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

The gas composition of breathing air is a very important stimulus for the control of breathing. The different partial pressures of O2 and CO2 independently trigger individually different reactions (respiratory response), which can be measured as a change of respiratory minute volume. Investigations of the respiratory control in patients with obstructive sleep apnoea (OSA) have up to now been restricted to an analysis of the breathing patterns at night. Therefore we have developed a computer-controlled device which allows a flexible composition of the air to be inhaled using a regulated feet-back circle. With this system it is possible to produce a hypercapnia test as well as a hyperoxia and an isocapnic hypoxia test. The simultaneous recording of all relevant respiratory parameters (AF, AMV, ETCO2, SpO2, FiO2) and the parallel recording of continuous blood pressure allow a quantitative description of the respiratory regulation of patients with OSA with exactly defined tests.
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PMID:[Measuring hypoxic and hypercapnic respiratory response in patients with obstructive sleep apnea]. 1246 25

Sleep hypoventilation (SH) may be important in the development of hypercapnic respiratory failure in chronic obstructive pulmonary disease (COPD). The prevalence of SH, associated factors, and overnight changes in waking arterial blood gases (ABG), were assessed in 54 stable hypercapnic COPD patients without concomitant sleep apnoea or morbid obesity. Lung function assessment, anthropomorphic measurements, and polysomnography with ABG measurement before and after sleep were conducted in all patients. Transcutaneous carbon dioxide tension (Pt,CO2) was measured in sleep, using simultaneous arterial carbon dioxide tension (Pa,CO2) for in vivo calibration and to correct for drift in the sensor. Of the patients, 43% spent > or = 20% of sleep time with Pt,CO2 > 1.33 kPa (10 mmHg) above waking baseline. Severity of SH was best predicted by a combination of baseline Pa,CO2, body mass index and per cent rapid-eye movement (REM) sleep. REM-related hypoventilation correlated significantly with severity of inspiratory flow limitation in REM, and with apnoea/hypopnoea index. Pa,CO2 increased mean+/-SD 0.70+/-0.65 kPa (5.29+/-4.92 mmHg) from night to morning, and this change was highly significant. The change in Pa,CO2 was strongly correlated with severity of SH. Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease, and related to baseline arterial carbon dioxide tension, body mass index and indices of upper airway obstruction. Sleep hypoventilation is associated with significant increases in arterial carbon dioxide tension night-to-morning, and may contribute to long-term elevations in arterial carbon dioxide tension.
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PMID:Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors. 1279 91

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

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

Sleep apnea syndromes are more common in men than in women. The ventilatory response to arousal from sleep may be an important determinant of respiratory stability/instability and could contribute to this sex difference. We therefore compared changes in ventilation, end-tidal carbon dioxide (CO2), upper airway resistance, heart rate, and finger photoplethysmogram pulse wave amplitude after both spontaneous and tone-induced arousal from non-rapid eye movement sleep in 13 men and 13 women. At sleep onset, ventilation fell and both upper airway resistance and end-tidal CO2 rose, but these changes were not different between sexes. Spontaneous arousal (duration, 6.6 +/- 0.2 seconds) resulted in a biphasic ventilatory response consisting of brief hyperventilation (5 seconds) followed by prolonged hypoventilation (30-40 seconds) on resumption of sleep. The biphasic ventilatory response was greater in men than in women and did not appear to be explained by different wake-to-sleep increments in end-tidal CO2 or upper airway resistance between sexes. Peripheral vasoconstriction with arousal was also greater in men than in women. Ventilatory responses were more marked after tone-induced versus spontaneous arousals and when subjects slept supine compared with the left lateral position. These results suggest that male sex and supine position are associated with greater ventilatory instability after arousal from sleep.
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PMID:Ventilatory response to brief arousal from non-rapid eye movement sleep is greater in men than in women. 1452 99

To assess the occurrence and nature of sleep-disordered breathing (SDB) in 26 adult, nonobese diabetics (18 with autonomic neuropathy (DAN+) (age 45 (41-50) yrs; body mass index (BMI) 24.1 (22-26) kg x m(-2)) and eight without autonomic neuropathy (DAN-) (age 45 (35-55) yrs; BMI 24.8 (23-26) kg x m(-2))) overnight full sleep studies and measurements of central and peripheral carbon dioxide (CO2) chemosensitivity were performed. DAN+ were divided in two subgroups, according to the presence (DAN+PH+; n=10) or absence (DAN+PH-; n=8) of postural hypotension. Ten normal subjects were studied as controls (age 42 (36-48) yrs; BMI 24.4 (23-25) kg x m(-2)). In contrast to DAN- and controls, who did not show SDB, five DAN+ (four DAN+PH- and one DAN+PH+) had an apnoea/hypopnoea index > or = 10 and four DAN+ (two DAN+PH- and two DAN+PH+) had an apnoea index > or = 5. All the events were obstructive, occurring mainly during rapid eye movement (REM) sleep. Ten DAN+ exhibited a mean lowest oxygen saturation < 90% during REM sleep. No periodic breathing or central sleep apnoeas were found in DAN+PH+, although they had an enhanced central chemoresponsiveness to CO2. Both DAN+ subgroups showed a marked reduction in peripheral CO2 chemosensitivity. In conclusion, adult nonobese diabetics with autonomic neuropathy, independent of the severity of their dysautonomy, have obstructive sleep apnoea/hypopnoea with a frequency > 30%. A decrease in peripheral carbon dioxide chemosensitivity prevents adult nonobese diabetics with autonomic neuropathy and postural hypotension from experiencing posthyperventilatory central sleep apnoea, despite an increased hypercapnic central drive.
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PMID:Sleep-disordered breathing in nonobese diabetic subjects with autonomic neuropathy. 1458 20

