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

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
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PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

A 51-year-old patient with COPD, obesity, and pulmonary hypertension underwent long-term prazosin therapy after a successful hemodynamic response to 1 mg of oral prazosin. The 18-month administration of prazosin, in a dose of 3 mg a day, resulted in continued hemodynamic and echocardiographic benefits.
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PMID:Long-term prazosin therapy for COPD pulmonary hypertension. 164 64

The purpose of this study was to assess the efficacy of bi-level positive airway pressure (BiPAP) ventilation through a nasal mask in the treatment of eight patients with hypoventilatory respiratory failure and nocturnal CO2 retention. Nocturnal CO2 retention was significantly reduced in all patients with the application of BiPAP during sleep (p less than 0.01). Daytime somnolence was relieved and dyspnea improved after three months of home BiPAP therapy. All patients tolerated home BiPAP therapy, and two patients who had previously been treated with volume ventilation via nasal mask found BiPAP more comfortable. There were no changes in FEV1 or FVC after three months of BiPAP. Daytime PaCO2 improved slightly or remained stable in all patients after three months of home BiPAP. BiPAP nasal ventilation is effective in reducing nocturnal CO2 retention short term in hypoventilatory respiratory failure due to obesity hypoventilation syndrome, chest wall restriction, or neuromuscular disease. Further studies in patients with COPD may be warranted.
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PMID:Nocturnal nasal intermittent positive pressure ventilation with bi-level positive airway pressure (BiPAP) in respiratory failure. 173 82

Intermittent mechanical ventilation via nasal CPAP mask was provided to 13 patients admitted to this institution for exacerbation of chronic respiratory failure. Ten suffered from COPD, two suffered from obesity hypoventilation syndrome (OHS), and one from severe hypothyroidism. All except one presented with dyspnea and hypercapnia due solely to progression of their underlying disease processes. Six of the patients with COPD and the patient with hypothyroidism responded to positive pressure ventilation by mask with improvements in blood gas values and clinical status. The remaining two patients with COPD and the two patients with OHS were unable to use the system. Four of the patients with COPD and chronic respiratory failure have been subsequently maintained on daily volume ventilation via nasal mask for about 20 months with persistent clinical and physiologic improvements. Application of volume ventilation through the nasal CPAP mask is a feasible strategy for providing long-term mechanical ventilation to selected patients with COPD and respiratory failure.
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PMID:Intermittent volume cycled mechanical ventilation via nasal mask in patients with respiratory failure due to COPD. 155 51

Interactions between sleep and respiration have been noticed in several lung diseases. In COPD (chronic obstructive pulmonary disease) patients, the night sleep is delayed or shortened and deep sleep is often reduced or even absent. These disturbances are associated with hypoxaemic episodes occurring either in light slow wave sleep or in REM sleep, the former being short in duration and mild but repetitive and related to ventilatory changes, the latter prolonged, often severe, and resulting from both decrease in ventilation and alterations of ventilation-perfusion ratios. Restrictive syndrome due to interstitial pneumonia, kyphoscoliosis, neuromuscular diseases or, more commonly, to obesity or even pregnancy also alter sleep in a non-specific manner. Most of them result in hypoxia during paradoxical sleep. Unquestionably, there exists a relationship between sleep and asthma (aggravation of dyspnoea at night, reduction of peak expiratory flow when awaking, stage 2 asthmatic attacks). This relationship is probably caused by multifactorial interactions.
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PMID:[Changes in sleep and night respiration in asthma and obstructive or restrictive lung diseases]. 214 79

Described is a 67-year-old man whose initial symptoms evoked an obesity-hypoventilation syndrome. Polysomnography showed hypopneas associated with O2 desaturation episodes, and no apnea; maximal changes were noted during REM sleep. A few months later, in spite of marked weight loss, acute alveolar hypoventilation occurred and necessitated mechanical ventilatory support. Tracheostomy was performed. The patient appeared to be dependent on nocturnal ventilatory assistance. Diaphragmatic paralysis was noted in addition to clinical and electrodiagnostic evidence of amyotrophic lateral sclerosis. While the patient was not ventilated, a nocturnal recording of SaO2 again revealed desaturation episodes partly corrected by O2 2 L/min administered through the tracheostomy tube. With volume-controlled ventilation, desaturations completely disappeared, although no oxygen enrichment of the air was provided. We speculate that sleep disorders with hypopneas and O2 desaturation episodes were the initial symptoms of amyotrophic lateral sclerosis. This leads us to suggest that nonspecific respiratory muscle fatigue frequently seen in COPD might be included in the hypothetic causes of nocturnal hypoxemia.
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PMID:Amyotrophic lateral sclerosis presenting with sleep hypopnea syndrome. 337 Nov 13

