Supine low-frequency power of heart rate variability reflects baroreflex function, not cardiac sympathetic innervation

2009 ◽  
Vol 76 (4 suppl 2) ◽  
pp. S51-S59 ◽  
Author(s):  
Jeffrey P. Moak ◽  
David S. Goldstein ◽  
Basil A. Eldadah ◽  
Ahmed Saleem ◽  
Courtney Holmes ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sympathetic Innervation ◽  
Low Frequency ◽  
Cardiac Sympathetic Innervation ◽  
Baroreflex Function ◽  
Low Frequency Power ◽  
Frequency Power

scholarly journals Supine low-frequency power of heart rate variability reflects baroreflex function, not cardiac sympathetic innervation

Heart Rhythm ◽  
2007 ◽  
Vol 4 (12) ◽  
pp. 1523-1529 ◽  
Author(s):  
Jeffrey P. Moak ◽  
David S. Goldstein ◽  
Basil A. Eldadah ◽  
Ahmed Saleem ◽  
Courtney Holmes ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sympathetic Innervation ◽  
Low Frequency ◽  
Cardiac Sympathetic Innervation ◽  
Baroreflex Function ◽  
Low Frequency Power ◽  
Frequency Power

Normalized Low Frequency Power of Heart Rate Variability Correlates Negatively With the SOFA Score in Severe Sepsis and Septic Shock

CHEST Journal ◽  
2011 ◽  
Vol 140 (4) ◽  
pp. 427A
Author(s):  
Subhasis Behera ◽  
Samuel Brown ◽  
Jason Jones ◽  
Michael Lanspa ◽  
Kathryn Kuttler ◽  
...  
Keyword(s):  
Heart Rate ◽  
Septic Shock ◽  
Heart Rate Variability ◽  
Severe Sepsis ◽  
Sofa Score ◽  
Low Frequency ◽  
Low Frequency Power ◽  
Sepsis And Septic Shock ◽  
Frequency Power

Reproducibility of Heart Rate Variability Measures in Patients with Chronic Heart Failure

1996 ◽  
Vol 91 (4) ◽  
pp. 391-398 ◽  
Author(s):  
Piotr Ponikowski ◽  
Massimo Piepoli ◽  
Aham A. Amadi ◽  
Tuan Peng Chua ◽  
Derek Harrington ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Chronic Heart Failure ◽  
Time Domain ◽  
Low Frequency ◽  
Variation Coefficient ◽  
Very Low Frequency ◽  
Low Frequency Power ◽  
Frequency Power

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.

Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity

1999 ◽  
Vol 276 (1) ◽  
pp. H215-H223 ◽  
Author(s):  
Melanie S. Houle ◽  
George E. Billman
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Ventricular Fibrillation ◽  
Sympathetic Activity ◽  
Low Frequency ◽  
Frequency Component ◽  
Atropine Sulfate ◽  
Low Frequency Power ◽  
Heart Rate Variability Spectrum ◽  
Frequency Power

The low-frequency component of the heart rate variability spectrum (0.06–0.10 Hz) is often used as an accurate reflection of sympathetic activity. Therefore, interventions that enhance cardiac sympathetic drive, e.g., exercise and myocardial ischemia, should elicit increases in the low-frequency power. Furthermore, because an enhanced sympathetic activation has been linked to an increased propensity for malignant arrhythmias, one might also predict a greater low-frequency power in animals that are susceptible to ventricular fibrillation than in resistant animals. To test these hypotheses, a 2-min coronary occlusion was made during the last minute of exercise in 71 dogs with healed myocardial infarctions: 43 had ventricular fibrillation (susceptible) and 28 did not experience arrhythmias (resistant). Exercise or ischemia alone provoked significant heart rate increases in both groups of animals, with the largest increase in the susceptible animals. These heart rate increases were attenuated by β-adrenergic receptor blockade. Despite the sympathetically mediated increases in heart rate, the low-frequency power decreased, rather than increased, in both groups, with the largest decrease again in the susceptible animals: 4.0 ± 0.2 (susceptible) vs. 4.1 ± 0.2 ln ms2 (resistant) in preexercise control and 2.2 ± 0.2 (susceptible) vs. 2.9 ± 0.2 ln ms2 (resistant) at highest exercise level. In a similar manner the parasympathetic antagonist atropine sulfate elicited significant reductions in the low-frequency power. Although sympathetic nerve activity was not directly recorded, these data suggest that the low-frequency component of the heart rate power spectrum probably results from an interaction of the sympathetic and parasympathetic nervous systems and, as such, does not accurately reflect changes in the sympathetic activity.

