Magnitude Of Respiratory Sinus Arrhythmia Research Articles

Feasibility of Spectral Analysis as a Tool in Nursing Research to Quantify Patterns of Respiration in Premature Infants.

Respiratory difficulties are a common concern in preterm infants, and they can lead to long-term health problems. Few studies have investigated the use of spectral analysis as a biomarker to quantify respiration patterns in preterm infants. To evaluate the feasibility of using spectral analysis of heart rate variability as a biomarker for the quantification of respiratory patterns in very-low-birth-weight preterm infants compared to direct observation. In a comparative, small-scale feasibility study, 18 preterm infants born during their 27th to 28th gestational week (weighing <1500 grams) participated by convenience. Respiratory patterns (regular or irregular; shallow or deep) were directly observed on the 28th week during playback of speech recording. Heart rate variability was simultaneously measured using spectral analysis of heart periods, from which the mean values influenced by respiratory sinus arrhythmia (frequencies of 0.30-1.0 Hz) were compared to each observed respiratory pattern. The magnitudes of respiratory sinus arrhythmia and the area under the curve were determined. The magnitude of respiratory sinus arrhythmia (frequencies of 0.30-1.0 Hz) in infants observed to be displaying irregular shallow respiration was greater than that in infants with regular deep respiration. Further, there was a shift from lower frequencies (frequency peak = 0.30 Hz) to higher frequencies (peak = 0.70 Hz). In contrast with direct observation, spectral analysis allowed for the quantification of respiratory patterns in a vulnerable population of preterm infants of interest to the nursing scientific and practice community. Future directions include applying this biomarker to evaluate both developmental and pathological trends in the respiratory patterns of preterm infants.

Abstract 14612: The Relationship Between Left Ventricular Geometry and Respiratory Sinus Arrhythmia in Patients With Vasovagal Syncope

Introduction: The study was prompted by our observation that a significant number of patients with vasovagal syncope (VVS) have marked respiratory sinus arrhythmia as well as thin left ventricular (LV) walls. We hypothesized that the geometry of the LV walls may play a role in the pathogenesis of VVS. Hypothesis: The aim of this study was to assess LV geometry in relationship to respiratory sinus arrhythmia in patients with VVS M ethods: We included 191 patients (age 52±20 years, 101 women) with VVS who had either a positive or negative response to tilt table testing TTT (n=64 TTT+, and n=127 TTT-). The VVS group was compared to a group of 75 patients with no syncope (NL) and similar age, sex and BMI distributions. Standard 12-lead electrocardiograms (ECG), vectorcardiograms, and transthoracic echocardiograms were performed to assess electrical activation as well as ventricular geometry and function. The magnitude of respiratory sinus rhythm arrhythmia was measured as the maximum percent change in RR interval on a 10 second 12-lead ECG (dRR) performed before the TTT. Results: When compared to NL group patients with VVS had significantly higher dRR and LV end diastolic diameter (12 ±8% vs 10±8%, p=0.047 and 44±5 vs 46±6mm p=0.006 respectively) The end-diastolic thickness of the interventricular septum (IVS) and that of the LV posterior wall (PWT) in the VVS group were significantly smaller than in the NL group (8.9±1.7mm vs 9.6±1.8mm p value=0.003 and 8.4±1.5mm vs 9.2±1.6mm p value=0.0002). The magnitude of respiratory sinus arrhythmia expressed as dRR correlated inversely and significantly with IVS (r=-0.32; p value=0.042). The was however no significant correlation between dRR and PWT. These results suggest that a more pronounced respiratory sinus arrhythmia could be related to more ample variations in right and left ventricular filling due to increased ventricular interdependence via a thinner and more compliant ventricular septum. Conclusions: The geometry of the LV as well as the cardiovascular impact of respiratory movements may play a role in the pathogenesis of VVS.

Respiratory sinus arrhythmia magnitude quantification as a potential marker of stress and pain in cows and sheep.

