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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

A 24-year-old woman was followed for about ten months with oral administration of prednisolone (22.5-35 mg/d) for autoimmune hepatitis. In June 1995, she noticed fatigue and appetite loss and blood chemistry revealed markedly deteriorated liver function. She was admitted to our hospital. The daily dose of prednisolone was increased to 60 mg. Her elevated levels of transaminases decreased gradually. Administration of azathioprine (100 mg/d) was started with tapering of prednisolone on August 18th. Ten days later, tender cervical lymphadenopathy and high fever occurred. Azathioprine administration was stopped immediately and intravenous antibiotics were given. On September 5th, 50 mg of azathioprine was administered again. Two hours later, the patient complained of intolerable pain from the lumbar region to the knee joints, which subsided following two injections of analgesics within a few hours. However, chills, high fever and hypotension (86/30 mmHg) subsequently developed. No bacterial growth was detected in blood culture. She was discharged on September 12th. On October 4th, she visited our out-patient clinic. The next day, she took one tablet (50 mg) of azathioprine at 10 o'clock. She noted intense pain from the thighs to the knees and calves around noon again. Her home doctor found that she exhibited shock (BP 67/?). She was immediately taken to our department. The same symptoms and signs as the above-mentioned occurred. Azathioprine was considered responsible for these two adverse reactions (shock) as an allergen. Later, systemic lupus eythematosus was diagnosed in 1996. And she died to pulmonary hypertension in May 1999. Physicians should be aware of the potential adverse effect of azathioprine administered in order to manage the patients with autoimmune disorders.
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PMID:[Autoimmune hepatitis complicated by intolerable pain of lower extremities and shock due to azathioprine]. 1086 28

An obese 23-year-old man with sleep-disordered breathing and primary pulmonary hypertension (PPH) had been administered oral beraprost sodium, anticoagulant warfarin, and home oxygen therapy, at another hospital as treatment for the PPH, but he had not experienced any symptomatic improvement. The patient had a body mass index of 32.4kg/m2, and complained of fatigue, shortness of breath on exertion, excessive daytime sleepiness, and snoring. Arterial blood gas analysis showed a PaO2 and a PaCO2 of 70.9 and 31.2mmHg, respectively. A polysomnographic study revealed central sleep apnea with an apnea-hypopnea index (AHI) of 29.7episodes/h. The patient showed improvement of daytime sleepiness after starting nocturnal nasal bilevel positive airway pressure (BiPAP) therapy for the central sleep apnea, but his pulmonary hypertension, measured in the daytime, worsened. The patient died suddenly while walking to the bathroom in the morning 1 month after initiation of BiPAP therapy. It is necessary to consider the possibility of sudden death when nasal BiPAP therapy is given to a PPH patient with central sleep apnea.
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PMID:Primary pulmonary hypertension with central sleep apnea: sudden death after bilevel positive airway pressure therapy. 1098 61

The patients with chronic thromboembolic pulmonary hypertension (CTEPH) usually shows impaired physical activity and poor prognosis, proportional to the degree of pulmonary hypertension. Effort dyspnea and fatigue, the major symptoms, are quite nonspecific, and the physical findings of pulmonary hypertension are easily overlooked until they are far advanced. The most important clue to the diagnosis is perfusion and ventilation lung scan which demonstrates more segmental sized or larger perfusion defects that are normally ventilated. The presence of precapillary pulmonary hypertension should be confirmed by right heart catheterization. Pulmonary angiography is essential not only for diagnosing CTEPH but also for defining thrombus extent and location. The current criteria for considering for surgery include: 1) significant exertional limitation defined as Hugh-Jones > or = III, or NYHA > or = III, 2) pulmonary hypertension defined as PAm > or = 30 mmHg, 3) thrombi located at least as proximally as the lobar level, 4) the absence of significant co-morbid disease, 5) a willingness of the patient and his family to accept the risks of surgery. Although the hemodynamic and symptomatic improvement associated with pulmonary thromboendarterectomy is apparent, the operative mortality is still high, especially in patients with severe hemodynamic disease. The accurate diagnosis and selection criteria for surgery are crucial.
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PMID:[Chronic thromboembolic pulmonary hypertension (CTEPH)]. 1141 Nov 31

