Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nadir of SaO2 during an obstructive apnea is dependent upon the apnea's duration and the rate of fall of saturation (dSaO2/dt). We postulated that a low Q, such as in patients with congestive heart failure with sleep apnea, or a reduction in Q, as seen in some humans during obstructive sleep apnea, might steepen dSaO2/dt. The mechanism postulated was lowering of SvO2 with increased pulmonary capillary blood oxygen uptake and faster depletion of alveolar oxygen. This study examines dSaO2/dt following the onset of apnea in eight spontaneously breathing adult baboons. Nonrepetitive obstructive apneas (30, 45, and 60 seconds) were created by clamping an indwelling cuffed endotracheal tube at the end of expiration. Following baseline measurements, the animals were given a bolus of a rapid-acting beta-adrenergic blocker followed by continuous infusion to reduce cardiac output and to limit the cardiovascular response to obstructive asphyxia. Fiberoptic catheters were used for continuous monitoring of SaO2, SvO2, and cardiac output. Esophageal pressure and relative thoracic gas volume (Respitrace) were monitored to insure equivalence of lung volume at the onset of apnea. Beta-adrenergic blockade reduced resting Q by a mean of 25 percent. The blocked vs unblocked dSaO2/dt was 0.73 vs 0.72 percent/s, 0.76 vs 0.73 percent/s, and 0.70 vs 0.71 percent/s for 30-second, 45-second, and 60-second apneas, respectively. Thus, mean dSaO2/dt for all durations of apneas was unaffected by beta-adrenergic blockade. We concluded that dSaO2/dt is not influenced by limited Q preceding or induced by obstructive asphyxia.
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PMID:Effect of cardiac output reduction on rate of desaturation in obstructive apnea. 167 Dec 12

Oesophageal pressure swings were analysed during complete occlusion of the upper airways in 8 patients with obstructive sleep apnoea. We hypothesed that in dependence of the apnoea type, there is a significant decrease in oesophageal inspiratory effort in REM vs. NREM that is caused by a decrease of the respiratory drive. We analysed in each patient 40 apnoeas in which the respiratory timing (Ti) and the inspiratory effort (Pin) were calculated and compared with the type of apnoea and the degree of oxygen desaturation. A significant decrease in inspiratory effort in REM vs NREM occurred only in mixed apnoeas but not in patients with mainly obstructive apnoeas. Additionally, all apnoeas with a decrease of inspiratory effort at the end of apnoea during NREM were seen in obstructive apnoeas only, whereas none occurred in mixed apnoeas. Due to the significant lower inspiratory timing during obstructive apnoeas vs mixed apnoeas we assume a decrease in respiratory drive in the patients suffering mainly from obstructive apnoeas.
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PMID:[Inspiratory intrathoracic pressure changes in obstructive and mixed sleep apnea]. 815 93

OSAS, a common cause of disrupted sleep and EDS, result from repetitive closure of the upper airway during sleep. It probably represents the most severe syndrome related to obstruction of the upper airway; less severe forms include UARS, a syndrome characterized by the need for increased effort to breath but no prominent apneas or hypopneas, and primary snoring. Initial clues to the presence of OSAS and related disorders are derived from the history and include loud snoring, EDS or insomnia, and witnessed apneas. Some patients, especially women, may complain mostly of tiredness or fatigue, and children may present with behavioral abnormalities. Obesity, a large neck circumference, and a crowded oropharynx are common on physical examination. Nonobese patients, in particular, often have retrognathia, a high-arched narrow palate, macroglossia, enlarged tonsils, temporomandibular joint abnormalities, or chronic nasal obstruction. The clinical suspicion of obstructed nocturnal breathing is confirmed by overnight polysomnography, and an MSLT may be used to assess sleepiness. Esophageal manometry during polysomnography facilitates diagnosis of UARS. Treatment most commonly consists of nasal CPAP or BPAP, although problems with compliance make surgical treatment preferable in some cases. Although UPPP eliminates sleep apnea only in a minority of patients, combining UPPP with maxillofacial procedures appears to improve outcomes. Other treatments such as the use of dental appliances or medications, weight loss, and positional therapy may be useful as adjunctive therapy for moderate to severe OSAS or as primary treatments for UARS or mild OSAS.
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PMID:Obstructive sleep apnea and related disorders. 887 78

