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Andrew Lefevre

Publications and source records attributed to Andrew Lefevre.

2 recordsLinked to original sources

Synchronization-dissipation dynamics in the cardiorespiratory system

Dissipative coupling is known to induce synchronization. Conversely it may be hypothesized that oscillators driven to synchronize may reduce power dissipation in their coupling. The latter scenario is realized in the human cardiorespiratory system where cardiac and respiratory rhythms are controlled by the central nervous system while interacting viscoelastically through the pulmonary vasculature. Here we examine the functional significance of this coupling which is observed in respiratory sinus arrhythmia (RSA). By modelling electrical and viscoelastic interactions within the cardiorespiratory system, we identify the conditions leading to synchronization. We demonstrate that, when present, synchronization reduces cardiac power losses by 10% in humans and up to 55% in other species. The predicted gain in cardiac output is compared to the gain observed in-vivo by pacing the heart with a device restoring RSA. It is therefore surmised that RSA may improve cardiac pumping efficiency by reducing dynamic stress and power dissipation in the pulmonary vasculature.

physics.bio-ph

Cardiorespiratory coupling improves cardiac pumping efficiency in heart failure

Recent trials of a neuronal pacemaker have shown that cardiac pumping efficiency increases when respiratory sinus arrhythmia (RSA) is artificially restored in animal models of heart failure. This novel device sheds new light on the functional role of RSA, which has long been debated, by allowing the strength of cardiorespiratory coupling to be artificially varied. Here we show that RSA minimizes the cardiac power dissipated within the cardiovascular network. The cardiorespiratory system is found to exhibit mode-locked synchronized regions within which viscoelastic dissipation is reduced relative to the scenario where cardiorespiratory coupling is absent. We determine the gain in cardiac output as the magnitude of RSA increases. We find that cardiac pumping efficiency improves up and until the cardiac frequency, within each breadth intake, is approximately 1.5 times greater than the cardiac frequency in the expiratory phase, at which point it reaches a plateau. RSA was found to be most effective at low cardiac frequencies, in good agreement with clinical evidence. Simulation of the cardiac power saved under RSA is in good agreement with the 17-20% increase in cardiac output observed in RSA-paced animal models.

q-bio.TO