Hypoventilation

Abstract: Obesity can profoundly alter pulmonary function and diminish exercise capacity by its adverse effects on respiratory mechanics, resistance within the respiratory system, respiratory muscle function, lung volumes, work and energy cost of breathing, control of breathing, and gas exchange. Weight loss can reverse many of the alterations of pulmonary function produced by obesity. Obesity places the patient at risk of aspiration pneumonia, pulmonary thromboembolism, and respiratory failure. It is the most common precipitating factor for obstructive sleep apnea and is a requirement for the obesity hypoventilation syndrome, both of which are associated with substantial morbidity and increased mortality. There are numerous medical and surgical therapies for obstructive sleep apnea and obesity hypoventilation. Weight reduction in the obese is among the most effective of these measures.

Abstract: We report four young women who developed acute psychiatric symptoms, seizures, memory deficits, decreased level of consciousness, and central hypoventilation associated with ovarian teratoma (OT) and cerebrospinal fluid (CSF) inflammatory abnormalities. Three patients recovered with treatment of the tumor or immunosuppression and one died of the disorder. Five other OT patients with a similar syndrome and response to treatment have been reported. Our patients' serum or CSF showed immunolabeling of antigens that were expressed at the cytoplasmic membrane of hippocampal neurons and processes and readily accessed by antibodies in live neurons. Immunoprobing of a hippocampal-expression library resulted in the isolation of EFA6A, a protein that interacts with a member of the two-pore-domain potassium channel family and is involved in the regulation of the dendritic development of hippocampal neurons. EFA6A-purified antibodies reproduced the hippocampal immunolabeling of all patients' antibodies and colocalized with them at the plasma membrane. These findings indicate that in a young woman with acute psychiatric symptoms, seizures, and central hypoventilation, a paraneoplastic immune-mediated syndrome should be considered. Recognition of this disorder is important because despite the severity of the symptoms, patients usually recover. The location and function of the isolated antigen suggest that the disorder is directly mediated by antibodies.

Abstract: Background Severe obesity is associated with hypoventilation, a disorder that may adversely affect morbidity and mortality. We sought to determine the prevalence and effects of obesity-associated hypoventilation in hospitalized patients. Methods Consecutive admissions to internal medicine services were screened over a 6-month period. In all eligible subjects with severe obesity (body mass index ≥35 kg/m 2 ), we administered a sleep questionnaire, and performed neuropsychological, arterial blood gas, and pulmonary function testing. Hospital course and mortality at 18 months was also determined. Results Of 4332 admissions, 6% (n = 277) of patients were severely obese, of whom 150 were enrolled, 75 refused to participate, and 52 met the exclusion criteria. Hypoventilation (mean [± SD] arterial partial pressure of carbon dioxide [PaCO 2 ], 52 ± 7 mm Hg) was present in 31% (n = 47) of subjects who did not have other reasons for hypercapnia. Decreased objective attention/concentration and increased subjective sleepiness were present in patients with obesity-associated hypoventilation compared with in severely obese hospitalized patients without hypoventilation (simple obesity group; mean PaCO 2 , 37 ± 6 mm Hg). There were higher rates of intensive care ( P = 0.08), long-term care at discharge ( P = 0.01), and mechanical ventilation ( P = 0.01) among subjects with obesity-associated hypoventilation. Therapy for hypoventilation at discharge was initiated in only 6 (13%) of the patients with obesity-associated hypoventilation. At 18 months following hospital discharge, mortality was 23% in the obesity-associated hypoventilation group as compared with 9% in the simple obesity group (hazard ratio=4.0; 95% confidence interval: 1.5 to 10.4]. Conclusion Hypoventilation frequently complicates severe obesity among hospitalized adults and is associated with excess morbidity and mortality.

