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

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.

Circadian affective, cardiopulmonary, and cortisol variability in depressed and nondepressed individuals at risk for cardiovascular disease

“…The parameters were transformed by natural logarithm to produce an approximately normal distribution. Since variations in respiration can bias the relationship between traditional spectral measures and vagal activity (Grossman & Taylor, 2007), transfer-function RSA (TF-RSA) was quantified as the magnitude of the transfer function relating RR-interval oscillations to tidal volume oscillations at the peak respiratory frequency (Saul et al, 1991). TF-RSA data were excluded if spectral coherence between tidal volume and RR-interval was below 0.5 (Rottenberg, Wilhelm, Gross, & Gotlib, 2002), because less coherence would indicate sources for RR-interval variation other than respiration.…”

Risk factors for atherogenesis and cardiovascular autonomic function in persons with spinal cord injury

“…Power spectral analysis of BPV provides another tool for assessing the relationship between the autonomic and vascular systems. 164,165 The low frequency systolic blood pressure (LF SBP ) component of BPV represents sympathetic vasomotor tone, while the high frequency (HF SBP ) component depicts the mechanical e ects of respiration on blood pressure. Because HRV methods only isolate cardiac vagal activity (HF RRI ), a combination of the LF SBP component of BPV and the HF RRI component of HRV provides a more complete picture of parasympathetic and sympathetic cardiovascular regulation.…”

Baroreflex sensitivity, blood pressure buffering, and resonance: what are the links? Computer simulation of healthy subjects and heart failure patients

“…It appears that BRS (the TF between 0.05 and 0.15 Hz) may lower with high sympathetic gain to the heart. This is caused by the differences in the latencies/time constants in the sympathetic (17,41) and vagal (6,48) limbs, bringing the vagal and the sympathetic effects in counterphase in the BRS frequency band. Hence, there are situations thinkable in which cancellation of vagal effects on heart rate by concurring sympathetic effects on heart rate in counterphase incorrectly suggest a deficient baroreflex.…”