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

The objective of this article is to review the available data on the relationship between sleep-disordered breathing (SDB) and pulmonary arterial hypertension (PAH), with a focus on the prevalence of SDB in patients with idiopathic PAH (IPAH); the prevalence of PAH in patients with SDB; and the effects of SDB treatment on PAH. The evidence to date suggests that PAH may occur in the setting of SDB, although the prevalence is low. However, pulmonary hypertension (PH) in SDB is most strongly associated with other risk factors, such as left-sided heart disease, parenchymal lung disease, nocturnal desaturation, and obesity. The limited data available also suggest that SDB is uncommon in patients with IPAH. Treatment of SDB with continuous positive airway pressure may lower pulmonary artery pressures when the degree of PH is mild.
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PMID:Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines. 1524 96

Chronic alveolar hypoventilation is a classic feature of the "pickwickian syndrome" (i.e. obesity-hypoventilation syndrome) but in fact hypercapnia is observed in a minority of obstructive sleep apnoea syndrome (OSAS) patients. Most recent studies having included large numbers of unselected, consecutive OSAS patients agree on a prevalence of 10-20% of alveolar hypoventilation. The mechanisms of hypercapnia in OSAS are not fully understood but the determining factors of daytime respiratory insufficiency are probably the presence of a marked obesity, leading to the obesity hypoventilation syndrome and, principally, the association of OSAS with chronic obstructive pulmonary disease. This association (the so-called "overlap syndrome") is observed in >10% of OSAS patients. Bronchial obstruction is generally mild to moderate and may be asymptomatic. The severity of the nocturnal events (apnoeas, hypopnoeas) and a (possible) diminished chemosensitivity to hypercapnic and hypoxic stimuli do not appear to be determining factors of hypercapnia. The most important consequence of chronic alveolar hypoventilation is pulmonary hypertension which is only observed in patients with daytime arterial blood gases disturbances, and which can lead to right heart failure. When nasal continuous positive airway pressure fails to correct sleep-related hypoxaemia, supplementary O, must be given or another way of assisted ventilation (BIPAP) must be considered. In the most severe patients (diurnal PaO(2) <55 mmHg) conventional O(2) therapy (>or=16h/24h) is required in addition to nocturnal ventilation.
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PMID:Daytime hypoventilation in obstructive sleep apnoea syndrome. 1531 Apr 91

Sleep has effects on breathing, including changes in respiratory control, airways resistance and muscular contractility. These sleep-related modifications in the respiratory system do not induce adverse effects in healthy subjects, but may cause problems in patients with chronic obstructive pulmonary disease (COPD). Hypo-ventilation causes the most important gas-exchange alteration during sleep in COPD patients, leading to hypercapnia and hypoxemia, especially during rapid-eye-movement (REM) sleep. Blood gases alterations lead to increased arousals, sleep disruption, pulmonary hypertension and higher mortality. The presence of other sleep-related breathing disorders, like sleep apnea syndrome, may induce a more pronounced impairment of gas exchange, both during sleep and wakefulness, and development of symptoms like excessive daytime somnolence. Nocturnal oximetry is recommended to evaluate gas exchange during sleep in COPD patients. Sleep studies are usually indicated when there is a possibility of sleep apnea or obesity-hypoventilation syndrome. The role of non-invasive mechanical ventilation in managing COPD patients with nocturnal hypoventilation is discussed.
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PMID:Sleep disordered breathing in patients with chronic obstructive pulmonary disease. 1533 44

In this article we summarize the available information regarding the epidemiology, the pathophysiology as well as the risk factors and complications of the sleep apnea syndrome (SAS). Central, obstructive and mixed forms of SAS are known, however, the obstructive form is (resulting from the actual high prevalence of obesity) definitely the most frequent. Latest years of experimental and clinical research have pointed towards the clinical importance of this sleep related breathing disorder. High prevalence in the population and especially the cardiovascular complications (e. g. systemic and pulmonary hypertension, atherosclerosis, arrhythmias) have contributed to the recent increase in knowledge about SAS. Nevertheless, there are numerous unsolved problems and unanswered questions in the pathophysiology of SAS. Future studies should, thus, provide us with more information and shed light on regarding the hidden mysteries of SAS.
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PMID:Sleep apnea syndrome and its complications. 1535 82

