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)

Episodes of sleep disordered breathing are surprisingly common in asymptomatic, middle-aged individuals. The majority of these events are hypopneas, rather than apneas. Even though these events cause rather modest decreases in arterial oxygen saturation, they evoke substantial increases in arterial pressure. In this population, mild to moderate sleep disordered breathing is associated with elevated daytime blood pressure. The mechanisms responsible for the acute and chronic cardiovascular effects of sleep disordered breathing are incompletely understood. Chemoreflex mechanisms appear to be more important than intrathoracic pressure changes in causing the acute elevation in arterial pressure that occurs after obstructive sleep apnea. Arousal from sleep may contribute to this pressor response, either in an additive or synergistic manner. Relatively brief exposure to combined hypoxia and hypercapnia during wakefulness can produce an increase in sympathetic outflow to skeletal muscle that persists after return to room air breathing. This lingering post-asphyxic effect on sympathetic outflow may be the basis of chronically elevated sympathetic nervous system activity which accompanies sleep apnea syndrome and may contribute to sustained hypertension in these individuals.
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PMID:Acute and chronic cardiovascular responses to sleep disordered breathing. 908 12

A 57-yr-old man with idiopathic central apnea is reported. He presented at our hospital complaining of excessive daytime sleepiness. Polysomnography, including esophageal pressure monitoring, confirmed central sleep apnea with an apnea index of 27/h. He had mild non-insulin-dependent diabetes mellitus (NIDDM) but no signs of diabetic neuropathy or other background diseases. The ventilatory responses to hypoxia and hypercapnia tested while he was awake indicated increased respiratory chemosensitivity. We applied nasal continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) in an attempt to compare the possible difference in therapeutic efficacy. Although nasal CPAP completely reversed central apnea, nasal BPAP adversely affected both apnea length and frequency in an applied pressure-dependent manner. Arterial blood gas analyses while he was being treated indicted alveolar hypoventilation with CPAP and hyperventilation with BPAP. Additionally, administration of a mixed gas containing 5% CO2 through a face mask had a significant effect on the disappearance of central apnea in this patient. These findings support the theory that the arterial PCO2 level is critical in generating idiopathic central apnea and that nasal CPAP therapy may be effective in eliminating central apnea by raising the PaCO2.
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PMID:Continuous versus bilevel positive airway pressure in a patient with idiopathic central sleep apnea. 910 99

Sleep has a physiological influence on respiration, which can have major adverse effects on gas exchange in patients with respiratory insufficiency. These effects relate largely to a reduction in various stimulant inputs to the brainstem respiratory centre. Conditions that may be associated with sleep-related respiratory insufficiency range from pulmonary disorders (such as chronic obstructive pulmonary disease (COPD)), to central respiratory insufficiency (such as central alveolar hypoventilation), neurological and neuromuscular disorders (such as polio and muscular dystrophy), and thoracic cage disorders (such as kyphoscoliosis). All these conditions have in common the finding of hypoxaemia and hypercapnia, which become more pronounced during sleep. The relative hypoventilation, which is common to each condition, is due to varying combinations of an inadequate respiratory drive and an increase in the work of breathing. Management of respiratory insufficiency during sleep should be directed first at optimizing the underlying disorder, then at correcting hypoxaemia with controlled low-flow supplemental oxygen. Pharmacological therapy may be effective in some instances, but the choice of agent varies with the underlying disorder. Assisted ventilation is an important part of the management of advanced cases, and the recent development of intermittent positive pressure ventilation by nasal mask (NIPPV) has been an important advance in this area. Use of NIPPV during the night is associated with beneficial effects during the day, particularly improved awake gas exchange and respiratory muscle strength, in addition to less dyspnoea and improved quality of life. Electrophrenic pacing of the diaphragm is helpful in highly selected cases, particularly patients with central respiratory insufficiency and high quadriplegia, but is frequently complicated by the development of obstructive sleep apnoea.
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PMID:Impact of sleep in respiratory failure. 915 Mar 36

Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.
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PMID:Effects of alcohol on sympathetic activity, hemodynamics, and chemoreflex sensitivity. 918 Jun 29

