Short‐term cardiovascular oscillations in man: measuring and modelling the physiologies

Abstract

Research into cardiovascular variabilities intersects both human physiology and quantitative modelling. This is because respiratory and Mayer wave (or 10 s) cardiovascular oscillations represent the integrated control of a system through both autonomic branches by systemic haemodynamic changes within a fluid‐filled, physical system. However, our current precise measurement of short‐term cardiovascular fluctuations does not necessarily mean we have an adequate understanding of them. Empirical observation suggests that both respiratory and Mayer wave fluctuations derive from mutable autonomic and haemodynamic inputs. Evidence strongly suggests that respiratory sinus arrhythmia both contributes to and buffers respiratory arterial pressure fluctuations. Moreover, even though virtual abolition of all R‐R interval variability by cholinergic blockade suggests that parasympathetic stimulation is essential for expression of these variabilities, respiratory sinus arrhythmia does not always reflect a purely vagal phenomenon. The arterial baroreflex has been cited as the mechanism for both respiratory and Mayer wave frequency fluctuations. However, data suggest that both cardiac vagal and vascular sympathetic fluctuations at these frequencies are independent of baroreflex mechanisms and, in fact, contribute to pressure fluctuations. Results from cardiovascular modelling can suggest possible sources for these rhythms. For example, modelling originally suggested low frequency cardiovascular rhythms derived from intrinsic delays in baroreceptor control, and experimental evidence subsequently corroborated this possibility. However, the complex stochastic relations between and variabilities in these rhythms indicate no single mechanism is responsible. If future study of cardiovascular variabilities is to move beyond qualitative suggestions of determinants to quantitative elucidation of critical physical mechanisms, both experimental design and model construction will have to be more trenchant.

Cardiovascular and cardiorespiratory coupling analyses: a review

“…Interactions of these physiological subsystems within the cardiovascular system can be described as closed loops with feed-forward (FF) and feed-back (FB) mechanisms. On the one hand, blood pressure changes detected by baroreceptors lead to changes in heart rate (HR) regulation through the arterial baroreflex control loop, and on the other hand, heart rate variations (HRVs) affect blood pressure via the Windkessel function [2]. Interactions within the cardiorespiratory system are mainly reflected in the respiratory sinus arrhythmia (RSA), the rhythmic fluctuation of cardiac cycle intervals (RR interval) in relation to respiration.…”

Clinical impact of evaluation of cardiovascular control by novel methods of heart rate dynamics

“…The high-frequency (from 0.18 to 0.4 Hz) fluctuations of heart rate (and blood pressure) are determined by respiration. These oscillations represent autonomic neural fluctuations and central blood volume alterations (Cohen & Taylor 2002). These high-frequency fluctuations are modified by the phenomenon called respiratory gating, whose magnitude depends on the level of stimulation of autonomic motor neurons.…”

“…When the level of the stimulation is low (low vagal activity at low arterial pressure), respiratory oscillations of vagal activity are also low (Eckberg 2003). The low-frequency (from 0.03 to 0.15 Hz) fluctuations of heart rate have been proposed to be derived from the arterial pressure Mayer waves, whose major determinant is considered to be sympathetic vasomotor activity (Cohen & Taylor 2002). The very-low-frequency fluctuations (below 0.03 Hz) have been attributed to the renin-angiotensin system, other humoral factors and thermoregulation.…”

Physiological System Identification with the Kalman Filter in Diffuse Optical Tomography

“…Anecdotal evidence was presented that certain principal components correlate with blood pressure and respiratory dynamics. This observation of statistically uncorrelated blood pressure and respiratory dynamics contradicts known respiratory interactions in blood pressure regulation [6]. Due to physiological interactions, the orthogonal projections in PCA are more likely to be mixtures of physiological effects.…”