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

The arterial baroreflex buffers slow (<0.05 Hz) blood pressure (BP) fluctuations, mainly by controlling peripheral resistance. Baroreflex sensitivity (BRS), an important characteristic of baroreflex control, is often noninvasively assessed by relating heart rate (HR) fluctuations to BP fluctuations; more specifically, spectral BRS assessment techniques focus on the BP-to-HR transfer function around 0.1 Hz. Skepticism about the relevance of BRS to characterize baroreflex-mediated BP buffering is based on two considerations: 1) baroreflex-modulated peripheral vasomotor function is not necessarily related to baroreflex-HR transfer; and 2) although BP fluctuations around 0.1 Hz (Mayer waves) might be related to baroreflex BP buffering, they are merely a not-intended side effect of a closed-loop control system. To further investigate the relationship between BRS and baroreflex-mediated BP buffering, we set up a computer model of baroreflex BP control to simulate normal subjects and heart failure patients. Output variables for various randomly chosen combinations of feedback gains in the baroreflex arms were BP resonance, BP-buffering capacity, and BRS. Our results show that BP buffering and BP resonance are related expressions of baroreflex BP control and depend strongly on the sympathetic gain to the peripheral resistance. BRS is almost uniquely determined by the vagal baroreflex gain to the sinus node. In conclusion, BP buffering and BRS are unrelated unless coupled gains in all baroreflex limbs are assumed. Hence, the clinical benefit of a high BRS is most likely to be attributed to vagal effects on the heart instead of to effective BP buffering.

Thoracic sympathectomy: effects on hemodynamics and baroreflex control.

UNLABELLED: Endoscopic thoracic sympathectomy at T2-T4 is an effective and safe treatment for primary axillary and palmar hyperhidrosis and facial blushing refractory to conventional treatment. T2 and T4 ganglia however are in the direct pathway of sympathetic innervation of the heart and part of the vasomotor nerves. In this study we investigate possible changes in steady-state hemodynamics as well as in beat-to-beat cardiovascular control after thoracoscopic sympathectomy of T2-T4. In 12 patients we measured continuously heart rate (HR) and blood pressure (BP) (non-invasively with Finapres) during rest and during deep inspiration, in supine and sitting position as well as during a change from lying to standing. Stroke volume (SV) and total peripheral resistance (TPR) were estimated from the BP recordings by the Modelflow method. Markers for cardiovascular control were obtained from power and cross-spectra of BP and HR. After sympathectomy, only in the sitting position was mean HR decreased, while TPR and BP (diastolic and mean) were lower in the supine as well as sitting positions. SV clearly increased. Low frequency power in HR and BP was significantly decreased, just like the max/min ratio in HR after standing up, indicating a diminished capacity in sympathetic vasomotor control. High frequency power of HR as well as baroreflex sensitivity, both parasympathetic markers, did not change in a statistically significant manner. CONCLUSION: Besides altering steady-state hemodynamics, a thoracic sympathectomy causes relatively small, though measurable changes in cardiovascular control, in particular of peripheral vasomotion.