We wished to determine the severity of posthypoxic ventilatory decline in patients with sleep apnea relative to normal subjects during sleep. We studied 11 men with sleep apnea/hypopnea syndrome and 11 normal men during non-rapid eye movement sleep. We measured EEG, electrooculogram, arterial O(2) saturation, and end-tidal P(CO2). To maintain upper airway patency in patients with sleep apnea, nasal continuous positive pressure was applied at a level sufficient to eliminate apneas and hypopneas. We compared the prehypoxic control (C) with posthypoxic recovery breaths. Nadir minute ventilation in normal subjects was 6.3 +/- 0.5 l/min (83.8 +/- 5.7% of room air control) vs. 6.7 +/- 0.9 l/min, 69.1 +/- 8.5% of room air control in obstructive sleep apnea (OSA) patients; nadir minute ventilation (% of control) was lower in patients with OSA relative to normal subjects (P < 0.05). Nadir tidal volume was 0.55 +/- 0.05 liter (80.0 +/- 6.6% of room air control) in OSA patients vs. 0.42 +/- 0.03 liter, 86.5 +/- 5.2% of room air control in normal subjects. In addition, prolongation of expiratory time (Te) occurred in the recovery period. There was a significant difference in Te prolongation between normal subjects (2.61 +/- 0.3 s, 120 +/- 11.2% of C) and OSA patients (5.6 +/- 1.5 s, 292 +/- 127.6% of C) (P < 0.006). In conclusion, 1) posthypoxic ventilatory decline occurred after termination of hypocapnic hypoxia in normal subjects and patients with sleep apnea and manifested as decreased tidal volume and prolongation of Te; and 2) posthypoxic ventilatory prolongation of Te was more pronounced in patients with sleep apnea relative to normal subjects.
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PMID:Posthypoxic ventilatory decline during NREM sleep: influence of sleep apnea. 1499 May 52

Since hypercapnia is a negative prognostic index in stable chronic obstructive pulmonary disease (COPD), the chance of applying non invasive ventilation (NIV) to COPD with CO2 retention has been investigated for the two last decades. Patho-physiologic basis of its employ are resting of respiratory muscles and/or resetting of respiratory centres. Due to its poor tolerability, negative pressure NIV has been taken over by positive pressure technique. As the results of the few available controlled studies aren't enthusiastic and univocal, it's not possible to draw guidelines about the domiciliary use of NIV in COPD. In conclusion, the author suggests that, in order to avoid useless waste of resources, the application of NIV to stable COPD should be reserved to very selected cases (significant hypercapnia, frequent nocturnal desaturations and/or sleep disordered breathing and/or hospital admissions) if its compliance and effectiveness are demonstrated.
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PMID:[Non invasive mechanical ventilation in the domiciliary treatment of chronic obstructive pulmonary disease]. 1503 41

Sleep apnea syndrome (SAS) is a prominent clinical feature in acute stroke patients. Diagnosis is usually established by polysomnography or cardio-respiratory polygraphy (CRP). Both diagnostic procedures produce high costs, are dependent on the access to a specialized sleep laboratory, and are poorly tolerated by patients with acute stroke. In this study we therefore investigated whether capnography may work as a simple screening tool in this context. In addition to conventional CRP, 27 patients with acute stroke were studied with capnography provided by our standard monitoring system. The trend graphs of the end-tidal CO(2) values (EtCO(2)) were used to determine the capnography-based estimate of the apnea-hypopnea index (AHI(CO2)). Index events were scored when the EtCO(2) value dropped for > 50% of the previous baseline value. We found that the AHI(CO2) correlated significantly with the apnea-hypopnea index measured with conventional CRP (AHI(CRP)) (r = 0.94; p < 0.001). An AHI(CO2) > 5 turned out to be highly predictive of an AHI(CRP) > 10. According to our findings, routinely acquired capnography may provide a reliable estimate of the AHI(CRP). The equipment needed for this screening procedure is provided by the monitoring systems of most intensive care units and stroke units where stroke patients are regularly treated during the first days of their illness. Therefore, early diagnosis of SAS in these patients is made substantially easier.
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PMID:Capnography screening for sleep apnea in patients with acute stroke. 1582 65

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10


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