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Journal articles on the topic 'Periodic breathing'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

KELLY, DOROTHY H., DAVID W. CARLEY, and DANIEL C. SHANNON. "Periodic Breathing." Annals of the New York Academy of Sciences 533, no. 1 The Sudden In (August 1988): 301–4. http://dx.doi.org/10.1111/j.1749-6632.1988.tb37259.x.

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2

Strohl, Kingman P. "Periodic breathing and genetics." Respiratory Physiology & Neurobiology 135, no. 2-3 (May 2003): 179–85. http://dx.doi.org/10.1016/s1569-9048(03)00036-3.

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3

Burleson, Mark L. "Periodic breathing in fishes." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 126 (July 2000): S20. http://dx.doi.org/10.1016/s0305-0491(00)80039-5.

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4

Fowler, A. C. "Periodic breathing at high altitude." Mathematical Medicine and Biology 19, no. 4 (December 1, 2002): 293–313. http://dx.doi.org/10.1093/imammb/19.4.293.

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5

Han, Fang, Shyam Subramanian, Edwin R. Price, Joseph Nadeau, and Kingman P. Strohl. "Periodic breathing in the mouse." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1133–40. http://dx.doi.org/10.1152/japplphysiol.00785.2001.

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The hypothesis was that unstable breathing might be triggered by a brief hypoxia challenge in C57BL/6J (B6) mice, which in contrast to A/J mice are known not to exhibit short-term potentiation; as a consequence, instability of ventilatory behavior could be inherited through genetic mechanisms. Recordings of ventilatory behavior by the plethsmography method were made when unanesthetized B6 or A/J animals were reoxygenated with 100% O2 or air after exposure to 8% O2 or 3% CO2-10% O2 gas mixtures. Second, we examined the ventilatory behavior after termination of poikilocapnic hypoxia stimuli in recombinant inbred strains derived from B6 and A/J animals. Periodic breathing (PB) was defined as clustered breathing with either waxing and waning of ventilation or recurrent end-expiratory pauses (apnea) of ≥2 average breath durations, each pattern being repeated with a cycle number ≥3. With the abrupt return to room air from 8% O2, 100% of the 10 B6 mice exhibited PB. Among them, five showed breathing oscillations with apnea, but none of the 10 A/J mice exhibited cyclic oscillations of breathing. When the animals were reoxygenated after 3% CO2-10% O2 challenge, no PB was observed in A/J mice, whereas conditions still induced PB in B6 mice. (During 100% O2 reoxygenation, all 10 B6 mice had PB with apnea.) Expression of PB occurred in some but not all recombinant mice and was not associated with the pattern of breathing at rest. We conclude that differences in expression of PB between these strains indicate that genetic influences strongly affect the stability of ventilation in the mouse.

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6

Ribeiro, Jorge P. "Periodic Breathing in Heart Failure." Circulation 113, no. 1 (January 3, 2006): 9–10. http://dx.doi.org/10.1161/circulationaha.105.590265.

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7

Agostoni, Piergiuseppe, Ugo Corrà, and Michele Emdin. "Periodic Breathing during Incremental Exercise." Annals of the American Thoracic Society 14, Supplement_1 (July 2017): S116—S122. http://dx.doi.org/10.1513/annalsats.201701-003fr.

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8

Liippo, K., H. Puolijoki, and E. Tala. "Periodic Breathing Imitating Hyperventilation Syndrome." Chest 102, no. 2 (August 1992): 638–39. http://dx.doi.org/10.1378/chest.102.2.638.

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9

Nugent, S. T., and J. P. Finley. "Spectral analysis of the EMG and diaphragmatic muscle fatigue during periodic breathing in infants." Journal of Applied Physiology 58, no. 3 (March 1, 1985): 830–33. http://dx.doi.org/10.1152/jappl.1985.58.3.830.

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Periodic breathing occurs commonly in full-term and preterm infants. The mechanisms which switch breathing on and off within a cycle of periodic breathing are not certain. Since immature infants may experience diaphragmatic muscle fatigue, one potential switching mechanism is fatigue. Power spectra of the electromyogram, uncontaminated by the electrocardiograph artifact, were studied for evidence of diaphragmatic muscle fatigue during spontaneous periodic breathing in infants. A fall in the high-frequency (103–600 Hz) power and an increase in the low-frequency (23–47 Hz) power during periodic as compared with normal breathing would indicate fatigue. This effect was not observed in any of the infants studied. Hence, there is no evidence that periodic breathing is the result of diaphragmatic muscle fatigue. This finding suggests that the effect of drugs such as theophylline in eliminating periodic breathing may be unrelated to the fact that they also reduce fatigue.

