UMLS:C0037315 - FACTA Search

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Query: UMLS:C0037315 (sleep apnea)
8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiology of obstructive sleep apnoea syndrome (OSAS) is complex and incompletely understood, but is principally based on an imbalance between the collapsing forces of the upper airway (UA) during inspiration and the counteracting dilating forces of the UA dilating muscles. A narrowed UA is very common among OSAS patients, which is usually due, in adults, to nonspecific factors such as fat deposition in the neck or abnormal bony morphology of the UA. Functional impairment of the UA dilating muscles is particularly important in the development of OSAS, and patients have a reduction in both tonic and phasic contraction of these muscles during sleep when compared to normal subjects. Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea because of a reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. A cyclical pattern of repetitive obstructive apnoeas may result. A better understanding of the integrated pathophysiology of obstructive sleep apnoea syndrome should help both in the choice of optimum therapy for each individual patient and also in the development of new therapeutic techniques.
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PMID:Implications of pathophysiology for management of the obstructive sleep apnoea syndrome. 986 12

We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25-35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21-43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (VT) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in VT to 155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/- 0.57 Torr. In men, induction of a central apnea required an increase in VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr (P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.
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PMID:Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep. 1090 52

Given that the apnea-ventilation cycle length during central sleep apnea (CSA) with congestive heart failure (CHF) is approximately 70 s, we hypothesized that rapidly responsive peripheral CO(2) ventilatory responses would be raised in CHF-CSA and would correlate with the severity of CSA. Sleep studies and single breath and rebreathe hypercapnic ventilatory responses (HCVR) were measured as markers of peripheral and central CO(2) ventilatory responses, respectively, in 51 subjects: 12 CHF with no apnea (CHF-N), 8 CHF with obstructive sleep apnea (CHF-OSA), 12 CHF-CSA, 11 CSA without CHF ("idiopathic" CSA; ICSA), and 8 normal subjects. Single breath HCVR was equally elevated in CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (0.58 +/- 0.09 [mean +/- SE] and 0. 58 +/- 0.07 versus 0.23 +/- 0.06, 0.25 +/- 0.04, and 0.27 +/- 0.02 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Similarly, rebreathe HCVR was elevated in both CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (5.80 +/- 1.12 and 3.53 +/- 0. 29 versus 2.00 +/- 0.25, 1.44 +/- 0.16, and 2.14 +/- 0.22 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Furthermore, in the entire CHF group, single breath HCVR correlated with central apnea-hypopnea index (AHI) (r = 0.63, p < 0.001) and percentage central/total apneas (r = 0.52, p = 0.022). Rebreathe HCVR correlated with awake Pa(CO(2)) (r = -0.61, p < 0.001), but not with central AHI or percentage central/total apneas independent of its relationship with single breath HCVR. In conclusion, in subjects with CHF, raised central CO(2) ventilatory response predisposes to CSA promoting background hypocapnia and exposing the apnea threshold to fluctuations in ventilation, whereas raised and faster-acting peripheral CO(2) ventilatory response determines the periodicity and severity of CSA.
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PMID:Peripheral and central ventilatory responses in central sleep apnea with and without congestive heart failure. 1111 37

Hypocapnia contributes to the genesis of Cheyne-Stokes respiration and central sleep apnoea in patients with congestive heart failure (CHF) and is associated with increased mortality. However, the cause of hypocapnia in patients with chronic stable CHF is unknown. Since pulmonary congestion can induce hyperventilation via stimulation of pulmonary vagal afferents, the present study tested the hypothesis that in patients with CHF (carbon dioxide tension in arterial blood (Pa,CO2)) is inversely related to pulmonary capillary wedge pressure (PCWP), and that alterations in PCWP would cause inverse changes in Pa,CO2. In 11 CHF patients undergoing diagnostic cardiac catheterization, haemodynamic variables and arterial blood gas tensions were measured simultaneously at baseline. In three patients, these measurements were repeated after coronary angiographic dye infusion and nitroglycerine infusion. At baseline, Pa,CO2 correlated inversely with PCWP (r=-0.80, p=0.003). In the three patients in whom multiple measurements were made, acute alterations in PCWP caused inversely proportional changes in Pa,CO2. The present study concludes that in patients with congestive heart failure, pulmonary capillary wedge pressure is an important determinant of carbon dioxide tension in arterial blood. These findings imply that hypocapnia in patients with chronic stable congestive heart failure is a respiratory manifestation of elevated left ventricular filling pressures.
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PMID:Relationship of carbon dioxide tension in arterial blood to pulmonary wedge pressure in heart failure. 1184 25