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Congenital heart disease can increase or decrease pulmonary blood flow, pulmonary vascular resistance (PVR) or pulmonary artery pressure (PAP). PAP is the product of PVR and pulmonary minute volume (Qp), such that pulmonary hypertension (PHT) may develop as a result of an increase in either PVR or Qp or both. Given that the pulmonary vascular bed is a low pressure system with high flow, any increase in resistance would generate PHT. The normal value of PVR is 2 Woods units (mm Hg/l/min). Increased PAP is due to hypoxic lesions of the endothelium, which release proteolytic enzymes that alter the balance of metabolites of arachidonic acid, regulators of pulmonary vasomotor tone. Hypoxia and acidosis cause intense pulmonary vasoconstriction (hypoxic vasoconstrictor reflex). An increase of PVR is due to a combination of vasoconstrictive processes and remodeling, with hypertrophy of the pulmonary artery. Structural lesions are related to hypertrophy of the endothelium, the transformation of fibroblasts to myocytes and the decrease of the alveolar/arteriolar ratio with the formation of new vessels.PHT may be primary or secondary to another disease. Primary PHT is a rare genetic disease. The most common secondary forms of PHT in pediatrics are due to persistence of neonatal anatomy (neonatal PHT), to heart diseases with left-right shunt (CIV, DAP, etc.), to diseases of the pulmonary parenchyma (interstitial viral infection, mucoviscidosis), and complications of heart surgery. All congenital heart diseases can lead to PHT if not treated promptly. Clinical signs of PHT are highly non-specific: dyspnea, fatigue, syncopes, exercise intolerance, precordialgia, cyanosis and edema. The best approaches to diagnosis and prognosis are echocardiography and cardiac catheterization with vasodilators. Anesthetics that do not alter PVR should be used in such patients, who are sensitive to changes in pulmonary ventilation, to changes in cardiac output and to anesthetics. The treatment of PHT during intra and postoperative pediatric surgery is based on the use of high inspirated oxygen concentration (100%), an adequate sedation and the use of vasodilators (prostaglandin I2, nitric oxide, sodium nitroprusiate and milrinone).
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PMID:[Pulmonary hypertension in pediatric heart surgery]. 1179 1

Sleep-related breathing disorders (SRBDs) represent a spectrum of abnormalities that range from simple snoring to upper airway resistance syndrome to sleep apnea. The clinical presentation may include obesity, snoring, neuropsychological dysfunction, and daytime hypersomnolence and tiredness. The acute hemodynamic alterations of obstructive sleep apnea include systemic and pulmonary hypertension, increased right and left ventricular afterload, and increased cardiac output. Earlier reports attributed the coexistence of SRBDs with cardiovascular diseases to the shared risk factors such as age, sex, and obesity. However, recent epidemiologic data confirm an independent association between SRBDs and the different manifestations of cardiovascular diseases. Possible mechanisms may include a combination of intermittent hypoxia and hypercapnia, repeated arousals, sustained increase in sympathetic tone, reduced baroreflex sensitivity, increased platelet aggregation, and elevated plasma fibrinogen and homocysteine levels. The strength of the association, its pathogenesis, and the impact of treatment of SRBDs on the health outcome of patients with cardiovascular diseases are issues to be addressed in future studies.
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PMID:Cardiovascular consequences of sleep-related breathing disorders. 1235 Feb 42