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10

Keyl, Cornelius, Peter Lemberger, Michael Pfeifer, Karin Hochmuth, and Peter Geisler. "Heart Rate Variability in Patients with Daytime Sleepiness Suspected of Having Sleep Apnoea Syndrome: A Receiver-Operating Characteristic Analysis." Clinical Science 92, no. 4 (April 1, 1997): 335–43. http://dx.doi.org/10.1042/cs0920335.

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1. Periodic breathing is known to be associated with cyclic fluctuations in heart rate. The purpose of this study was to evaluate the capability of spectral analysis of heart rate variability to identify episodes with periodic breathing in patients suspected of having sleep apnoea syndrome. 2. Forty-eight subjects complaining of chronic daytime sleepiness were studied using polysomnography and additional monitoring of Holter-ECG and synchronized pulse oximetry. The recordings were divided into 20 min episodes which were identified as recordings registered during normal breathing, periodic breathing, and periods of both normal and abnormal breathing. Power spectral analysis was performed on episodes which met the criteria of stationarity of data (313 episodes with normal breathing, 264 episodes with continuous periodic breathing, 80 episodes with both normal and periodic breathing pattens). 3. The ability of parameters, derived from analysis of heart rate variability, to discriminate between episodes with normal and periodic breathing was assessed by receiver-operating characteristic analysis. 4. The spectral power component in the frequency range 0.01–0.07 Hz revealed the greatest accuracy for discriminating between normal and periodic breathing (area under the receiver-operating characteristic curve = 0.929; standard error = 0.009). The analysis of the episodes classified as false-positive at a given test sensitivity of 90% and a corresponding specificity of 77% revealed that half of these episodes had been recorded during transient central nervous arousal reactions related to periodic leg movements or heavy snoring. 5. We concluded that power spectral analysis of heart rate variability offers a possible means of identifying episodes of sleep-related breathing disorders or periodic leg movements. Therefore, analysis of heart rate variability may be a valuable additional diagnostic tool in patients undergoing Holter-ECG recording.

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11

Cherniack, Neil S. "Apnea and Periodic Breathing during Sleep." New England Journal of Medicine 341, no. 13 (September 23, 1999): 985–87. http://dx.doi.org/10.1056/nejm199909233411310.

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12

Bartsch, Stephen, and Philippe Haouzi. "Periodic Breathing With No Heart Beat." Chest 144, no. 4 (October 2013): 1378–80. http://dx.doi.org/10.1378/chest.12-2950.

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13

Naughton, Matthew T. "Periodic breathing: Fine tuning the phenotype." Respirology 25, no. 3 (August 7, 2019): 240–41. http://dx.doi.org/10.1111/resp.13657.

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14

Roberts, John L., and David M. Rowell. "Periodic respiration of gill-breathing fishes." Canadian Journal of Zoology 66, no. 1 (January 1, 1988): 182–90. http://dx.doi.org/10.1139/z88-025.

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Rhythmic and arrhythmic patterns of breathing are common among gill-breathing fishes. Irregular, short bouts of apnea occur in most fishes during feeding, while long apneic periods are routine for many open-water fishes such as scombrids, which ram ventilate during cruise swimming. During ram ventilation, the work of gill ventilation is transferred from the respiratory to the swimming musculature, with energy savings due to reductions in drag and inertial losses. Noncontinuous swimmers, such as some benthic and midwater marine and freshwater species, seldom cease rhythmic respiratory movements or resort to ram ventilation. When quiescent, they may adopt patterns of secondary cycling, alternating between respiratory pauses and short periods of rhythmic branchial pumping. Types and locations of chemo- and mechano-receptors that trigger changes in respiratory patterns of fish are being identified, as are the reflex pathways linking them to brainstem respiratory centers. A new mechanoreceptor is described that overlies the adductor mandibulae jaw muscles and may be of use in the modulation of cyclic respiratory movements. Respiratory switching control between rhythmic and ram gill ventilation is discussed.

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15

Wißkirchen and Teschler. "Central sleep apnea and periodic breathing." Therapeutische Umschau 57, no. 7 (July 1, 2000): 458–62. http://dx.doi.org/10.1024/0040-5930.57.7.458.

