Abstract
Spontaneous oscillations of blood pressure (BP) and interbeat interval (IBI) may reveal important information on the underlying baroreflex control and regulation of BP. We evaluated the method of continuously measured instantaneous baroreflex sensitivity by cross correlation (xBRS) validating its mean value against the gold standard of phenylephrine (Phe) and nitroprusside (SNP) bolus injections, and focusing on its spontaneous changes quantified as variability around the mean. For this purpose, we analyzed data from an earlier study of eight healthy males (aged 25–46 years) who had received Phe and SNP in conditions of baseline and autonomic blocking agents: atropine, propranolol, and clonidine. Average xBRS corresponds well to Phe/SNP‐BRS, with xBRS levels ranging from 1.2 (atropine) to 102 msec/mmHg (subject asleep under clonidine). Time shifts from BP‐ to IBI‐signal increased from ≤1 sec (maximum correlations within the current heartbeat) to 3–5 sec (under atropine). Plotted on a logarithmic vertical scale, xBRS values show 40% variability (defined as SD/mean) over the whole range in the various conditions, except twice when the subjects had fallen asleep and it dropped to 20%. The xBRS oscillates at frequencies of 0.1 Hz and lower, dominant between 0.02–0.05 Hz. Although xBRS is the result of IBI/BP‐changes, no linear coherence was found in the cross‐spectra of the xBRS‐signal and IBI or BP. We speculate that the level of variability in the xBRS‐signal may act as a probe into the central nervous condition, as evidenced in the two subjects who fell asleep with high xBRS and only 20% of relative variation.
Highlights
The sensitivity of the arterial baroreceptor-heart rate reflex or cardiac baroreflex sensitivity (BRS) is calculated from the ratio of the heart period changes subsequent to systolic blood pressure changes in msec/ mmHg
It was predicted that the timeaveraged values of xBRS would follow the Phe/SNP BRS-results, that the variance of xBRS would change in relation to its mean level and that reflex delay would increase from 0 to 1 sec at normal resting heart rates to 3–4 sec under atropine and it would decrease to the shortest values at longer resting intervals, under propranolol and clonidine (Cividjian et al 2011)
The strength of the effect of atropine is variable per subject ranging from a factor 5 to 27 (5–34 for xBRS)
Summary
The sensitivity of the arterial baroreceptor-heart rate reflex or cardiac baroreflex sensitivity (BRS) is calculated from the ratio of the heart period changes subsequent to systolic blood pressure changes in msec/ mmHg. We applied xBRS to this data set to assess xBRS for accuracy and its apparent reflex delay in establishing “true” baroreflex sensitivity, while at the same time assessing the variability of the values under various forms of autonomic blockade. It was predicted that the timeaveraged values of xBRS would follow the Phe/SNP BRS-results, that the variance of xBRS would change in relation to its mean level and that reflex delay would increase from 0 to 1 sec at normal resting heart rates to 3–4 sec under atropine and it would decrease to the shortest values at longer resting intervals, under propranolol and clonidine (Cividjian et al 2011). We applied a Fourier transform to the sequentially measured BRS-values to unmask possibly recurrent oscillations in an ostensibly random signal, comparing this to the underlying interbeat interval – and blood pressure signals by cross-spectral analysis
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