scholarly journals Apnea and periodic breathing in bed-sharing and solitary sleeping infants

1998 ◽  
Vol 84 (4) ◽  
pp. 1374-1380 ◽  
Author(s):  
Christopher A. Richard ◽  
Sarah S. Mosko ◽  
James J. McKenna
Keyword(s):  
Respiratory Control ◽  
Random Order ◽  
Periodic Breathing ◽  
Developmental Differences ◽  
Behavioral Effects ◽  
Sleep Laboratory ◽  
Physiological Effects ◽  
Central Apnea ◽  
Bed Sharing

Mother-infant bed sharing, compared with the solitary sleeping condition, has recently been associated with several physiological and behavioral effects. Because the physiological effects of bed sharing may also include respiratory changes, we compared the incidence of central and obstructive apneas and periodic breathing in bed-sharing and solitary sleeping infants. Twenty routinely bed-sharing mother-infant pairs and fifteen routinely solitary sleeping pairs slept for 3 nights in a sleep laboratory. After an initial adaptation night, each pair spent 1 night bed sharing and 1 night in solitary sleep in random order. Apnea and periodic breathing were scored from polysomnographic recordings. The frequency of central apnea was significantly increased on the bed-sharing night, compared with the solitary night, regardless of routine sleeping arrangement. There were significantly fewer obstructive apneas on the bed-sharing night than on the solitary night, but only in routinely solitary sleeping infants. In both groups, there was a significantly higher frequency of periodic breathing events on the bed-sharing night than on the solitary night. These findings demonstrate that the bed-sharing environment can have a significant impact on respiratory control in the infant. Evidence is also presented to suggest that routine bed sharing may result in subtle neurophysiological and/or developmental differences in infants.

Incidence of Apnea in Siblings of Sudden Infant Death Syndrome Victims Studied at Home

PEDIATRICS ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 128-131
Author(s):  
Dorothy H. Kelly ◽  
Joseph Twanmoh ◽  
Daniel C. Shannon
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Chronic Hypoxia ◽  
Breathing Pattern ◽  
Respiratory Control ◽  
Periodic Breathing ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Sudden Infant ◽  
Sibling Group

Victims of sudden infant death syndrome (SIDS) have been shown to have pathologic abnormalities consistent with chronic hypoxia.1-7 Two groups of infants at high risk of dying of SIDS, near miss infants and subsequent siblings of SIDS victims, have been studied in attempts to demonstrate physiologic abnormalities that could account for these pathologic findings. Investigators have found abnormalities in breathing pattern and the respiratory control system in the former consisting of prolonged sleep apnea, excessive short apnea, periodic breathing, hypoventilation, and depressed response to hypercarbia.8-13 However, studies in the SIDS sibling group have demonstrated varying results of excessive periodic breathing in the home14 and decreased apnea in the laboratory.15

Relative stability of human respiration during progressive hypoxia

1988 ◽  
Vol 65 (3) ◽  
pp. 1389-1399 ◽  
Author(s):  
D. W. Carley ◽  
D. C. Shannon
Keyword(s):  
Mathematical Model ◽  
Control System ◽  
Relative Stability ◽  
Respiratory Control ◽  
Periodic Breathing ◽  
Adult Males ◽  
Human Respiration ◽  
Progressive Hypoxia ◽  
The Mean ◽  
Breathing Room

We have systematically studied the relationship between the relative stability (R) of respiration and the loop gain (LG) of the CO2 control system in 15 healthy awake adult males during progressive hypoxia. R was measured by the ventilatory oscillations after brief (less than 10 s) CO2 challenges. Control theory suggests that such oscillations are completely governed by LG. A significant positive correlation was found between R and LG (r = 0.74, P less than 0.01, n = 85). A minimal mathematical model of respiratory control was used to predict R as a function of LG. Serial correlation analysis (r = 0.09, P greater than 0.1) of the residuals indicated statistical agreement between predictions and observations. The mean residual (0.011) was not significantly different from zero (P greater than 0.1). Also, as the model predicted, sustained periodic breathing (PB) occurred whenever the estimated LG was greater than unity. The mean LG breathing room air was 0.51 and for the 13 epochs of PB was 1.17 (range 0.71-1.65). It is concluded that PB is a quantitative extension of the relative stability continuum and corresponds to unstable operation of the CO2 control system. Furthermore, relative stability can be quantitatively predicted for each subject by a minimal mathematical model.

