Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnea
Among patients with similar degrees of obstructive sleep apnea (OSA) there is considerable variability in the degree of associated nocturnal hypoxemia. The factors responsible for this variability have not been clearly defined. Therefore we studied 44 patients with OSA to identify the physiological determinants of nocturnal arterial O2 saturation (SaO2). All patients underwent pulmonary function testing, arterial blood gas analysis, and overnight polysomnography. Mean nocturnal SaO2 ranged from 96 to 66% and apnea-hypopnea index from 11 to 128 per hour of sleep. Several anthropometric, respiratory physiological, and polysomnographic variables that could be expected to influence nocturnal SaO2 were entered into a stepwise multiple linear regression analysis, with mean nocturnal SaO2 as the dependent variable. Three variables [awake supine arterial PO2 (PaO2), expiratory reserve volume, and percentage of sleep time spent in apnea] were found to correlate strongly with mean nocturnal SaO2 (multiple R, 0.854; P less than 0.0001) and accounted for 73% of its variability among patients. Body weight, other lung volumes, and airflow rates influenced awake PaO2 and expiratory reserve volume but had no independent influence on nocturnal SaO2. In a further group of 15 patients with OSA a high correlation was obtained between measured nocturnal SaO2 and that predicted by the model (r = 0.87; P less than 0.001). We conclude that derangements of pulmonary mechanics and awake PaO2 (generally attributable to obesity and diffuse airway obstruction) are of major importance in establishing the severity of nocturnal hypoxemia in patients with OSA.
Available from: Izabela Grabska-Kobylecka
- "Due to repeated apnea and/or hypopnea episodes, nocturnal PaO2 can fall below 50 mmHg in OSAS patients [11,12] and thus favor activation and enhance ROS production by means of blood phagocytes. Scanty and conflicting data concerning ROS production by blood phagocytes in the course of OSAS have been published so far [13-16]. "
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ABSTRACT: Obstructive sleep apnea syndrome (OSAS) is a recognized risk factor for cardiovascular morbidity and mortality, perhaps due to causative exacerbations of systemic oxidative stress. Putative oxidative stress related to numerous episodes of intermittent hypoxia, may be an oxidants chief driving force in OSAS patients.
We assessed the resting and n-formyl-methionyl-leucyl-phenylalanine (fMLP)- induced whole blood chemiluminescence (as a measure of oxidant production by polymorphonuclear leukocytes and monocytes), ferric reducing ability of plasma (FRAP) and H2O2 generation in the whole blood of 27 untreated OSAS patients, 22 subjects after a night of CPAP therapy and 11 controls without OSAS. All of them were matched to age, BMI (body mass index) and smoking habits. All parameters were measured before and after polysomnography-controlled sleep, individual results were obtained as a mean from duplicated experiments.
No significant differences were distinguished between evening and morning blood chemiluminescence, H2O2 activity and FRAP within and between all three study groups.For instance patients with untreated OSAS had similar morning and evening resting whole blood chemiluminescence (2.3 +/- 2.2 vs. 2.4 +/- 2.2 [aU.10-4 phagocytes]), total light emission after stimulation with fMLP (1790 +/- 1371 vs. 1939 +/- 1532 [aU.s.10-4 phagocytes]), as well as FRAP after 3 min. plasma incubation (602 +/- 202 vs. 671 +/- 221 [uM]). Although, in the subgroup of 11 patients with severe OSAS (apnea/hypopnea index 58 +/- 18/h and oxygen desaturation index 55 +/- 19/h), the morning vs. evening resting chemiluminescence and total light emission after stimulation with fMLP observed a propensity to elevate 2.5 +/- 2.7 vs. 1.9 +/- 1.8 [aU.10-4 phagocytes] and 1778 +/- 1442 vs. 1503 +/- 1391 [aU.s.10-4 phagocytes], respectively, these did not attain statistical significance (p > 0.05).
Our investigation exposed no evidence in the overproduction of oxidants via circulating phagocytes, once considered a culprit in the oxidative stress of OSAS patients.
Journal of Negative Results in BioMedicine 12/2008; 7(1):10. DOI:10.1186/1477-5751-7-10 · 1.47 Impact Factor
Available from: unc.edu
- "Previous studies in middle-aged adults (30-50 years) report that when associated with apneas, EEG arousals evoke such large increases in the amplitude of breathing cycles that they shorten the duration of desaturations during sleep (Badr et al., 1997; Basner, Onal, Stepanski, & Lopata, 1995; D. M. Carlson, Carley, Onal, Lopata, & Basner, 1994). Similar studies in young adults indicate that it is the magnitude of the increase in the amplitude of breathing cycles that follow an apnea or hypopnea event that is predictive of the rate of return of the oxygen level to normal following the event (Bradley et al., 1985; Findley et al., 1983). Given that arousals are important for restoring ventilation after desaturations during sleep, prolonged desaturations might be a result of either failure to initiate an arousal or an inability to alter breathing patterns when an arousal occurs. "
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ABSTRACT: The aim of this exploratory study was to examine the relationship of electroencephalogram (EEG) arousals to breathing patterns and the relationship of both arousals and breathing patterns to arterial oxygenation during sleep in older adults. Five older adults were monitored using standard polysomnography. Records were divided into 5-min segments and breathing patterns identified based on the level of respiratory periodicity and the variability in the frequency of breathing cycles. Standard criteria were used to determine sleep states and occurrence of EEG arousals. High respiratory periodicity was seen in 23% of the segments, whereas 24% had low respiratory periodicity with minimal variability in the frequency of breathing (Type A low respiratory periodicity) and 53% had low respiratory periodicity with high variability in the frequency of breathing (Type B low respiratory periodicity). Nearly all (97%) segments with high respiratory periodicity had EEG arousals, whereas fewer segments (33%) with low respiratory periodicity had arousals, regardless of the stage of sleep. Desaturations occurred more often in segments with high respiratory periodicity, F((2,4)) = 57.3, p < .001, but overall, the mean SaO(2) of segments with high respiratory periodicity did not differ from levels seen in segments with low respiratory periodicity, F((2,4)) = 0.77, ns. Our findings suggest that high respiratory periodicity is a common feature of EEG arousals and, in older adults, may be important for maintaining oxygen levels during desaturations during sleep.
Biological Research for Nursing 04/2007; 8(4):249-60. DOI:10.1177/1099800406298072 · 1.43 Impact Factor
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ABSTRACT: This review addresses some current controversies and issues of interest in sleep-related disorders of breathing.
Abnormalities of respiratory control may influence the degree of obstructive sleep apnea but it is likely that abnormalities
of pharyngeal size are of far greater significance.
Central sleep apnea is a heterogeneous condition. Examples of all the causes one would postulate leading to cessation of drives
to breathe do occur, hence appropriate therapies also vary.
It is not yet known what aspect of, and how much, disordered breathing during sleep leads to morbidity, thus fixed definitions
of normality are not helpful.
Recurrent nocturnal asphyxia alone is unlikely to result in chronic respiratory failure. Associated diffuse airways obstruction
or impaired respiratory muscle function is probably necessary before this complication arises.
The recurent REM sleep-induced dips of Sao2 in patients with chronic airways obstruction may be due to physiological inhibition of accessory muscles of respiration.
This leads to considerable hypoventilation and recurrent activation of an intact, but displaced, hypoxic drive, resulting
in the characteristic oscillations of Sao2.
Beiträge zur Klinik der Tuberkulose 02/1986; 164(1):17-31. DOI:10.1007/BF02713626 · 2.27 Impact Factor
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