Effects of chronic intermittent asphyxia on rat diaphragm and limb muscle contractility

OBJECTIVE: In obstructive sleep apnea (OSA), there is intermittent upper airway (UA) collapse due to an imbalance between the collapsing force generated by the diaphragm and the stabilizing force of the UA muscles. This results in chronic intermittent asphyxia (CIA). We have previously shown that CIA affects UA muscle fatigue, but little is known about the effects of chronic hypoxia on diaphragm or on limb muscle contractile properties and structure. DESIGN: Rats were exposed to asphyxia and normoxia twice per minute for 8 h/d for 5 weeks to simulate the intermittent asphyxia of OSA in humans. Isometric contractile properties were determined from strips of isolated diaphragm, extensor digitorum longus (EDL), and soleus muscles in Krebs solution at 30 degrees C. EDL and soleus type 1 (slow, fatigue resistant), type 2A (fast, fatigue resistant), and type 2B (fast, fatigable) fiber distribution was determined using adenosine triphosphatase staining. RESULTS: CIA caused a significant increase in diaphragm, EDL, and soleus fatigue, and reduced recovery from fatigue. Most of the other contractile properties were unaffected aside from a small reduction in diaphragm half-relaxation time and EDL twitch tension and a small shift to the left in the EDL force-frequency curve. There was no change in soleus fiber-type distribution and a small increase in EDL type 2A fibers (46.1 +/- 1.2% vs 49.9 +/- 1.4%, control vs CIA [mean +/- SD]). CONCLUSIONS: CIA increases diaphragm, EDL, and soleus muscle fatigue. We speculate that if this also occurs in OSA, it would contribute to the pathophysiology of the condition.     

Phasic respiratory muscle patterns and sleep-disordered breathing during rapid eye movement sleep in the English bulldog

Basic mechanisms of sleep-disordered breathing (SDB) during rapid-eye-movement sleep (REMS) have been little investigated, despite the fact that events are often more prolonged and SaO2 nadirs lower during REMS. We predicted that the mechanisms of SDB in REMS would be related to the normal phasic changes in respiratory control in that state, rather than to cyclic arousals or responses to hypoxia as postulated for non-REMS SDB. Recordings of the EMG of the diaphragm (DIA) and the sternohyoid (SH), an upper airway dilating muscle, were made in five English bulldogs during sleep. We found that, as predicted, SDB events were associated with phasic influences rather than with arousals or response to hypoxia. The onset of SDB was significantly related to suppression of drive to both the DIA (p less than 0.01) and the SH (p less than 0.01). The mean drive of the DIA was suppressed to 42% of normal and of the SH to 17% of normal; the suppression of the SH was significantly greater than that of the DIA (p less than 0.05). Events were associated with changes in respiratory muscle EMG patterns typical of phasic REMS (p less than 0.01 for each muscle). The occurrence and duration of events exhibited no clear pattern or relationship to arousal or SaO2. Rather, as would be expected of phenomena associated with phasic REMS, the onset and termination of events were unpredictable. The association of SDB in REMS with phasic REMS influences rather than arousal or hypoxia suggests new directions for therapeutic approaches.     

Upper airway collapsibility, dilator muscle activation and resistance in sleep apnoea.

The calibre of the upper airway is thought to be dependant upon its passive anatomy/collapsibility and the activation of pharyngeal dilator muscles. During awake periods, the more collapsible upper airway in obstructive sleep apnoea (OSA) increases the dilator muscle activity through a negative-pressure reflex. A direct correlation between the critical closing pressure (P(crit)), as a measure of anatomy/collapsability and electromyogram (EMG) activity of genioglossus EMG (GG-EMG) and tensor palatini EMG (TP-EMG), was hypothesised. The relationship between these indices and pharyngeal resistance (R(phar)) was also examined. The study involved eight males with a mean age of 48 (interquartile range 46-52) yrs with OSA, and an apnoea/hypopnoea index of 75 (65-101).hr(-1) on two nights breathing normally and on nasal continuous positive airway pressure (nCPAP). The P(crit )was measured during nonrapid eye movement sleep on nCPAP using brief, incremental reductions in mask pressure. GG-EMG and TP-EMG were measured breath-by-breath, awake, during sleep onset and on nCPAP. R(phar) was measured using airway pressures and flow. Wakeful GG-EMG, early sleep TP-EMG and the sleep decrement in TP-EMG were directly related to P(crit). Muscle activation was negatively correlated with R(phar) for TP-EMG awake and GG-EMG early in sleep. In conclusion these results confirm that dilator muscle activation is directly related to airway narrowing and reduces resistance across patients with obstructive sleep apnoea.     

