Hemodynamic regulation: investigation by spectral analysis

TLDR

We investigated whether beat‑to‑beat variability in hemodynamic parameters reflects the dynamic interplay between ongoing circulatory perturbations and short‑term cardiovascular control, and proposed a simple closed‑loop model evaluated via pharmacological blockades of parasympathetic, alpha‑, beta‑sympathetic, and renin‑angiotensin systems to examine spectral changes. Spontaneous fluctuations in heart rate, arterial blood pressure, and respiration were analyzed by spectral analysis in the 0.02–1 Hz range, and a simple closed‑loop model of short‑term cardiovascular control was evaluated using pharmacological blockades and atrial pacing to isolate blood‑pressure variability independent of heart rate. Respiratory‑frequency heart‑rate fluctuations are parasympathetically mediated, while corresponding blood‑pressure fluctuations arise mainly from centrally mediated heart‑rate changes; the sympathetic system is too sluggish to mediate respiratory‑frequency variations, whereas low‑frequency heart‑rate fluctuations are jointly mediated by parasympathetic and beta‑sympathetic activity and compensate for low‑frequency blood‑pressure fluctuations, which are largely due to vasomotor variability damped by the renin‑angiotensin system and remain unchanged by alpha‑adrenergic blockade.

Abstract

We investigated the hypothesis that beat-to-beat variability in hemodynamic parameters reflects the dynamic interplay between ongoing perturbations to circulatory function and the compensatory response of short-term cardiovascular control systems. Spontaneous fluctuations in heart rate (HR), arterial blood pressure, and respiration were analyzed by spectral analysis in the 0.02- to 1-Hz frequency range. A simple closed-loop model of short-term cardiovascular control was proposed and evaluated in a series of experiments: pharmacological blockades of the parasympathetic, alpha-sympathetic, beta-sympathetic, and renin-angiotensin systems were used to open the principal control loops in order to examine changes in the spectral pattern of the fluctuations. Atrial pacing was used to examine blood pressure variability in the absence of HR variability. We found that respiratory frequency fluctuations in HR are parasympathetically mediated and that blood pressure fluctuations at this frequency result almost entirely from the direct effect of centrally mediated HR fluctuations. The sympathetic nervous system appears to be too sluggish to mediate respiratory frequency variations. Low-frequency (0.02-0.09 Hz) fluctuations in HR are jointly mediated by the parasympathetic and beta-sympathetic systems and appear to compensate for blood pressure fluctuations at this frequency. Low-frequency blood pressure fluctuations are probably due to variability in vasomotor activity which is normally damped by renin-angiotensin system activity. Blockade of the alpha-adrenergic system, however, does not significantly alter low-frequency blood pressure fluctuations.