Continuous versus bilevel positive airway pressure in a patient with idiopathic central sleep apnea

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.     

Effects of nasal continuous positive airway pressure on breathing pattern and respiratory drive in patients with obstructive sleep apnea syndrome

To examine the influence of continuous positive airway pressure (CPAP) therapy on respiratory center drive in patients with obstructive sleep apnea syndrome (OSAS), 20 normocapnic OSAS patients (group 0) and 20 simple snoring patients were studied. In the first night, diagnostic polysomnography (PSG) was performed. Before and after PSG monitoring, mouth occlusion pressure (P0.1), tidal volume (VT), minute ventilation (VE), respiratory rate (RR), inspiratory time (Ti), expiratory time (Te), total cycle duration (Ttot), inspiratory duty cycle (Ti/Ttot), mean inspiratory flow (VT/Ti) and effective inspiratory impedance (P0.1/VT/Ti, Ieff) were measured while they were breathing room air. In the following night the OSAS patients were treated with nasal CPAP and PSG monitoring and the above mentioned measurements were repeated. The results showed that pre-PSG values of P0.1, RR and P0.1/VT/Ti in the OSAS patients were significantly higher than those in the snoring patients, while VT, Ti, Te and Ttot values were lower. In the first night, the post-PSG P0.1 value in the OSAS patients increased markedly as compared with the pre-PSG. After overnight nasal CPAP therapy, the respiratory disorder index in the OSAS patients decreased markedly, the nadir SaO2 increased markedly, but the post-PSG P0.1 value did not increase significantly. It is concluded that, before sleep, OSAS patients exhibit a higher respiratory drive and a shallow and frequent breathing pattern as compared with simple snoring patients. After nocturnal sleep, the respiratory drive of OSAS patients increases significantly, the breathing pattern becomes more shallow and frequent. Nasal CPAP may effectively relieve the sleep apnea and hypopnea as well as the resulting hypoxemia and therefore correct the changes in breathing pattern and respiratory drive through nocturnal sleep in patients with OSAS.     

Sleep-induced breathing instability. University of Wisconsin-Madison Sleep and respiration Research Group

We present a view of the neuromechanical regulation of breathing and causes of breathing instability during sleep. First, we would expect transient increases in upper airway resistance to be a major cause of transient hypopnea. This occurs in sleep because a hypotonic upper airway is more susceptible to narrowing and because the immediate excitatory increase in respiratory motor output in response to increased loads is absent in non-REM sleep. Secondly, sleep predisposes to an increased occurrence of ventilatory "overshoots", in part because abruptly changing sleep states cause transient changes in upper airway resistance and in the gain of the respiratory controller. Following these ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include: a) hypocapnia-if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptors and cause apnea; b) a persistent inhibitory effect from lung stretch; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may partially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitatory stimuli have risen well above their apneic thresholds, and these prolonged apneas are commonly accompanied by tonic EMG activation of expiratory muscles of the chest wall and upper airway.     

Surgical maxillofacial treatment of obstructive sleep apnea

Obstructive sleep apnea is the most common sleep-related breathing disorder, with a surprisingly high prevalence. The treatment of choice is nasal continuous positive airway pressure (CPAP) ventilation during sleep, which has to be applied throughout the patient's whole life. Because of various underlying pathomechanisms in patients with certain craniofacial disorders--narrow posterior airway space and maxillary-mandibular deficiency--surgical therapy by craniofacial osteotomies seems possible. A series of 38 consecutive patients were treated by 10-mm maxillomandibular advancement by retromolar sagittal split osteotomy and Le Fort I osteotomy, respectively. Obstructive sleep apnea syndrome was improved considerably in all patients; there was no significant difference compared to the results under nasal CPAP. In 37 of 38 patients, the postoperative apnea-hypopnea index was reduced clearly to under 10 per hour, oxygen saturation rose, and sleep quality improved. This was achieved by maxillomandibular advancement of 10 mm without secondary refinements in all but 2 patients. In one patient, the apnea-hypopnea index could only be reduced to 20 per hour, probably because of insufficient maxillary advancement. These results indicate that successful surgical treatment is possible in a high percentage of selected patients with certain craniofacial characteristics. In addition to cardiorespiratory polysomnography, there should be routine cephalometric evaluation of all patients. Maxillomandibular advancement should be offered as an alternative therapy to all patients with maxillary and/or mandibular deficiency or dolichofacial type in combination with narrow posterior airway space.     

