Cardiorespiratory coupling improves cardiac pumping efficiency in heart failure

TL;DR

This study demonstrates that artificially restoring respiratory sinus arrhythmia enhances cardiac efficiency in heart failure models by reducing energy dissipation and increasing cardiac output, especially at low heart rates.

Contribution

It provides new insights into the functional role of RSA and shows how modulating cardiorespiratory coupling can improve cardiac performance in heart failure.

Findings

RSA reduces cardiac power dissipation.

Cardiac output increases with RSA magnitude.

RSA is most effective at low cardiac frequencies.

Abstract

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.