Effects of sleep deprivation on respiratory events during sleep in healthy infants

1989 ◽  
Vol 66 (3) ◽  
pp. 1158-1163 ◽  
Author(s):  
E. Canet ◽  
C. Gaultier ◽  
A. M. D'Allest ◽  
M. Dehan
Keyword(s):  
Sleep Deprivation ◽  
Total Duration ◽  
Periodic Breathing ◽  
Central Apnea ◽  
Quiet Sleep ◽  
Term Infants ◽  
Event Time ◽  
Respiratory Events ◽  
Healthy Infants ◽  
Respiratory Event

This study was designed to determine the effects of sleep deprivation on respiratory events during sleep in healthy infants. Ten unsedated full-term infants (1–6 mo) were monitored polygraphically during “afternoon naps” on a control day and on the day after sleep deprivation. Respiratory events, i.e., central apnea, obstructive apnea and hypopnea, and periodic breathing were tabulated. Results for respiratory events were expressed as 1) indexes of the total number of respiratory events and of specific respiratory events per hour of total sleep (TST), “quiet” sleep (QS) and “active” sleep (AS) times; 2) total duration of total and specific respiratory events, expressed as a percentage of TST, QS, and AS times. After sleep deprivation, significant increases were observed for 1) respiratory event (P less than 0.001), central apnea (P less than 0.05), and obstructive respiratory event (P less than 0.01) indexes; 2) respiratory event time as a percentage of TST (P less than 0.002) and as a percentage of AS time (P less than 0.001); 3) obstructive respiratory event time as a percentage of TST (P less than 0.01), QS (P less than 0.05), and AS times (P less than 0.002). The present study shows that short-term sleep deprivation in healthy infants increases the number and timing of respiratory events, especially obstructive events in AS.

Possible mechanisms of periodic breathing during sleep

1988 ◽  
Vol 64 (3) ◽  
pp. 1000-1008 ◽  
Author(s):  
K. R. Chapman ◽  
E. N. Bruce ◽  
B. Gothe ◽  
N. S. Cherniack
Keyword(s):  
Control System ◽  
Respiratory Control ◽  
Periodic Breathing ◽  
Nrem Sleep ◽  
Loop Gain ◽  
Hypoxic Conditions ◽  
Spontaneous Oscillations ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Stage 1

To determine the effect of respiratory control system loop gain on periodic breathing during sleep, 10 volunteers were studied during stage 1-2 non-rapid-eye-movement (NREM) sleep while breathing room air (room air control), while hypoxic (hypoxia control), and while wearing a tight-fitting mask that augmented control system gain by mechanically increasing the effect of ventilation on arterial O2 saturation (SaO2) (hypoxia increased gain). Ventilatory responses to progressive hypoxia at two steady-state end-tidal PCO2 levels and to progressive hypercapnia at two levels of oxygenation were measured during wakefulness as indexes of controller gain. Under increased gain conditions, five male subjects developed periodic breathing with recurrent cycles of hyperventilation and apnea; the remaining subjects had nonperiodic patterns of hyperventilation. Periodic breathers had greater ventilatory response slopes to hypercapnia under either hyperoxic or hypoxic conditions than nonperiodic breathers (2.98 ± 0.72 vs. 1.50 ± 0.39 l.min-1.Torr-1; 4.39 ± 2.05 vs. 1.72 ± 0.86 l.min-1.Torr-1; for both, P less than 0.04) and greater ventilatory responsiveness to hypoxia at a PCO2 of 46.5 Torr (2.07 ± 0.91 vs. 0.87 ± 0.38 l.min-1.% fall in SaO2(-1); P less than 0.04). To assess whether spontaneous oscillations in ventilation contributed to periodic breathing, power spectrum analysis was used to detect significant cyclic patterns in ventilation during NREM sleep. Oscillations occurred more frequently in periodic breathers, and hypercapnic responses were higher in subjects with oscillations than those without. The results suggest that spontaneous oscillations in ventilation are common during sleep and can be converted to periodic breathing with apnea when loop gain is increased.