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Anders als die obstruktive Schlafapnoe ist die zentrale Schlafapnoe nicht durch einen Kollaps der oberen Atemwege im Schlaf gekennzeichnet, sondern basiert meist auf einer Instabilität der Atemregulation mit periodisch oszillierendem oder ausfallendem Atemantrieb, wofür eine Vielzahl von Erkrankungen ursächlich in Betracht kommen. Die Patienten fallen gewöhnlich nicht durch Hypersomnolenz, sondern insomnische Beschwerden auf. Die häufigste zentrale Schlafapnoe ist die periodische Atmung oder Cheyne-Stokes-Atmung. Sie findet sich überwiegend bei schwerer Herzinsuffizienz und zerebralen Erkrankun-gen mit Hirnstammbeteiligung. Bei herzinsuffizienten Patienten hat das Auftreten einer periodischen Atmung prognostische Bedeutung. An validierten Therapieformen stehen zur Zeit die nasale Sauerstoffgabe, die Anwendung von nasal kontinuierlichem Atemwegsdruck (sog. nCPAP) und medikamentöse Therapien zur Verfügung. Neuere Beatmungsverfahren werden zur Zeit erprobt.

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16

Agostoni, Piergiuseppe, and Elisabetta Salvioni. "Exertional Periodic Breathing in Heart Failure." Clinics in Chest Medicine 40, no. 2 (June 2019): 449–57. http://dx.doi.org/10.1016/j.ccm.2019.02.016.

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17

Ghazanshahi, Shahin D., and Michael C. K. Khoo. "Optimal ventilatory patterns in periodic breathing." Annals of Biomedical Engineering 21, no. 5 (September 1993): 517–30. http://dx.doi.org/10.1007/bf02584334.

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18

Gleeson, K., and C. W. Zwillich. "Adenosine infusion and periodic breathing during sleep." Journal of Applied Physiology 72, no. 3 (March 1, 1992): 1004–9. http://dx.doi.org/10.1152/jappl.1992.72.3.1004.

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Intravenously administered adenosine may increase ventilation (VI) and the ventilatory response to CO2 (HCVR). Inasmuch as we have previously hypothesized that those with higher HCVR may be more prone to periodic breathing during sleep, we measured VI and HCVR and monitored ventilatory pattern in seven healthy subjects before and during an infusion of adenosine (80 micrograms.kg-1.min-1) during uninterrupted sleep. Adenosine increased the mean sleeping VI (7.6 +/- 0.4 vs. 6.5 +/- 0.4 l/min, P less than 0.05) and decreased mean end-tidal CO2 values (42.4 +/- 1.2 vs. 43.7 +/- 1.0 Torr, P = 0.06, paired t test) during stable breathing. In six of seven subjects, periodic breathing occurred during this infusion. The amplitude (maximum VI--mean VI) and period length of this periodic breathing was variable among subjects and not predicted by baseline HCVR [correlation coefficients (r) = 0.64, P = 0.17 and r = -0.1, P = 0.9, respectively]. Attempts to measure HCVR during adenosine infusion were unsuccessful because of frequent arousals and continued periodic breathing despite hyperoxic hypercapnia. We conclude that adenosine infusion increases VI and produces periodic breathing during sleep in most normal subjects studied.

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19

Agostoni, Piergiuseppe, Michele Emdin, Fabiana De Martino, Anna Apostolo, Marco Masè, Mauro Contini, Cosimo Carriere, Carlo Vignati, and Gianfranco Sinagra. "Roles of periodic breathing and isocapnic buffering period during exercise in heart failure." European Journal of Preventive Cardiology 27, no. 2_suppl (November 26, 2020): 19–26. http://dx.doi.org/10.1177/2047487320952029.

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In heart failure, exercise – induced periodic breathing and end tidal carbon dioxide pressure value during the isocapnic buffering period are two features identified at cardiopulmonary exercise testing strictly related to sympathetic activation. In the present review we analysed the physiology behind periodic breathing and the isocapnic buffering period and present the relevant prognostic value of both periodic breathing and the presence/absence of the identifiable isocapnic buffering period.

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20

Miller, M. J., W. A. Carlo, J. M. DiFiore, and R. J. Martin. "Airway obstruction during periodic breathing in premature infants." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2496–500. http://dx.doi.org/10.1152/jappl.1988.64.6.2496.