The aim of this review was to analyse the effects of intermittent hypoxia (IH) on pulmonary haemodynamics, comparing results of animal experiments with results of clinical studies. In animal investigations even short hypoxic exposure, continuously or in short repeated episodes mimicking obstructive sleep apnoea (OSA), leads to pulmonary artery remodelling and to pulmonary hypertension (PH). Results of investigations on effects of nocturnal IH on pulmonary haemodynamics in patients with chronic obstructive pulmonary disease (COPD) are discordant. Earlier studies reported the development of mild PH in subjects desaturating during sleep, while more recent investigations did not confirm those findings. Alveolar IH developing during apnoeic episodes during sleep in OSA patients is a disease-induced model to study its effects on pulmonary haemodynamics. In the majority of studies in OSA patients pulmonary arterial pressure remained within normal values. PH was found in patients with OSA accompanied by COPD and/or extreme obesity. People commuting between lowland and high altitude due to their employment, are also repeatedly exposed to IH. Results of clinical investigations suggest that it did not lead to the development of permanent PH. The mechanisms of discrepancies between effects of intermittent hypoxia in animal models and in humans remain to be studied.
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PMID:Effects of intermittent hypoxia on pulmonary haemodynamics: animal models versus studies in humans. 1564 Mar 39

The pathophysiology of upper-airway obstruction (UAO) is complex. Possible causes of UAO that may lead to acute respiratory failure, are as follows: infections like acute epiglottitis and croup, obstructing tumors in the base of the tongue, larynx or hypopharynx, aspirated food or liquid contents, obesity and anatomical variations. Management changes according to the pathogenesis of the disorder. In patients with severe carbon dioxide retention or apnea, emergency endotracheal intubation must be carried out. Hereby, we describe a 23-year-old patient with susceptible upper-airway anatomy and UAO occurred following an upper respiratory infection and complicated with pulmonary hypertension and pulmonary edema. Our patient seems to be one of the complicated UAO cases, with an unusual but critical clinical presentation, evaluated in a wide spectrum and nicely returned to life.
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PMID:Pulmonary hypertension and acute pulmonary edema in a 23-year-old male with a history of an upper respiratory tract infection. 1576 90

The role of sleep-disordered breathing (SDB) in the development of persistent daytime pulmonary hypertension (PH) and cor pulmonale is controversial and has not been extensively studied. In this review we discuss the physiological changes that occur during SDB in the cardiovascular system, as well as review the most recent literature examining the relationship between SDB and PH/cor pulmonale. The literature suggests that much of the PH and right heart dysfunction seen in SDB is related to concurrent obesity and underlying lung disease, although it does appear that isolated SDB (in the form of obstructive sleep apnea) may be responsible for a small but significant degree of PH. The clinical consequences of this, however, remain unclear.
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PMID:Cardiovascular abnormalities in sleep-disordered breathing. 1608 52