Respiratory sinus arrhythmia (RSA) provides a quantitative evaluation of 'vagal tone' and may be used for pain and stress assessment in livestock. The aim was to quantify the magnitude of RSA in cows and sheep. In 7 cows and 4 sheep standing at rest we measured the 3-lead electrocardiogram (ECG) together with the pneumogram, to identify inspiration and expiration. For each breath, RSA was the difference in instantaneous heart rate (HR) between the inspiratory peak and the expiratory trough, in percent of mean HR. The resting breathing rates (28 ± 2 and 32 ± 5 breaths/min in cows and sheep, respectively) were about twice those expected for similar size non-ruminants, in conformity with previous reports. Both species had long-period (>15s) HR fluctuations. The average values of RSA, 1.4 ± 0.2% in cows and 7.8 ± 3.1 in sheep, were lower than those previously computed by an identical approach in humans (12%), dogs (40%) and horses (9%).In conclusion, by breath-by-breath analysis of instantaneous HR we measured RSA in both cows and sheep. Results from the present study represent a preliminary step in assessing whether or not RSA could be used as a biomarker for stress or pain in ruminants.

Stroke volume variation as an index of fluid responsiveness can be impaired by mental stress.

Cardiac stroke volume variation (SVV) measurement is one of the techniques to detect fluid-responsive hypovolemia in patients under mechanical ventilation. There is an ongoing effort to apply SVV for this purpose also in conscious patients. However, the effect of mental stress often occurring in conscious patients as a potential confounding factor on SVV is not known. The aim of our study was to compare effect of simulated hypovolemia and mental stress on SVV in healthy volunteers in the context of potential confounders - breathing pattern, respiratory sinus arrhythmia magnitude and sex. We examined 102 young healthy volunteers (58 females), mean age 18.6 years. Finger arterial blood pressure was recorded by volume-clamp photoplethysmographic method (Finometer Pro, FMS, Amsterdam, Netherland). From the blood pressure curve, a built in ModelFlow algorithm calculated stroke volume values (SV) for each heartbeat. Respiratory volume was recorded using calibrated respiratory inductive plethysmography (RespiTrace, NIMS, Miami Beach, FL, USA). During four phases of examination protocol (supine rest, head-up tilt (HUT), supine recovery, mental arithmetic task (MA)) we analyzed SVV related to respiratory activity. While during HUT we found an expected increase in SVV together with mean SV decrease, SVV significantly decreased during MA. The observed changes during MA could be attributed to an increased respiratory rate and/or decreased respiratory sinus arrhythmia. Sex related differences in SVV responses to HUT and MA were observed. We conclude that mental stress together with respiratory sinus arrhythmia and respiratory pattern changes can significantly influence SVV as a potential index of fluid responsiveness in conscious patients.

The Effect of Inspired Hypoxia and Hyperoxia on Respiratory Sinus Arrhythmia Reactivity

Respiratory sinus arrhythmia (RSA) is the normal fluctuation in heart rate (HR) in phase with the respiratory cycle, whereby HR increases during inspiration and decreases during expiration. The underlying mechanisms and potential utility remain elusive. RSA magnitude is thought to be affected by autonomic balance, whereby a dominant parasympathetic nervous system (NS) at rest facilitates RSA, and sympathetic NS activation attenuates its magnitude. Carotid body stimulation via acute hypoxia elicits sympathetic activation, whereas hyperoxia facilitates sympathetic withdrawal. In addition, RSA has been hypothesized to facilitate improvements in ventilation/perfusion (V/Q) matching, improving oxygenation when hypoxic. We hypothesized that (a) acute hypoxia and hyperoxia would increase and decrease the magnitude of RSA reactivity, respectively and (b) when hypoxic, those with larger RSA magnitude during deep breathing would have larger improvements in oxygen saturation (SpO2). Healthy participants (n=13) were instrumented with a pneumotachometer and coached to breathe at three percentages (30, 40 and 50%) of their forced vital capacity (FVC) using visual cues while inspiring room air (21% FIO2), hypoxia (13.5% FIO2), hyperoxia (100% FIO2). RSA was quantified via the peak‐valley approach, and RSA reactivity (RSAR) was quantified via linear regression to calculate the slope of changes in RSA magnitude across all three FVC levels. RSA magnitude increased linearly with increases in inspired tidal volume in all three gases (R2&gt;0.98). No significant differences were found in RSAR slopes between room air (0.32±0.2 ΔBPM/%FVC), hypoxia (0.33±0.26 ΔBPM/%FVC), and hyperoxia (0.34±0.26 ΔBPM/%FVC; P=0.97). There was also no correlation between RSA magnitude during deep breathing (50%FVC) and the associated improvements in SpO2 in hypoxia (r=−0.11, P=0.72). Given that RSAR is not affected by oxygen availability, our data provides evidence that hypoxic stimulation of the carotid bodies elicits activation of both arms of the autonomic nervous system, maintaining autonomic balance and normal heart rate variability. In addition, RSA magnitude does not appear to bestow advantages on V/Q matching in the context of acute hypoxia.Support or Funding InformationMRU Faculty of Science and Technology

Respiratory Sinus Arrhythmia as an Index of Cardiac Vagal Control in Mitral Valve Prolapse.