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.
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PMID:Respiratory muscles and ventilatory failure: 1993 perspective. 850 1

Nocturnal oximetry can show nocturnal oxygen desaturation. This examination was proposed as an investigation for the early detection of the sleep apnoea syndrome (SAS). We have compared the results of nocturnal oximetry and polysomnography in 329 consecutive patients seen in the department of thoracic medicine for the early detection of the SAS between June 1990 and June 1995. The diagnosis of SAS was confirmed at the time of polysomnography using an hypopnoea/apnoea index (IAH) greater or equal to 15 per hour. Two parameters of oximetry were well correlated with IAH less than 15 per hour: if the mean oxygen saturation is greater than 92% and for less than five per cent of the time of the examination there was a saturation of less than 90%. The sensitivity was 89.7% and the specificity was 57.8%. Among the 48 false positive cases on oximetry 17 patients were found to be suffering from COPD and 31 patients were probably suffering from a syndrome of upper airways resistance or possibly from the hypoventilation obesity syndrome. Amongst the 22 false, negatives to oximetry 10 non COPD patients with an IAH of greater than 30 per hour and diurnal somnolence had important anomalies of the oro-pharyngeal pathway as the origin of their nocturnal apnoea. The 12 other false negatives were patients with moderate SAS with an IAH of between 15 and 20 per hour. Logistical analysis has shown the association of the two oximetric criteria (mean oxygen saturation or percentage of time with a saturation of less than 5%) with clinical criteria (body mass index and formation on diurnal somnolence from a questionnaire) would enable a probable diagnosis of SAS in 75% of cases. Our study shows that nocturnal oximetry used an early diagnosis test, associated with clinical and respiratory function data enables the number of requests for polysomnography to be reduced.
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PMID:[Role of nocturnal oximetry in screening for sleep apnea syndrome in pulmonary medicine. Study of 329 patients]. 941 97

The incidence of peri-operative pulmonary complications varies, depending on surgery and patient related determinants. Risk factors include upper abdominal or thoracic surgery, duration of anaesthesia, age, obesity, smoking history and underlying respiratory diseases such as COPD. The preoperative evaluation of patients undergoing general surgery is predominantly based on medical history and physical examination. A preoperative chest radiograph and pulmonary function tests are indicated in some high risk patient groups, and in all patients about to undergo lung resection surgery. If in this latter group, the preoperative lung function is severely compromised, a quantitative perfusion scan and exercise testing may be useful for the assessment of the operative risk. Prevention of postoperative pulmonary complications should begin with discontinuation of smoking at least 8 weeks prior to surgery. In high risk patients preoperative chest physiotherapy, including incentive spirometry, is clearly beneficial.
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PMID:Preoperative pulmonary evaluation. 948 24

Obstructive Sleep Apnea (OSA), Obesity-Linked Hypoventilation (OLH)--a hypoventilation which is independent of apneas and increased by sleep--, and COPD are mechanisms for respiratory failure in obese patients. We thought nasal bi-level positive airway pressure to be a suitable treatment: EPAP is useful to maintain upper airway patency and IPAP-EPAP difference to correct OLH and COPD hypoventilation. Our purpose is to report the results of such a therapeutic approach. We included 41 patients that we first treated by nasal bi-level positive airway pressure for a respiratory failure with an uncompensated respiratory acidosis. The initial setting was about 4 cm H2O for EPAP and 16 for IPAP. Under supervision of a real-time printed oximetry tracing, we furthermore increased EPAP until disappearance of repetitive dips in oxygen saturation (that we assimilated to obstructive events) and IPAP until obtaining an acceptable level of steady saturation (we assimilated a low level to a steady hypoventilation). Age (mean +/- SD) was 63 +/- 11 years, BMI 42 +/- 9 kg/m2, pH 7.32 +/- 0.04, PaCO2 71 +/- 13 mmHg, PaO2 45 +/- 7 mmHg. Thirty-nine out of 41 patients returned home without need for tracheal intubation. At 7 days of treatment, PaCO2 was 50 +/- 6 mmHg. Thus, nasal bi-level position airway pressure appears to be an efficient treatment in these patients.
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PMID:[Management of obesity and respiratory insufficiency. The value of dual-level pressure nasal ventilation]. 967 35


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