Interactions of atrial and brain natriuretic peptides at pathophysiological levels in normal men

1995 ◽  
Vol 269 (6) ◽  
pp. R1397-R1403 ◽  
Author(s):  
P. J. Hunt ◽  
E. A. Espiner ◽  
A. M. Richards ◽  
T. G. Yandle ◽  
C. Frampton ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Random Order ◽  
Normal Male ◽  
Metabolic Clearance ◽  
Physiological Effects ◽  
Brain Natriuretic Peptides ◽  
Normal Humans ◽  
Normal Men

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are both circulating plasma hormones that are secreted by the heart and have similar physiological effects. We have shown previously that abrupt increases in plasma BNP in normal humans impair the clearance of ANP from plasma and result in additive physiological effects. Because large increases in plasma ANP are reported to have no effect on plasma BNP levels in patients with heart failure, we have studied ANP-BNP interactions in eight normal male subjects receiving background infusions of BNP (2 pmol.kg-1.min-1 for 5 h). Each subject also received a coinfusion of ANP ("active" day, 2 pmol.kg-1.min-1 for 2 h) or vehicle ("placebo" day) using a balanced random order, single-blind design. Metabolic clearance rate of ANP (mean 4.1 +/- 0.6 l/min) and disappearance rate from the plasma (t1/2 3.4 +/- 0.3 min) were similar to values measured previously in the absence of exogenous BNP. In contrast, steady-state plasma BNP levels were reversibly increased (mean BNP increment 10 pmol/l) during the administration of ANP (P = 0.038). Associated with these changes were significant (additive) physiological effects. Thus the addition of ANP increased plasma and urine guanosine 3',5'-cyclic monophosphate (P < 0.001 for both) and lowered systolic blood pressure (P = 0.049). When ANP was coinfused, significant differences were also observed in urine volume (P = 0.001) and sodium excretion (P = 0.043) between the infusion period (when urine volume and sodium excretion were enhanced) and postinfusion period (when values decreased). Taken together, our findings of similar interactions between ANP-BNP and BNP-ANP infusions occurring at pathophysiological concentrations of these two peptides, suggest that the interactions result from dissociation of prebound hormone, presumably from biological or clearance receptors.

Maturational effect of enkephalin on respiratory control in newborn rabbits

1982 ◽  
Vol 53 (5) ◽  
pp. 1063-1070 ◽  
Author(s):  
M. M. Grunstein ◽  
J. S. Grunstein
Keyword(s):  
Respiratory Control ◽  
Periodic Breathing ◽  
Opioid Peptide ◽  
Time Profile ◽  
Central Inspiratory Activity ◽  
Age Dependent ◽  
Inspiratory Activity ◽  
Afferent Influence ◽  
The Stability ◽  
Age Range

The respiratory responses to systemic infusion of the opioid peptide, [D-Ala2, D-Leu5]enkephalin (ENK) were determined in 39 unanesthetized tracheotomized rabbits (age range 1–20 days). At all ages, ventilation (VE), measured in a body plethysmograph, was depressed after ENK infusion in association with a decrease in CO2 elimination (VCO2) and body temperature. The degree of VE depression varied inversely with increasing age and was directly related to changes in mean inspiratory flow (i.e., VT/TI) while the ratio of inspiratory to total breath duration (TI/TT) was unaltered, except in rabbits under about 1 wk of age. Maturational differences in the VE response to ENK were related to age-dependent variation in the stability of the central inspiratory activity, which was manifested as periodic breathing with apnea in rabbits under about 5 days of age. Since the initial inspiratory volume-time profile was little affected by ENK and vagal afferent influence on respiration was not diminished, the depression in VE could be explained by an inhibition of the central inspiratory “off-switch” threshold and delay in central inspiratory “on-switching.” All effects of ENK were reversed by the opiate antagonist, naloxone.