We studied 134 patients with Steinert's myotonic dystrophy (MD) in order to determine the prevalence of chronic hypercapnia, the level of muscle weakness and forced expiratory volume at which hypercapnic respiratory failure is likely to occur, and how clinical assessment might help predict hypercapnic respiratory failure. Subjects were divided into five classes with a muscular disability rating scale (MDRS): 0 = no clinical impairment (n = 9), I = minimal signs of impairment (n = 11), II = distal weakness (n = 41), III = moderate proximal weakness (n = 62), and IV = nonambulatory (n = 11). The prevalence of hypercapnia (PaCO2 > or = 43 mm Hg) was found to be 0%, 27%, 29%, 45% and 55% for MDRS 0 to 4, respectively (p = 0.03). A multiple regression analysis limited to clinical data showed that daytime hypersomnolence was a significant cofactor with the MDRS (p = 0.01) in predicting PaCO2 (r = 0.40). Among respiratory parameters, FVC, respiratory muscle strength (RMS), and maximal inspiratory pressure against occluded airways (PImax) were found to be predictors of nearly equal strength, explaining 16%, 15%, and 14% of the PaCO2 variance, respectively. In multiple regression analysis, sex, daytime sleepiness, and the expected/observed FVC ratio for a given RMS were found to be significant cofactors with PImax in predicting PaCO2 (r = 0.51). It is concluded that respiratory insufficiency should be suspected in MD patients with proximal weakness or daytime sleepiness. The likelihood of hypercapnia also increases with volume restriction and respiratory muscle weakness. Our study suggests that the combination of inspiratory muscle weakness and loading plays a predominant role in the pathogenesis of chronic alveolar hypoventilation in MD patients. The occurrence of daytime hypersomnolence suggests that other factors, such as low central ventilatory drive or sleep apnea, might play an additional role.
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PMID:Relationship between chronic hypercapnia and inspiratory-muscle weakness in myotonic dystrophy. 923 Jul 37

Even if different mechanisms of various interactions during sleep are known, it is still unsolved by which mechanisms physiological reactions during sleep may start a pathophysiological course. Hypoxia, Hypercapnia and repetitive sympathetic elevations are well known elements in the control of the arterial resistance. Furthermore investigations in patients with sleep apnea showed changes of the pulsatile secretion pattern within the renin-angiotensin-system and the antinatriuretic peptides. These changes were reversible under nasal CPAP-therapy, nycturia as a frequent symptom disappeared. Nevertheless neither hypoxia nor intrathoracic pressure changes nor the arousals can assert the longterm influence on the blood pressure alone, a multifactorial confluence must be assumed. Further it is unclear how a tonic increase of the arterial blood pressure may occur in dependence of the REM- and NREM-sleep cycle changes as well as during daytime. First investigations in sleeping man seem to indicate, that a disturbance of the physiological coupling of breathing and circulation may present a pathogenetic element. Finally it remains open, whether the changes of the cardiorespiratory coupling during sleep of control persons and of patients with OSA are comparable, and whether they may be procured for an explanation of the pathogenesis of arterial and pulmonary hypertension. Further investigations in the control mechanisms of breathing and circulation related to the circuits of chemo- and baroreception, thresholds during wakefulness and sleep may be of decisive help to process the question, to what extent clinical states find a correlate in a disturbed cardiorespiratory coupling and, much more significantly, whether a disturbance in the physiological cardiorespiratory coupling appears already in early states of a disease. Sleep with ist complex physiology as well as with its characteristic pathophysiological phenomenon of sleep related breathing disorders has opened a new interdisciplinary field where tools like the polysomnography and electronic data analysis are used by physiologists, pathophysiologists as well as by physicians.
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PMID:[Cardiorespiratory coupling in obstructive sleep apnea (OSA)]. 924 90

Apnea and hypopnea during sleep are often viewed as different expressions of the same sleep-related breathing disorder. In our point of view, both symptoms are two different entities which can occur in the same patient. We discuss the hypothesis that sleep apnea is a disorder associated with recurrent arousals and chronic activation of the sympathetic nervous system, leading to daytime sleepiness and disturbances in the autonomic system. Hypoventilation results from reduced alveolar ventilation and is associated with hypercapnia. In rare cases it is caused by genuine disorders of the breathing center, like Odine's curse. In most cases, hypoventilation is secondary to an underlying disease and a strategy of the body, to avoid respiratory muscle failure. Treatment trials of hypoventilation of the respiratory muscles by stimulating the breathing center failed to be beneficial. However, unloading treatment with long-term oxygen and/or home mechanical ventilation improves arterial blood gases, physical activity and prognosis.
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PMID:How important is the differentiation between apnea and hypopnea? 938 Sep 56

The authors have studied chemical control of breathing in 37 normocapnic patients with OSA. These patients had increased apnea-hypopnea index (AHI = 51 +/- 22), obesity (BMI = 32.4 +/- 5.6 kg/m2) and normal lung function tests. Control group consisted of 20 healthy subjects with normal weight (BMI = 23.1 +/- 2.4 kg/m2). Respiratory responses (ventilatory and P0.1) to hypercapnic and hypoxic stimulation during rebreathing tests were measured with computerized methods. The obtained results in OSA patients were compared with the data of the control group. The results exceeding mean values of the control group above 1.64 SD were recognized as hyperreactive responses. The majority e.g. 26 patients (OSA-N) had normal respiratory responses during hypercapnic stimulation. delta V/delta PCO2 = 16.8 +/- 4.5 L/min/kPa, P0.1/delta PCO2 = 3.5 +/- 2.4 cm H2O/kPa/. In remaining 11 patients (OSA-H) respiratory responses were significantly increased delta V/delta PCO2 = 39.1 +/- 18.8 L/min/kPa, P0.1/delta PCO2 = 8.6 +/- 3.9 cm H20/kPa). During isocapnic hypoxic stimulation majority e.g. 25 patients (OSA-H) had significantly increased respiratory responses delta V/delta SaO2 = 3.28 +/- 1.63 L/min/%, delta P0.1/delta SaO2 = 0.54 +/- 0.43 cm H2O/%/. In remaining 12 patients (OSA-N) respiratory responses were within normal limits delta V/SaO2 = 1.2 +/- 0.28 L/min/%, delta P0.1/ delta SaO2 = 0.21 +/- 0.07 cm H2O/%/. The above results indicated, that majority OSA patients (67.5%) had increased ventilatory and P0.1 responses to hypoxic stimulation. Among them also 11 patients had increased respiratory responses to hypercapnia. It seems, that increased respiratory responses to hypoxic stimulus in OSA patients are symptoms of protective reaction to hypoxaemia occurring during repetitive sleep apnoea and reveals increased neuro-muscular output.
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PMID:[Chemical control of breathing in patients with obstructive sleep apnea]. 941 Feb 80