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To characterize changes in pulmonary resistance, timing, and respiratory drive during periodic breathing, we studied 10 healthy preterm infants (body wt 1,340 +/- 240 g, postconceptional age 35 +/- 2 wk). Periodic breathing in these infants was defined by characteristic cycles of ventilation with intervening respiratory pauses greater than or equal to 2 s. Nasal airflow was recorded with a pneumotachometer, and esophageal or pharyngeal pressure was recorded with a fluid-filled catheter. Pulmonary resistance at half-maximal tidal volume, inspiratory time (TI), expiratory time (TE), and mean inspiratory flow (VT/TI) were derived from computer analysis of five cycles of periodic breathing per infant. In 80% of infants periodic breathing was accompanied by completely obstructed breaths at the onset of ventilatory cycles; the site of airway obstruction occurred within the pharynx. The first one-third of the ventilatory phase of each cycle was accompanied by the highest airway resistance of the entire cycle (168 +/- 98 cmH2O.l-1.s). In all infants TI was greatest at the onset of the ventilatory cycle, VT/TI was maximal at the midpoint of the cycle, and TE was longest in the latter two-thirds of each cycle. A characteristic increase and subsequent decrease of 4.5 +/- 1.9 ml in end-expiratory volume also occurred within each cycle. These results demonstrate that partial or complete airway obstruction occurs during periodic breathing. Both apnea and periodic breathing share the element of upper airway instability common to premature infants.

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21

Canet, Emmanuel, Jean-Paul Praud, and Michel A. Bureau. "Periodic breathing induced on demand in awake newborn lamb." Journal of Applied Physiology 82, no. 2 (February 1, 1997): 607–12. http://dx.doi.org/10.1152/jappl.1997.82.2.607.

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Canet, Emmanuel, Jean-Paul Praud, and Michel A. Bureau.Periodic breathing induced on demand in awake newborn lamb. J. Appl. Physiol. 82(2): 607–612, 1997.—Spontaneous periodic breathing, although a common feature in fullterm and preterm human infants, is scarce in other newborn mammals. The aim of this study was to induce periodic breathing in lambs. Four 10-day-old and two <48-h-old awake lambs were instrumented with jugular catheters connected to an extracorporeal membrane lung aimed at controlling arterial [Formula: see text]([Formula: see text]). Arterial[Formula: see text]([Formula: see text]) was set and maintained at the desired level by changing inspired O2 fraction and providing O2 through a small catheter into the “apneic” lung. At a critical[Formula: see text]/[Formula: see text]combination, the four 10-day-old lambs exhibited periodic breathing that could be initiated, terminated, and reinitiated on demand. In the 2-day-old lambs with low chemoreceptor gain, periodic breathing was hardly seen, regardless of the trials done to find the critical[Formula: see text]/[Formula: see text]combination. We conclude that periodic breathing can be induced in lambs and depends on critical[Formula: see text]/[Formula: see text]combinations and maturity of the chemoreceptors.

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22

Chapman, K. R., E. N. Bruce, B. Gothe, and N. S. Cherniack. "Possible mechanisms of periodic breathing during sleep." Journal of Applied Physiology 64, no. 3 (March 1, 1988): 1000–1008. http://dx.doi.org/10.1152/jappl.1988.64.3.1000.

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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.

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23

Onal, E., D. L. Burrows, R. H. Hart, and M. Lopata. "Induction of periodic breathing during sleep causes upper airway obstruction in humans." Journal of Applied Physiology 61, no. 4 (October 1, 1986): 1438–43. http://dx.doi.org/10.1152/jappl.1986.61.4.1438.

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To test the hypothesis that occlusive apneas result from sleep-induced periodic breathing in association with some degree of upper airway compromise, periodic breathing was induced during non-rapid-eye-movement (NREM) sleep by administering hypoxic gas mixtures with and without applied external inspiratory resistance (9 cmH2O X l-1 X s) in five normal male volunteers. In addition to standard polysomnography for sleep staging and respiratory pattern monitoring, esophageal pressure, tidal volume (VT), and airflow were measured via an esophageal catheter and pneumotachograph, respectively, with the latter attached to a tight-fitting face mask, allowing calculation of total pulmonary system resistance (Rp). During stage I/II NREM sleep minimal period breathing was evident in two of the subjects; however, in four subjects during hypoxia and/or relief from hypoxia, with and without added resistance, pronounced periodic breathing developed with waxing and waning of VT, sometimes with apneic phases. Resistive loading without hypoxia did not cause periodicity. At the nadir of periodic changes in VT, Rp was usually at its highest and there was a significant linear relationship between Rp and 1/VT, indicating the development of obstructive hypopneas. In one subject without added resistance and in the same subject and in another during resistive loading, upper airway obstruction at the nadir of the periodic fluctuations in VT was observed. We conclude that periodic breathing resulting in periodic diminution of upper airway muscle activity is associated with increased upper airway resistance that predisposes upper airways to collapse.