Respiratory sinus arrhythmia (RSA), i.e. heart rate (HR) variations during inspiration and expiration, is considered as a noninvasive index of cardiac vagal control. Mitral valve prolapse (MVP) could be associated with increased cardiovascular risk; however, the studies are rare particularly at adolescent age. Therefore, we aimed to study cardiac vagal control indexed by RSA in adolescent patients suffering from MVP using short-term heart rate variability (HRV) analysis. We examined 12 adolescents (girls) with MVP (age 15.9±0.5 years) and 12 age and gender matched controls. Resting ECG was continuously recorded during 5 minutes. Evaluated HRV indices were RR interval (ms), rMSSD (ms), pNN50 (%), log HF (ms(2)), peak HF (Hz) and respiratory rate (breaths/min). RR interval was significantly shortened in MVP group compared to controls (p=0.004). HRV parameters-rMSSD, pNN50 and log HF were significantly lower in MVP compared to controls (p=0.017, p=0.014, p= 0.015 respectively). Our study revealed reduced RSA magnitude indicating impaired cardiac vagal control in MVP already at adolescent age that could be crucial for early diagnosis of cardiovascular risk in MVP.

Respiratory Sinus Arrhythmia Mechanisms in Young Obese Subjects.

Autonomic nervous system (ANS) activity and imbalance between its sympathetic and parasympathetic components are important factors contributing to the initiation and progression of many cardiovascular disorders related to obesity. The results on respiratory sinus arrhythmia (RSA) magnitude changes as a parasympathetic index were not straightforward in previous studies on young obese subjects. Considering the potentially unbalanced ANS regulation with impaired parasympathetic control in obese patients, the aim of this study was to compare the relative contribution of baroreflex and non-baroreflex (central) mechanisms to the origin of RSA in obese vs. control subjects. To this end, we applied a recently proposed information-theoretic methodology – partial information decomposition (PID) – to the time series of heart rate variability (HRV, computed from RR intervals in the ECG), systolic blood pressure (SBP) variability, and respiration (RESP) pattern measured in 29 obese and 29 age- and gender-matched non-obese adolescents and young adults monitored in the resting supine position and during postural and cognitive stress evoked by head-up tilt and mental arithmetic. PID was used to quantify the so-called unique information transferred from RESP to HRV and from SBP to HRV, reflecting, respectively, non-baroreflex and RESP-unrelated baroreflex HRV mechanisms, and the redundant information transferred from (RESP, SBP) to HRV, reflecting RESP-related baroreflex RSA mechanisms. Our results suggest that obesity is associated: (i) with blunted involvement of non-baroreflex RSA mechanisms, documented by the lower unique information transferred from RESP to HRV at rest; and (ii) with a reduced response to postural stress (but not to mental stress), documented by the lack of changes in the unique information transferred from RESP and SBP to HRV in obese subjects moving from supine to upright, and by a decreased redundant information transfer in obese compared to controls in the upright position. These findings were observed in the presence of an unchanged RSA magnitude measured as the high frequency (HF) power of HRV, thus suggesting that the changes in ANS imbalance related to obesity in adolescents and young adults are subtle and can be revealed by dissecting RSA mechanisms into its components during various challenges.

The magnitude of respiratory sinus arrhythmia of a large mammal (the horse) is like that of humans

Heart rate (FH) accelerates in inspiration and decelerates in expiration, a phenomenon known as Respiratory Sinus Arrhythmia (RSA). Although the presence of RSA has been documented in many species, how its magnitude compares among species is unknown. We asked whether the magnitude of RSA in a large mammal, the horse, differed from that of previously measured humans. From electrocardiogram and pneumography, the peaks and troughs of FH were identified breath-by-breath in four horses (Italian Saddlebred geldings) during resting wakefulness. RSA was computed as the peak-trough FH difference, in percent of mean FH. Horses had lower FH and respiratory frequency (FR) than humans, but similar FH/FR. RSA ranged between 6% and 15%, with an average of 9 ± 2%, not statistically different from the mean value in humans (12 ± 1%). Like in humans, in horses the FH/FR values below the mean had correspondingly lower RSA, while values above the mean had correspondingly higher RSA. If confirmed in other species, these results suggest that RSA is body size-independent. The correlation with FH/FR, rather than FH or FR, supports the view that RSA optimizes the coupling between pulmonary blood flow and ventilation.