Determinants of poststimulus potentiation in humans during NREM sleep

1992 ◽  
Vol 73 (5) ◽  
pp. 1958-1971 ◽  
Author(s):  
M. S. Badr ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Control Period ◽  
Periodic Breathing ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Central Apnea ◽  
Inhibitory Effects ◽  
Arterial Pco2 ◽  
End Tidal ◽  
Sustained Hypoxia

To test whether active hyperventilation activates the “afterdischarge” mechanism during non-rapid-eye-movement (NREM) sleep, we investigated the effect of abrupt termination of active hypoxia-induced hyperventilation in normal subjects during NREM sleep. Hypoxia was induced for 15 s, 30 s, 1 min, and 5 min. The last two durations were studied under both isocapnic and hypocapnic conditions. Hypoxia was abruptly terminated with 100% inspiratory O2 fraction. Several room air-to-hyperoxia transitions were performed to establish a control period for hyperoxia after hypoxia transitions. Transient hyperoxia alone was associated with decreased expired ventilation (VE) to 90 +/- 7% of room air. Hyperoxic termination of 1 min of isocapnic hypoxia [end-tidal PO2 (PETO2) 63 +/- 3 Torr] was associated with VE persistently above the hyperoxic control for four to six breaths. In contrast, termination of 30 s or 1 min of hypocapnic hypoxia [PETO2 49 +/- 3 and 48 +/- 2 Torr, respectively; end-tidal PCO2 (PETCO2) decreased by 2.5 or 3.8 Torr, respectively] resulted in hypoventilation for 45 s and prolongation of expiratory duration (TE) for 18 s. Termination of 5 min of isocapnic hypoxia (PETO2 63 +/- 3 Torr) was associated with central apnea (longest TE 200% of room air); VE remained below the hyperoxic control for 49 s. Termination of 5 min of hypocapnic hypoxia (PETO2 64 +/- 4 Torr, PETCO2 decreased by 2.6 Torr) was also associated with central apnea (longest TE 500% of room air). VE remained below the hyperoxic control for 88 s. We conclude that 1) poststimulus hyperpnea occurs in NREM sleep as long as hypoxia is brief and arterial PCO2 is maintained, suggesting the activation of the afterdischarge mechanism; 2) transient hypocapnia overrides the potentiating effects of afterdischarge, resulting in hypoventilation; and 3) sustained hypoxia abolishes the potentiating effects of after-discharge, resulting in central apnea. These data suggest that the inhibitory effects of sustained hypoxia and hypocapnia may interact to cause periodic breathing.

scholarly journals 475 Automatic detection of self-similarity and prediction of CPAP failure

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A187-A187
Author(s):  
Eline Oppersma ◽  
Wolfgang Ganglberger ◽  
Haoqi Sun ◽  
Robert Thomas ◽  
Michael Westover
Keyword(s):  
Sleep Apnea ◽  
Significant Risk ◽  
Periodic Breathing ◽  
Driving Mechanism ◽  
Central Apnea ◽  
Loop Gain ◽  
Breathing Patterns ◽  
Self Similarity ◽  
High Loop ◽  
Cpap Failure

