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

A child with respiratory failure and cor pulmonale secondary to the obesity hypoventilation syndrome (OHS) was found to have abnormal beta-endorphin levels in cerebrospinal fluid (CSF) and serum. A single iv dose of 10 microgram/kg of naloxone early in the course of respiratory failure resulted in dramatic improvement which lasted approximately 3 to 4 h. The patient failed to response to progesterone, and because of deteriorating respiratory status a low-dose continuous infusion of naloxone, 2 microgram/kg.h, was begun and gradually increased to 10 microgram/kg.h, during which time there was a dramatic improvement in respiratory status and clinical condition. After 5 days, naloxone infusion was discontinued and progressive respiratory deterioration recurred. The child died of over-whelming sepsis and disseminated intravascular coagulation.
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PMID:Narcotic antagonist therapy of the obesity hypoventilation syndrome. 628 52

Previous reports underestimate the morbidity of a lipectomy, having focused on mortality statistics. Alterations of respiratory kinetics leading to complications do not always correlate with the usual signs and symptoms of respiratory failure. Patients at increased risk, namely, those with obesity, a smoking history, or lung disease, deserve special attention, including appropriate pulmonary function studies in the preoperative and postoperative phase. The following studies are indicated in the preoperative assessment of the high-risk patient: (1) vital capacity, (2) arterial blood gases, and (3) chest radiograph.
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PMID:Pulmonary complications following abdominal lipectomy. 685 97

The normoxic ventilatory drive contributes to the normal level of ventilation, and the hypoxic ventilatory drive contributes to the maintenance of adequate gas exchange in the presence of ventilation/blood flow maldistribution and increased mechanical load to breathing. This respiratory drive arises principally from stimuli at the carotid chemoreceptors. The reflex cardiovascular responses to hypoxia also contribute to the delivery of O2 to vital organs, and their efficacy depends on the integrity of the respiratory response and the autonomic nervous system as well as the function of the vascular system. Prolonged exposure to hypoxemia from altitude, cyanotic congenital heart disease, and chronic pulmonary disease impair the ventilatory response to hypoxia. In addition, the respiratory and cardiovascular responses to hypoxemia are impaired by familial or acquired abnormalities of the autonomic effector system. There is growing evidence that impaired respiratory response to hypoxemia is a major factor in recurrent respiratory failure in obesity, obstructive pulmonary disease, idiopathic or familial "hypoventilation," and contributes to disturbances in oxygenation during sleep [152, 189, 192, 202]. Although the ventilatory response to hypoxemia was traditionally thought to be resistant to the effects of inhalational anesthetics, barbiturates, and narcotics, there is abundant evidence that in fact the ventilatory response to hypoxia is more sensitive to depression by drugs than the ventilatory response to CO2. In addition, the hemodynamic responses to hypoxia are modified by anesthesia and anesthetic techniques. The clinical implications of these observations are wide. The ventilatory and cardiovascular response to hypoxemia will be altered, and usually depressed by age, disease processes, premedicant and anesthetic drugs, and autonomic blocking drugs. The cardiovascular responses will be modified indirectly by altered ventilatory control due to neuromuscular blocking drugs and controlled ventilation. Thus, not only will the responses to hypoxemia be depressed by anesthesia but the early clinical hemodynamic signs will be modified or absent, or indeed the cardiovascular response will further impair oxygen delivery. Furthermore, it is not only anesthetic doses that impair the reflex respiratory responses, but also subanesthetic doses of inhalational anesthetics and premedicant doses of barbiturates and narcotics. Hence the patient in the perioperative period continues to have impaired respiratory response to hypoxemia. As anesthetic and surgical care extends to older patients, patients with systemic disease, and recipients of cardiovascular peripheral and central drugs, the clinical implications of the impairment of ventilatory and cardiovascular responses to hypoxia, and the maintenance of organ and system function, escalate. Only a few hesitant steps have been taken into this vast arena of clinical and experimental research.
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PMID:Respiratory and cardiovascular responses to hypoxemia and the effects of anesthesia. 702 55

We studied 10 obese volunteers, mean age 36.5 +/- 10.3 years, who weighed 123.56 +/- 28.7 g and were 69.96 +/- 22.5 kg overweight. The subjects did not have diabetes, arterial hypertension or signs of cardiac and respiratory failure or disease and all underwent right- and left-heart catheterization. cardiac output and stroke volume were high, according to increased oxygen consumption and to the degree of obesity. Ventricular end-diastolic and atrial pressures ranged from normal to high and correlated with body weight, signs of volume overloading and reduced left ventricular (LV) compliance. The mean pulmonary artery pressure was elevated and correlated well with weight, pulmonary resistance being normal; mean aortic pressure did not correlate with weight, and systemic arterial resistance tended to have a negative correlation. The LV function curve showed impaired ventricular function, particularly for the heaviest subjects, in whom Vmax and the ratio of the stroke work index to LV end-diastolic pressure were reduced. These indexes correlated well with each other and both correlated negatively with the degree of obesity. In contrast, maximal dP/dt was normal and did not correlate with excess weight. These observations show that depressed LV function is already present in relatively young obese people, even if they are free from signs of cardiopathy and other associate diseases. The degree of impairment of heart function seems to parallel the degree of obesity.
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PMID:Obesity and cardiac function. 726 Dec 80

