Respiratory heart rate variability may improve cardiac power efficiency

In humans, the cardiac and respiratory rhythms are controlled by the central nervous system and interact viscoelastically through the pulmonary vasculature. The former coupling gives rise to respiratory sinus arrhythmia (RSA) which is characterised by a lower heart rate during the expiratory phase and phasic synchronization of heart beats to the respiratory cycle. The functional significance of RSA has however remained unclear. Here, we aim to address this question by computing the cardiac power dissipated in the pulmonary vasculature under RSA pacing and by comparing it to the power dissipated under monotonic pacing. We find that RSA decreases the workload of the right ventricle by minimizing the dynamic stress on alveoli capillaries. Our simulation predicts a power gain comparable to that observed in-vivo when RSA is restored by a pacemaker.