RR interval-respiratory signal waveform modeling in human slow paced and spontaneous breathing.

Our aim was to model the dependence of respiratory sinus arrhythmia (RSA) on the respiratory waveform and to elucidate underlying mechanisms of cardiorespiratory coupling. In 30 subjects, RR interval and respiratory signal were recorded during spontaneous and paced (0.1Hz/0.15Hz) breathing and their relationship was modeled by a first order linear differential equation. This model has two parameters: a0 (related to the instantaneous degree of abdominal expansion) and a1 (referring to the speed of abdominal expansion). Assuming that a0 represents slowly adapting pulmonary stretch receptors (SARs) and a1 SARs in coordination with other stretch receptors and central integrative coupling; then pulmonary stretch receptors relaying the instantaneous lung volume are the major factor determining cardiovagal output during inspiration. The model's results depended on breathing frequency with the least error occurring during slow paced breathing. The role of vagal afferent neurons in cardiorespiratory coupling may relate to neurocardiovascular diseases in which weakened coupling among venous return, arterial pressure, heart rate and respiration produces cardiovagal instability.