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At least 19 recordsLinked to original sources
PubMed1984

Spectral analysis of fetal heart rate in sheep: the occurrence of respiratory sinus arrhythmia.

Respiratory sinus arrhythmia is a pattern of rhythmic variation in the heart rate that occurs at the frequency of respiration and is mediated principally by the vagus nerve. Spectral analysis can decompose the variance of a series of sequential measures into constituent frequencies to measure and verify whether there is respiratory sinus arrhythmia in utero in the fetal lamb. Recordings of heart period were obtained from electrodes implanted under fetal skin in six chronic preparations. Respiratory rate and heart period were recorded immediately after delivery and daily for the next 5 days. Respiratory sinus arrhythmia was clearly demonstrated in the neonatal lambs, and the same frequency of respiratory sinus arrhythmia was observed in the fetus and in the newborn lamb (0.8 to 0.1 Hz). There was a reproducible pattern of change in respiratory sinus arrhythmia from 27 days before delivery until term, with a decline in the amplitude of respiratory sinus arrhythmia 4 to 8 days before delivery. We conclude that respiratory sinus arrhythmia was demonstrated in fetal sheep and may serve as an indicator of the integrity of the central nervous system in the fetus and the neonate.

Animals↗
PubMed1960

Computer analysis of reflex control and organization: respiratory sinus arrhythmia.

Respiratory sinus arrhythmia in waking man is described by differential equations which relate thorax circumference acceleration to instantaneous heart rate. Consequent experiments show that the arrhythmia is initiated by stretch receptors within the thorax rather than by hemodynamic or central factors, and that it is due mainly to superimposed biphasic inspiratory heart rate transients of about 15 seconds' duration. Analysis of respiration heart rate reflex provides a new quantitative physiological tool.

Arrhythmia, Sinus↗
PubMed1992

Self-regulation of respiratory sinus arrhythmia.

Respiratory sinus arrhythmia (RSA)--the peak-to-peak variations in heart rate caused by respiration--can be used as a noninvasive measure of parasympathetic cardiac control. In the present study four strategies to increase RSA amplitude are investigated: (1) biofeedback of RSA amplitude, (2) biofeedback of RSA amplitude plus respiratory instructions, (3) respiratory biofeedback, and (4) respiratory instructions only. All four procedures produce a significant increase of RSA amplitude from the first physiological control trial compared to baseline. This increase is faster for the groups that received respiratory biofeedback and respiratory instructions only than for the two groups that received biofeedback of RSA amplitude, the increases being equivalent for the four groups in the third session. All subjects of the group that received biofeedback of RSA amplitude only reported respiratory strategies in order to achieve the increase in RSA. Possible clinical implications of these results for parasympathetic cardiac control and cardiovascular disorders are discussed.

Adult↗
PubMed1998

Acute effects of bisoprolol on respiratory sinus arrhythmia.

Respiratory sinus arrhythmia (RSA) is often quantified by computing the spectra of heart period (HP) or of its reciprocal heart rate (HR) at the respiratory frequency. This study was undertaken to describe the effect of an acute beta-blockade achieved with bisoprolol on RSA, obtained during a calibrated breathing (breathing frequency 0.25 Hz, tidal volume VT 500 or 700 mL) in 15 normal volunteers, using a double-blind, placebo-controlled, cross-over method. The two heart signals were computed and the RSA values were compared to the individual estimates of vagal tone obtained using an additional atropine injection. The difference between the HP (or HR) value obtained after beta-blockade and the HP (or HR) value observed following the double blockade (bisoprolol plus atropine) was taken as an index of cardiac vagal tone. Bisoprolol administration resulted in a significant reduction in HR reaching 60.3 +/- 1.4 bpm at VT of 500 mL (compared to 70.5 +/- 1.8 bpm with placebo, P < 0.001). Changes in HP were also significant with an increase in HP reaching 1004.5 +/- 22.2 msec at this controlled VT (compared to 860.3 +/- 21.5 msec with placebo, P < 0.001). Similar changes were observed at a VT of 700 mL. The relationship between RSA in bpm and vagal tone was not significant for HR while a significant positive relationship was observed between RSA in msec and vagal tone for the two respiratory patterns (r = 0.65 for a tidal volume of 500 mL, P < 0.01, and r = 0.62 for 700 mL, P < 0.05). This demonstrates that the detection of the variability effect highly depends upon the unit. The parallelism between vagal tone and RSA supports the view that the HF component of HRV in msec quantifies the vagal tone. The increased RSA during beta-blockade could well reflect this vagotonic effect of this class of drugs.