Heart Rate Variability as a Predictor of Cardiac Dysrhythmias During Weaning From Mechanical Ventilation

2015 ◽  
Vol 24 (2) ◽  
pp. 118-127 ◽  
Author(s):  
Muna H. Hammash ◽  
Debra K. Moser ◽  
Susan K. Frazier ◽  
Terry A. Lennie ◽  
Melanie Hardin-Pierce
Keyword(s):  
Heart Rate ◽  
Mechanical Ventilation ◽  
Heart Rate Variability ◽  
Low Frequency ◽  
Weaning From Mechanical Ventilation ◽  
Cardiac Dysrhythmias ◽  
Ectopic Beats ◽  
The Mean ◽  
Low Frequency Power ◽  
Frequency Power

BackgroundWeaning from mechanical ventilation to spontaneous breathing is associated with changes in the hemodynamic and autonomic nervous systems that are reflected by heart rate variability. Although cardiac dysrhythmias are an important manifestation of hemodynamic alterations, the impact of heart rate variability on the occurrence of dysrhythmias during weaning has not been specifically studied.ObjectivesTo describe differences in heart rate variability spectral power and occurrence of cardiac dysrhythmias at baseline and during the initial trial of weaning from mechanical ventilation and to evaluate the impact of heart rate variability during weaning on occurrence of dysrhythmias.MethodContinuous 3-lead electrocardiographic recordings were collected from 35 patients receiving mechanical ventilation for 24 hours at baseline and during the initial weaning trial. Heart rate variability was evaluated by using spectral power analysis.ResultsLow-frequency power increased (P = .04) and high-frequency and very-low-frequency power did not change during weaning. The mean number of supraventricular ectopic beats per hour during weaning was higher than the mean at baseline (P &lt; .001); the mean of ventricular ectopic beats did not change. Low-frequency power was a predictor of ventricular and supraventricular ectopic beats during weaning (P &lt; .001). High-frequency power was predictive of ventricular and supraventricular (P = .02) ectopic beats during weaning. Very-low-frequency power was predictive of ventricular ectopic beats (P &lt; .001) only.ConclusionHeart rate variability power spectra during weaning were predictive of dysrhythmias. (American Journal of Critical Care. 2015;24:118–127)

scholarly journals Heart Rate Variability Analysis in Patients with Allergic Rhinitis

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Ming-Ying Lan ◽  
Guo-She Lee ◽  
An-Suey Shiao ◽  
Jen-Hung Ko ◽  
Chih-Hung Shu
Keyword(s):  
Heart Rate ◽  
Allergic Rhinitis ◽  
Heart Rate Variability ◽  
Nervous System ◽  
Low Frequency ◽  
Sitting Position ◽  
Rr Intervals ◽  
Hrv Analysis ◽  
Low Frequency Power ◽  
Frequency Power

Background. Very few studies investigate the role of the autonomic nervous system in allergic rhinitis. In this study, we evaluated the autonomic nervous system in allergic rhinitis patients using heart rate variability (HRV) analysis.Methods. Eleven patients with allergic rhinitis and 13 healthy controls, aged between 19 and 40 years old, were enrolled in the study. Diagnosis of allergic rhinitis was based on clinical history, symptoms, and positive Phadiatop test. Electrocardiographic recordings on the sitting and supine positions were obtained for HRV analysis.Results. In the supine position, there were no significant statistical differences in very-low-frequency power (VLF, ≤0.04 Hz), low-frequency power (LF, 0.04–0.15 Hz), high-frequency power (HF, 0.15–0.40 Hz), and the ratio of LF to HF (LF/HF) between the patient and control groups. The mean RR intervals significantly increased, while LF% and LF/HF significantly decreased in the patient group in the sitting position. Moreover, mean RR intervals, LF, and LF/HF, which were significantly different between the two positions in the control group, did not show a significant change with the posture change in the patient group.Conclusion. These suggest that patients with allergic rhinitis may have poor sympathetic modulation in the sitting position. Autonomic dysfunction may therefore play a role in the pathophysiology of allergic rhinitis.

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