Transfer function analysis of the circulation: unique insights into cardiovascular regulation

TLDR

A simple circulatory control model based on previously published transfer functions explains most of the observed findings. The study aimed to investigate how the autonomic nervous system shapes respiratory sinus arrhythmia and its complex interactions with arterial pressure by measuring transfer functions among respiration, heart rate, and various arterial pressure components in 14 healthy subjects during controlled, erratic breathing. Transfer‑function analysis was performed while applying pharmacological autonomic blockade (atropine, propranolol, or both) and altering posture to delineate sympathetic and vagal contributions and to separate mechanical respiration–pressure links from RSA effects. The results showed that sympathetic heart‑rate responses were attenuated above 0.1 Hz with phase delay, vagal modulation had higher magnitude without delay, and both mechanical respiration–pressure links and RSA significantly influenced arterial pressure, with RSA effects prominent under vagal modulation, mechanical effects tied to negative lung‑volume change, larger during systole, and greater in standing than supine.

Abstract

We have demonstrated previously that transfer function analysis can be used to precisely characterize the respiratory sinus arrhythmia (RSA) in normal humans. To further investigate the role of the autonomic nervous system in RSA and to understand the complex links between respiratory activity and arterial pressure, we determined the transfer functions between respiration, heart rate (HR), and phasic, systolic, diastolic, and pulse arterial pressures in 14 healthy subjects during 6-min periods in which the respiratory rate was controlled in a predetermined but erratic fashion. Pharmacological autonomic blockade with atropine, propranolol, and both, in combination with changes in posture, was used to characterize the sympathetic and vagal contributions to these relationships, as well as to dissect the direct mechanical links between respiration and arterial pressure from the effects of the RSA on arterial pressure. We found that 1) the pure sympathetic (standing + atropine) HR response is characterized by markedly reduced magnitude at frequencies greater than 0.1 Hz and a phase delay, whereas pure vagal (supine + propranolol) modulation of HR is characterized by higher magnitude at all frequencies and no phase delay; 2) both the mechanical links between respiration and arterial pressure and the RSA contribute significantly to the effects of respiration on arterial pressure; 3) the RSA contribution to arterial pressure fluctuations is significant for vagal but not for sympathetic modulation of HR; 4) the mechanical effects of respiration on arterial pressure are related to the negative rate of change of instantaneous lung volume; 5) the mechanical effects have a higher magnitude during systole than during diastole; and 6) the mechanical effects are larger in teh standing than the supine position. Most of these findings can be explained by a simple model of circulatory control based on previously published experimental transfer functions from our laboratory.