Pathophysiology of pediatric obstructive sleep apnea

Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.     

Functional contribution of mandibular advancement to awake upper airway patency in obstructive sleep apnea

In the narrowed upper airway of patients with obstructive sleep apnea (OSA), a neuromuscular compensatory mechanism augments the activity of the upper airway dilator muscles in defense of upper airway patency, particularly during inspiration. We hypothesized that mechanical enlargement of the upper airway by a mandibular advancement oral appliance would permit a reduction in this neuromuscular compensation during wakefulness. To test this hypothesis, we focused on changes in the cross-sectional (CS) area of the upper airway before and after emplacement of a ventrally titrated oral appliance in 12 awake OSA patients. The CS areas at the end of tidal expiration (CS area-EET) and at the nadir of intraluminal pressure during inspiration (CS area-IN) were obtained using videoendoscopy. The median apnea–hypopnea index decreased with mandibular advancement. Before mandibular advancement, there was no difference between CS area-EET and CS area-IN in the velopharynx, oropharynx, and hypopharynx. This indicates that upper airway dilator muscle activity increased during inspiration to counteract the intraluminal negative pressure of the upper airway. After mandibular advancement, CS area-EET increased in the velopharynx, oropharynx, and hypopharynx, but CS area-IN was unchanged at any level and was less than CS area-EET in the velopharynx and oropharynx. These findings suggest that mandibular advancement enlarges the upper airway and may reduce upper airway dilator muscle activity during inspiration. We conclude that oral appliances act to return the upper airway towards a normal configuration and pattern of muscle function in OSA patients.     

Electromyographic study of some accessory muscles of respiration in children with obstructive sleep apnea

To further elucidate the pathogenesis of obstructive sleep apnea (OSA), we recorded sternocleidomastoid (SCM), genioglossal (GG), and abdominal (ABD) muscle activity, using surface electromyograms (EMGs), during 45 polygraphic studies in 39 children referred for possible OSA. For each muscle, an index of electromyographic (EMG) activity was developed, allowing an interpatient regression analysis of EMG amplitude versus highest PACO2 and lowest transcutaneous O2 tension (tcPO2) during sleep. Phasic inspiratory SCM activity was present during more than 50% of sleep time in 16 of 20 patients with OSA versus only 2 of 15 patients without OSA; SCM EMG activity increased with increasing PACO2 (r = 0.45, p less than 0.02) and decreasing tcPO2 (r = 0.51, p less than 0.01). Phasic inspiratory GG activity was present during more than 50% of sleep time in 15 of 18 patients with OSA versus none of 4 without OSA; GG EMG activity increased with increasing PACO2 (r = 0.51, p less than 0.05) and with decreasing tcPO2 (r = 0.60, p less than 0.02). Phasic expiratory ABD activity was present during more than 50% of sleep time in 10 to 20 patients with OSA versus 1 of 12 patients without OSA. These findings suggest the following conclusions: (1) inspiratory (SCM), airway-maintaining (GG), and expiratory (ABD) muscles contract during sleep-related partial airway obstruction in children; (2) augmented GG activity during periods of sleep-related partial airway obstruction suggests that pediatric OSA involves pathogenic mechanisms other than GG hypotonia; (3) expiratory ABD muscle activity suggests that some children with OSA have increased expiratory, as well as inspiratory, airway resistance during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of nasal obstruction on upper airway muscle activation in normal subjects

It is not known whether nasal occlusion produces obstructive sleep apnea (OSA) by decreasing upper airway muscle activation via nasal reflexes or by increasing upper airway resistance and hence lowering the pressure in the pharnyx. The purpose of this study was to determine the effect of nasal occlusion on upper airway muscle activation. We studied seven men and measured alae nasi (AN) and genioglossal (GG) electromyograms (EMGs) during two nights of sleep, one with their nose open and the other with their nose occluded. Nasal occlusion produced OSA in all subjects and also increased the percentage of time during sleep in which phasic AN and GG EMG activity was present. Apneas tended to occur at the nadirs of EMG activity. This suggests that nasal occlusion generally increases respiratory drive to upper airway muscles during sleep and that it does not cause OSA by merely decreasing respiratory drive to these muscles.     