Abstract Introduction Sleep disordered breathing is a significant risk factor for cardiometabolic and neurodegenerative diseases. Tolerance and efficacy of continuous positive airway pressure (CPAP), the primary form of therapy for sleep apnea, is often poor. High loop gain (HLG) is a driving mechanism of central sleep apnea or periodic breathing. The current study aimed to develop a computational approach to detect HLG based on self-similarity in respiratory oscillations during sleep solely using breathing patterns, measured via Respiratory Inductance Plethysmography (RIP). To quantify the potential utility of the developed similarity metric, the presented algorithm was used to predict acute CPAP failure. Methods We developed an algorithm for detecting apneas as periods with reduced breathing effort, manifested in the RIP signal as low signal amplitude. Our algorithm calculates self-similarity in breathing patterns between consecutive periods of apnea or hypopnea. Working under the assumption that high loop gain induces self-similar respiratory oscillations and increases the risk of failure during CPAP, the full night similarity, computed during diagnostic non-CPAP polysomnography (PSG), was used to predict failure of CPAP, which we defined as titration central apnea index (CAI)&gt;10. Central apnea labels are obtained both from manual scoring by sleep technologists, and from an automated algorithm developed for this study. The Massachusetts General Hospital (MGH) sleep database was used, including 2466 PSG pairs of diagnostic and CPAP titration PSG recordings. Results Diagnostic CAI based on technologist labels predicted failure of CPAP with an AUC of 0.82 ±0.03. Based on automatically generated labels, the combination of full night similarity and automatically generated CAI resulted in an AUC of 0.85 ±0.02. A subanalysis was performed on a population with technologist labeled diagnostic CAI&gt;5. Full night similarity predicted failure with an AUC of 0.57 ±0.07 for manual and 0.65 ±0.06 for automated labels. Conclusion This study showed that central apnea labels can be derived in an automated way. The proposed self-similarity feature, as a surrogate estimate of expressed respiratory high loop gain and computed from easily accessible effort signals, can detect periodic breathing regardless of admixed obstructive features such as flow-limitation, and can aid prediction of CPAP failure or success. Support (if any):

Description of central apnea and periodic breathing in children

2020 ◽  
Author(s):  
Sergio Ghirardo ◽  
Alessandro Amaddeo ◽  
Sonia Khirani ◽  
Lucie Griffon ◽  
Brigitte Fauroux
Keyword(s):  
Periodic Breathing ◽  
Central Apnea

scholarly journals Physiological Effects of Different Recruitment Maneuvers in a Pig Model of ARDS

2020 ◽  
Author(s):  
Feiping Xia ◽  
Chun Pan ◽  
Lihui Wang ◽  
Ling Liu ◽  
Songqiao Liu ◽  
...  
Keyword(s):  
Random Order ◽  
Pig Model ◽  
Physiological Effects ◽  
Impedance Tomography ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Recruitment Maneuvers ◽  
Sustained Inflation ◽  
Significant Difference ◽  
Before And After

Abstract Background: In acute respiratory distress syndrome (ARDS), lung recruitment maneuvers can recruit collapsed alveoli in gravity-dependent lung regions, improving the homogeneity of ventilation distribution. This study used electrical impedance tomography (EIT) to investigate the physiological effects of different recruitment maneuvers for alveolar recruitment in a pig model of ARDS. Methods: ARDS was induced in ten healthy male pigs with repeated bronchoalveolar lavage until the arterial partial pressure of oxygen (PaO2)/fraction of inspired oxygen (FiO2) (P/F ratio) was < 100 mmHg and remained stable for 30 minutes (TARDS). ARDS pigs underwent three sequential recruitment maneuvers, including sustained inflation (SI), increments of positive end-expiratory pressure (PEEP) (IP), and pressure-controlled ventilation (PCV) applied in random order, with 30 mins at a PEEP of 5 cmH2O between maneuvers. Respiratory mechanics, hemodynamics, arterial blood gas, and EIT were recorded at baseline, TARDS, and before and after each recruitment maneuver.Results: In all ten pigs, ARDS was successfully induced with a mean 2.8±1.03L (2800±1032.80ml) bronchoalveolar lavages. PaO2, SO2, P/F, and compliance were significantly improved after recruitment with SI, IP or PCV (all p<0.05), and there were no significant differences between maneuvers. Global inhomogeneity (GI) was significantly decreased after recruitment with SI, IP, or PCV. There were no significant differences in GI before or after recruitment with the different maneuvers. The decrease in GI (ΔGI) was significantly greater after recruitment with IP compared to SI (p=0.023), but there was no significant difference in ΔGI between IP and PCV.Conclusion: SI, IP, and PCV increased oxygenation, and regional and global compliance of the respiratory system, and decreased inhomogeneous gas distribution in ARDS pigs. IP significantly improved inhomogeneity of the lung compared to SI.

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