Activity of phosphatidylinositol-specific phospholipase C from Bacillus cereus with thiophosphate analogs of dimyristoylphosphatidylinositol

We examined the effects of nasal continuous positive airway pressure (CPAP) on exercise performance in patients with obstructive sleep apnea (OSA). Six patients were treated with nasal CPAP on seven successive days and underwent overnight sleep studies and multiple sleep latency test (MSLT) at the beginning and after the last day of the treatment. The subjects also performed incremental exercise testing using a bicycle ergometer followed by 0-w, 25-w, 50-w,--(3 minutes each) until maximum level. Arterial oxygen pressure, arterial carbon dioxide pressure at rest while awake, apnea/ hypopnea index, longest apnea duration, the lowest percutaneous oxygen saturation measured by a pulse oximeter and the value of MSLT were significantly improved after nasal CPAP. Moreover, maximal oxygen consumption was significantly increased from 1841 ml/min +/- 350 to 2125 ml/min +/- 351 (p < 0.05); however, other cardiorespiratory parameters did not change significantly. The improvement of exercise performance by short-term nasal CPAP treatment in OSA patients may correlate with the improvement of sleepiness.     

Upper airway resistance syndrome

Many clinicians are familiar with the clinical symptoms and signs of obstructive sleep apnea (OSA). In its most blatant form, OSA is complete airway obstruction with repetitive, prolonged pauses in breathing, arterial oxyhemoglobin desaturation; followed by arousal with resumption of breathing. Daytime symptoms of this disorder include excessive daytime somnolence, intellectual dysfunction, and cardiovascular effects such as systemic hypertension, angina, myocardial infarction, and stroke. It has been recently recognized that increased pharyngeal resistance with incomplete obstruction can lead to a constellation of symptoms identical to OSA called "upper airway resistance syndrome" (UARS). The typical findings of UARS on sleep study are: (1) repetitive arousals from EEG sleep coinciding with a (2) waxing and waning of the respiratory airflow pattern and (3) increased respiratory effort as measured by esophageal pressure monitoring. There may be few, if any, obvious apneas or hypopneas with desaturation, but snoring may be a very prominent finding. Treatment with nasal positive airway pressure (NCPAP) eliminates the symptoms and confirms the diagnosis. Herein we describe two typical cases of UARS.     

The effect of nasal CPAP on nocturnal reflux in patients with aperistaltic esophagus

It has been shown that nasal continuous positive airway pressure (nasal CPAP) significantly reduces nocturnal reflux both in patients with sleep apnea and in patients without sleep apnea but consistent abnormal nocturnal reflux. The mechanism by which CPAP is thought to reduce reflux includes the elevation of the resting lower esophageal sphincter (LES) pressure. In this study, we tested the effect of nasal CPAP in two groups of patients with aperistaltic esophagus but with different resting LES pressure. Seven patients with scleroderma esophagus and six patients treated for achalasia were tested over a 48-h period. On the first night, the patients were untreated; on the second night, both groups received applied nasal CPAP at 8 cm H2O pressure. The percentage of time the pH < 4.0, the number of reflux events > 5 min, and the length of the longest reflux event were all significantly reduced in the patients with achalasia (p < 0.03), but not in the scleroderma group (p > 0.20). These results suggest that a residual resting LES pressure greater than that demonstrated by patients with scleroderma (> 10 mm Hg) may be necessary for nasal CPAP to affect nocturnal reflux.     

Therapeutic leukapheresis in the patient with leukemia

OBJECTIVE: To predict and optimal level of continuous positive airway pressure (CPAP) in the menagement of obstructive sleep apnea syndrome (OSAS) by relating certain parameters of respiratory disturbance and sleep hypoxemia. METHODS: 18 patients with OSAS (all male, aged 48 +/- 11 yrs) were enrolled in the study. Their actual levels of CPAP (Pm) were determined by a RHK-5500 mode polysomnographic system plus BiPAP (ST/D) system. The actuual Pm was related to the respiratory disturbance index (RDI) or total time of SaO2 < or = 90% (T S90). The correlation regression equations were calculated. 6 patients with OSAS (Group A) were treated with the predicted nasal CPAP (predicted Pm) which was derived from the regression equation, 8-10 hours per night, for 5-7 nights. 13 patients (Group B) receiving nasal CPAP treatment using the actually measured Pm served as control. RESULTS: There was a close positive linear correlation between RDI or T S90 and actual Pm. Symptoms and polysomnographic parameters improved significantly after one course of CPAP treatment in Group A. The efficacy showed no signifcant different as compared with that in Group B. CONCLUSIONS: It was suggested that RDI or T S90 are of value and simple in predicting the pressuure level of CPAP in the management of OSAS with nasal CPAP.     

Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea

We hypothesized that reductions in arterial PCO2 (PaCO2) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during room air breathing (N1), alternating room air and CO2 breathing (N2), CO2 breathing all night (N3), and addition of dead space via a face mask all night (N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous PCO2, which virtually eliminated apneas and hypopneas; they decreased from 43.7 +/- 7.3 apneas and hypopneas/h on N1 to 5.8 +/- 0.9 apneas and hypopneas/h during N3 (P < 0.005), from 43.8 +/- 6.9 apneas and hypopneas/h during room air breathing to 5.9 +/- 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 (P < 0.005). Because raising PaCO2 through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in PaCO2 below the apnea threshold.     

Starling resister and stability of sleep ventilation

The upper airway can be described as a collapsible segment (the pharynx) interposed between two rigid bony (the cavum) or cartilaginous (the trachea) segments. Due to this structure, the pharynx behaves as a collapsible tube, in which airflow does not depend on the downstream pressure, but is limited to a maximum value which depends only on the upstream pressure and on the pressure surrounding the collapsible segment; this behavior, known as a Starling resistor can be modeled by the waterfall effect. Thus, the upper airways can be in three different conditions: an occluded condition, in which no flow is possible, a patent condition, in which flow depends on the difference between upstream and downstream pressures (according to Poiseuille's law), and a situation in which flow is limited. The behavior of the upper airway is largely dependent on its anatomic structure, but functional factors play a critical role. Among these sleep state is both a determinant of the collapsibility of the pharynx, and determined by the simulation of upper airway mechanoreceptors whose activity depends on the activity of respiratory muscles. Thus the interplay of three factors: ventilatory drive, upper airway collapsibility, and arousal threshold can predict most of the situations of stable and unstable ventilatory behavior during sleep. The level of the arousal threshold governs the stability of the ventilatory pattern, as it determines whether a combination of slow, respiratory effort, and blood gases can be maintained or is interrupted by an arousal.     

Obstructive sleep apnea and related disorders

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.     

Obstructive sleep apnea during pregnancy resulting in pulmonary hypertension

Obesity is known to increase maternal morbidity and mortality. We describe a case of obstructive sleep apnea due to obesity and discuss our treatment of the resulting pulmonary hypertension. A patient was transferred to our hospital at 29 weeks' gestation with severe anasarca and more than a 100-pound weight gain during pregnancy. Pulmonary hypertension due to obstructive sleep apnea was diagnosed. The patient was treated with nasal continuous positive airway pressure (CPAP) during sleep and remained in the hospital the remainder of her pregnancy. She had a massive spontaneous diuresis during her hospital stay and lost more than 100 pounds. She was delivered at term via cesarean section because of transverse lie. Preoperative hemodynamic monitoring confirmed the diagnosis of pulmonary hypertension. This represents the first case in the literature of obstructive sleep apnea leading to pulmonary hypertension in pregnancy. This patient responded well to nasal CPAP as evident by the massive diuresis and good maternal outcome.     

A cost-effective and rational surgical approach to patients with snoring, upper airway resistance syndrome, or obstructive sleep apnea syndrome

The past decade has seen several innovations in the surgical techniques available for treatment of patients with sleep-disordered breathing. Outpatient techniques such as laser-assisted uvulopalatoplasty (LAUP) and more aggressive procedures designed to address hypopharyngeal and base of tongue obstruction (genioglossus advancement and hyoid myotomy) have been developed and proven successful. We describe the efficacy of LAUP for snoring (72.7%), upper airway resistance syndrome (81.8%), and mild (mean [+/-SD] respiratory disturbance index [RDI] = 12 +/- 8.1) obstructive sleep apnea (41.7%) in 56 patients who underwent 132 LAUP procedures in a 26-month period. Thirty-two patients with more significant obstructive sleep apnea (mean RDI = 41.8 +/- 23.1) underwent multilevel pharyngeal surgery consisting of genioglossus advancement and hyoid myotomy combined with uvulopalatopharyngoplasty. The surgical success rate in this group of patients was 85.7% when commonly accepted criteria were applied. We recommend a stratified surgical approach to patients with sleep-disordered breathing. Progressively worse airway obstruction marked by multilevel pharyngeal collapse and more severe sleep-disordered breathing is treated with incrementally more aggressive surgery addressing multiple areas of the upper airway.     