Oesophageal pressure (Pes) and oronasal flow are necessary to describe upper airway obstruction in patients with obstructive sleep apnoea syndrome (OSAS), but Pes interferes with sleep. We developed a device applying an oscillating flow (20 Hz) through a nasal mask. An additional flow (2.6 l/min) is needed to reduce dead space and humidity. 24 patients (age 55.8 +/- 8.3 years, BMI 28.6 +/- 3.9, RDI 38.6 +/- 19.4, Raw 0.27 +/- 0.07 kPa/s/l) underwent polygraphy (oronasal flow, thoracic and abdominal effort, oxygen saturation, microphone, heart rate). Pes and oscillatory impedance (OI) were measured simultaneously. During snoring, hypopnoeas and apnoeas we compared Pes, OI and effort values for the detection of number and period of airway obstruction. The average Pes during habitual snoring was -3.2 +/- 0.8, during hypopnoeas -3.9 +/- 1.1 and during apnoeas -4.4 +/- 1.6 kPa. We found no significant difference in respect of the number and period of obstruction in patients with apnoeas, whereas in patients with incomplete obstruction (hypopnoea) Pes and OI were found to be more sensitive in detecting obstruction than effort (period: 27.0 +/- 9.1 sec (Pes), 29.0 +/- 4.8 sec (OI) vs. 20.0 +/- 6.8 sec (effort); number: 34.0 +/- 9.1 (Pes), 35.0 +/- 8.5 (OI) vs. 23.0 +/- 9.5 (effort). There is a significant correlation between Pes and OI (r = 0.89). OI is shown to be equally sensitive in identifying Upper Airway Resistance Syndrome as compared to Pes. This method is more convenient than conventional measurements such as Pes and it could be an alternative.
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PMID:[Comparative study of thoracic and abdominal effort, respiratory oscillatory impedance (ROI) and intrathoracic pressure in sleep apnea syndrome]. 934 Jun 34

Cardiorespiratory decompensation or even death may result from dysfunction of upper airway reflexes during sleep. This could manifest, for example, as a lack of pharyngeal dilation in obstructive sleep apnoea or failure of autoresuscitation by gasping in sudden infant death syndrome. Data obtained from experiments in anaesthetized cats suggest several clinicophysiological applications for upper airway reflexes possessing important pathogenetic and therapeutic potentials. Such reflex effects include: 1. Pharyngeal dilation as additional treatment in obstructive sleep apnoea. 2. Bronchodilation after deep nasal breathing in asthmatic attacks. 3. Oesophageal sphincter relaxation alleviating gastro-oesophageal reflux. 4. Provocation of sniff- and gasp-like aspiration for reversal of central apnoea. 5. Arousal from sleep increasing the general reactivity. 6. Increase in muscle tone underlying behavioural defence reactions. 7. Increase in sympathetic activity contributing to powerful cardiopulmonary-cerebral resuscitation. 8. Adrenergic reaction mediated by catecholamine secretion.
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PMID:Contribution of upper airway reflexes to apnoea reversal, arousal, and resuscitation. 1121 78

Gastroesophageal reflux disease (GERD) and laryngopharyngeal reflux (LPR) are sibling diseases that are a modern-day plague. Millions of Americans suffer from their sequelae, ranging from subtle annoyances to life-threatening illnesses such as asthma, sleep apnea, and cancer. Indeed, the recognized prevalence of GERD alone has increased threefold throughout the 1990s. Knowledge of the precise etiologies for GERD and LPR is becoming essential for proper treatment. This review focuses on the anatomical, physiological, neurobiological, and cellular aspects of these diseases. By definition, gastroesophageal reflux (GER) is the passage of gastric contents into the esophagus; when excessive and damaging to the esophageal mucosa, GERD results. Reflux that advances to the laryngopharynx and, subsequently, to other regions of the head and neck such as the larynx, oral cavity, nasopharynx, nasal cavity, paranasal sinuses, and even middle ear results in LPR. While GERD has long been identified as a source of esophageal disease, LPR has only recently been implicated in causing head and neck problems. Recent research has identified four anatomical/physiological "barriers" that serve as guardians to prevent the cranial incursion of reflux: the gastroesophageal junction, esophageal motor function and acid clearance, the upper esophageal sphincter, and pharyngeal and laryngeal mucosal resistance. Sequential failure of all four barriers is necessary to produce LPR. While it has become apparent that GER must precede both GERD and LPR, the head and neck distribution of the latter clearly separates these diseases as distinct entities warranting specialized focus and treatment.
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PMID:Anatomy of reflux: a growing health problem affecting structures of the head and neck. 1710 21