Patients undergoing major lower-extremity orthopedic surgery such as total hip replacement (THR) and total knee replacement (TKR) are at an increased risk of venous thromboembolism (VTE). Routine prophylaxis is necessary to reduce the risk of deep vein thrombosis (DVT), which may progress to potentially fatal pulmonary embolism and secondary complications such as postthrombotic syndrome, recurrent DVT, and chronic pulmonary hypertension. Prophylaxis in patients undergoing TKR, THR, and hip fracture surgery is now standard practice and generally involves anticoagulant treatment with either low-molecular-weight heparin (LMWH) or warfarin for a period of 7 to 10 days, with extended prophylaxis in those with ongoing risk factors such as obesity, cancer, or previous VTE. Data from clinical practice suggest that there is a general trend toward longer postsurgical prophylaxis and shorter hospital stays, making practicality of treatment an important consideration. LMWH is effective for the prophylaxis of VTE, but the parenteral route of administration is not convenient for use in the outpatient setting. Warfarin, on the other hand, can be administered orally but requires the infrastructure for careful patient monitoring and dose adjustments because of its unpredictable dose-response relationship. The development of new anticoagulants has been pursued with the aim of improving efficacy, predictability, consistency of response, safety, and convenience. A recently approved anticoagulant, fondaparinux, has been proven to provide superior efficacy for the prevention of VTE compared with LMWH, but this agent requires parenteral administration and does not overcome the convenience issue. Ximelagatran is the oral form of the direct thrombin inhibitor melagatran, which is available for subcutaneous administration. Ximelagatran has a consistent anticoagulant response allowing fixed oral dosing without the need for coagulation monitoring. The efficacy and safety profile of melagatran/ximelagatran prophylaxis for VTE following THR and TKR has compared favorably with standard LMWH prophylaxis, as seen in the European METHRO II and III trials and EXPRESS trial, and with warfarin prophylaxis, as seen in the North American EXULT A and B trials. Several prophylactic treatment regimens have been evaluated in the European trials to determine the optimal dosing and timing of first dose of melagatran to achieve the best balance of efficacy and safety. Preoperative initiation of melagatran was more effective than when prophylactic treatment was initiated postoperatively, and the lowest rates of bleeding were associated with a postoperative initiation of prophylaxis. Early administration of the first postoperative melagatran dose (4 to 8 hours) was also associated with better prophylactic efficacy relative to a later postoperative start (8 to 12 hours). The results of the comprehensive international clinical trial program and in particular the optimal balance of efficacy/safety data provided by the METHRO III study have led to approval of melagatran/ximelagatran in 2004 in the European Union for the prevention of VTE in patients undergoing elective hip or knee replacement surgery. Ximelagatran has the potential to maximize the use of anticoagulation in patients discharged following major lower-extremity orthopedic surgery.
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PMID:Ximelagatran for the prevention of venous thromboembolism following elective hip or knee replacement surgery. 1612 14

The obesity hypoventilation syndrome, which is defined as a combination of obesity and chronic hypoventilation, utimately results in pulmonary hypertension, cor pulmonale, and probable early mortality. Since the classical description of this syndrome nearly fifty years ago, research has led to a better understanding of the pathophysiologic mechanisms involved in this disease process, and to the development of effective treatment options. However, recent data indicate the obesity hypoventilation syndrome is under-recognized, and under-treated. Because obesity has become a national epidemic, it is critical that physicians are able to recognize and treat obesity-associated diseases. This article reviews current definitions of the obesity hypoventilation syndrome, clinical presentation and diagnosis, present understanding of the pathophysiology, and treatment options.
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PMID:The obesity hypoventilation syndrome. 1720 68

The management of the patient with pulmonary hypertension is a challenge for the anesthesiologists because the risk of right-sided heart failure is markedly increased. We experienced a case of general anesthesia for a patient with pulmonary hypertension (mean pulmonary arterial pressure 39 mmHg), bronchial asthma and obesity. A 31-year-old woman was scheduled for arytenoid rotation for left recurrent nerve palsy. We applied routine monitors (noninvasive blood-pressure, five-lead electrocardiogram, pulse oximeter), and direct blood pressure monitoring through the radial artery. Anesthesia was induced with midazolam 4 mg, fentanyl 100 microg and sevoflurane 5%, and maintained with sevoflurane (1-2%) and nitrous oxide in oxygen. Surgery was completed in 100 minutes without any complications. We could successfully perform general anesthesia in a patient complicated by pulmonary hypertension, bronchial asthma and obesity, without invasive right-sided heart catheterization.
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PMID:[General anesthesia for a patient with pulmonary hypertension, bronchial asthma and obesity]. 1623 70


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