Very-low-frequency oscillations in heart rate and blood pressure in periodic breathing: role of the cardiovascular limb of the hypoxic chemoreflex

2000 ◽  
Vol 99 (2) ◽  
pp. 125-132 ◽  
Author(s):  
Darrel P. FRANCIS ◽  
L. Ceri DAVIES ◽  
Keith WILLSON ◽  
Piotr PONIKOWSKI ◽  
Andrew J. S. COATS ◽  
...  

In chronic heart failure, very-low-frequency (VLF) oscillations (0.01–0.04 Hz) in heart rate and blood pressure may be related to periodic breathing, although the mechanism has not been fully characterized. Groups of ten patients with chronic heart failure and ten healthy controls performed voluntary periodic breathing with computer guidance, while ventilation, oxygen saturation, non-invasive blood pressure and RR interval were measured. In air, voluntary periodic breathing induced periodic desaturation and prominent VLF oscillations when compared with free breathing in both patients [RR interval spectral power from 179 to 358 ms2 (P < 0.05); systolic blood pressure (SBP) spectral power from 3.44 to 6.25 mmHg2 (P < 0.05)] and controls [RR spectral power from 1040 to 2307 ms2 (P < 0.05); SBP spectral power from 3.40 to 9.38 mmHg2 (P < 0.05)]. The peak in RR interval occurred 16–26 s before that in SBP, an anti-baroreflex pattern. When the patients followed an identical breathing pattern in hyperoxic conditions to prevent desaturation, the VLF RR interval spectral power was 50% lower (179.0±51.7 ms2; P < 0.01) and the VLF SBP spectral power was 44% lower (3.51±0.77 mmHg2; P < 0.01); similar effects were seen in controls (VLF RR power 20% lower, at 1847±899 ms2, P < 0.05; VLF SBP power 61% lower, at 3.68±0.92 mmHg2, P = 0.01). Low- and high-frequency spectral powers were not significantly affected. Thus periodic breathing causes oxygen-sensitive (and by implication chemoreflex-related) anti-baroreflex VLF oscillations in RR interval and blood pressure in both patients with chronic heart failure and normal controls.

1997 ◽  
Vol 272 (1) ◽  
pp. H438-H447 ◽  
Author(s):  
P. Ponikowski ◽  
T. P. Chua ◽  
M. Piepoli ◽  
A. A. Amadi ◽  
D. Harrington ◽  
...  

Factors responsible for very low frequency oscillations (VLF; cycle > 30 s) in the cardiovascular system remain obscure. We tested the hypothesis that increased peripheral chemosensitivity is important in the pathogenesis of VLF oscillations in patients with chronic heart failure (CHF). Fourteen male patients with stable, moderate to severe CHF (age 60 +/- 1.1 yr, ejection fraction 23 +/- 11%) and reproducible VLF oscillations in heart rate underwent a protocol consisting of three consecutive 20-min phases during which they breathed air, hyperoxia (O2 via mask, 60% O2 concn), and air again. Autoregressive spectral analysis of R-R intervals, blood pressure, and respiration was used to quantify total oscillatory power (TP), VLF, low (0.04-0.15 Hz)- and high (0.15-0.40Hz)-frequency power, and the coherence between these signals. Peripheral chemosensitivity was studied by assessing the ventilatory response to hypoxia using transient inhalations of pure N2. Discrete VLF rhythms were seen in R-R intervals in all 14 patients, in blood pressure in 7 of 14, and in respiration in 8 of 14 patients. A significant coherence (> 0.5) between heart rate and systolic blood pressure within the VLF band with mean phase value of -140 degrees, suggesting an antibaroreflex relationship, was seen in six subjects. Transient hyperoxia abolished the VLF oscillations in most subjects (12 of 14 in R-R intervals) and decreased R-R variability power within the VLF band. This response significantly correlated with peripheral chemoreceptor sensitivity (r = 0.77, P = 0.014). This study suggests that in CHF, enhanced peripheral chemoreceptor activity may facilitate slow oscillations in the cardiorespiratory signals.


2000 ◽  
Vol 99 (2) ◽  
pp. 125 ◽  
Author(s):  
Darrel P. FRANCIS ◽  
L. Ceri DAVIES ◽  
Keith WILLSON ◽  
Piotr PONIKOWSKI ◽  
Andrew J.S. COATS ◽  
...  

1996 ◽  
Vol 91 (4) ◽  
pp. 391-398 ◽  
Author(s):  
Piotr Ponikowski ◽  
Massimo Piepoli ◽  
Aham A. Amadi ◽  
Tuan Peng Chua ◽  
Derek Harrington ◽  
...  

