Beat to beat variability in cardiovascular variables: Noise or music?

Abstract

Cardiovascular variables such as heart rate, arterial blood pressure, stroke volume and the shape of electrocardiographic complexes all fluctuate on a beat to beat basis. These fluctuations have traditionally been ignored or, at best, treated as noise to be averaged out. The variability in cardiovascular signals reflects the homeodynamic interplay between perturbations to cardiovascular function and the dynamic response of the cardiovascular regulatory systems. Modern signal processing techniques provide a means of analyzing beat to beat fluctuations in cardiovascular signals, so as to permit a quantitative, noninvasive or minimally invasive method of assessing closed loop hemodynamic regulation and cardiac electrical stability. This method promises to provide a new approach to the clinical diagnosis and management of alterations in cardiovascular regulation and stability.

Characteristics of Autonomic Nervous System Activity in Men With Lower Urinary Tract Symptoms (LUTS): Analysis of Heart Rate Variability in Men With LUTS

“…Efferent vagal activity is a major contributor to the HF component, as is seen in clinical and experimental observations of autonomic maneuvers such as electrical vagal stimulation, muscarinic receptor blockade, and vagotomy. [17][18][19] More controversial is the interpretation of the LF component, which is considered by some investigators [19][20][21][22] to be a marker of sympathetic modulation (especially when expressed in normalized units) and considered by others 17,23 to be a parameter that includes both sympathetic and vagal influences. Finally, most investigators believe that LF and HF mean the activity of sympathetic and parasympathetic activity in short-term HRV.…”

Effects of physical training on autonomic cardiac modulation in hypertension: assessment by heart rate variability analysis

“…[1][2][3] An indirect assessment of the alterations in cardiovascular autonomic modulation accompanying essential hypertension is also possible through the analysis of BP and heart rate (HR) variability (BPV, HRV), which represent a simple, non-invasive means to quantify the amplitude of BP and HR fluctuations occurring at specific frequency regions, which are known to reflect BP and HR modulation by neural autonomic influences. [4][5][6][7][8][9] Most studies have focused on HRV only, mainly because of its ability to reflect both sympathetic and parasympathetic cardiac modulation and because its beat-by-beat fluctuations are easily recorded though the use of one electrocardiographic lead. In the frequency domain, current spectral analysis techniques allow for quantification of the power of HR variations in the very-low (VLF, 0.025-0.05 Hz), low (LF, 0.05-0.15 Hz) and high frequency (HF, 0.15-0.5 Hz) regions of the HR spectra, as well as calculation of other autonomic indices by normalizing these powers vs. total variance or by computing the ratio between the powers reflecting sympathetic and vagal drive (that is, LF/HF ratio).…”

“…In the frequency domain, current spectral analysis techniques allow for quantification of the power of HR variations in the very-low (VLF, 0.025-0.05 Hz), low (LF, 0.05-0.15 Hz) and high frequency (HF, 0.15-0.5 Hz) regions of the HR spectra, as well as calculation of other autonomic indices by normalizing these powers vs. total variance or by computing the ratio between the powers reflecting sympathetic and vagal drive (that is, LF/HF ratio). [4][5][6][7][8] These indices have proven to be useful in characterizing the alterations in cardiac autonomic modulation occurring in essential hypertension and even in pre-hypertensive states, 10 and have also demonstrated their prognostic value in predicting the development of CV disease and events in large population-based studies 11 or in specific clinical settings (that is, post-myocardial infarction and heart failure patients). 12 The spectral analysis of HRV has also been proposed as a tool to quantify changes in autonomic cardiac modulation in response to treatment.…”

“…6,7,19 Although changes in the HF (0.15-0.5 Hz) spectral power of HRV seem to be primarily caused by the modulation of cardiac parasympathetic efferent activity, 5,[19][20][21] at respiratory frequencies below nine breaths per minute sympathetic modulation of respiratoryinduced HR changes also occurs, together with some degree of mechanical stimulation of the sinus node by ventilation cycles. Thus, HR HF power is considered a satisfactory, but incomplete, measure of parasympathetic cardiac control.…”

“…Thus, HR HF power is considered a satisfactory, but incomplete, measure of parasympathetic cardiac control. The specificity of HR LF power (0.05-0.15 Hz) in reflecting sympathetic cardiac modulation of HR has been reported to be even lower because it may also depend on vagal influences (as demonstrated by the reductions in LF HR power achieved by either parasympathetic or sympathetic pharmacological blockade) 5,20 and on a variety of other factors, including thermoregulation, atrial stretch by periodic breathing and hemodynamic instability. 22 In recognition of the limited specificity of HR LF and HF powers as respective markers of sympathetic and vagal cardiac drive and based on the assumption that sympathetic and vagal cardiac influences are normally altered in opposite directions, 6,23-25 the LF/HF ratio was proposed as an index of sympathovagal balance and has proven to be useful in providing information in a number of clinical conditions.…”