Heart rate variability is thought to be mediated by both vagal and sympathetic activity, through both phasic and tonic stimulation of the sino-atrial node. Decomposition of heart rate variability by power spectral analysis techniques has shown fluctuations related to the respiratory pattern, expression of respiratory sinus arrhythmia (RSA) and oscillations related to blood pressure (between 0.03 and 0.15 Hz). Under physiologic conditions, low- and high frequency peaks can be considered as relative markers of sympathetic and parasympathetic activity, respectively.

The purpose of our study was to investigate whether high frequency oscillations are dependent on vagal activity also in critical conditions (i.e. low heart rate variability). In 6/6 recently heart-transplantated subjects we found a residual RSA which increased during moderate bicycle exercise. To assess its mechanical determinants, in 15 urethane-anaesthetized, vagotomized and mechanically-ventilated rabbits we measured the influence on RSA of changes in right atrial pressure, induced by changes in tidal volumes (Vt: 20-60m1) and respiratory frequency (RF: 10-30/min). RSA was present in all recordings, it was dependent on both RF and Vt (p<0.01 and p<0.001, respectively) and correlated with right atrial pressure variability (r=0.62, p<0.001).

Similarly, patients with severe autonomic dysfunction and low heart rate variability show a well evident RSA which can not be abolished by injection of atropine. In absence of parasympathetic drive to the heart RSA does persist and is proportional to changes in ventilation through phasic changes in right atrial pressure, supporting the hypothesis that atrial stretch can be a secondary source of RSA.