Abstract: Summary In a patient showing a typical pickwickian syndrome a study was made of respiratory functions and arterial gasometry, with polygraphic registrations carried out during the day and at night in an attempt to evaluate sleep, respiration, blood oxyhaemoglobin and CO2 concentration of the expiratory air. It was demonstrated that, at the onset of an authentic pickwickian syndrome, the symptomatology may be confined to obesity and diurnal drowsing episodes of the type described by Dickens in his novel. This means that the permanent alveolar hypoventilation regarded by some authors as an indispensable feature of the syndrome, In the patient under discussion, the numerous episodes of diurnal slumber which characterized his condition and occurred while the blood oxyhaemoglobin saturation and alveolar CO2 concentration were entirely normal, cannot be explained on the basis of hypoxia and hypercapnia as suggested by a majority of authors. One must resort to other hypotheses, bearing in mind that the one does not necessarily exclude the other. A first hypothesis suggests that the subject drowses during the day as a result of a primary disturbance of centres in the brain stem which regulate wakefulness and sleep by a mechanism not yet understood. According to this hypothesis, we are confronted with some sort of narcolepsy. A second hypothesis holds that the subject drowses during the day because he does not sleep sufficiently at night as a result of an exaggeration of the physiological phenomenon of hypnic hypoventilation. Nocturnal polygraphic registrations disclosed respiratory pauses which occurred in the initial phase of sleep, quite apart from hypotonia of the muscles of the floor of the mouth, so rapid and pronounced that the tongue moves back and causes the obstructive apnoea responsible for a hypoxia which arouses the subject, who returns to sleep after a short while. The cyclic repetition of arousal and slumber reduces nocturnal sleep to 2–3 h a night. This loss of nocturnal sleep is held responsible for the diurnal somnolence. Unfortunately the subject's diurnal sleep is disturbed even more than his nocturnal sleep because the slightest slumber immediately produces episodes of central or obstructive apnoea. Regardless of the respective values of these two hypotheses, the authors are convinced that the majority of individuals suffering from the pickwickian syndrome drowse during the day and sleep badly at night because of a primary disturbance in the wakefulness-sleep regulation which as such is based on their obesity. This affords an obvious explanation of the established fact that the only way to suppress hypnic disturbances in pickwickian patients is to have them lose weight.

Abstract: Children with Down syndrome have many predisposing factors for the obstructive sleep apnea syndrome (OSAS), yet the type and severity of OSAS in this population has not been characterized. Fifty-three subjects with Down syndrome (mean age 7.4 +/- 1.2 [SE] years; range 2 weeks to 51 years) were studied. Chest wall movement, heart rate, electroculogram, end-tidal PO2 and PCO2, transcutaneous PO2 and PCO2, and arterial oxygen saturation were measured during a daytime nap polysomnogram. Sixteen of these children also underwent overnight polysomnography. Nap polysomnograms were abnormal in 77% of children; 45% had obstructive sleep apnea (OSA), 4% had central apnea, and 6% had mixed apneas; 66% had hypoventilation (end-tidal PCO2 greater than 45 mm Hg) and 32% desaturation (arterial oxygen saturation less than 90%). Overnight studies were abnormal in 100% of children, with OSA in 63%, hypoventilation in 81%, and desaturation in 56%. Nap studies significantly underestimated the presence of abnormalities when compared to overnight polysomnograms. Seventeen (32%) of the children were referred for testing because OSAS was clinically suspected, but there was no clinical suspicion of OSAS in 36 (68%) children. Neither age, obesity, nor the presence of congenital heart disease affected the incidence of OSA, desaturation, or hypoventilation. Polysomnograms improved in all 8 children who underwent tonsillectomy and adenoidectomy, but they normalized in only 3. It is concluded that children with Down syndrome frequently in have OSAS, with OSA, hypoxemia, and hypoventilation. Obstructive sleep apnea syndrome is seen frequently in those children in whom it is not clinically suspected. It is speculated that OSAS may contribute to the unexplained pulmonary hypertension seen in children with Down syndrome.