Local mechanisms drive genioglossus activation in obstructive sleep apnea

Individuals with obstructive sleep apnea (OSA) require increased pharyngeal muscle dilator activation during wakefulness to maintain upper airway patency. Negative pressure is one potential stimulus for this neuromuscular compensation. Individuals with OSA who have previously undergone tracheostomy provide an opportunity to study upper airway physiology in both the presence and absence of upper airway respiratory stimuli. If negative pressure (or another local airway stimulus) were important in driving pharyngeal dilator muscle activation, one would predict that during nasal breathing, the pharynx of a tracheostomized patient would be exposed to negative pressure, and that high levels of muscle activation would therefore be measured. Conversely, during breathing by the patient through the tracheal stoma, one would expect low levels of muscle activation in the absence of local stimuli. We measured a number of respiratory variables, including genioglossus activation under both nasal and tracheal stomal breathing conditions, in five patients. In all five patients there was a significant and substantial decrease in both peak phasic (100 +/- 0 to 53.4 +/- 9.2 arbitrary units [mean +/- SEM], p < 0.01) and tonic genioglossus activation (36.3 +/- 5.3 to 20.7 +/- 3.9 arbitrary units, p < 0.05) during stomal breathing as compared with nasal breathing. We conclude that local upper airway respiratory stimuli, possibly negative pressure, are important in mediating the increased pharyngeal dilator muscle activation seen in sleep apnea patients during wakefulness.     

Recent advances of the impact of obstructive sleep apnea on systemic hypertension

Obstructive sleep apnea (OSA) is a common clinical condition in the general population, especially among patients with cardiovascular diseases. More than just a local phenomenon of upper respiratory tract obstruction, OSA leads to systemic consequences that may include intermittent hypoxia, sudden reduction of the intrathoracic pressure, and the occurrence of micro-awakenings with sleep fragmentation. In the past decades, innumerous evidences have consistently pointed to OSA as an important factor related to the presence of cardiovascular diseases. In particular, the relationship between OSA and systemic hypertension (SH) is the one supported by the largest body of evidence. Currently, there are data suggesting that OSA is an important secondary cause of SH. More importantly, OSA is independently associated with poorer blood pressure control, changes in sleep dip, and presence of target-organ damage such as left ventricular hypertrophy and microalbuminuria. Randomized studies suggest that the management of OSA, especially with continuous positive airway pressure (CPAP) - which is considered the standard treatment for OSA - promotes a significant 24-hour blood pressure reduction, and this effect is more significant in the subgroup of patients with uncontrolled SH and drug-resistant SH. Despite all those evidences, OSA has still been underdiagnosed. The objective of this review is to discuss the recent advances in the pathophysiological mechanisms, clinical presentation, and treatment of OSA, as well as the benefits this treatment can bring on blood pressure.     

Effects of respiratory stimulation on alae nasi electromyograms and respiratory changes in length in dogs

The relationship between the electrical and mechanical activity of the nasal dilator muscle was assessed in 8 pentobarbital-anesthetized, tracheostomized, supine dogs. Alae nasi electromyograms (EMGs) were recorded with bipolar fine wire electrodes, and respiratory changes in muscle length were recorded contralaterally using sonomicrometry. During both resting and stimulated breathing, the intrabreath pattern of muscle shortening closely paralleled the intrabreath pattern of EMG activity. Increases in both alae nasi EMG and alae nasi inspiratory shortening occurred in response to single-breath airway occlusions, brief periods of asphyxia, progressive hyperoxic hypercapnia, and intravenous nicotine sulfate administration. With all interventions, the increases in mechanical activation of the alae nasi paralleled the increases in alae nasi electrical activity. These results indicate that alae nasi EMGs, closely reflect respiratory changes in alae nasi length under conditions in which no mechanical load is placed in the nasal muscle.     