Acute-Phase Reaction↗
PubMed2005

Respiratory sinus arrhythmia during stress predicts resting respiratory sinus arrhythmia 3 years later in a pediatric sample.

The author examined whether respiratory sinus arrhythmia (RSA) responses to stress predicted resting RSA approximately 3 years later in children and adolescents. A total of 149 children and adolescents (49% girls and women, 44% African Americans) participated in 2 laboratory protocols approximately 3 years apart. RSA reactivity during tasks was consistent within participants across tasks during each session. Resting RSA at Visit 1 explained 17% of the variance in resting RSA at Visit 2 when body mass index, duration between visits, race, gender, and age were controlled for. Visit 1 RSA reactivity explained an additional 5% of the variance in resting RSA at Visit 2. The positive relationship between Visit 1 reactivity and Visit 2 resting levels suggests that larger decreases in RSA during stress predicted lower resting RSA. Conversely, increases in RSA during stress were associated with higher resting RSA an average of 3 years later.

Adolescent↗
PubMed2006

Methodological issues in the quantification of respiratory sinus arrhythmia.

Although respiratory sinus arrhythmia (RSA) is a commonly quantified physiological variable, the methods for quantification are not consistent. This manuscript questions the assumption that respiration frequency needs to be manipulated or monitored to generate an accurate measure of RSA amplitude. A review of recent papers is presented that contrast RSA amplitude with measures that use respiratory parameters to adjust RSA amplitude. In addition, data from two studies are presented to evaluate empirically both the relation between RSA amplitude and respiration frequency and the covariation between RSA frequency and respiration frequency. The literature review demonstrates similar findings between both classes of measures. The first study demonstrates, during spontaneous breathing without task demands, that there is no relation between respiration frequency and RSA amplitude and that respiration frequency can be accurately derived from the heart period spectrum (i.e., frequency of RSA). The second study demonstrates that respiration frequency is unaffected by atropine dose, a manipulation that systematically mediates the amplitude of RSA, and that the tight linkage between the RSA frequency and respiration frequency is unaffected by atropine. The research shows that the amplitude of RSA is not affected by respiration frequency under either baseline conditions or vagal manipulation via atropine injection. Respiration frequency is therefore unlikely to be a concern under these conditions. Research examining conditions that produce (causal) deviations from the intrinsic relation between respiratory parameters and the amplitude of RSA combined with appropriate statistical procedures for understanding these deviations are necessary.

Adolescent↗
PubMed1991

Mathematical model of cellular basis for the respiratory sinus arrhythmia.

The respiratory sinus arrhythmia (RSA) is a vagally mediated oscillation in cardiac cycle length at the frequency of breathing. We developed a mathematical model that predicted the temporal and frequency dependence of the RSA. We used the mathematical model to examine the underlying cellular basis for the RSA at the level of the sinus node. We alternated efferent vagal activity between a low and a high frequency at the frequency of breathing. This oscillation caused the rate of acetylcholine (ACh) release to oscillate between a low and a high rate at the frequency of breathing. ACh degradation followed linear pharmacokinetics for physiological concentrations of ACh. Therefore, the concentration of ACh in neuroeffector junctions of the sinus node oscillated at the frequency of breathing. Membrane potential responded rapidly to changes in the concentration of ACh relative to the rate of ACh degradation. Thus, the time course of the RSA depended on the rate of ACh degradation. Membrane potential oscillated at several integer multiples of frequency of breathing and at various higher frequencies, which were integer multiples of the frequency of breathing and the frequencies of firing of the sinus node. However, computing cardiac cycle length from membrane potential eliminated the higher frequencies. Therefore, cardiac cycle length oscillated at several integer multiples of the frequency of breathing, but not at these higher frequencies.

Acetylcholine↗
PubMed2002

Preserved parasympathetic cardiac innervation after atrioventricular node modification: evidence from circle maps of respiratory sinus arrhythmia.