Diagnostic and treatment implications of nasal obstruction in snoring and obstructive sleep apnea

LEARNING OBJECTIVES: The purpose of this review is to highlight fundamental aspects of obstructive sleep apnea (OSA), and to present an overview of the medical literature that pertains to the clinical interplay between various allergy-related disorders, nasal patency, and OSA. This should enable the reader to play a more proactive role in the diagnosis, management, and prevention of OSA. DATA SOURCES: Relevant reviews, texts, and articles. The MEDLINE database was used to find related literature. CONCLUSIONS: In predisposed individuals, OSA, sleep fragmentation, and the sequelae of disturbed sleep often result from nasal obstruction. Since breathing through the nose appears to be the preferred route during sleep, nasal obstruction frequently leads to nocturnal mouth breathing, snoring, and ultimately to OSA. Allergists can thus play a vital role in assessing sleep problems in their patients with allergic rhinitis and other upper respiratory disorders, in treating these problems more aggressively, and in some instances, in preventing them.     

Upper airway assessment: radiographic and other imaging techniques

Upper airway imaging is a powerful technique to study the mechanisms underlying the pathogenesis and biomechanics of sleep apnea and the mechanisms underlying the efficacy of therapeutic interventions in patients with sleep disordered breathing. The primary upper airway imaging modalities include nasopharyngoscopy, cephalometrics, CT scanning, and MR imaging. Imaging studies using these modalities have provided important insights into the static and dynamic structure and function of the upper airway and surrounding soft-tissue structures during wakefulness and sleep. Such imaging studies have highlighted the importance of the lateral pharyngeal walls in mediating upper airway caliber. These imaging modalities have also been used to study the effect of respiration, weight loss, mandibular repositioning devices, and upper airway surgery on the upper airway. Three-dimensional reconstruction of the airway and surrounding soft-tissue structures can be performed with MR imaging and CT scanning. Clinical indications for upper airway imaging are evolving such that imaging studies should be considered in patients with sleep apnea who are being treated with dental appliances or upper airway surgery.     

Surgical options for obstructive sleep apnea

The pathology associated with obstructive sleep apnea is cumulative and progressive. When patients fail to improve with continuous nasal airway pressure or other, less-invasive treatments, surgery should be considered. The initial approach to the surgical patient is identification of all areas of potential obstruction. There are often several sites of obstruction, which can occur anywhere in the upper respiratory tract. One or more procedures may be needed to address these areas. The objective of surgery is to relieve these obstructing sites without interfering with the normal functionality of the upper airway.     

Donor site morbidity following vascularized fibular grafting

Nasal continuous positive airway pressure (CPAP) therapy is usually effective in the treatment of obstructive sleep apnea (OSA), reversing the excessive daytime sleepiness associated with OSA. We investigated how polysomnography and maintenance of wakefulness test (MWT) predicted response to CPAP therapy in 10 patients with obstructive sleep apnea and 10 healthy controls. After a full polysomnography and MWT the patients were started on CPAP. MWT was repeated to quantify the treatment effect. Oxygen desaturation index and the percentage of slow wave sleep were the best predictors for baseline S1 latency in MWT. Baseline S1 latency in the MWT was the most important determinant of improvement in MWT S latency after CPAP, followed by the latency to 10 min of continuous nocturnal sleep, arousal index and CPAP use. We suggest that in mild sleep apnea, knowledge of sleep architecture is not necessary before deciding whether or not to initiate CPAP treatment.     