Upper airway muscle activation is augmented in patients with obstructive sleep apnea compared with that in normal subjects

Although phasic electromyographic (EMG) activity of upper airway muscles in patients with obstructive sleep apnea (OSA) decreases at apnea onset, the presence of phasic activity in normal subjects has not been studied and compared with that in patients. We consequently compared the percentage of total sleep time in which phasic activity of the genioglossal EMG activity was present in 8 adult patients with OSA and 3 control groups without OSA, one consisting of 6 young, normal subjects, one matched for age, and one matched for age and obesity. From wakefulness to sleep, genioglossal EMG phasic activity time increased in patients but not in control subjects. Patients with OSA had more phasic genioglossal group EMG activity during non-REM sleep than did control subjects. At apnea onset, phasic EMG activity decreased in patients but remained greater than zero. In many control subjects, phasic activity was not detected, yet their pharyngeal airway remained patent. We conclude that phasic genioglossal group EMG activity occurs more frequently during sleep in patients with OSA than in control subjects, suggesting that it is a compensatory mechanism that occurs when patency of the pharyngeal airway is precarious.     

Sympathetic chemoreflex responses in obstructive sleep apnea and effects of continuous positive airway pressure therapy

BACKGROUND: Sympathetic nerve activity is increased in awake and regularly breathing patients with obstructive sleep apnea (OSA). Over time, repetitive hypoxic stress could alter sympathetic chemoreflex function in OSA. METHODS: We determined the responses to acute hypoxia (fraction of inspired oxygen of 0.1, for 5 min), static handgrip exercise, and the cold pressor test (CPT) in 24 patients with OSA (age, 50 +/- 3 years [mean +/- SEM]; apnea-hypopnea index, 47 +/- 6 events per hour) and in 14 age- and weight-matched nonapneic control subjects. Muscle sympathetic nerve activity (MSNA) [peroneal microneurography], BP, and ventilation were monitored. RESULTS: Basal MSNA was higher in OSA patients compared to control subjects (45 +/- 4 bursts per minute vs 33 +/- 4 bursts per minute, respectively; p < 0.05). Furthermore, compared to control subjects, the MSNA responses to hypoxia were markedly enhanced in OSA (p < 0.001). Whereas the ventilatory responses to hypoxia tended to be increased in OSA (p = 0.06), the BP responses did not differ between the groups (p = 0.45). The neurocirculatory reflex responses to handgrip exercise and to the CPT were similar in the two groups (p = not significant). In OSA patients who were retested after 1 to 24 months of continuous positive airway pressure (CPAP) therapy (n = 11), basal MSNA (p < 0.01) and the responses of MSNA to hypoxia (p < 0.01) decreased significantly, whereas the ventilatory responses remained unchanged (p = 0.82). CONCLUSION: These data suggest that the sympathetic responses to hypoxic chemoreflex stimulation are enhanced in OSA and may normalize in part following CPAP therapy.     

Severe OSA Leading to Long Pauses in 24-h Holter ECG Reversed with CPAP

Introduction Sleep-related problems like sleep apnea are increasing tremendously mostly owing to the disordered lifestyle the present generation is leading which is added like a topping on the base of obesity and metabolic syndrome. The burden on the society is huge taking into consideration the work-time loss and health-related financial issues arising out of these sleep disorders with obstructive sleep apnea (OSA) leading the way. Early diagnosis can prevent several complications of OSA. Cardiovascular diseases, including various arrhythmias, arising due to OSA, are described previously.Case Presentation Herein, an interesting case of OSA, whose pacemaker installation to rectify the long pause could be avoided by simple correction of his OSA using continuous positive airway pressure, is presented. This 49-year-old male patient was diagnosed with severe OSA by using polysomnography and all his significant sinus pauses (highest one with 7.8 sec) during holter ECG monitoring were found to be occurring at night and correcting his OSA with continuous positive airway pressure (CPAP) treatment reverted all those sinus pauses and the need for any further intervention with pacemaker was discarded.Discussion OSA is caused by either partial or complete obstruction of the upper airway, and there is the simultaneously attenuated upper airway dilator muscle tone while the patient is sleeping. The gold standard test designed for the assessment of OSA is polysomnography, as approved by the American Academy of Sleep Medicine and CPAP has been found to be universally beneficial in treating OSA related complications. Physiologically, the ACC/AHA guidelines recommend pacing only in patients with prolonged asymptomatic pauses occurring during wakefulness. This case report proved the above mentioned claim of CPAP treatment.     