The lower esophageal sphincter (LES) is the primary barrier to gastroesophageal reflux. Reflux is associated with periods of LES relaxation, as occurs during swallowing. Continuous positive airway pressure (CPAP) has been shown to reduce reflux in individuals with and without sleep apnea, by an unknown mechanism. The aim of this study was to determine the effect of CPAP on swallow-induced LES relaxation. Measurements were made in 10 healthy, awake, supine individuals. Esophageal (Pes), LES (Ples), gastric (Pg), and barrier pressure to reflux (Pb = Ples - Pg) were recorded using a sleeve catheter during five swallows of 5 ml of water. This was repeated at four levels of CPAP (0, 5, 10, and 15 cmH(2)O). Pressures were measured during quiet breathing and during the LES relaxation associated with a swallow. Duration of LES relaxation was also recorded. During quiet breathing, CPAP significantly increased end-expiratory Pes, Ples, Pg, and Pb (P < 0.05). The increase in Pb was due to a disproportionate increase in Ples compared with Pg (P < 0.05). During a swallow, CPAP increased nadir Ples, Pg, and Pb and decreased the duration of LES relaxation (4.1 s with 0-cmH(2)O CPAP to 1.6 s on 15-cmH(2)O CPAP, P < 0.001). Pb increased with CPAP by virtue of a disproportionate increase in Ples compared with Pg. This may be due to either reflex activation of LES smooth muscle, or nonspecific transmission of pressure to the LES. The findings suggest CPAP may make the LES less susceptible to reflux by increasing Pb and decreasing the duration of LES relaxation.
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PMID:The impact of continuous positive airway pressure on the lower esophageal sphincter. 1723 90

For a given neural drive, oesophageal pressure during apnoeic episodes may differ from that during airflow, since inspiratory airflow and increased lung volume both reduce pressure generation. It was, therefore, hypothesised that diaphragm electromyography (EMG) may provide additional data to oesophageal pressure when used for the assessment of neural drive in patients with obstructive sleep apnoea, whose breathing is associated with variable airflow and changes in lung volume. Neural respiratory drive was assessed using diaphragm EMG recorded from multipair oesophageal electrodes in 12 patients with obstructive sleep apnoea. Oesophageal pressure was also recorded. The mean+/-sd inspiratory oesophageal pressure swing was 11.0+/-3.7 cmH(2)O during wakefulness, 38.2+/-15.7 cmH(2)O at the end of the apnoea and reduced to 28.5+/-10.4 cmH(2)O at the beginning of arousal. The mean peak inspiratory diaphragm EMG signal was 21.8+/-6.5 muV during wakefulness, 38.6+/-14.0 muV at the end of the apnoea and further increased to 59.6+/-32.0 muV at the beginning of arousal. It was concluded that the pattern of neural drive assessed by oesophageal pressure differs from that measured by diaphragm electromyography during apnoeic events and, therefore, that diaphragm electromyography may be a useful adjunct to measurement of oesophageal pressure for the assessment of neural drive in patients with obstructive sleep apnoea.
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PMID:Neural respiratory drive during apnoeic events in obstructive sleep apnoea. 1803 43

The differentiation between obstructive and central respiratory events is one of the most recurrent tasks in the diagnosis of sleep disordered breathing. Esophageal pressure measurement is the gold-standard method to assess respiratory effort and identify these events. But as its invasiveness discourages its use in clinical routine, non-invasisve systems have been proposed for differentiation. However, their adoption has been slow due to their limited clinical validation, as the creation of manual, gold-standard validation sets by human experts is a cumbersome procedure. In this study, a new system is proposed for an objective automatic, gold-standard differentiation between obstructive and central hypopneas with the esophageal pressure signal. First, an overall of 356 hypopneas of 16 patients were manually scored by a human expert to create a gold-standard validation set. Then, features were extracted from each hypopnea to train and test classifiers (Discriminant Analysis, Support Vector Machines and adaboost classifiers) to differentiate between central and obstructive hypopneas with the gold-standard esophageal pressure signal. The automatic differentiation system achieved promising results, with a sensitivity of 0.88, a specificity of 0.93 and an accuracy of 0.90. Hence, this system seems promising for an automatic, gold-standard differentiation between obstructive and central hypopneas.
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PMID:Automatic differentiation of obstructive and central hypopneas with esophageal pressure measurement during sleep. 1996 45

The differentiation of obstructive and central respiratory events is a major challenge in the diagnosis of sleep disordered breathing. Esophageal pressure (Pes) measurement is the gold-standard method to identify these events but its invasiveness deters its usage in clinical routine. Flattening patterns appear in the airflow signal during episodes of inspiratory flow limitation (IFL) and have been shown with invasive techniques to be useful to differentiate between central and obstructive hypopneas. In this study we present a new method for the automatic non-invasive differentiation of obstructive and central hypopneas solely with nasal airflow. An overall of 36 patients underwent full night polysomnography with systematic Pes recording and a total of 1069 hypopneas were manually scored by human experts to create a gold-standard annotation set. Features were automatically extracted from the nasal airflow signal to train and test our automatic classifier (Discriminant Analysis). Flattening patterns were non-invasively assessed in the airflow signal using spectral and time analysis. The automatic non-invasive classifier obtained a sensitivity of 0.71 and an accuracy of 0.69, similar to the results obtained with a manual non-invasive classification algorithm. Hence, flattening airflow patterns seem promising for the non-invasive differentiation of obstructive and central hypopneas.
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PMID:Automatic non-invasive differentiation of obstructive and central hypopneas with nasal airflow compared to esophageal pressure. 2109 44


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