In contrast to the obstructive sleep apnoea syndrome (OSA) the obesity-hypoventilation syndrome (OHS) is characterized by persistent hypercapnia during the day. After positive pressure ventilation (PPV) patients with OHS the daytime blood gases normalize after a short time. The aim of this study was to investigate whether blood gases at the end of a standardized exercise test separate both OSA and OHS after 3 months of PPV. Fourteen patients with OHS (12 males, 53.2 +/- 9.5 years, BMI: 41.7 +/- 9.6 kg/m2, PCO2: 50.7 +/- 4.5 mmHg) and 28 patients with severe OSA (27 males, 54.5 +/- 8.3 years, BMI: 35.7 +/- 4.9 kg/m2, PCO2: 37.3 +/- 3.3 mmHg) were studied. Blood gases before and after 4 minutes constant load exercise test were measured. The exercise level for patients with OSA was 2/3 of the predicted maximal work load. Since in OHS the load tolerance was compromised, the exercise test was performed at 2/3 of the maximal exercise level which was investigated before. The identical exercise load was done before and 3 months after beginning the PPV. Compared to the OSA-group the load tolerance of the OHS-group was lower (112 +/- 20 Watt [2/3 of predicted maximal work load] versus 81 +/- 26 Watt [39.9 +/- 8.3% of predicted maximal work load], p < 0.0001). Both before and after 3 months of PPV all patients with OHS showed an exercise induced increase of PCO2 (Before PPV: from 50.7 +/- 4.5 to 56.6 +/- 5.8 mmHg; after PPV: from 39.1 +/- 2.7 to 45.6 +/- 2 mmHg, each p < 0.0001). Correspondingly the PCO2 decreased significantly. In OSA neither before nor after 3 months PPV the blood gases changed significantly during the exercise test. We conclude that the OHS associated hypercapnia during exercise is further on a reliable indicator for the diagnosis despite the daytime normocapnia during rest after PPV. However after PPV the PCO2-values of patients with OHS at rest are in the normal range.
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PMID:[Ergometry separates sleep apnea syndrome from obesity-hypoventilation after therapy positive pressure ventilation therapy]. 948 73

Patients with obstructive sleep apnea experience repetitive apneic events during sleep, with consequent hypoxia and hypercapnia. Hypoxia and hypercapnia, acting via the chemoreflexes, elicit increases in sympathetic nerve activity. The sympathetic responses to hypoxia and hypercapnia are potentiated during apnea, when the sympathetic inhibitory influence of the thoracic afferent nerves is eliminated. As a consequence of the sympathetic vasoconstrictor response to apneic events, patients with obstructive sleep apnea manifest marked increases in blood pressure during sleep, especially evident at the end of the apnea. The increases in sympathetic activity and blood pressure during sleep in these patients appear to carry over into the daytime such that patients with sleep apnea have an increased prevalence of hypertension and high levels of sympathetic nerve activity. Although the mechanism underlying the persistent elevation in sympathetic activity during the daytime is not known, it is likely that the increased sympathetic drive is implicated in the higher daytime blood pressures in these patients. Whereas patients with sleep apnea have an increased prevalence of hypertension, in those patients with sleep apnea who do have hypertension, the sympathetic response to apneic events may be potentiated. This may be secondary to impaired baroreflex sensitivity, since the baroreflexes exert an inhibitory influence on the chemoreflex responses to hypoxia. Treatment with continuous positive airway pressure results in an acute reduction in blood pressure and sympathetic activity during sleep. Prolonged effective treatment of sleep apnea may also reduce daytime blood pressure levels. This review examines the physiology of the chemoreflex responses to hypoxia, hypercapnia and apnea, as well as the physiologic responses to sleep in normal humans. These physiologic responses are compared with the pathophysiologic sympathetic and hemodynamic responses that characterize obstructive sleep apnea. Increases in sympathetic activity and blood pressure in patients with obstructive sleep apnea may play a role in linking sleep apnea to hypertension and cardiac and vascular events.
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PMID:The sympathetic nervous system and obstructive sleep apnea: implications for hypertension. 948 12

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