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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 182 episodes with ARF (PaCO2 > 50 torr) in 400 episodes of COPD patients who were admitted to Chulalongkorn Hospital during the period 1982 to 1986, despite conservative treatment, 66 developed severe acute respiratory failure requiring assisted ventilation. Patients with a history of chronic cough, pneumonia as a precipitating factor and more severe ARF on admission, as indicated by palpitation, headache, cyanosis, alteration of consciousness, cor-pulmonale and decompensated acidosis (pH < 7.30), were likely to require mechanical ventilation. Indications for mechanical ventilation were carbon dioxide narcosis (43 episodes), severe hypoxemia despite on a high FIO2 (one episode), various combination parameters of respiratory muscle fatigue, cardiovascular instability (22 episodes). The major complications of mechanical ventilation were pneumonia, sepsis, pneumothorax, UGI bleeding of 16, 8, 5 and 9 episodes, respectively. The average duration of assisted ventilation and hospitalization were 15.8 and 19.02 days, respectively. The mortality rate was 50 per cent in the mechanical ventilation group compared with 9.8 per cent in the non-mechanical ventilation group. Increased mortality rate was found in those with pneumonia as the precipitating factor (68.4 vs 14.3%, respectively, in comparing the two groups). Complications of mechanical ventilation, which included pneumonia, sepsis, fluid overload, hyponatremia and persistent acidosis, were high-risk factors for the non-surviving group.
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PMID:Mechanical and non-mechanical ventilation of respiratory failure in chronic obstructive pulmonary disease. 822 88

A 20-year-old man underwent total cavopulmonary shunt for univentricular heart type A (A.L.L.) with hemiazygos connection six years ago. Four years later, his condition deteriorated with easy fatigue and cyanosis. Cardiac catheterization showed recanalization of ligated SVC. Chest CT showed tight adhesion between the chest wall and the ascending aorta. We approached the heart through left anterolateral thoracotomy in order to avoid injury of the aorta and the ventricle during redo median sternotomy. Total cavopulmonary connection with intraatrial conduit was performed under circulatory arrest and retrograde cardioplegia without aortic cross clamp. His postoperative course was satisfactory. Left thoracotomy was useful for total cavopulmonary connection following total cavopulmonary shunt associated with postoperative adhesion.
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PMID:[A case report of total cavopulmonary connection following total cavopulmonary shunt]. 899 47

A 43-y-old Caucasian female applied 4 ounces of dimethyl sulfoxide (DMSO) to her lower abdomen for treatment of interstitial cystitis. Within 24 h she developed fatigue, cyanosis and dyspnea with mild exertion. She sought medical attention 10 d later, at which time initial laboratory tests revealed a methemoglobin level of 47%. Two doses of 1 mg methylene blue/kg i.v. were given without significant improvement in either her cyanosis or methemoglobin level. Repeat analysis the day following admission using an outside lab demonstrated a sulfhemoglobin level of 6.2% and a methemoglobin level of < 0.1%. No prior reports have associated sulfhemoglobin formation with DMSO application. Carbon monoxide-oximetry may falsely identify sulfhemoglobin as methemoglobin; sulfhemoglobinemia should be considered in cases of methemoglobinemia refractory to methylene blue therapy.
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PMID:Sulfhemoglobinemia after dermal application of DMSO. 955 60

Ebstein's anomaly is a malformation of the tricuspid valve characterized from the clinical view point by dysnea, evolutive cyanosis and fatigue. Is it characterized anatomically by a downward displacement of the tricuspid valve into the right ventricle due to anomalous attachment of the tricuspid leaflets. Because of the abnormally situated tricuspid orifice, a portion of the right ventricle lies between the atrioventricular ring and the origin of the valve, that is, an "atrialized" segment of the ventricle, and they have a functionally small ventricular chamber. Roentgenographic studies, usually demonstrate a characteristic enlarged heart. The globular-shaped heart on a chest X-ray may closely resemble the picture usually associated with a large pericardial effusion. The ecocardiographic study is more specific for the differential diagnosis, and usually eliminates one pathology but confirms the other. The patient that we are presenting is unusual, and, as far as we know, it is the only in the literature case in which there is a coexistence of the important pericardial effusion and the Ebstein's anomaly. We review the functional abnormalities of the right ventricle with Doppler and two-dimensional echocardiography in this patient.
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PMID:[Ebstein's anomaly related with significant pericardial effusion. Report and analysis of a case]. 978 92

