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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During hypercapnia-induced hyperventilation, obese patients with a prior history of alveolar hypoventilation appear to have significantly more blunted ventilatory response than simply obese patients who never retained carbon dioxide. In addition, these patients with former obesity-hypoventilation syndrome have decreased neuromuscular responses as measured by way of the mouth occlusion technique when compared with either the patients with simple obesity or normal subjects. The patients with simple obesity appear to have augmented responses in comparison with normal subjects. Simple mechanical considerations and baseline breathing variables failed to distinguish the simple obesity group from the group with former obesity-hypoventilation syndrome. Thus, the decreased neuromuscular responsiveness to carbon dioxide (mouth-occlusion pressure/end-tidal carbon dioxide pressure) among the group with former obesity-hypoventilation syndrome when compared with that in the group with simple obesity is a consequence of a blunted neural (central) drive, and not due to any apparent worse mechanical limitations. The augmented mouth-occlusion pressure/end-tidal carbon dioxide pressure and increased integrated, rectified electromyographic signal of the diaphragm found in the group with simple obesity presumably reflect their attempt to maintain ventilatory homeostasis in the presence of severe respiratory loads. Neuromechanical coupling values, as reflected in the integrated electromyographic signal of the diaphragm versus transdiaphragmatic pressure and mouth-occlusion pressure versus mean inspiratory flow, are identical in the two groups. On the basis of these studies, it would appear that although mechanical loads put all obese patients at a disadvantage, the addition of an acute extra load on the respiratory system produces the obesity-hypoventilation syndrome in those obese persons who have truly blunted central hypercapnic responses.
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PMID:Neuromechanical properties in obese patients during carbon dioxide rebreathing. 640 17

To define the roles of mechanical loading, respiratory neuromuscular control, and sleep apnea in the pathogenesis of obesity hypoventilation, respiratory muscle drive and output, assessed by diaphragmatic electromyogram (EMGdi) and mouth occlusion pressure (P 0.15), respectively, were determined during CO2 chemostimulation in nonobese volunteers who were subjected to abdominal mass loading, and in three groups of markedly obese patients: eucapnic obese without sleep apnea (O), eucapnic obese with sleep apnea (OSA), and hypercapnic obese with sleep apnea (OH). The P0.15 responses were decreased in OSA and OH, but the EMGdi responses were not significantly different from those in control subjects. In O patients EMGdi responses were significantly greater than those in control subjects as well as those in OSA and OH patients. EMGdi and P0.15 responses increased in all nonobese subjects when they were subjected to mass loading. We conclude that both OSA and OH patients were equally unable to develop the expected increase in respiratory muscle drive and output. The presence of sleep apnea, possibly by causing nocturnal hypoxemia and/or sleep fragmentation, may result in impaired mass load compensation and predispose obese patients to develop hypercapnia.
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PMID:Mass loading, sleep apnea, and the pathogenesis of obesity hypoventilation. 681 71

Four morbidly obese men who had been found to have significant sleep-disordered breathing and oxygen desaturation were restudied after an average weight loss of 108 kg (range 53-155 kg). In all subjects, weight loss was accompanied by a significant reduction in the number of episodes per hour of sleep-disordered breathing events. In three of the four subjects, there was improvment in the severity of desaturation accompanying abnormal breathing. The two subjects with daytime somnolence and hypercapnia prior to weight loss showed the most dramatic improvement in desaturation. This suggests that obesity is a cause, rather than an effect, of the sleep apnea syndrome.
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PMID:The effect of weight loss on sleep-disordered breathing and oxygen desaturation in morbidly obese men. 710 55

A sex-, age-, obesity, and protease inhibitor-matched study of pulmonary function and ventilatory control was performed on 26 sons of 19 patients with chronic obstructive pulmonary disease (COPD) and 26 control subjects. Mean values for FEV1/FVC and V25 were significantly lower and CV/VC was significantly higher in sons of patients than in the controls. VC, airway resistance, static pulmonary compliance. delta N2, arterial blood gases and pH were not different between sons and controls. When the sons of patients were divided into two groups according to the arterial blood gases of their parents, sons of hypoxemic, hypercapnic parents showed significantly lower hypoxic ventilatory responses than sons of normoxemic, normocapnic parents. Hypercapnic ventilatory responses were not different between sons and controls. Abnormal pulmonary function and low ventilatory responses were more frequently detected in sons than in controls. The association of smoking with abnormalities of pulmonary function was not clearly seen in sons. These results suggest that familial factors (either genetic or environmental) play a significant role in determining the pathogenesis and clinical types of COPD.
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PMID:Familial aggregation of abnormal ventilatory control and pulmonary function in chronic obstructive pulmonary disease. 722 84

The obese Zucker rat, an autosomally genetic model of obesity, represents a good model of relatively early onset human obesity. Although factors associated with the control of metabolism and thermoregulation have been studied extensively in these animals, pulmonary mechanics and ventilation have not been documented and form the basis of this investigation. Studies were carried out in 16 obese and 18 lean female littermates (698 +/- 79 versus 304 +/- 24 g, p < 0.001). Pulmonary function, including lung volumes and respiratory system compliance, was evaluated in supine anesthetized animals. With the exception of residual volume, all other lung volumes, including function residual capacity, total lung capacity, expiratory reserve volume, and inspiratory capacity, were significantly reduced (p < 0.05 or better) in the obese phenotype compared with volumes in the lean littermates. Pressure-volume relationships of the intact respiratory system and the excised lung were also determined. Although lung compliance was similar between the phenotypes, respiratory system compliance was significantly lower (0.85 +/- 0.06 versus 0.67 +/- 0.09 ml/cm H2O, p < 0.01) in the obese rats. Oxygen consumption and ventilatory parameters (including respiratory rate, tidal volume, minute ventilation, inspiratory time, and expiratory time) were similar between phenotypes breathing room air, and the minute ventilation in response to hypoxia was similar in both groups. In marked contrast, obese animals exhibited a blunted ventilatory response to hypercapnia (221 +/- 38 versus 135 +/- 44 ml/min, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary ventilation and mechanics in morbidly obese Zucker rats. 804 15