1. In patients with chronic heart failure, heart rate variability is reduced with relative preservation of very-low-frequency power (< 0.04 Hz). Heart rate variability has been measured without acceptable information on its stability and the optimal recording periods for enhancing this reproducibility. 2. To this aim and to establish the optimal length of recording for the evaluation of the very-low-frequency power, we analysed 40, 20, 10 and 5 min ECG recordings obtained on two separate occasions in 16 patients with chronic heart failure. The repeatability coefficient and the variation coefficient were calculated for the heart rate variability parameters, in the time-domain (mean RR, SDRR and pNN50), and in the frequency-domain: very low frequency (< 0.04 Hz), low frequency (0.04–0.15 Hz), high frequency (0.15–0.40 Hz), total power (0–0.5 Hz). 3. Mean RR remained virtually identical over time (variation coefficient 8%). The reproducibility of time-domain (variation coefficient 25–139%) and of spectral measures (variation coefficient 45–111%) was very low. The stability of the heart rate variability parameters was only apparently improved after square root and after log transformation. 4. Very-low-frequency values derived from 5 and 10 min intervals were significantly lower than those calculated from 40 and 20 min intervals (P < 0.005). Discrete very-low-frequency peaks were detected in 11 out of 16 patients on the first 40, 20 and 10 min recording, but only in seven out of 16 when 5 min segments were analysed. 5. The reproducibility of both time or frequency-domain measures of heart rate variability in patients with chronic heart failure may vary significantly. Square root or log-transformed parameters may be considered rather than absolute units in studies assessing the influence of management on heart rate variability profile. Recordings of at least 20 min in stable, controlled conditions are to be recommended to optimize signal acquisition in patients with chronic heart failure, if very-low-frequency power in particular is to be studied.


2012 ◽  
Vol 302 (5) ◽  
pp. R541-R550 ◽  
Author(s):  
Siqi Wang ◽  
David C. Randall ◽  
Charles F. Knapp ◽  
Abhijit R. Patwardhan ◽  
Kevin R. Nelson ◽  
...  

Cardiac and vascular dysfunctions resulting from autonomic neuropathy (AN) are complications of diabetes, often undiagnosed. Our objectives were to: 1) determine sympathetic and parasympathetic components of compromised blood pressure (BP) regulation in patients with peripheral neuropathy and 2) rank noninvasive indexes for their sensitivity in diagnosing AN. We continuously measured electrocardiogram, arterial BP, and respiration during supine rest and 70° head-up tilt in 12 able-bodied subjects, 7 diabetics without, 7 diabetics with possible, and 8 diabetics with definite, sensory, and/or motor neuropathy (D2). During the first 3 min of tilt, systolic BP (SBP) of D2 decreased [−10.9 ± 4.5 (SE) mmHg] but increased in able-bodied (+4.8 ± 5.4 mmHg). Compared with able-bodied, D2 had smaller low-frequency (0.04–0.15 Hz) spectral power of diastolic BP, lower baroreflex effectiveness index (BEI), and more SBP ramps. Except for low-frequency power of SBP, D2 had greater SBP and smaller RR interval harmonic and nonharmonic components at rest across the 0.003- to 0.45-Hz region. In addition, our results support previous findings of smaller HF RR interval power, smaller numbers of baroreflex sequences, and lower baroreflex sensitivity in D2. We conclude that diabetic peripheral neuropathy is accompanied by diminished parasympathetic and sympathetic control of heart rate and peripheral vasomotion and diminished baroreflex regulation. A novel finding of this study lies in the sensitivity of BEI to detect AN, presumably because of its combination of parameters that measure reductions in both sympathetic control of vasomotion and parasympathetic control of heart rate.


2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Ping Cao ◽  
Bailu Ye ◽  
Linghui Yang ◽  
Fei Lu ◽  
Luping Fang ◽  
...  

Objective. The deceleration capacity (DC) and acceleration capacity (AC) of heart rate, which are recently proposed variants to the heart rate variability, are calculated from unevenly sampled RR interval signals using phase-rectified signal averaging. Although uneven sampling of these signals compromises heart rate variability analyses, its effect on DC and AC analyses remains to be addressed. Approach. We assess preprocessing (i.e., interpolation and resampling) of RR interval signals on the diagnostic effect of DC and AC from simulation and clinical data. The simulation analysis synthesizes unevenly sampled RR interval signals with known frequency components to evaluate the preprocessing performance for frequency extraction. The clinical analysis compares the conventional DC and AC calculation with the calculation using preprocessed RR interval signals on 24-hour data acquired from normal subjects and chronic heart failure patients. Main Results. The assessment of frequency components in the RR intervals using wavelet analysis becomes more robust with preprocessing. Moreover, preprocessing improves the diagnostic ability based on DC and AC for chronic heart failure patients, with area under the receiver operating characteristic curve increasing from 0.920 to 0.942 for DC and from 0.818 to 0.923 for AC. Significance. Both the simulation and clinical analyses demonstrate that interpolation and resampling of unevenly sampled RR interval signals improve the performance of DC and AC, enabling the discrimination of CHF patients from healthy controls.