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24

Tomcsányi, J., K. Karlócai, and L. Papp. "Disappearance of periodic breathing after heart operations." Journal of Thoracic and Cardiovascular Surgery 107, no. 1 (January 1994): 317–18. http://dx.doi.org/10.1016/s0022-5223(94)70495-3.

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25

Bradley, T. Douglas. "The ups and downs of periodic breathing." Journal of the American College of Cardiology 41, no. 12 (June 2003): 2182–84. http://dx.doi.org/10.1016/s0735-1097(03)00470-4.

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26

Canet, E., J. L. Carroll, and M. A. Bureau. "Hypoxia-induced periodic breathing in newborn lambs." Journal of Applied Physiology 67, no. 3 (September 1, 1989): 1226–33. http://dx.doi.org/10.1152/jappl.1989.67.3.1226.

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This study was designed to elucidate the effect of hypoxia on the breathing rhythmicity and the effect of hypoxia on periodic breathing (PB) in two groups of newborn lambs (less than 2 days and 10 days of age). Lambs undergoing a hypoxic ventilatory test [0.08 inspired O2 fraction (FIo2) for 13 min] experienced no apnea or PB in hypoxia, but all developed PB during the 1-min period immediately after their abrupt return to 0.21 FIo2. This PB occurred when alternation of arterial PO2 and PCO2 in mild hypoxic and hypocapnic conditions induced an overshoot-undershoot response of the chemical drive to breathe. The magnitude of PB was found to be greater in the animals with a higher peripheral chemoreflex sensitivity to hypoxia but ceased altogether when the hypoxic-hypocapnic conditions were resolved. When these conditions were removed more quickly, that is, when the animals were returned either to 0.50 FIo2 or to 0.03 FIco2, no PB was observed. To clarify the role of hypoxia as a central depressant on the genesis of PB, we tested to determine whether additional central tissue hypoxia, using carboxyhemoglobin (30%), would worsen the episodes of PB. No effect on breathing rhythmicity was observed. These findings suggest not only that, in newborn animals and adults, the mechanisms of post-hypoxia-induced PB are identical but that the PB elicited in mild hypoxic conditions is a peripheral chemoreflex-mediated event rather than a centrally mediated one.

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27

Schulz, R., G. Baseler, H. A. Ghofrani, F. Grimminger, H. Olschewski, and W. Seeger. "Nocturnal periodic breathing in primary pulmonary hypertension." European Respiratory Journal 19, no. 4 (April 2002): 658–63. http://dx.doi.org/10.1183/09031936.02.00225102.

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28

Bourque, Danielle K., David A. Dyment, Ian MacLusky, Kristin D. Kernohan, and Hugh J. McMillan. "Periodic breathing in patients with NALCN mutations." Journal of Human Genetics 63, no. 10 (July 3, 2018): 1093–96. http://dx.doi.org/10.1038/s10038-018-0484-1.

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29

Marcus, Carole L. "Periodic Breathing in an Infant with Hydrocephalus." New England Journal of Medicine 334, no. 24 (June 13, 1996): 1577. http://dx.doi.org/10.1056/nejm199606133342405.

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30

Nugent, Sherwin T., and John P. Finley. "Periodic Breathing in Infants: A Model Study." IEEE Transactions on Biomedical Engineering BME-34, no. 6 (June 1987): 482–85. http://dx.doi.org/10.1109/tbme.1987.326059.

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31

Welborn, Leila G., Nina Ramirez, Tae Hee Oh, Urs E. Ruttimann, Robertt Fink, Philip Guzzetta, and Burton S. Epstein. "Postanesthetic Apnea and Periodic Breathing in Infants." Anesthesiology 65, no. 6 (December 1, 1986): 658–61. http://dx.doi.org/10.1097/00000542-198612000-00015.

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32

Shannon, Daniel C., David W. Carley Phd, and Dorothy H. Kelly. "Periodic breathing: Quantitative analysis and clinical description." Pediatric Pulmonology 4, no. 2 (1988): 98–102. http://dx.doi.org/10.1002/ppul.1950040207.

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33

Glotzbach, S. F., P. A. Tansey, R. B. Baldwin, and R. L. Ariagno. "Periodic Breathing Cycle Duration in Preterm Infants." Pediatric Research 25, no. 3 (March 1989): 258–61. http://dx.doi.org/10.1203/00006450-198903000-00007.

