Abstract
Cardioventilatory coupling is the temporal alignment between inspiratory onset and preceding heart beat, and is a determinant of ventilatory timing. Although investigated in anaesthetised and resting individuals, as well as animals, few studies have examined cardioventilatory coupling during sleep. This thesis aimed to further work in this area by investigating the cardioventilatory coupling during sleep.
In the first study, 30 healthy individuals (14 male; 16 female) aged 18-35 years and nine healthy individuals (4 male; 5 female) aged 60-75 years underwent a level II polysomnographic study in their own home. Cardioventilatory coupling was observed to some degree in all healthy individuals. In young adults, strength of coupling (χ2(3) = 12.71, p = 0.005) and the proportion of the night spent coupling (χ2(3) = 9.80, p = 0.02) differed significantly between wakefulness, light sleep, slow wave sleep (SWS) and REM sleep. Post hoc analyses indicated that coupling strength and the proportion of the night spent coupling during light sleep and slow wave sleep, was significantly different to that during wakefulness. Decreased strength of cardioventilatory coupling was observed with increasing time post sleep onset (Spearman, r = 0.20, p = 0.003). Cardioventilatory coupling did not differ between the young and older age groups, or with gender.
In the second study, 14 (6 male; 8 female) of these individuals aged 18-35 years underwent an additional home-based polysomnographic study, 14 days after the first study. In these individuals, both strength of cardioventilatory coupling (ICC = 0.671, p = 0.003), and proportion of the night spent coupling (ICC = 0.770, p < 0.001), were moderately repeatable from Night 1 to Night 2.
In the third study, cardioventilatory coupling was examined in 151 individuals with sleep-disordered breathing (SDB). Cardioventilatory coupling was observed to some degree in all but one individual with SDB. Decreased strength of coupling (Spearman, r = -0.33, p < 0.001) and decreased proportion of the night spent coupling (Spearman, r = -0.39, p < 0.001) was observed with increasing apnoea hypopnoea index. As with healthy individuals, both the strength of coupling (χ2(3) = 12.95, p = 0.005) and the proportion of the night spent coupling (χ2(3) = 19.37, p < 0.001) differed significantly between wakefulness, light sleep, SWS and REM sleep, in individuals with SDB. Coupling strength was increased during light sleep, compared to wakefulness and REM sleep.
It is concluded that cardioventilatory coupling is a phenomenon observed in most individuals during sleep, but a large degree of inter-individual variability is exhibited in strength of coupling and the proportion of the night spent coupling. In healthy individuals, coupling is observed as a moderately repeatable phenomenon from night-to-night. Increasing severity of SDB is associated with decreased cardioventilatory coupling, which may be reflective of changes in autonomic activity observed with SDB. Together, these findings have identified a number of areas for future investigation, which could provide useful insights into ventilatory control during sleep.