The use of nasal CPAP in newborns with respiratory distress syndrome

The efficiency of applying continuous positive airway pressure (CPAP) by the nasal route was retrospectively nalyzed in 32 newborns with RDS (23 uncomplicated HMD with additional cardiac or pulmonary complications and 7 RDS of non-hyaline membrane etiology) who underwent nasal CPAP treatment at the Kinderspital Zurich from 1972--1974. 16 of the 23 infants with uncomplicated HMD were successfully treated with CPAP. They showed a significant rise in PaO2 as well as a significant drop in respiratory frequency during nasal CPAP application, the PaCO2 did not change significantly. The remaining 7 infants in this group (7/23) had to be intubated and mechanically ventilated owing to a persistent high FIO2 (4 infants), technical difficulties (1) or nasal hypersecretion (2). Two of these 23 infants died, one of meningitis, one of cerebral hemorrhage. The two infants with HMD and additional cardiac or pulmonary complications and 3 of 7 infants with RDS of non-hyaline membrane etiology had to be intubated and mechanically ventilated after failure of nasal CPAP. All 9 infants in these two groups survived. The nasal CPAP system as described is a simple, inexpensive and effective method of applying CPTPP in newborns with uncomplicated HMD, except radiological stage IV. In HMD with additional cardiac or pulmonary complications and in RDS of non-hyaline membrane etiology the results of nasal CPAP treatment were not convincing.     

Long-term evolution of daytime somnolence in patients with sleep apnea/hypopnea syndrome treated by continuous positive airway pressure

We demonstrated in a previous study that excessive daytime sleepiness (EDS) in patients who have sleep apnea/hypopnea syndrome (SAHS) and are undergoing continuous positive airway pressure (CPAP) treatment improved differently in two groups of patients: in group I, multiple sleep latency tests (MSLT) were normalized after 50 days of treatment (individual value > 10 minutes), whereas they remained low (individual value < 10 minutes) in group II, with a significant difference between groups. To evaluate the long-term evolution of daytime somnolence under nasal CPAP treatment, five patients from group I and seven patients from group II underwent a new polysomnography and MSLT 4 years after the previous study. Clinical, polysomnographic and MSLT results obtained at baseline before treatment (T1), after the initial 50-day period of CPAP treatment (T2), and after 4 years (T3) were compared. The significant difference in mean MSLT value between the two groups previously observed at T1 and T2 disappeared at T3 (group I: 12.4+/-5.9 minutes; group II: 9.7+/-5.9 minutes). We found that this long-term improvement in excessive daytime somnolence was independent of the initial MSLT value, the severity of SAHS, and the initial MSLT changes under nasal CPAP. Long-term MSLT evolution was significantly correlated to CPAP compliance. These results demonstrate that even in the absence of a significant increase in MSLT at the beginning of CPAP treatment, further improvement is still possible several years later, which may encourage the regular, long-term use of nasal CPAP by patients.     

Respiratory arousal from sleep: mechanisms and significance

The mechanisms by which respiratory stimuli induce arousal from sleep and the clinical significance of these arousals have been explored by numerous studies in the last two decades. Evidence to date suggests that the arousal stimulus in nonrapid eye movement sleep (NREM) is related to the level of inspiratory effort rather than the individual stimuli that contribute to ventilatory drive. A component of the arousal stimulus proportional to the level of inspiratory effort may originate in mechanoreceptors either in the upper airway or respiratory pump. Medullary centers responsible for ventilatory drive may also send a signal proportionate to the level of drive to higher centers in the brain which are responsible for arousal. Thus, the arousal stimulus may consist of multiple components, each increasing as inspiratory effort increases. The level of effort triggering arousal is an index of the arousability of the brain (arousal threshold). A deeper stage of sleep, central nervous system depressants, prior sleep fragmentation, and the presence of obstructive sleep apnea (OSA) have been observed to increase the arousal threshold to airway occlusion. Less information is available concerning the mechanisms of arousal from rapid eye movement (REM) sleep. While REM sleep is associated with the longest obstructive apneas in patients with OSA, normal human subjects appear to have a similar or lower arousal threshold to respiratory stimuli in REM compared to NREM sleep. Recent studies have challenged the assumption that the termination of all obstructive apnea is dependent on arousal from sleep. Improvements in methods to detect and quantitate changes in the cortical electroencephalogram (EEG) may better define the relationship between arousal and apnea termination. This may result in improved criteria for identifying EEG changes of clinical significance. While little is known concerning the mechanisms of arousal in central sleep apnea, arousal may play an important role in inducing this type of apnea in some patients.