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34

Barrington, Keith J., and Neil N. Finer. "Periodic Breathing and Apnea in Preterm Infants." Pediatric Research 27, no. 2 (February 1990): 118–21. http://dx.doi.org/10.1203/00006450-199002000-00003.

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35

Cherniack, Neil S. "Putting Numbers to Theories about Periodic Breathing." American Journal of Respiratory and Critical Care Medicine 167, no. 2 (January 15, 2003): 112–13. http://dx.doi.org/10.1164/rccm.2210004.

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36

Lee, S., Y. Kim, S. Kim, and K. Im. "0430 CENTRAL PERIODIC BREATHING IN ACUTE STROKE." Sleep 40, suppl_1 (April 28, 2017): A160. http://dx.doi.org/10.1093/sleepj/zsx050.429.

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37

Mohr, Mary A., Karen D. Fairchild, Manisha Patel, Robert A. Sinkin, Matthew T. Clark, J. Randall Moorman, Douglas E. Lake, John Kattwinkel, and John B. Delos. "Quantification of periodic breathing in premature infants." Physiological Measurement 36, no. 7 (May 27, 2015): 1415–27. http://dx.doi.org/10.1088/0967-3334/36/7/1415.

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38

Tarakanov, I. A., V. A. Safonov, G. A. Semkina, and E. A. Golovatyuk. "Experimental model of apneusis and periodic breathing." Bulletin of Experimental Biology and Medicine 114, no. 1 (July 1992): 936–39. http://dx.doi.org/10.1007/bf00790047.

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39

Levine, M., J. P. Cleave, and C. Dodds. "Can periodic breathing have advantages for oxygenation?" Journal of Theoretical Biology 172, no. 4 (February 1995): 355–68. http://dx.doi.org/10.1006/jtbi.1995.0033.

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40

Patel, Manisha, Mary Mohr, Douglas Lake, John Delos, J. Randall Moorman, Robert A. Sinkin, John Kattwinkel, and Karen Fairchild. "Clinical associations with immature breathing in preterm infants: part 2—periodic breathing." Pediatric Research 80, no. 1 (March 22, 2016): 28–34. http://dx.doi.org/10.1038/pr.2016.58.

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41

West, J. B., R. M. Peters, G. Aksnes, K. H. Maret, J. S. Milledge, and R. B. Schoene. "Nocturnal periodic breathing at altitudes of 6,300 and 8,050 m." Journal of Applied Physiology 61, no. 1 (July 1, 1986): 280–87. http://dx.doi.org/10.1152/jappl.1986.61.1.280.

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Nocturnal periodic breathing was studied in eight well-acclimatized subjects living at an altitude of 6,300 m [barometric pressure (PB) 350–352 Torr] for 3–5 wk and in four subjects during one night at 8,050 m altitude (PB 281–285 Torr). The measurements at 6,300 m included tidal volume by inductance plethysmography, arterial O2 saturation by ear oximetry (calibrated by arterial blood samples), electrocardiogram (ECG), and electrooculogram. At 8,050 m, periodic breathing was inferred from the cyclical variation in heart rate obtained from a night-long ECG record. All subjects at 6,300 m altitude showed well-marked periodic breathing with apneic periods. Cycle length averaged 20.5 s with 7.9 s apnea. Minimal arterial O2 saturation averaged 63.4% corresponding to a PO2 of approximately 33 Torr, i.e., approximately 6 Torr lower than the normal value at rest during daytime. This was probably the most severe hypoxemia of the 24-h period. At 8,050 m altitude, the cycle length averaged 15.4 s, much longer than predicted by a theoretical model. Cyclical variations in heart rate caused by periodic breathing occurred in all subjects, but abnormal cardiac rhythms such as ventricular premature contractions were uncommon. The severe arterial hypoxemia caused by periodic breathing may be an important determinant of tolerance to these great altitudes.

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42

Bissonnette, John M., and Sharon J. Knopp. "Effect of inspired oxygen on periodic breathing in methy-CpG-binding protein 2 (Mecp2) deficient mice." Journal of Applied Physiology 104, no. 1 (January 2008): 198–204. http://dx.doi.org/10.1152/japplphysiol.00843.2007.