INTRODUCTION: Respiratory sinus arrhythmia (RSA) and heart rate variability (HRV) are parameters of autonomic cardiac innervation. They decrease with age and after atrioventricular nodal modification (AVNM) suggesting vagal denervation in both situations. We hypothesized, however, that AVNM causes only a transient, functional decline in vagal activity, whereas aging causes permanent vagal denervation. A new method of analyzing RSA phase dynamics based on circle maps (CM) can potentially differentiate between both forms of reduced vagal activity. METHODS: In 18 younger and 14 older healthy control subjects 24-hour Holter ECGs were recorded for HRV analysis. Repeated measurements of RSA were acquired during paced breathing (PB). In 16 consecutive patients undergoing AVNM the same measurements were applied before, 1 day and 3 months after the procedure. CM were calculated from consecutive RR intervals and the similarity between different CM quantified by the Kullback information gain (KIG). RESULTS: HRV analysis revealed lower HF bands, LF bands and RSA amplitudes in older vs. younger control subjects. KIG revealed less similarity between younger and older control subjects than within the respective age groups. After AVNM a decrease in HF bands was noted in HRV analysis. Three months after AVNM, HF bands returned to pre-ablation values. CM obtained before and 1 day after AVNM displayed comparable similarity to CM acquired 1 day before and 3 months after ablation. CONCLUSIONS: In contrast to conventional HRV parameters, CM of RSA are not altered by ablation in the posteroseptal space but by aging. Thus, this new method appears to differentiate between transient autonomic modification and chronic denervation.

Adult↗
PubMed1991

Prediction of tonic parasympathetic cardiac control using respiratory sinus arrhythmia: the need for respiratory control.

Respiratory sinus arrhythmia (RSA) has received much attention in recent years due to the large body of evidence indicating that variations in this phenomenon represent alterations in parasympathetic cardiac control. Although it appears that respiratory sinus arrhythmia is mediated by vagal mechanisms, the extent to which the well-known respiratory influences (i.e., rate and tidal volume) on respiratory sinus arrhythmia (in altering its magnitude) may moderate the relationship between RSA and cardiac vagal tone has never been systematically studied. We addressed this issue by examining intraindividual relationships among RSA magnitude, respiration (rate and tidal volume), and heart period among six healthy male adults after intravenous administration of 10 mg propranolol, a beta-adrenergic blocker. Subjects were exposed to various behavioral tasks which altered all physiological variables measured. Variations in heart period after beta blockade were assumed to be predominantly vagally mediated. Within-subject regression analyses consistently showed that respiratory parameters influenced RSA magnitude, but not tonic variations in beta-blocked heart period, suggesting that respiratory-mediated RSA alterations are not associated with changes in cardiac vagal tone. Only when respiratory variables were statistically controlled was there evidence of a reasonable correspondence between beta-blocked heart period and RSA amplitude, providing support for the idea that respiratory parameters need to be controlled when using RSA amplitude as an index of cardiac vagal tone. Repeated-measures analyses of variance of mean levels of heart period and respiratory sinus arrhythmia across subjects supplemented and supported the intraindividual results. These findings point to the importance of controlling for respiratory parameters when using respiratory sinus arrhythmia as a cardiac vagal index.

Adult↗
PubMed1976

Variation of respiratory sinus arrhythmia with age.

Respiratory sinus arrhythmia was measured on 24 male subjects whose ages ranged from 21 to 65 yr, using a technique in which respiration was coupled to heart rate, so that there were 6 heartbeats per inspiration and 6 heartbeats per expiration. This voluntary cardiorespiratory coupling reduced the variance of heart rates measured at various points in the respiratory cycle. Fourier analysis was used to obtain the fundamental of heart rate and respiratory volume. A high correlation coefficient (-0.83) was found between percent of variation of heart rate from the average heart rate (PB) and the age of the subject. Linear regression analysis performed on these data produced the equation: PB = 23.2-0.35 (age). Since sinus arrhythmia at the low respiratory frequencies used probably reflects the viability of the cardiorespiratory control systems, we believe this provides a simple noninvasive method for the study of the overall competence of the system responsible for respiratory sinus arrhythmia.

Adult↗
PubMed1985

Effects of carotid sinus nerve stimulation on respiratory sinus arrhythmia and respiratory blood pressure waves of the dog.

The effect on the amplitudes of RSA and RBPW of the time of the stimulus in the cardiac cycle, and also of continuous stimulation were studied. When the stimulus train was applied near peak systole the amplitudes of RSA and RBPW decreased. Stimulation in late systole increased both RSA and RBPW. Continuous stimulation did not exert any effects on RSA and RBPW.

Animals↗
PubMed1996

Respiratory sinus arrhythmia and central respiratory drive in humans.