We describe herein a successful biventricular repair in a 21-year-old male who had severe hypoplasia of isomeric right appendages. He had previously undergone the conventional Glenn procedure at the age of one and a half years. Although he had grown uneventfully until adolescence, cyanosis as well as fatigue than gradually became worse. When referred to us for further treatment, we deemed a Fontan type procedure to be contraindicated, because of the hypoplastic nature of the right pulmonary artery, and the presence of abundant collateral arteries supplying the right lung. In terms of ventricular morphology, however, because both apical components were present, separated by the hypoplastic septum, biventricular repair seemed feasible. Initially, the Glenn anastomosis was taken down, and systemic-to-pulmonary shunts were constructed via a median sternotomy to both the right and left pulmonary arteries. This was followed by surgical division of the developed collaterals to the right lung via the right thoracotomy. Definitive biventricular repair was then carried out by reconstructing the pulmonary arteries and right ventricular outflow tact, separating and rerouting within the ventricles using a EPTFE patch, and achieving redirection of blood within the atriums using bovine pericardium. Such staged surgical approaches, although extensive, can provide useful options when seeking definitive repair in grown-up patients with complicated malformations.
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PMID:[A successful biventricular repair in an adult case with "common ventricle" and isomeric atrial appendages previously undergoing the conventional Glenn procedure]. 988 73

Congenitally corrected transposition of the great arteries is a rare cardiac anomaly with a poor prognosis. In this report, the authors describe an 81-year-old man admitted to the hospital with generalized fatigue, chest pain, and cyanosis. Computed tomography and cardiac catheterization revealed corrected transposition of the great arteries. Transesophageal echocardiography disclosed moderate right atrioventricular regurgitation and a right-to-left shunt across a patent foramen ovale during systole. Because this patient had no other congenital cardiac anomalies, the right-to-left shunt through the patent foramen ovale was thought to be the major cause of cyanosis.
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PMID:Congenitally corrected transposition of the great arteries with a patent foramen ovale in an 81-year-old man--a case report. 992 92

The suggested role of oxidative stress in the pathogenesis of heart failure is largely based on utilizing left heart failure models. The present study on rats evaluated changes in antioxidants as well as oxidative stress in relation to hemodynamic function subsequent to the right heart failure induced by monocrotaline (50 mg/kg, i.p.). During the post-injection period, monocrotaline (MCT)-treated rats demonstrated a persistent growth depression. Two to three weeks after the injection, MCT-treated rats showed signs of fatigue, peripheral cyanosis and dyspnea. In these rats, right heart hypertrophy was confirmed by a significant increase in right ventricular weight as well as right ventricle to body weight ratio. In MCT-treated rats, there was also a significant increase in right ventricular systolic as well as end diastolic pressures. No change in lung and liver wet/dry weight ratios between MCT-treated and control animals was observed. Based on the hemodynamic data as well as other clinical observations, the functional stage achieved was compensated heart failure. Myocardial antioxidant enzymes, catalase, glutathione peroxidase and superoxide dismutase, in the MCT-treated rats were not different compared to control rats. Vitamin E levels were significantly depressed in the RV and there was no change in retinol levels. There was a significant increase in lipid hydroperoxide concentrations in MCT-treated rats as compared to the control group. These data provide evidence that right heart failure is associated with an increase in oxidative stress.
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PMID:Myocardial oxidative stress changes during compensated right heart failure in rats. 1044 2

This is a case report of a double-outlet left ventricle associated with tricuspid atresia and hypoplasia of the right ventricle, diagnosed during echocardiography with color-flow imaging, in a three-month-old child who presented with fatigue and cyanosis. The child underwent palliative pulmonary arterial banding without an invasive procedure, and showed sustained improvement during follow-up.
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PMID:Double-outlet left ventricle. Echocardiographic diagnosis. 1144 96

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

An 11-year-old male with total anomalous systemic venous return had surgical repair except for the hepatic venous return, which drained to the left atrium. He developed progressive cyanosis and fatigue and was diagnosed with large pulmonary arteriovenous malformations (PAVMs) during cardiac catheterization with the use of bubble contrast echocardiography. After surgical redirection of hepatic venous flow to the right heart and pulmonary arterial system, resolution of these PAVMs was demonstrated clinically and by contrast echocardiography. This unique case report demonstrates the development of PAVMs with exclusion of hepatic venous return through the pulmonary vascular bed while pulsatile pulmonary blood flow remains intact. It reinforces the likelihood of the absence of an as yet unidentified hepatic vasoactive substance as the source for development of PAVMs.
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PMID:Resolution of acquired pulmonary arteriovenous malformations in a patient with total anomalous systemic venous return. 1188 37


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