Poincare Analysis of Spontaneous Respiratory Sinus Arrhythmia during High Altitude Ascent: Effects on oxygenation

Respiratory sinus arrhythmia (RSA) is the transient fluctuation in heart rate (HR) in phase with the respiratory cycle. Poincare spectral analysis is used to (a) quantify heart rate variability (HRV) through short term (SD1; i.e., RSA) and long term (SD2) fluctuations in heart rate and (b) determine components of autonomic nervous system activity (low and high frequency; LF and HF; sympathetic and parasympathetic, respectively). Although RSA likely represents the dominance of the parasympathetic nervous system at rest, there is controversy regarding the mechanisms underlying RSA, as well as the possible physiological utility. RSA may improve ventilation and perfusion (V/Q) matching in the lungs, and may protect against oxygen desaturation in the context of hypoxic exposure. We aimed to investigate the relationship between RSA magnitude and peripheral oxygen saturation (SpO2) during incremental ascent to high altitude (4370m). We hypothesized that (a) RSA magnitude (SD1/SD2) ratio would decrease during ascent to high altitude as a result of sympathetic nervous system activation and (b) individuals with a larger SD1/SD2 ratio during ascent would have increased SpO2 through improved V/Q matching. Measurements were conducted over eleven days at 1045m (baseline, day 1), 3440m (day 7), 3860m (day 9), and 4370m (day 11) during a trek to altitude in the Nepal Himalaya. Participants (26±2.1 years; BMI 23.8±1.1 kg/m2; 9 females, n=12) were instrumented with an ECG and finger pulse oximeter (SpO2 %) and tested on rest days after one night at each altitude. Spontaneous RSA was measured from the ECG periods during the last 7‐min of a 10‐min baseline and evaluated using Poincare plots. There was no significant difference between the SD1/SD2 ratio during incremental ascent to 4370m (P=0.65). There was also no significant difference observed in the LF/HF ratios during ascent to 4370m (P=0.66), suggesting that the sympathetic/parasympathetic ratio remained unchanged with ascent. Additionally, we correlated SD1/SD2 ratio and SpO2 at 4370m when individuals were most hypoxic at rest (SpO2 87.2±0.8%) and found no significant correlation (r=0.32, P=0.31). Our data suggests that during slow incremental ascent to high altitude, there is no difference in spontaneous RSA or the balance between sympathetic and parasympathetic nervous system activity. Individuals with larger SD1/SD2 ratios do not have improved SpO2, suggesting that RSA magnitude does not improve V/Q matching during high altitude ascent.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada, Student Temporary Employment Program of Alberta, Alberta Innovates Health Solutions Summer Studentship,

Respiratory sinus arrhythmia as a non-invasive index of 'brain-heart' interaction in stress.

Respiratory sinus arrhythmia (RSA) is accepted as a peripheral marker of cardiac-linked parasympathetic regulation. According to polyvagal theory, the RSA is also considered as the index of emotion regulation. The neurovisceral integration model posits that parasympathetic modulation of the heart marked by RSA is related to complex nervous regulation associated with emotional and cognitive processing. From this perspective, high resting RSA amplitude associated with a greater withdrawal during stressors and subsequent recovery could represent a flexible and adaptive physiological response system to a challenge. Conversely, low resting RSA accompanied by an inadequate reactivity to stress might reflect maladaptive regulatory mechanisms. The RSA reactivity is different with various types of stressors: while the RSA decreases to cognitive tasks indicating a vagal withdrawal, the RSA magnitude increases to emotional challenge indicating an effective cognitive processing of emotional stimuli. The RSA reactivity to stress could have important implications for several mental disorders, e.g. depressive or anxiety disorder. It seems that the study of the RSA, as a non-invasive index of ‘brain-heart’ communication, could provide important information on the pathway linked to mental and physical health.

Respiratory sinus arrhythmia stabilizes mean arterial blood pressure at high-frequency interval in healthy humans.