1. The influence of central inspiratory drive on heart rate variability was investigated in young human subjects using power spectral analysis of R-R intervals. 2. The area of the high-frequency component occurring at the respiratory frequency (0.2-0.25 Hz) in the power spectral density curves was used as an index of respiratory sinus arrhythmia. 3. Central inspiratory drive was increased by breathing a CO2-enriched (5%) gas mixture and this condition was compared with a similar degree of ventilation produced voluntarily. 4. Tests were conducted on eight young subjects with and without low-dose scopolamine (scopoderm TTS) in a double-blind cross-over trial. 5. Scopolamine decreased heart rate and increased the high-frequency peak, suggesting that its main action on the cardiac vagal pathway was a peripheral one, possibly increasing the efficacy of vagal impulses on the cardiac pacemaker. 6. With scopolamine, CO2 breathing increased the area of the high-frequency component significantly more than a similar degree of ventilatory movements produced by voluntary hyperventilation. 7. It is concluded that respiratory sinus arrhythmia in humans is at least partly dependent on a central respiratory-cardiac coupling, most probably similar to that shown in animal studies.

Administration, Inhalation↗
PubMed1996

The effect of exposure to increased hydrostatic pressure up to 46 ATA on respiratory sinus arrhythmia in humans.

Respiratory sinus arrhythmia (RSA) has been used as a non-invasive estimate of vagal tone to determine whether the reduction in resting heart rate commonly seen when humans are exposed to increases in the ambient pressure is associated with changes in vagal autonomic control. Two sets of divers (n = 4) were examined during two simulated saturation dives, one to 46 atmospheres absolute (ATA) and another to 37 ATA. A significant reduction in resting heart rate was seen in both dives upon exposure to high pressure compared with controls at 1 ATA. The reduction in heart rate seen at increased pressure was consistent regardless of respiratory rate, indicating that moderate changes in respiratory rate do not affect heart rate under these conditions. No changes in the overall magnitude of RSA were observed over a range of respiratory rates during either dive compared with control values at 1 ATA. During both dives, RSA was significantly larger (P < 0.05) at low respiratory rates compared with higher rates for both 1 ATA controls and at high pressure. The presence of a hyperbaric bradycardia strongly suggests that vagal tone is altered during hyperbaric exposure; however, the lack of change in the magnitude of RSA at high pressure brings into question the viability of using RSA as an accurate indicator of vagal tone and this lack of correspondence deserves further investigation.

Adult↗
PubMed1992

Effects of consecutive administration of central and peripheral anticholinergic agents on respiratory sinus arrhythmia in normal subjects.

Respiratory sinus arrhythmia is thought to be vagally mediated, since it disappears after atropine, but the site of action of the drug (central vs. peripheral) accounting for this effect has not been elucidated. To investigate the effects of anticholinergic agents on respiratory arrhythmia, ten healthy subjects received an intravenous bolus of tropatepine (a presumed central antagonist) at a dose of 0.08 mg per kg of body weight, then, 7 min later, prifinium (a peripheral antagonist) at a dose of 0.1 mg per kg of body weight. Respiratory sinus arrhythmia during controlled breathing was evaluated as the area under the high-frequency peak of the heart rate variability spectrum coinciding with the respiratory frequency +/- 0.02 Hz. The power of this high-frequency peak decreased by 55% after tropatepine (P less than 0.05) with a concomitant increase of the mean RR interval from 930 to 1072 ms (P less than 0.01). When prifinium was added, a further but non-significant decrease of respiratory arrhythmia was observed, while the mean RR interval decreased from 1072 to 714 ms (P less than 0.01). The low-frequency components (0.05 to 0.15 Hz) of the power spectrum, significantly decreased (P less than 0.05) after infusion of both drugs. In conclusion, tropatepine depresses respiratory sinus arrhythmia with a paradoxical concomitant bradycardia. This suggests that tropatepine acts like a pure central muscarinic antagonist, in support of the hypothesis that a central cholinergic receptor is involved in the respiratory modulation of heart rate.

Adult↗
PubMed1996

Postural effect on respiratory sinus arrhythmia with various respiratory frequencies.