Effects of upper airway carbon dioxide on upper airway resistance and muscle activity in young guinea-pigs.

The upper airway (UA) of adult animals is known to contain carbon dioxide-sensitive receptors and UA CO2 reflexly affects breathing, UA dilator muscle activity and UA resistance. These effects may function in the control of UA patency. There is evidence that some UA reflexes are stronger in young than in adult animals, but it is not known whether CO2-sensitive receptors are present in the UA of young animals, and the effects of UA CO2 on UA resistance and on UA dilator muscle activity have not been investigated in young animals. The responses of ventilation, UA resistance and geniohyoid muscle electromyographic activity to warm air containing 10% CO2 applied to the isolated UA were measured in anaesthetized, vagotomized young guinea-pigs breathing spontaneously through a low-cervical tracheostomy. Upper airway carbon dioxide caused an increase in ventilation (46.7+/-16.3 to 49.9+/-16.8 mL x min(-1) x 100 g body weight(-1)) and upper airway resistance (56.8+/-14.8 to 63.7+/-17.7 cmH2O x L(-1) x s(-1) x kg body weight(-1)). Similar effects were obtained following vagotomy. Geniohyoid activity became apparent following vagotomy and this activity was reduced by upper airway carbon dioxide. These responses were abolished by topical anaesthesia of the upper airway. This suggests that the reflexes seen are due to carbon dioxide-sensitive receptors in the upper airway.     

Relationship between upper airway and inspiratory pump muscle force in obstructive sleep apnea

BACKGROUND: Upper airway (UA) patency during inspiration is determined by the balance between dilating forces generated by UA dilator muscle activity and collapsing forces related to the decreased intraluminal pressure that accompanies flow generated by inspiratory muscle activity. It is possible that the relative strengths of UA dilator and inspiratory pump muscles could be an important determinant of the susceptibility to UA collapse during sleep (ie, obstructive sleep apnea [OSA]). METHODS: Measurements of tongue protrusion (TP) force and maximum inspiratory pressure (Pimax) were obtained in 94 patients admitted for overnight polysomnography for suspected OSA, quantified by apnea-hypopnea index (AHI). RESULTS: There was a direct linear relationship between TP force and Pimax (r(2) = 0.37, p < 0.001). A high ratio of TP force to Pimax (greater than group 90th percentile, 0.027 kg/cm H(2)O) appeared to protect against OSA, as moderate-to-severe OSA (AHI > 20/h) was not observed in any individual with a ratio above this threshold. AHI was not linearly related to TP force, Pimax, or the ratio of TP force to Pimax. CONCLUSIONS: UA muscle strength is linearly related to inspiratory pump muscle strength. The ratio of UA muscle strength (TP force) and inspiratory pump muscle strength (Pimax) was not different between individuals with and without OSA; however, a high wakeful ratio of TP force to Pimax appears to be associated with a reduced propensity to moderate-to-severe OSA.     

Obstructive sleep apnea syndrome and fatty liver: Association or causal link?

Obstructive sleep apnea (OSA) is a complex disorder that consists of upper airway obstruction, chronic intermittent hypoxia and sleep fragmentation. OSA is well known to be associated with hypoxia, insulin resistance and glucose intolerance, and these factors can occur in the presence or absence of obesity and metabolic syndrome. Although it is well established that insulin resistance, glucose intolerance and obesity occur frequently with non-alcoholic fatty liver disease (NAFLD), it is now becoming apparen...     