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Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the X-linked gene methyl-CpG-binding protein 2 ( Mecp2) that encodes a DNA binding protein involved in gene silencing. Periodic breathing (Cheyne-Stokes respiration) is commonly seen in RTT. Freely moving mice were studied with continuous recording of pleural pressure by telemetry. Episodes of periodic breathing in heterozygous Mecp2 deficient (Mecp2+/−) female mice (9.4 ± 2.2 h−1) exceeded those in wild-type (Mecp2+/+) animals (2.5 ± 0.4 h−1) ( P = 0.010). Exposing Mecp2+/− animals to 40% oxygen increased the amount of periodic breathing from 118 ± 25 s/30 min in air to 242 ± 57 s/30 min ( P = 0.001), and 12% oxygen tended to decrease it (67 ± 29 s/30 min, P = 0.14). Relative hyperoxia and hypoxia did not affect the incidence of periodic breathing in Mecp2+/+ animals. The ventilation/apnea ratio (V/A) was less at all levels of oxygen in heterozygous Mecp2+/− females compare with wild type ( P = 0.003 to P < 0.001), indicating that their loop gain is larger. V/A in Mecp2+/− fell from 2.42 ± 0.18 in normoxia to 1.82 ± 0.17 in hyperoxia ( P = 0.05) indicating an increase in loop gain with increased oxygen. Hyperoxia did not affect V/A in Mecp2+/+ mice (3.73 ± 0.28 vs. 3.5 ± 0.28). These results show that periodic breathing in this mouse model of RTT is not dependent on enhanced peripheral chemoreceptor oxygen sensitivity. Rather, the breathing instability is of central origin.

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Khan, Akram, Mansour Qurashi, Kim Kwiatkowski, Don Cates, and Henrique Rigatto. "Measurement of the CO2 apneic threshold in newborn infants: possible relevance for periodic breathing and apnea." Journal of Applied Physiology 98, no. 4 (April 2005): 1171–76. http://dx.doi.org/10.1152/japplphysiol.00574.2003.

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We measured the Pco2 apneic threshold in preterm and term infants. We hypothesized that, compared with adult subjects, the Pco2 apneic threshold in neonates is very close to the eupneic Pco2, likely facilitating the appearance of periodic breathing and apnea. In contrast with adults, who need to be artificially hyperventilated to switch from regular to periodic breathing, neonates do this spontaneously. We therefore measured the apneic threshold as the average alveolar Pco2 (PaCO2) of the last three breaths of regular breathing preceding the first apnea of an epoch of periodic breathing. We also measured the PaCO2 of the first three breaths of regular breathing after the last apnea of the same periodic breathing epoch. In preterm infants, eupneic PaCO2 was 38.6 ± 1.4 Torr, the preperiodic PaCO2 apneic threshold was 37.3 ± 1.4 Torr, and the postperiodic PaCO2 was 37.2 ± 1.4 Torr. In term infants, the eupneic PaCO2 was 39.7 ± 1.1 Torr, the preperiodic PaCO2 apneic threshold was 38.7 ± 1.0 Torr, and the postperiodic value was 37.9 ± 1.2 Torr. This means that the PaCO2 apneic thresholds were 1.3 ± 0.1 and 1.0 ± 0.2 Torr below eupneic PaCO2 in preterm and term infants, respectively. The transition from eupneic PaCO2 to PaCO2 apneic threshold preceding periodic breathing was accompanied by a minor and nonsignificant increase in ventilation, primarily related to a slight increase in frequency. The findings suggest that neonates breathe very close to their Pco2 apneic threshold, the overall average eupneic Pco2 being only 1.15 ± 0.2 Torr (0.95–1.79, 95% confidence interval) above the apneic threshold. This value is much lower than that reported for adult subjects (3.5 ± 0.4 Torr). We speculate that this closeness of eupneic and apneic Pco2 thresholds confers great vulnerability to the respiratory control system in neonates, because minor oscillations in breathing may bring eupneic Pco2 below threshold, causing apnea.

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Eleuteri, Michela, Erica Ipocoana, Jana Kopfová, and Pavel Krejčí. "Periodic solutions of a hysteresis model for breathing." ESAIM: Mathematical Modelling and Numerical Analysis 54, no. 1 (January 2020): 255–57. http://dx.doi.org/10.1051/m2an/2019060.

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We propose to model the lungs as a viscoelastic deformable porous medium with a hysteretic pressure–volume relationship described by the Preisach operator. Breathing is represented as an isothermal time-periodic process with gas exchange between the interior and exterior of the body. The main result consists in proving the existence of a periodic solution under an arbitrary periodic forcing in suitable function spaces.

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Wellman, Andrew, Atul Malhotra, Robert B. Fogel, Jill K. Edwards, Karen Schory, and David P. White. "Respiratory system loop gain in normal men and women measured with proportional-assist ventilation." Journal of Applied Physiology 94, no. 1 (January 1, 2003): 205–12. http://dx.doi.org/10.1152/japplphysiol.00585.2002.