Recent epidemiological data indicate that obstructive sleep apnoea (OSA) and related conditions are extremely common in the middle-aged population. Obesity is an important aetiological factor in sleep-disordered breathing with a multifactorial role in the pathogenesis of upper airway occlusion. One extreme of the spectrum of sleep-disordered breathing is obesity-hypoventilation syndrome (one type of OSA with awake respiratory failure). Sleep-disordered breathing has a number of clinical consequences, including excess cardiovascular morbidity. Obesity is an important confounder of this association. Treatment of these disorders has been revolutionized by the use of nasal continuous positive airway pressure (CPAP). Weight reduction reduces apnoea severity but is not curative in most obese patients with sleep apnoea.
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PMID:Sleep-disordered breathing and obesity. 798 Mar 49

A 47 year old man with a long history of chronic loud snoring and daytime sleepiness presented with hypercapnic respiratory failure and right ventricular failure. The diagnosis of obstructive sleep apnoea (OSA) leading to the 'obesity-hypoventilation syndrome', was supported by the findings of an overnight cardio-respiratory monitoring during sleep. His symptoms and arterial blood gases improved following treatment with nocturnal nasal continuous positive airway pressure (CPAP).
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PMID:Cor pulmonale due to obstructive sleep apnoea. 818 51

Several disorders of the thoracic cage are known to cause respiratory failure, by means of relatively simple mechanisms, such as the increased work of breathing, which results in alveolar hypoventilation. A variety of pathogenic mechanisms may be considered, as functions of the types of thoracic disorders present. As causes of these additional potential mechanisms, we considered the following: 1) ventilation-perfusion (V/Q) inhomogeneity; 2) inability to cough; 3) malformation or acquired defect of the respiratory centres; and 4) excess blood volume and fluid retention, which aggravate work of breathing and V/Q inhomogeneity. All of these disorders can be grouped into two major categories (which nevertheless have some of the pathophysiology in common): the mechanical syndrome and the neuromuscular or paralytic syndrome. In this paper we discuss chest wall diseases falling into the first category; namely, kyphoscoliosis, fibrothorax, thoracoplasty, ankylosing spondylitis and obesity-hypoventilation. Congenital deformities of the thoracic cage, which do not have important effects on ventilatory apparatus (e.g. pectus excavatum and pectus carinatum), were also considered.
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PMID:Classification of chest wall diseases. 847 68

A 32-year-old, hypertensive, morbidly obese (BMI 49 kg/m2) woman was referred to us suspected of sleep-disordered breathing. Polycythaemia, right heart and respiratory failure, restrictive ventilatory impairment, decreased hypercapnic respiratory drive, high number of very short apneas mostly of central origin (698 vs 530 obstructive), and overnight hypoxaemia were found. The diagnosis of obesity-hypoventilation syndrome was established and the treatment with almitrine, aminophylline and low-calorie diet was started. After 6 months body weight decreased significantly (BMI 38 kg/m2). RBC, spirometry, blood gas analysis, overnight oximetry, hypercapnic respiratory drive and polysomnography showed results within normal limits. Causes, pathophysiology and possible treatment of obesity-hypoventilation syndrome are discussed.
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PMID:[Obesity and hypoventilation syndrome; effects of weight loss and treatment with respiratory stimulants]. 899 66

A 72-year-old man was admitted to our hospital because of a tumor-like shadow on a chest X-ray film. At the initial examination, he had clinical signs of Cushing's syndrome: moon face, central obesity, and hypertension. A computed tomographic scan of chest showed an abnormal shadow in the lung (5 x 6 cm) with involvement of the right paratracheal and anterior tracheal lymph nodes, and a right-sided pleural effusion. Small cell lung cancer (extended disease; T2N2M6 stage IV) was diagnosed after a transbronchial biopsy. The concentrations of adrenocorticotropic hormone, cortisol, and parathyroid hormone in plasma were markedly elevated, and there was no circadian rhythm (336 pg/ml. more than 60.1 micrograms ml. and 805 pg/ml, respectively). Fluid obtained by thoracentasis had malignant cells, and the levels of adrenocorticotropic hormone and parathyroid hormone in the effusion (1120 pg/ml and 1810 pg/ml, respectively) were higher than those in serum, which indicates that these hormones were produced by the tumor cells. The patient received chemotherapy and responded well, but he died of respiratory failure 26 months later. The response rate to chemotherapy in elderly patients with lung cancer is said to be comparable to that in younger patients, but treatment may be difficult because of poor performance status and diminished physical capacity. Although patients with lung cancer complicated by Cushing's syndrome have a poor prognosis, this patient survived for more than 2 years after the disease was diagnosed.
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PMID:[Cushing's syndrome due to small cell lung cancer with ectopic production of adrenocorticotropic and parathyroid hormone]. 915 97

Sleep is characterized by many changes in the respiratory system, including a reduction in respiratory motor output associated with the loss of wakefulness, increased upper airway resistance, and blunted protective reflexes (such as load compensation), that result in reduced alveolar ventilation. The development of carbon dioxide retention appears to be linked to the exaggeration of sleep-related changes on ventilation by coexistent respiratory system disorders. Sleep-disordered breathing is becoming increasingly recognized in subjects with neuromuscular diseases, who may be prone to nocturnal respiratory events due to diaphragm and bulbar muscle weakness, abnormal central respiratory control, obesity, and sleep position restrictions. Nocturnal gas exchange deterioration may occur in patients with chronic obstructive pulmonary disease, particularly during rapid eye movement sleep when activity of the respiratory muscles other than the diaphragm is inhibited. Concurrent obstructive sleep apnea syndrome may further compromise nocturnal ventilation, thereby contributing to the development of acute or chronic respiratory failure. The use of noninvasive nocturnal ventilation at night has resulted in significant improvements in symptoms of hypoventilation and daytime carbon dioxide retention in various clinical settings, yet important questions remain about implementation of this modality.
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PMID:Sleep-wake cycles and the management of respiratory failure. 936 92


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