Genioglossal and diaphragmatic EMG responses to hypoxia during sleep

Activation of pharyngeal dilator muscles, such as the genioglossus, during hypoxia must be sufficient to overcome the increased subatmospheric pressure generated by the diaphragm. This is particularly important during sleep, when upper airway resistance is greater. We measured ventilatory, genioglossal (EMGgg) and diaphragmatic (EMGdi) electromyogram responses to isocapnic hypoxia during wakefulness (W), slow-wave sleep (SWS), and rapid eye movement (REM) sleep in seven chronically instrumented adult goats. We also compared the EMG responses to hypoxia to response to CO2 during W. delta EMGdi/delta SaO2 decreased progressively from W to SWS (p less than 0.05) to REM sleep (p less than 0.05 versus SWS), paralleling the corresponding ventilatory responses. EMGgg was activated only below an SaO2 threshold, similar during W (69.8 +/- 6.3%) and SWS (67.2 +/- 4.3%), beyond which there was a brisk linear increase. During REM sleep, arousal preceded activation of EMGgg in each animal, although SaO2 at arousal (61.3 +/- 4.4%) was less than the SaO2 threshold for EMGgg activation during W or SWS (p less than 0.05). Despite state-related differences in the individual muscle responses, simultaneous EMGgg and EMGdi during hypoxia or hypercapnia in W, and during hypoxia in SWS and REM sleep, were linked in a constant manner. This suggests common integration of central and peripheral chemoreceptor inputs. Furthermore, these relationships are unaffected by either SWS or REM sleep.     

Upper airway resistance during progressive hypercapnia and progressive hypoxia in normal awake subjects

Ventilatory motor output is known to influence the upper airway. Although inspiratory upper airway resistance decreases during progressive hypoxia or hypercapnia, the effects of hypoxia and hypercapnia on expiratory upper airway resistance remain unknown. In the present study, we attempted to examine whether the expiratory and the inspiratory upper airway resistances were modified in the same way by progressive hyperoxic hypercapnia or by progressive normocapnic hypoxia. Nine healthy subjects (five males, four females, 33+/-9 years) participated in the study. Inspiratory upper airway (iUAR) and expiratory upper airway resistances (eUAR) were calculated at flow 300 ml x s(-1). Both resistances were obtained during a baseline period and during progressive hyperoxic hypercapnia or progressive normocapnic hypoxia. In all subjects, iUAR and eUAR decreased significantly during hypercapnic or hypoxic challenge (P<0.05). eUAR was always lower than iUAR during hypercapnic challenge (P<0.0001) and during hypoxic challenge (P<0.0001). The authors conclude that expiratory upper airway resistance, as with inspiratory resistance, decreases during progressive hypercapnia or during progressive hypoxia. Pharyngeal dilator or constrictor muscle activities may be implicated.     

阻塞性睡眠呼吸暂停低通气综合征患者上气道扩张肌的中枢调控

阻塞性睡眠呼吸暂停低通气综合征患者的主要病理生理基础是长期间断低氧,低氧可导致上气道扩张肌功能紊乱及大脑皮质抑制及神经元的损伤.在睡眠时极易出现呼吸暂停,在觉醒时由于肌肉的中枢代偿作用被破坏也会出现呼吸暂停.用TMS技术已证实上气道扩张肌活动与颏舌肌运动皮质区的依赖性,有增强颏舌肌活性的可能,使阻塞性睡眠呼吸暂停低通气综合征患者不出现呼吸暂停.     

Recent advances in understanding the pathogenesis of obstructive sleep apnea

PURPOSE OF REVIEW: The pathogenesis of obstructive sleep apnea (OSA) is incompletely understood. Historically it was believed that patients with OSA have a small upper airway (often due to obesity) that is kept patent during wakefulness by the activity of upper airway dilating muscles. With the reduction in muscle tone at sleep onset, the airway collapses and causes apnea. While this appears to be the case for many patients with OSA, other patients show no major airway anatomic defects or minimal obesity. RECENT FINDINGS: This has led to the concept that other factors such as unstable ventilatory control and changes in lung volume during sleep may be involved in the pathogenesis of OSA. Recently there have been several advances in our understanding of how these mechanisms are involved in OSA pathogenesis. SUMMARY: A more complete understanding of apnea pathogenesis may improve therapeutic techniques and reduce the consequences of OSA.