2001 ◽  
Vol 101 (4) ◽  
pp. 429-438 ◽  
Author(s):  
Gianfranco PICCIRILLO ◽  
Mauro CACCIAFESTA ◽  
Marco LIONETTI ◽  
Marialuce NOCCO ◽  
Vincenza DI GIUSEPPE ◽  
...  

As QT variability increases and heart rate variability diminishes, the QT variability index (QTVI)-a non-invasive measure of beat-to-beat fluctuations in QT interval on a single ECG lead-shows a trend towards positive values. Increased QT variability is a risk factor for sudden death. Aging lengthens the QT interval and reduces RR-interval variability. In the present study we investigated the influence of aging and the autonomic nervous system on QT-interval variability in healthy subjects. We studied 143healthy subjects, and divided them into two age ranges (younger and older than 65 years). For each subject we measured two QTVIs: from the q wave to the end of the T wave (QTeVI) and to the apex of the T wave (QTaVI). Both indexes were calculated at baseline and after sympathetic stress. In 10 non-elderly subjects, both QTVIs were determined after β-adrenoreceptor blockade induced by intravenous infusion of propranolol or sotalol. The QTVI was higher in elderly than in younger subjects (P < 0.001). QTVIs obtained during sympathetic stress remained unchanged in the elderly, but became more negative in the younger group (P < 0.05). QTeVI and QTaVI at baseline were correlated positively with age (P < 0.01) and anxiety scores (P < 0.05), but inversely with the low-frequency spectral power of RR-interval variability (P < 0.001). QTVIs were higher in subjects with higher anxiety scores. In younger subjects, sotalol infusion increased both QTVIs significantly, whereas propranolol infusion did not. In conclusion, aging increases QT-interval variability. Whether this change is associated with an increased risk of sudden death remains unclear. The association of abnormal QT-interval variability with anxiety and with reduced low-frequency spectral power of heart rate variability merits specific investigation. In healthy non-elderly subjects, acute sympathetic stress (tilt) decreases the QTVI. β-Adrenoreceptor blockade inhibits this negative trend, thus showing its sympathetic origin. Because a negative trend in QTVI induced by sympathetic stress increases only in younger subjects, it could represent a protective mechanism that is lost with aging.


1997 ◽  
Vol 92 (6) ◽  
pp. 543-550 ◽  
Author(s):  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
John S. Floras

1. There is a substantial non-harmonic or fractal component to the variability of both heart rate and blood pressure in normal subjects. Heart rate is the more complex of these two signals, with respect to the slope, β, of the 1/fβ relationship. In congestive heart failure, heart rate spectral power is attenuated, but the fractal and harmonic components of heart rate and systolic blood pressure variability have not been characterized. 2. Two groups, each comprising 20 men, were studied during 15 min of supine rest and spontaneous respiration: one with functional class II—IV heart failure (age 52 ± 2 years; mean ± SEM) and a second group of healthy men (age 46 ± 2 years). 3. Total spectral power for heart rate was significantly reduced in heart failure (P < 0.02), whereas total spectral power for systolic blood pressure was similar in the two groups. In both heart failure and normal subjects, 65–80% of total spectral power in these two signals displayed fractal characteristics. 4. In heart failure, the slope of the 1/fβ relationship for heart rate was significantly steeper than in normal subjects (1.40 ± 0.08 compared with 1.14 ± 0.05; P < 0.05), indicating reduced complexity of the fractal component of heart rate variability. There was no significant difference in the 1/fβ slope for systolic blood pressure variability between these two groups, but the blood pressure signals were less complex than heart rate variations in both heart failure (2.31 ± 0.15; P < 0.006) and normal subjects (2.47 ± 0.15; P < 0.0001). 5. Parasympathetic nervous system activity, as estimated from heart rate variability was reduced (P < 0.01) in patients with heart failure, whereas trends towards increased sympathetic nervous system activity and decreased non-harmonic power were not significant. 6. The non-harmonic components of cardiac frequency are reduced in heart failure. Non-harmonic power is not attenuated, but the complexity of the heart rate signal is less than in subjects with normal ventricular function. A reduction in parasympathetic modulation appears to contribute to this loss of complexity of heart rate. Consequently, the heart rate signal comes to resemble that of blood pressure. In contrast, the variability and complexity of the systolic blood pressure signal is similar in heart failure and normal subjects. This reduced complexity of heart rate variability may have adverse implications for patients with heart failure.


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