Mechanism of blood pressure and R-R variability: insights from ganglion blockade in humans

Abstract

Spontaneous blood pressure (BP) and R-R variability are used frequently as 'windows' into cardiovascular control mechanisms. However, the origin of these rhythmic fluctuations is not completely understood. In this study, with ganglion blockade, we evaluated the role of autonomic neural activity versus other 'non-neural' factors in the origin of BP and R-R variability in humans. Beat-to-beat BP, R-R interval and respiratory excursions were recorded in ten healthy subjects (aged 30 +/- 6 years) before and after ganglion blockade with trimethaphan. The spectral power of these variables was calculated in the very low (0.0078-0.05 Hz), low (0.05-0.15 Hz) and high (0.15-0.35 Hz) frequency ranges. The relationship between systolic BP and R-R variability was examined by cross-spectral analysis. After blockade, R-R variability was virtually abolished at all frequencies; however, respiration and high frequency BP variability remained unchanged. Very low and low frequency BP variability was reduced substantially by 84 and 69 %, respectively, but still persisted. Transfer function gain between systolic BP and R-R interval variability decreased by 92 and 88 % at low and high frequencies, respectively, while the phase changed from negative to positive values at the high frequencies. These data suggest that under supine resting conditions with spontaneous breathing: (1) R-R variability at all measured frequencies is predominantly controlled by autonomic neural activity; (2) BP variability at high frequencies (> 0.15 Hz) is mediated largely, if not exclusively, by mechanical effects of respiration on intrathoracic pressure and/or cardiac filling; (3) BP variability at very low and low frequencies (< 0.15 Hz) is probably mediated by both sympathetic nerve activity and intrinsic vasomotor rhythmicity; and (4) the dynamic relationship between BP and R-R variability as quantified by transfer function analysis is determined predominantly by autonomic neural activity rather than other, non-neural factors.

Figure 1

Representative changes in arterial pressure (ABP) and heart rate (HR) during the Valsalva manoeuvre. A, before ganglion blockade; B, after ganglion blockade.

Figure 2

Representative time series of systolic pressure (SBP) and R-R interval before (A and C) and after (B and D) ganglion blockade.

Figure 3

Representative spectra of SBP and R-R interval variability before (A and C) and after (B and D) ganglion blockade. Data are from the same subject as in Fig. 2. Note that the y-axis scale of D is 1/20 of that of C after ganglion blockade.

Figure 4

Group averaged spectra of SBP (A) and R-R interval (B) variability before (continuous lines) and after (dashed lines) ganglion blockade. Dotted lines, s.e.m. Note that the plots in the insets have ‘zoomed’ scales at the frequencies from 0.15 to 0.35 Hz for the SBP spectrum in A and for the R-R spectrum in B.

Figure 5

Group averaged transfer function gain (A), phase (B) and coherence (C) before (continuous lines) and after (dashed lines) ganglion blockade. Dotted lines, s.e.m.

Figure 6

Direct recordings of ABP, R-R interval and respiration at baseline (left), and during trimethaphan (middle) and trimethaphan plus phenylephrine (right) infusion.

Figure 7

Group averaged spectra of SBP (A) and R-R interval (B) variability from three subjects at baseline (continuous lines), and during trimethaphan (dashed lines) and trimethaphan plus phenylephrine (dotted lines) infusion.