequency (LF) and very low frequency (VLF) band. The spectral composition of the R–R interval (RRI) and systolic arterial blood pressure (SAP) in the frequency range below 0.15 Hz were carefully analyzed using three different spectral methods: Fast Fourier transform (FFT), Wigner-Ville distribution (WVD), and autoregression (AR). All spectral methods were used to create time–frequency plots to uncover the principal spectral components that are least dependent on time. The accurate frequencies of these components were calculated from the pole decomposition of the AR spectral density after determining the optimal model order – the most crucial factor when using this method – with the help of FFT and WVD methods.

          Results

          Spectral analysis of the RRI and SAP of 12 healthy subjects revealed that there are always at least three spectral components below 0.15 Hz. The three principal frequency components are 0.026 ± 0.003 (mean ± SD) Hz, 0.076 ± 0.012 Hz, and 0.117 ± 0.016 Hz. These principal components vary only slightly over time. FFT-based coherence and phase-function analysis suggests that the second and third components are related to the baroreflex control of blood pressure, since the phase difference between SAP and RRI was negative and almost constant, whereas the origin of the first component is different since no clear SAP–RRI phase relationship was found.

          Conclusion

          The above data indicate that spontaneous fluctuations in heart rate and blood pressure within the standard low-frequency range of 0.04–0.15 Hz typically occur at two frequency components rather than only at one as widely believed, and these components are not harmonically related. This new observation in humans can help explain divergent results in the literature concerning spontaneous low-frequency oscillations. It also raises methodological and computational questions regarding the usability and validity of the low-frequency spectral band when estimating sympathetic activity and baroreflex gain.

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          Most cited references15

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          Spectral Analysis of Blood Pressure and Heart Rate Variability in Evaluating Cardiovascular Regulation: A Critical Appraisal

          Blood pressure variability includes rhythmic and nonrhythmic fluctuations that, with the use of spectral analysis, appear as clear peaks or broadband power, respectively. This review offers a concise and critical description of the spectral methods most commonly used (fast Fourier transform versus autoregressive modeling, time-varying versus broadband spectral analysis) and an evaluation of their advantages and disadvantages. It also provides insight into the problems that still affect the physiological and clinical interpretations of data provided by spectral analysis of blood pressure and heart rate variability. In particular, the assessment of blood pressure and heart rate spectra aimed at providing indexes of autonomic cardiovascular modulation is discussed. Evidence is given that multivariate models--which allow evaluation of the interactions between changes in blood pressure, heart rate, and other biological signals (such as respiratory activity) in the time or frequency domains--offer a more comprehensive approach to the assessment of cardiovascular regulation than that represented by the separate analysis of fluctuations in blood pressure or heart rate only.
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            Hemodynamic regulation: investigation by spectral analysis.

            We investigated the hypothesis that beat-to-beat variability in hemodynamic parameters reflects the dynamic interplay between ongoing perturbations to circulatory function and the compensatory response of short-term cardiovascular control systems. Spontaneous fluctuations in heart rate (HR), arterial blood pressure, and respiration were analyzed by spectral analysis in the 0.02- to 1-Hz frequency range. A simple closed-loop model of short-term cardiovascular control was proposed and evaluated in a series of experiments: pharmacological blockades of the parasympathetic, alpha-sympathetic, beta-sympathetic, and renin-angiotensin systems were used to open the principal control loops in order to examine changes in the spectral pattern of the fluctuations. Atrial pacing was used to examine blood pressure variability in the absence of HR variability. We found that respiratory frequency fluctuations in HR are parasympathetically mediated and that blood pressure fluctuations at this frequency result almost entirely from the direct effect of centrally mediated HR fluctuations. The sympathetic nervous system appears to be too sluggish to mediate respiratory frequency variations. Low-frequency (0.02-0.09 Hz) fluctuations in HR are jointly mediated by the parasympathetic and beta-sympathetic systems and appear to compensate for blood pressure fluctuations at this frequency. Low-frequency blood pressure fluctuations are probably due to variability in vasomotor activity which is normally damped by renin-angiotensin system activity. Blockade of the alpha-adrenergic system, however, does not significantly alter low-frequency blood pressure fluctuations.
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              Transfer function analysis of the circulation: unique insights into cardiovascular regulation.

              We have demonstrated previously that transfer function analysis can be used to precisely characterize the respiratory sinus arrhythmia (RSA) in normal humans. To further investigate the role of the autonomic nervous system in RSA and to understand the complex links between respiratory activity and arterial pressure, we determined the transfer functions between respiration, heart rate (HR), and phasic, systolic, diastolic, and pulse arterial pressures in 14 healthy subjects during 6-min periods in which the respiratory rate was controlled in a predetermined but erratic fashion. Pharmacological autonomic blockade with atropine, propranolol, and both, in combination with changes in posture, was used to characterize the sympathetic and vagal contributions to these relationships, as well as to dissect the direct mechanical links between respiration and arterial pressure from the effects of the RSA on arterial pressure. We found that 1) the pure sympathetic (standing + atropine) HR response is characterized by markedly reduced magnitude at frequencies greater than 0.1 Hz and a phase delay, whereas pure vagal (supine + propranolol) modulation of HR is characterized by higher magnitude at all frequencies and no phase delay; 2) both the mechanical links between respiration and arterial pressure and the RSA contribute significantly to the effects of respiration on arterial pressure; 3) the RSA contribution to arterial pressure fluctuations is significant for vagal but not for sympathetic modulation of HR; 4) the mechanical effects of respiration on arterial pressure are related to the negative rate of change of instantaneous lung volume; 5) the mechanical effects have a higher magnitude during systole than during diastole; and 6) the mechanical effects are larger in teh standing than the supine position. Most of these findings can be explained by a simple model of circulatory control based on previously published experimental transfer functions from our laboratory.
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                Author and article information

                Journal
                BMC Physiol
                BMC Physiology
                BioMed Central (London )
                1472-6793
                2003
                13 October 2003
                : 3
                : 11
                Affiliations
                [1 ]Department of Physics, University of Turku, 20014 Turku, Finland
                [2 ]Department of Clinical Pharmacology, Tampere University Hospital, 33521 Tampere, Finland
                [3 ]Tampere University, 33014 Tampere, Finland
                [4 ]Department of Clinical Physiology, Tampere University Hospital, 33521 Tampere, Finland
                Article
                1472-6793-3-11
                10.1186/1472-6793-3-11
                270047
                14552660
                31a27587-c8cf-413c-8d33-2bb1c526ba3b
                Copyright © 2003 Kuusela et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
                History
                : 21 May 2003
                : 13 October 2003
                Categories
                Research Article

                Anatomy & Physiology
                Anatomy & Physiology

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