Arterial blood pressure variations are an independent risk factor for end organ failure. Respiratory sinus arrhythmia (RSA) is a sign of a healthy cardiovascular system. However, whether RSA counteracts arterial blood pressure variations during the respiratory cycle remains controversial. We restricted normal RSA with non-invasive intermittent positive pressure ventilation (IPPV) to test the hypothesis that RSA normally functions to stabilize mean arterial blood pressure. Ten young volunteers were investigated during metronome-paced breathing and IPPV. Heart rate (ECG), mean arterial blood pressure and left stroke volume (finger arterial pressure curve) and right stroke volume (pulsed ultrasound Doppler) were recorded, while systemic and pulmonary blood flow were calculated beat-by-beat. Respiratory variations (high-frequency power, 0.15-0.40 Hz) in cardiovascular variables were estimated by spectral analysis. Phase angles and correlation were calculated by cross-spectral analysis. The magnitude of RSA was reduced from 4.9 bpm(2) (95% CI 3.0, 6.2) during metronome breathing to 2.8 bpm(2) (95% CI 1.1, 5.0) during IPPV (p = 0.03). Variations in mean arterial blood pressure were greater (2.3 mmHg(2) (95% CI 1.4, 3.9) during IPPV than during metronome breathing (1.0 mmHg(2) [95% CI 0.7, 1.3]) (p = 0.014). Respiratory variations in right and left stroke volumes were inversely related in the respiratory cycle during both metronome breathing and IPPV. RSA magnitude is lower and mean arterial blood pressure variability is greater during IPPV than during metronome breathing. We conclude that in healthy humans, RSA stabilizes mean arterial blood pressure at respiratory frequency.

Body position does not affect respiratory sinus arrhythmia magnitude (1103.4)

Body position does not affect respiratory sinus arrhythmia magnitude Respiratory sinus arrhythmia (RSA) is the normal fluctuation in heart rate in phase with respiration. Instantaneous heart rate (IHR) increases with inspiration and decreases with expiration. The mechanisms underlying RSA are unclear, but some evidence suggests that central brainstem mechanisms drive RSA, independent of afferent feedback. Cardiac loading associated with inspiration or gravity may also trigger the Bainbridge reflex, although the contribution of this reflex is unclear in humans. We investigated the effects of incremental increases in inspired volume on RSA magnitude during both 45° head‐up and head‐down tilt (HUT, HDT). Six healthy subjects were positioned on a tilt table and instrumented with ECG to measure IHR (60/period) and a pnuemotachometer to measure respiratory volumes. Following a forced vital capacity (FVC) measurement, subjects were coached to breathe 30 consecutive breaths at each inspiratory volume of 10, 15, 20, 25 and 30% of FVC using a computer screen for visual feedback. The average RSA magnitude of the middle 10 breaths of each trial was plotted against the inspired volume, and linear regression was performed. The increase in RSA magnitude with inspired volume was highly linear in HUT and HDT (R2&gt;0.9), but the mean slopes were not different between positions. We have determined a range of inspired volumes that generate a linear RSA magnitude response. Further, our data demonstrate that gravity‐dependent cardiac loading does not influence RSA magnitude associated with increases in inspired volume.

Deep Breathing Heart Rate Variability is Associated with Inspiratory Muscle Weakness in Chronic Heart Failure

There is a synchronism between the respiratory and cardiac cycles. However, the relationship of inspiratory muscle weakness in chronic heart failure (CHF) on cardiac autonomic modulation is unknown. The purpose of the present investigation was to evaluate the impact of inspiratory muscle strength on the magnitude of respiratory sinus arrhythmia. Ten CHF (62 ± 7 years--left ventricle eject fraction of 40 ± 5% and New York Heart Association class I-III) and nine matched-age healthy volunteers (64 ± 5 years) participated in this study. Heart rate variability (HRV) was obtained at rest and during deep breathing manoeuvre (DB-M) by electrocardiograph. CHF patients demonstrated impaired cardiac autonomic modulation at rest and during DB-M when compared with healthy subjects (p < 0.05). Moreover, significant and positive correlations between maximal inspiratory pressure and inspiratory-expiratory differences (r = 0.79), expiratory/inspiratory ratio (r = 0.83), root mean square of the successive differences (r = 0.77), standard deviation of NN intervals (r = 0.77), low frequency (r = 0.77), and high frequency (r = 0.70) were found during DB-M. At rest, significant correlations were found also. Patients with CHF presented impaired cardiac autonomic modulation at rest. In addition, cardiac autonomic control of heart rate was associated with inspiratory muscle weakness in CHF. Based on this evidence, recommendations for future research applications of respiratory muscle training can bring to light a potentially valuable target for rehabilitation.

