Origin of heart rate variability and turbulence: an appraisal of autonomic modulation of cardiovascular function

Abstract

Heart period constantly changes on a beat to beat basis, due to autonomic influences on the sinoatrial node, and changes can be quantified as heart rate variability (HRV). In addition, after a premature ventricular beat, there are reproducible variations in RR interval, also due to baroreflex mediated autonomic influences on the sinoatrial node, that can be measured as heart rate turbulence (HRT). Impaired autonomic function as measured by HRV and HRT has proven to predict adverse outcomes in clinical settings. The ability of reduced HRV and HRT to predict adverse outcomes has been explained by their dependency on vagal mechanisms that could reflect an increased sympathetic and a reduced vagal modulation of sinus node, thus favoring cardiac electrical instability. Analysis of non-linear dynamics of HRV has also been utilized to describe the fractal like characteristic of the variability signal and proven effective in identify patients at risk for sudden cardiac death. Despite the clinical validity of these measures, it has also been evident that the relationship between neural input and sinus node responsiveness is extremely complex and variable in different clinical conditions. Thus, abnormal HRV or HRT on a clinical Holter recordings may reflect non-neural as well as autonomic mechanisms, and this also needs to be taken into account when interpreting any findings. However, under controlled conditions, the computation of the low and high frequency components of HRV and of their normalized powers or ratio seems capable of providing valid information on sympatho-vagal balance in normal subjects, as well as in most patients with a preserved left ventricular function. Thus, analysis of HRV does provide a unique tool to specifically assess autonomic control mechanisms in association with various perturbations. In conclusion, HRV measures are of substantial utility to identify patients with an increased cardiac mortality and to evaluate autonomic control mechanisms, but their ability to capture specific levels of autonomic control may be limited to controlled laboratory studies in relatively healthy subjects.

Keywords: autonomic modulation; baroreflex mechanisms; non-invasive evaluation of cardiac function; spectral analysis; sympathetic and vagal control.

Figure 1

RR interval time series during resting controlled conditions before and after autonomic blockade (atropine 0.04 mg/kg and propranolol 0.2 mg/kg).

Figure 2

Spectral analysis of short-term heart rate, arterial pressure and respiration variability. Signal recordings are presented in the left part of the figure. In the central panels, the time series of RR interval, systolic arterial pressure and respiratory movements are displayed. In the right panels the power spectrum of heart rate, systolic arterial pressure and respiration are presented. Two distinct components at low (LF: ∼0.01 Hz) and high (HF: ∼0.25 Hz) frequency are detectable (shadowed areas) in the autospectra of heart rate and systolic arterial pressure variability. A single HF component characterizes respiration. EKG, electrocardiogram; AP, arterial pressure; RES, respiratory movements.

Figure 3

Spectral analysis of ln transformed 24 h heart rate variability. Almost 90% of the power is distributed within the ultra low (ULF) and very low (VLF) frequency ranges. The slope of the relationship between ln power and frequency between 10⁻² and 10⁻⁴ Hz is indicated and provides the value of 1/f slope.

Figure 4

Schematic representation of the RR interval changes induced by a premature ventricular contraction that are used to compute the two indexes of heart rate turbulence: turbulence onset (TO) and turbulence slope (TS).