A 59-year-old man had undergone aortic and mitral valve replacement (DVR) for rheumatic aortic and mitral valve stenosis 15 years ago. At that time, echocardiography did not detect tricuspid regurgitation (TR), and catheterization data showed right atrial pressure v wave of 8 mmHg and pulmonary artery pressure of 27/12 (17) mmHg. One year after DVR, hepatomegaly and jugular venous dilatation appeared, and after 5 years edema of both legs became apparent. After 7 years, chest X-ray showed an increase of cardio-thoracic ratio, and for the first time, echocardiography detected mild TR. Fifteen years after DVR, severe general fatigue, shortness of breath and hepatomegaly could not be controlled with medication. Catheterization data showed right atrial pressure v wave of 23 mmHg and pulmonary artery pressure of 28/13 (17) mmHg. Right ventriculography showed progression of severe TR. Tricuspid valve replacement (TVR) was performed using a St. Jude Medical 31 M mechanical valve under natural cooling and heart beating. The tricuspid valve was only slightly thickened and no subvalvular abnormalities were seen other than a severely dilated tricuspid annulus. Postoperative course was uneventful and he was discharged 44 days after the TVR. He is currently doing well 6 years after the TVR. All terms, he did not have pulmonary hypertension or left-side heart problems. We suspect that the cause of TR was not secondary, and was included in the category of isolated TR. If the left heart is completely treated, as in this case, it is important to follow-up for signs of right heart failure, before TR is detected.
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PMID:[Severe tricuspid regurgitation late after aortic and mitral double valve replacement; report of a case]. 1247 68

The problem of kyphoscoliosis in combination with pregnancy is uncommon and published cases are rare. Until now, little and controversial information on the outcome, optimal management and course of pregnancy in patients with kyphoscoliosis has been available. The majority of maternal deaths seem to be attributed to cardiorespiratory failure, while obstetric complications account for relatively few complications. We present the case of a 34-year old pregnant woman with congenital kyphoscoliosis and a forced vital capacity (FVC) of about one liter. A further deterioration of lung function was expected. In fact, severe limitations in exercise capacity (bed rest), fatigue and hypersomnolence, as well as a severe increase in pulmonary hypertension occurred during the second and third trimester. Nasal intermittent positive pressure ventilation (NIP-PV) with bilevel positive airway pressure (BiPAP) was started in the 20th week of gestation and adapted throughout pregnancy. Nasal BiPAP was well-tolerated and corrected exercise tolerance, fatigue and nocturnal oxygen desaturations. At 32 weeks of gestation, the patient was admitted for an elective Caesarean section under combined spinal-epidural anaesthesia with ongoing NIPPV, and delivered a healthy baby. Home nocturnal ventilatory support was continued as nocturnal episodic desaturations were also assessed during the postpartum period. At time of discharge, the patient's exercise capacity and lung function were nearly equal to levels before pregnancy. We conclude that pregnancy in selected kyphoscoliotic patients with severe limitations in lung function is relatively safe for both the mother and the child when NIPPV is used for overcoming respiratory deterioration and for preventing further cardiorespiratory failure.
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PMID:Management of respiratory deterioration in a pregnant patient with severe kyphoscoliosis by non-invasive positive pressure ventilation. 1250 80

Liver disease affects the lungs. The majority of patients exhibit mild to moderate arterial hypoxaemia essentially attributable to an alteration in ventilation/perfusion matching and limited by an increase in ventilation. A minority (some 10%) of patients exhibit a "hepatopulmonary syndrome" defined by severe hypoxaemia with arterial PO2 below 60 mm Hg, dyspnoea, cyanosis, digital clubbing, orthodeoxia, platypnoea and demonstrable pulmonary vascular dilatations causing a true pulmonary shunt and a diffusion/perfusion imbalance. The hepatopulmonary syndrome is incurable but resolves over time after liver transplantation. An even lower proportion of patients, approximately 1%, develop pulmonary hypertension. Clinically this "portopulmonary hypertension" resembles primary pulmonary hypertension, with dyspnoea and fatigue as the main symptoms, histopathology and response to prostacyclin therapy. Portopulmonary hypertension is irreversible. Liver transplantation mortality in patients with portopulmonary hypertension ranges from 50 to 100%. The common cause of the hepatopulmonary syndrome and portopulmonary hypertension is portal hypertension and portosystemic shunting, indicating that vasoactive and angiogenetic factors originating from the liver normally control the pulmonary circulation.
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PMID:Hepatopulmonary syndrome and portopulmonary hypertension. 1271 85


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