Effect of Postural Changes on Cardiorespiratory Coordination in Humans

In this study we assessed the effect of body postural changes from the supine (Sup) to the upright (Up) position on the magnitude and phase of respiratory sinus arrhythmia (RSA) and the phase-locking between the heart rhythm and respiration. In eight healthy human subjects, electrocardiograms (ECG) and respiratory signals were recorded. The magnitude and phase of RSA were evaluated by selective averaging of R-R interval changes from multiple respiratory cycles over the respiratory phase. For the assessment of cardiorespiratory coordination, we analyzed the phase-locking between heart rate, computed from R-R intervals of ECG, and respiratory rate, computed from intervals of inspiratory onsets of respiration, using Hilbert transform. A significant decrease in the magnitude of RSA and percentage and duration of phase-locking between heart rate and respiratory rate was observed during Up as compared to Sup. Further, there was a significant increase in the phase of RSA during Up as compared to Sup. In conclusion, measures of RSA and interaction between cardiac and respiratory rhythms are affected by body posture in humans.

Respiratory sinus arrhythmia in conscious humans during spontaneous respiration

Respiratory sinus arrhythmia (RSA) is the beat-to-beat fluctuation in heart rate at the frequency of the respiratory cycle. While it is common to study RSA under conditions of controlled breathing, where respiratory frequency, and sometimes tidal volume and inspiratory:expiratory ratio are controlled, the effect of controlled breathing on RSA is not clear. While not all studies exploring the effects of controlled breathing on RSA magnitude are consistent, some of the best-designed studies addressing this question did find a significant effect. In addition to respiratory timing influencing heartbeats, there is evidence that cardiac timing also influences respiratory timing, termed cardioventilatory coupling. Thus, the timing interactions between the cardiac and respiratory systems are complex, and bi-directional. Controlled breathing eliminates one aspect of this relationship, and studies designed to understand cardiorespiratory physiology conducted under these conditions need to be interpreted with an understanding that they may not represent normal physiology.

Does respiratory sinus arrhythmia serve a buffering role for diastolic pressure fluctuations?

Though many consider the magnitude of respiratory sinus arrhythmia as an index of cardiac vagal control, its physiological origins remain unclear. One influential model postulates that the systolic pressure rise within a given beat stimulates the baroreflex arc to adjust the following heart period such that diastolic pressure is "stabilized" and hence displays lesser fluctuation. Accordingly, the magnitude of diastolic pressure fluctuations with respiration should change reciprocally after augmentation or inhibition of respiratory sinus arrhythmia. To test this, we augmented and subsequently inhibited respiratory sinus arrhythmia with vagotonic and vagolytic atropine administration in 19 healthy young volunteers to assess the relation between respiratory R-R interval and diastolic pressure fluctuations. Respiratory diastolic pressure fluctuations showed parallel rather than inverse changes in relation to those in respiratory sinus arrhythmia: they increased with augmented respiratory sinus arrhythmia (138 and 190% of baseline in the frequency and time domains, both P < 0.05) and tended to decrease with inhibited respiratory sinus arrhythmia (82 and 93% of baseline in frequency and time domains, P = 0.20 and P = 0.07). Furthermore, >60% of the change in diastolic pressure fluctuations was explained by the change in respiratory sinus arrhythmia (R(2) = 0.62; P < 0.001), that is, an approximately 50-ms increase or decrease in respiratory sinus arrhythmia resulted in a parallel approximately 1-mmHg change in diastolic pressure fluctuations. Thus, in young healthy individuals during supine rest, respiratory fluctuations in R-R interval do not buffer against diastolic pressure fluctuations but actually cause diastolic pressure fluctuations. Therefore, our data provide little evidence for a predominant role of a baroreflex feedback mechanism underlying respiratory sinus arrhythmia during supine rest.