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We hypothesized that increased chemical control instability (CCI) in men could partially explain the male predominance in obstructive sleep apnea (OSA). CCI was assessed by sequentially increasing respiratory control system loop gain (LG) with proportional-assist ventilation (PAV) in 10 men (age 24–48 yr) and 9 women (age 22–36 yr) until periodic breathing or awakening occurred. Women were studied in both the follicular and luteal phases of the menstrual cycle. The amount by which PAV amplified LG was quantified from the tidal volume amplification factor [(VtAF) assisted tidal volume/unassisted tidal volume]. LG was calculated as the inverse of the VtAF occurring at the assist level immediately preceding the emergence of periodic breathing (when LG × VtAF = 1). Only 1 of 10 men and 2 of 9 women developed periodic breathing with PAV. The rest were resistant to periodic breathing despite moderately high levels of PAV amplification. We conclude that LG is low in the majority of normal men and women and that higher volume amplification factors are needed to determine whether gender differences exist in this low range.

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FRANCIS, Darrel P., L. Ceri DAVIES, Keith WILLSON, Piotr PONIKOWSKI, Andrew J. S. COATS, and Massimo PIEPOLI. "Very-low-frequency oscillations in heart rate and blood pressure in periodic breathing: role of the cardiovascular limb of the hypoxic chemoreflex." Clinical Science 99, no. 2 (July 10, 2000): 125–32. http://dx.doi.org/10.1042/cs0990125.

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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.

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Kim, T. S., and M. C. Khoo. "Estimation of cardiorespiratory transfer under spontaneous breathing conditions: a theoretical study." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (August 1, 1997): H1012—H1023. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h1012.

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Using simulated noisy sequences of respiration and heart rate, we assessed the accuracy of the respiratory sinus arrhythmia transfer function (RSATF) estimation under three kinds of spontaneous breathing patterns: regular or tidal breathing, periodic breathing with apnea, and broadband breathing. Estimation employing the cross-power and autopower spectra of the simulated data produced RSATF estimates that were generally more variable than those computed with an autoregressive modeling approach. Variability and bias errors in the RSATF estimates became larger as respiratory bandwidth decreased when the breathing pattern changed from broadband to periodic to regular breathing. However, between frequencies of 0.1 and 0.3 Hz, these errors fell within 12% in all breathing patterns. Error in the RSATF estimates was only slightly increased, with reductions in data length to as low as 90 s. The results suggest the feasibility of obtaining accurate estimates of RSATF between 0.1 and 0.8 Hz from a wide variety of conditions, such as in different sleep-wake states where voluntary control of breathing is not possible and the ventilatory pattern may vary substantially.

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Ribeiro, Jorge Pinto, Anders Knutzen, Michael B. Rocco, L. Howard Hartley, and Wilson S. Colucci. "Periodic Breathing during Exercise in Severe Heart Failure." Chest 92, no. 3 (September 1987): 555–56. http://dx.doi.org/10.1378/chest.92.3.555.

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Luo, Weili, and Tengda Du. "Periodic breathing oscillations and instabilities in ferrofluids (abstract)." Journal of Applied Physics 79, no. 8 (1996): 6034. http://dx.doi.org/10.1063/1.362080.

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Shogilev, Daniel J., John B. Tanner, Yuchiao Chang, and N. Stuart Harris. "Periodic Breathing and Behavioral Awakenings at High Altitude." Sleep Disorders 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/279263.

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Objectives. To study the relationship between nocturnal periodic breathing episodes and behavioral awakenings at high altitude.Methods. Observational study. It is 6-day ascent of 4 healthy subjects from Besisahar (760 meters) to Manang (3540 meters) in Nepal in March 2012. A recording pulse oximeter was worn by each subject to measure their oxygen saturation and the presence of periodic breathing continuously through the night. An actigraph was simultaneously worn in order to determine nocturnal behavioral awakenings. There were no interventions.Results. 187-hour sleep at high altitude was analyzed, and of this, 145 hours (78%) had at least one PB event. At high altitude, 10.5% (95% CI 6.5–14.6%) of total sleep time was spent in PB while 15 out of 50 awakenings (30%, 95% CI: 18–45%) occurring at high altitudes were associated with PB (P<0.001).Conclusions. Our data reveals a higher than expected number of behavioral awakenings associated with PB compared to what would be expected by chance. This suggests that PB likely plays a role in behavioral awakenings at high altitude.

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