Respiratory sinus arrhythmia in humans: an obligatory role for vagal feedback from the lungs

Abstract

Respiratory sinus arrhythmia (RSA) is used as a noninvasive measure of vagal cardiac input, but its causative mechanisms in humans remain undetermined. We compared the RSA of five lung-denervated double-lung transplant patients with intact hearts to six normal (N) control subjects, five heart-denervated patients, and two liver transplant patients at matched tidal volumes (VT's) and breathing frequencies. In N and liver transplant subjects, RSA was significant during eupnea and increased two- to threefold with increasing VT and inspiratory effort. In heart- and lung-denervated subjects, RSA at eupnea was significant but was only 53% of that in N subjects and was not respondent to changing VT, inspiratory effort, or breathing frequency. We also compared the RSA of N subjects during voluntary (active) and passive positive pressure ventilation at normocapnia. RSA was reduced from 11 +/- 2.2 beats/min during active ventilation to 5.4 +/- 0.8 beats/min during PPV. We conclude that vagal feedback from pulmonary stretch receptors is obligatory for the generation of a neurally mediated RSA in awake humans at normal and raised levels of VT and respiratory motor output. In intact humans, we also hypothesize an important effect for nonpulmonary central and/or peripheral modulation of RSA. It is likely that the key mechanisms for neurally mediated RSA in unanesthetized humans are mutually dependent.

CO2-dependent components of sinus arrhythmia from the start of breath holding in humans

“…to sinus arrhythmia are reduced during breath holding [with the absence of pulmonary stretch (7) and the ensuing mechanical sequelae (4,8,9,45)]. We also confirmed previous studies (37,40,47) showing that there is also significantly more power 0.01 to 0.5 Hz below the eupneic frequency range during breath holding, demonstrating that a number of oscillators may continue to have some influence on sinus arrhythmia at a range of frequencies during breath holding.…”

“…SINUS ARRHYTHMIA IS PRONOUNCED during spontaneous breathing (11,35,36,46); its respiratory frequency components follow changes in breathing frequency (5,20,27,35,45) and have pronounced CO 2 dependency (41). This evidence suggests that sinus arrhythmia receives a substantial contribution from the central respiratory rhythm.…”

Compression on trigger points in the leg muscle increases parasympathetic nervous activity based on heart rate variability

“…Burst firing of the parasympathetic nerve (vagal nerve) disappears or decreases during inspiration, and the HR variability associated with the disappearance or decrease of the burst firing is observed as the HF component (i.e., respiratory sinus arrhythmia). Thus, the HF component of HR variability is dependent on breathing, and the influence of respiration on HR variability is considered to be an index of the influence of parasympathetic activity on HR variability [29][30][31]. Therefore, we analyzed a transfer function between ILV and HR.…”

Quantification of Cardiorespiratory Interactions Based on Joint Symbolic Dynamics

“…8 Neural RSA mechanisms are well established: it is vagally mediated, with inputs to cardiac vagal neurons from both central pattern generator 35 and from peripheral airways and lung stretch receptors. 46 Cardiorespiratory phase coordination/synchronization is a phenomenon, which was initially described as short intermittent periods 22,44 during which the phases of heart rate and respiratory rate coincide with different integer ratios known as phase locking ratios. 13,31,43 Cardiorespiratory phase coordination/ synchronization has been reported in healthy adults, 28,31 athletes, 43,44 infants, 34 and in anesthetized 45 and conscious rats.…”