Ventilation serves the exchange of gases between the organism and the environment. Oxygen uptake and CO2 elimination are controlled by feedback loops, that keep fluctuations in arterial CO2 pressure (PaCO2) within narrow limits Disorders in the central regulation of breathing, or impairment of the respiratory apparatus, may result in a mismatch between metabolic CO2 production and ventilatory CO2, elimination and thus in fluctuations in the PaCO2: inappropriately increased ventilation (hyperventilation) causes hypocapnia, and reduced ventilation (hypoventilation) causes hypercapnia. In order to detect such disorders during sleep, PCO2 measurement is of great importance, but direct and continuous measurement of the PaCO2 is invasive and thus unsuitable in the clinical setting. An alternative is capnography, the continuous measurement of PCO2 in inhaled and exhaled air on the basis of ultrared light absorption. This paper reviews the method, its features and limitations, and the possibilities of improving capnography to better detect sleep-related breathing disorders. In addition, data obtained from 57 patients with predominantly normal lung function, but suspected sleep disordered breathing are presented. Simultaneous measurements of capnography PETCO2) and capillary PaCO2 revealed a PETCO2 difference of +0.63 +/- 3.3 (SD) Torr. PaCO2 (38.8 +/- 4.1 Torr) and PETCO2 (38.1 +/- 4.3 Torr) were not significantly different with a correlation coefficient of r = 0.68 (p < 0.001). Thus 46% of the variation in PETCO2 was explained by changes in PaCO2. Currently the literature contains few further data on capnography during sleep. It is concluded that, provided the limitations of the method are respected and comparison with the PETCO2 is made, capnography may be a useful, noninvasive and continuous measuring method for assessing ventilation during sleep in patients with suspected sleep related breathing disorders.
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PMID:[Method for measuring respiration in sleep: capnography for determining ventilation]. 1286 57

Altered chemoresponsiveness has been postulated to explain the gender difference in the incidence of sleep disordered breathing (SDB). The purpose of this investigation was to ascertain a gender difference in the effect of hypocapnic hypoxia on ventilation. Hypocapnic hypoxia was induced in stable NREM sleep for 3 min periods. In the first analysis, hypoxic ventilatory response in a steady state (SHVR) was defined as the amount of change in minute ventilation (VI) between mean room air (RA) and hypoxia divided by the change in Sa O2 between RA and hypoxia (DeltaVI/DeltaSa O2). The mean group SHVR values were 0.23+/-0.15 and 0.20+/-0.10 L/min per %SaO2, for men and women, respectively (P = ns). In the second analysis, we analyzed the decline in ventilatory parameters after the cessation of hypoxia. There was no difference in VI between the genders (men, 5.6+/-1.7 L/min vs. women, 4.9+/-1.9 L/min, P = ns). We conclude that the gender difference in SDB is not explained by a difference in the ventilatory response to hypocapnic hypoxia.
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PMID:Lack of gender difference in ventilatory chemoresponsiveness and post-hypoxic ventilatory decline. 1287 76

Sleep apnea is attributable, in part, to an unstable ventilatory control system and specifically to a narrowed "CO2 reserve" (i.e., the difference in P(a)CO2 between eupnea and the apneic threshold). Findings from sleeping animal preparations with denervated carotid chemoreceptors or vascularly isolated, perfused carotid chemoreceptors demonstrate the critical importance of peripheral chemoreceptors to the ventilatory responses to dynamic changes in P(a)CO2. Specifically, (i) carotid body denervation prevented the apnea and periodic breathing that normally follow transient ventilatory overshoots; (ii) the CO2 reserve for peripheral chemoreceptors was about one half that for brain chemoreceptors; and (iii) hypocapnia isolated to the carotid chemoreceptors caused hypoventilation that persisted over time despite a concomitant, progressive brain respiratory acidosis. Observations in both humans and animals are cited to demonstrate the marked plasticity of the CO2 reserve and, therefore, the propensity for apneas and periodic breathing, in response to changing background ventilatory stimuli.
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PMID:The essential role of carotid body chemoreceptors in sleep apnea. 1289 6