Heart rate variations during steady state respiration with various frequencies were studied on seven healthy male students at two different body positions. Respiration was controlled at four different frequencies (0.083, 0.100, 0.200, 0.250Hz), and the tidal volume was simultaneously controlled at 1500ml (0.083, 0.100Hz) or 1000ml (0.200, 0.250Hz). A tilting bed was used for changing body position, and the measurements were conducted at horizontal and vertical position. RSA (respiratory sinus arrhythmia) amplitude at 0.250Hz was significantly decreased at vertical position compared with horizontal position. At 0.200Hz the significant decrease could not be obtained although some tendency of decrease appeared. Contrary to these high frequencies, the amplitudes at low frequencies (0.083, 0.100Hz) were significantly increased (p < 0.01) during vertical position. This postural effect on the low frequency RSA could be regarded as a similar result on MWSA (Mayer wave relate sinus arrhythmia) which reflects sympathetic nervous activity. Furthermore, the ratio between the amplitude at 0.100Hz and that at 0.250Hz was significantly correlated with mean heart rate (n = 56, r = 0.73). From these results it was assumed that the RSA amplitude at low frequency associate a with not only parasympathetic nerves but also sympathetic nerves whereas the amplitude at high frequency was solely mediated by parasympathetic nerves.

Adult↗
PubMed1998

Respiratory sinus arrhythmia in children with severe cyanotic and pallid breath-holding spells.

In this study we investigated centrally mediated parasympathetic regulation of modulated cardiac vagal tone among children with severe cyanotic and pallid breath-holding spells by examining respiratory sinus arrhythmia. Respiratory sinus arrhythmia was evaluated in 41 children; 17 subjects with cyanotic breath-holding spells (6 boys, 11 girls; mean age 37.1 months), 7 subjects with pallid breath-holding spells (2 boys, 5 girls; mean age 33.0 months), and 17 controls (8 boys, 9 girls; mean age 41.2 months). Subjects had recurrent (more than 3) severe breath-holding spells. Each subject's electrocardiogram was recorded in a quiet room and digitized by an 80386 personal computer during five 1-minute periods. R-R intervals within each 1-minute period were converted to heart rate in 120 successive 0.5-second intervals. The resultant heart rate time series was converted to its underlying frequency composition by a fast Fourier transform and averaged across minutes. Respiratory sinus arrhythmia was defined as the variability in the time series over a frequency range (0.096 Hz to 0.48 Hz) corresponding to a range of respiratory rates from 6 to 30 breaths per minute. ANCOVA adjusting for age and sex was conducted with the subject group as the independent measure. There were no significant differences between subjects with cyanotic breath-holding spells and controls. Pallid breath-holding spell subjects had a marked difference in respiratory sinus arrhythmia from either controls or subjects with cyanotic breath-holding spells, demonstrating less variability in respiratory sinus arrhythmia (P < .042) This study supports the hypothesis that there exists autonomic dysregulation in pallid breath-holding spells, caused by a primary central parasympathetic disturbance distinct from the dysregulation found in cyanotic breath-holding spells.

Apnea↗
PubMed2000

Analysis of respiratory sinus arrhythmia with respect to respiratory phase.

We evaluated the respiratory modulation of heart rate, i.e., respiratory sinus arrhythmia (RSA), with respect to respiratory phase derived from an analytic signal from the lung volume curve, during spontaneous breathing and paced breathing with different patterns. The magnitudes and waveforms of RSA in the phase domain were similar regardless of breathing pattern, even including spontaneous breathing. An examination of the occurrence of heart beats with respect to the respiratory phase revealed that synchronized patterns recently reported in the literature (Nature 392: 239, 1998) were observed during paced breathing with breath holding periods whereby the respiratory phase advanced more slowly. It was concluded that the phase domain approach might be useful in extracting RSA during spontaneous breathing and for elucidating detailed mechanisms for RSA. However, the use of this technique for studies investigating cardio-respiratory coupling should be approached cautiously, as the results may be influenced by breathing patterns.

Adult↗
PubMed2002

Direct effect of Pa(CO2) on respiratory sinus arrhythmia in conscious humans.

Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2 directly affects RSA in conscious humans even when changes in tidal volume (V(T)) and breathing frequency (F(B)), which indirectly affect RSA, are prevented. In seven healthy subjects, we adjusted end-tidal PCO2 (PET(CO2)) to 30, 40, or 50 mmHg in random order at constant V(T) and F(B). The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with PET(CO2) (P < 0.001). Mean R-R interval did not differ at PET(CO2) of 40 and 50 mmHg but was less at 30 mmHg (P < 0.05). Because V(T) and F(B) were constant, these results support our hypothesis that increased CO2 directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.

Adult↗