Abstract
The precise mechanisms connecting the cardiovascular system and the cerebrospinal fluid (CSF) are not well understood in detail. This paper investigates the couplings between the cardiac and respiratory components, as extracted from blood pressure (BP) signals and oscillations of the subarachnoid space width (SAS), collected during slow ventilation and ventilation against inspiration resistance. The experiment was performed on a group of 20 healthy volunteers (12 females and 8 males; BMI kg/m; age years). We analysed the recorded signals with a wavelet transform. For the first time, a method based on dynamical Bayesian inference was used to detect the effective phase connectivity and the underlying coupling functions between the SAS and BP signals. There are several new findings. Slow breathing with or without resistance increases the strength of the coupling between the respiratory and cardiac components of both measured signals. We also observed increases in the strength of the coupling between the respiratory component of the BP and the cardiac component of the and vice versa. Slow breathing synchronises the SAS oscillations, between the brain hemispheres. It also diminishes the similarity of the coupling between all analysed pairs of oscillators, while inspiratory resistance partially reverses this phenomenon. BP–SAS and SAS–BP interactions may reflect changes in the overall biomechanical characteristics of the brain.
Highlights
Variations in beat-to-beat interval evoked by rhythmic breathing that occurs during a respiratory cycle were described in the middle of the nineteenth century [1]
We recently demonstrated that ventilation at 0.1 Hz diminishes cardiac component of the blood pressure (BP) and subarachnoid space width (SAS) oscillations
Negative value of D(t) means that respiration mode drives the cardiac mode and this is a predominant direction of coupling for those signals
Summary
Variations in beat-to-beat interval evoked by rhythmic breathing that occurs during a respiratory cycle were described in the middle of the nineteenth century [1]. The heart rate (HR) decelerates during expiration and accelerates during inspiration [2]. It is a well known phenomena in physiology—respiratory sinus arrhythmia (RSA). When the breathing frequency slows down to 6 breaths/min, the amplitude of the heart rate variability (HRV) reaches its maximum. Slow breathing has been believed to have a beneficial effects on mental relaxation through the enhancement of autonomic, cerebral and psychological flexibility (reviewed in [5]). Hinterberge et al (2019) demonstrated that decelerated breathing at 0.1 Hz promotes synchronisation between breathing, RSA and slow cortical potentials. Respiratory activity crucially regulates the flow of cerebrospinal fluid (CSF, see the review in [6,7])
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