Arousals from sleep result in hyperventilation and hypocapnia that can lead to sleep apnoea. We have investigated whether sleep apnoea in the elderly is associated with more arousals compared with younger people. Additionally, the impact of arousals on daytime symptoms was noted. Four groups (n = 11) of elderly (> 65 years) and young (< 39 years) apnoeic (EA and YA), and age-matched non-apnoeics (EN and YN) were studied. The arousal index (AI) and apnoea/hypopnoea index were determined from polysomnography. Sleepiness (Epworth Sleepiness Scale) and Quality of life (QoL, SF-36) were assessed. The mean (SD) AI was: EN 23.1 (7.6), EA 46.5 (8.8), YN 13.2 (6.6), YA 38.5 (12.1) events/h. AI was higher in the elderly (P = 0.002) and in apnoeics (P = 0.001); however, the increase in AI associated with sleep apnoea was not age dependent (P = 0.73). The influence of sleep apnoea on sleepiness was similar in both age groups. YA but not EA reported reduced physical functioning (P = 0.04), vitality (P = 0.007) and general health (P = 0.04) compared to non-apnoeics. We conclude that (1) the effect of sleep apnoea on arousal is no greater in the elderly compared to the young (2) despite similar levels of sleepiness, elderly apneoics perceive a reduced loss of QoL compared to younger patients.
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PMID:Sleep apnoea and daytime function in the elderly--what is the impact of arousal frequency? 1456 Oct 17

Sleep unmasks a highly sensitive hypocapnia-induced apnoeic threshold, whereby apnoea is initiated by small transient reductions in arterial CO(2) pressure (P(aCO(2))) below eupnoea and respiratory rhythm is not restored until P(aCO(2)) has risen significantly above eupnoeic levels. We propose that the 'CO(2) reserve' (i.e. the difference in P(aCO(2)) between eupnoea and the apnoeic threshold (AT)), when combined with 'plant gain' (or the ventilatory increase required for a given reduction in P(aCO(2))) and 'controller gain' (ventilatory responsiveness to CO(2) above eupnoea) are the key determinants of breathing instability in sleep. The CO(2) reserve varies inversely with both plant gain and the slope of the ventilatory response to reduced CO(2) below eupnoea; it is highly labile in non-random eye movement (NREM) sleep. With many types of increases or decreases in background ventilatory drive and P(aCO(2)), the slope of the ventilatory response to reduced P(aCO(2)) below eupnoea remains unchanged from control. Thus, the CO(2) reserve varies inversely with plant gain, i.e. it is widened with hyperventilation and narrowed with hypoventilation, regardless of the stimulus and whether it acts primarily at the peripheral or central chemoreceptors. However, there are notable exceptions, such as hypoxia, heart failure, or increased pulmonary vascular pressures, which all increase the slope of the CO(2) response below eupnoea and narrow the CO(2) reserve despite an accompanying hyperventilation and reduced plant gain. Finally, we review growing evidence that chemoreceptor-induced instability in respiratory motor output during sleep contributes significantly to the major clinical problem of cyclical obstructive sleep apnoea.
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PMID:The ventilatory responsiveness to CO(2) below eupnoea as a determinant of ventilatory stability in sleep. 1528 45

During sleep, maintenance of rhythmic breathing is critically dependent on the level of PCO(2), such that if the prevailing spontaneous PCO(2) decreases below the apneic threshold, central sleep apnea (CSA) occurs. Several studies have shown that in patients with systolic heart failure (SHF), presence of a low, awake arterial PCO(2) (Pa(CO(2))) increases the likelihood of developing CSA during sleep. We therefore sought to determine if a low Pa(CO(2)) is a predictor of CSA in patients with cirrhosis of the liver and with normal left ventricular systolic function. In 13 hypocapnic (Pa(CO(2)) < 36 mm Hg, mean = 33 mm Hg) patients with SHF and a mean left ventricular ejection fraction of 23%, the mean apnea-hypopnea index, was 28/hour. CSA accounted for most of the breathing disorders. In 10 hypocapnic (Pa(CO(2)) < 36 mm Hg, mean = 32 mm Hg) patients with cirrhosis and a normal left ventricular ejection fraction (60%), the mean apnea-hypopnea index was 2/hour. The maximum central apnea index was 0.2/hour. There were no significant differences in age, demographics, pulmonary function tests, Pa(O(2)), Pa(CO(2)), minute and alveolar ventilation, and ventilatory responses to CO(2) between the two groups. We conclude that, in contrast to SHF, presence of hypocapnia does not predict CSA in cirrhosis.
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PMID:Hypocapnia is not a predictor of central sleep apnea in patients with cirrhosis. 1565 65

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