Vagus nerve stimulation induces changes in respiratory sinus arrhythmia of epileptic children during sleep

This study analyzed the direct short-term effect of vagus nerve stimulation (VNS) on respiratory sinus arrhythmia (RSA) in children with pharmacoresistant epilepsy. RSA magnitude is calculated as the ratio between maximum and minimum heart rate for each respiratory cycle-before, during, and after the actual VNS period. In 10 children, changes in RSA magnitude were evaluated on polysomnographic recordings, including electrocardiography (ECG), electroencephalography (EEG), thoracoabdominal distension, nasal airflow, and VNS artifacts. Measurements during stimulation were compared with those at baseline, immediately preceding the VNS periods and individually for each patient. During VNS, respiratory frequency increased and respiratory amplitude decreased with a variable effect on cardiac activity. The coupling between heart rate and respiratory rate was disturbed and RSA magnitude decreased significantly in 6 of 10 children during VNS. These changes in RSA magnitude varied from one child to another. The observed changes for respiratory and cardiac activity were concomitant with changes in RSA but were not correlated. Together with disorders of respiration, cardiac activity, and oxygen saturation (SaO(2)) described previously. VNS also modifies synchronization between cardiac and respiratory activity, resulting in poor optimization of oxygen delivery to tissues that can be regarded as an additive side effect, which should be considered in patients with already altered brain function. This interaction between the effects of VNS and potential autonomic nervous system (ANS) dysfunction already reported in epileptic patients should be considered to be potentially life-threatening. In addition, evaluation of changes in respiratory parameters can also provide reliable markers for further evaluation of the effectiveness of VNS.

Right anterior cingulate cortical volume covaries with respiratory sinus arrhythmia magnitude in combat veterans

Existing data suggest anterior cingulate cortex (ACC) plays a role in autonomic regulation. In persons with posttraumatic stress disorder (PTSD), autonomic regulation appears impaired and smaller mean ACC volume has been reported. This study examined relationships between ACC volume and the magnitude of respiratory sinus arrhythmia (RSA) in 77 U.S. combat veterans at rest, 40 of whom met criteria for PTSD. RSA magnitude did not differ in combat survivors with and without PTSD, which contradicts studies comparing civilians with PTSD to nontraumatized controls. RSA magnitude was positively correlated with right but not left hemisphere ACC volume. This finding was statistically independent of the presence or absence of PTSD.

Estimating heart rate and RSA from the mattress‐recorded kinetocardiogram

This article describes a method for extracting heart rate (HR) and respiratory sinus arrhythmia (RSA) from the kinetocardiogram (KCG) recorded from accelerometers embedded in a mattress topper. Validation has been performed via comparison with simultaneously recorded ECG. All-night estimates of HR and RSA magnitude derived from both methods were highly correlated. KCG-derived estimates of HR were slightly lower, and those of RSA magnitude higher, than those derived from ECG. These biases are consistent with the need to constrain KCG estimation to periods free of body movement. Mattress actigraphy represents a zero-burden method of obtaining intensive longitudinal indices of cardiac status.

Vagal nerve activity contributes to improve the efficiency of pulmonary gas exchange in hypoxic humans

The aim of this study was to test our hypothesis that both phasic cardiac vagal activity and tonic pulmonary vagal activity, estimated as respiratory sinus arrhythmia (RSA) and anatomical dead space volume, respectively, contribute to improve the efficiency of pulmonary gas exchange in humans. We examined the effect of blocking vagal nerve activity with atropine on pulmonary gas exchange. Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit with a respiratory analyser. Arterial partial pressure of O(2) (P(aO(2))) and arterial oxygen saturation (S(pO(2))) were measured, and alveolar-to-arterial P(O(2)) difference (D(A-aO(2))) was calculated. Anatomical dead space (V(D,an)), alveolar dead space (V(D,alv)) and the ratio of physiological dead space to tidal volume (V(D,phys)/V(T)) were measured. Electrocardiogram was recorded, and the amplitude of R-R interval variability in the high-frequency component (RRIHF) was utilized as an index of RSA magnitude. These parameters of pulmonary function were measured before and after administration of atropine (0.02 mg kg(-1)). Decreased RRIHF (P < 0.01) was accompanied by decreases in P(aO(2)) and S(pO(2)) (P < 0.05 and P < 0.01, respectively) and an increase in D(A-aO(2)) (P < 0.05). Anatomical dead space, V(D,alv) and V(D,phys)/V(T) increased (P < 0.01, P < 0.05 and P < 0.01, respectively) after atropine administration. The blockade of the vagal nerve with atropine resulted in an increase in V(D,an) and V(D,alv) and a deterioration of pulmonary oxygenation, accompanied by attenuation of RSA. Our findings suggest that both phasic cardiac and tonic pulmonary vagal nerve activity contribute to improve the efficiency of pulmonary gas exchange in hypoxic conscious humans.