The cardio-respiratory complications of sleep apnea syndrome have been prospectively assessed in 60 patients with massive obesity and free of chronic obstructive lung disease while the associated cardiovascular diseases and the alterations of pulmonary function were taken into account. These cardio-respiratory complications were observed only in patients with a number of apneas per hour of sleep greater than 20. The sleep apneas induced nocturnal hypoxemia that is frequently severe and independently correlated to the apnea index, diurnal hypoxemia and hypercapnia that are usually moderate, and presumably left ventricular hypertrophy that is not related to the development of daytime hypertension. However the nocturnal apneas were not associated with the development of an impairment of right or left ventricular function, or with the occurrence of cardiac arrhythmias or conduction disturbances. The absence of severe cardiac complications in this study may be related to the fact that the patients were relatively young and that the sleep apnea syndrome was diagnosed at an early stage of evolution. The findings of this study could help to define a more rationale approach in several therapeutic indications of sleep apnea syndrome.
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PMID:[Cardio-respiratory complications of sleep apnea in obese patients]. 822 Nov 69

Massive obesity may be accompanied by severe and sometimes lethal respiratory complications. The restrictive ventilatory deficit which results from a decrease in thoracic wall compliance and perhaps also from diaphragmatic dysfunction is more severe in males and in subjects with abdominal obesity. Diurnal hypoxaemia results from 2 mechanisms: diminution of the ventilation/perfusion ratio at the base of the lung, and alveolar hypoventilation. Hypercapnia is a fairly frequent complication of massive obesity. Although usually moderate, hypercapnia is a major indicator as it is very often associated with sleep apnoea syndrome. The most severe respiratory complication of massive obesity is this syndrome which must be looked for systematically by questioning the patient and her husband or his wife before serious cardiopulmonary and neuropsychic disorders appear. The effects of weight loss of nocturnal apnoea are inconsistent and variable. Continuous positive pressure ventilation by means of a nasal mask is the choice treatment of sleep apnoea syndrome, especially since the results of rhino-laryngeal surgery are often disappointing.
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PMID:[Respiratory function in massive obesity]. 831 Feb 44

The medical hazards of obesity are discussed. Risks include insulin resistance, diabetes mellitus, hypertriglyceridemia, decreased levels of high-density lipoprotein cholesterol, and increased levels of low-density lipoprotein cholesterol. Obesity is also associated with gallbladder disease and some forms of cancer as well as sleep apnea, chronic hypoxia and hypercapnia, and degenerative joint disease. Obesity is an independent risk factor for death from coronary heart disease. A central distribution of body fat enhances the risk for most of these conditions.
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PMID:Medical hazards of obesity. 836 92

Weight loss reduces many of the health hazards associated with obesity including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, sleep apnea, hypoxemia and hypercarbia, and osteoarthritis. Potential adverse effects of weight loss include a greater risk for gallstone formation and cholecystitis, excessive loss of lean body mass, water and electrolyte problems, mild liver dysfunction, and elevated uric acid levels. Less consequential problems such as diarrhea, constipation, hair loss, and cold intolerance may also occur. The short-term adverse effects are not severe enough to contraindicate weight loss, nor do they outweigh its short-term benefits.
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PMID:Short-term medical benefits and adverse effects of weight loss. 836 5

We hypothesized that obese children with a history of breathing difficulty during sleep would demonstrate (1) evidence of complete and partial obstructive sleep apnea (OSA) with hypercarbia and/or hypoxemia; and (2) correlation between symptoms, degree of obesity, adenoid and tonsil size, and polysomnography (PSG) results. We evaluated 32 obese children [% ideal body weight (IBW), 196 +/- 45%] with a sleep history questionnaire, airway radiographs, electrocardiograms (ECG), and PSG. By history, we found snoring (100%), difficulty breathing (59%), sweating (44%), restlessness (53%), arousals (41%), apnea (50%), worsening with upper respiratory infection (URI) (81%), hypersomnolence (59%), and mouth breathing (59%). We found adenoid and/or tonsil enlargement on 75% of airway x-ray pictures. ECGs were abnormal in 5 patients. Among all patients, mean sleep study oxyhemoglobin saturation (SaO2) was 85 +/- 16% and mean end-tidal CO2 (PetCO2) was 51 +/- 7 torr; 84% had paradoxical inward movement of the chest on inspiration, 59% had OSA, and 66% had partial OSA. In those with > or = 200% IBW and adenotonsillar enlargement, elevated PetCO2 and the presence of hypoxemia (SaO2 < 90%) for > or = 5% of the total sleep time (TST) were correlated, unlike in patients of similar weight but without adenotonsillar enlargement. Individuals symptoms did not correlate with the severity of PSG abnormalities. By discriminant analysis, using three variables (IBW, presence of adenotonsillar tissue, and presence of > or = 5 symptoms), we could predict PSG abnormalities with up to 81% reliability. Our findings indicate that in obese children, particularly those with %IBW > or = 200 and adenotonsillar hypertrophy, with sleep-disordered breathing evaluation by polysomnography should be considered.
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PMID:Polysomnography in obese children with a history of sleep-associated breathing disorders. 836 18


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