Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A quasi steady-state noninvasive, radioisotopic technique for measuring regional lung water distribution in man is described. The method depends upon the dilution principle. 123I labelled human serum albumin (HSA) and sodium iodide (NaI) were injected intravenously, allowed to mix completely within the body fluids and then counted externally over the chest. The size of each compartment to which the markers are confined was calculated from the external count rate and the isotopic concentration of the marker in plasma. 123I-HSA was used to estimate intravascular water and 123I-NaI extracellular water. Ratio analysis of the differential attenuation of the two photoenergies of 123Iodine (29 keV, 159 keV) by the lung and chest wall was used to estimate the absolute amount of isotope in the lung, independent of chest wall contribution, after validation by phantom studies. Regional pulmonary plasma (PPVr) and interstitial (PIVr) fluid volumes in normal subjects were 7.1 +/- 1.4 and 7.6 +/- 1.3 ml.100 cm-3 lung (mean +/- SD; n = 13) at mid-tidal volume, respectively. In patients with the adult respiratory distress syndrome, PPVr and PIVr were 7.0 +/- 2.9 and 15.9 +/- 4.6 ml.100 cm-3 lung (n = 18), respectively. The pulmonary artery wedge (Paw) pressure was normal (12.5 +/- 2.5 mmHg; n = 5). In patients with pulmonary oedema due to left heart disease, PPVr and PIVr were 7.2 +/- 2.7 and 12.1 +/- 3.7 ml.100 cm-3 lung (n = 8), respectively. The mean Paw pressure in this group was high (28.5 +/- 3.9 mmHg).
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PMID:Noninvasive measurement of regional lung water distribution in healthy man and in pulmonary oedema. 369 23

Extravascular lung water (EVLW) was measured in 16 patients with congenital heart disease by the cold green dye, double indicator dilution technique. Five patients with optimally corrected tetralogy of Fallot served as controls, and EVLW in this group was 4.7 +/- 0.5 ml/kg (111 +/- 13 ml/m2) (mean +/- standard deviation). In 5 asymptomatic patients with atrial septal defect (ASD), normal pulmonary artery (PA) pressure and increased pulmonary blood flow, EVLW was 5.7 +/- 2.8 ml/kg (132 +/- 63 ml/m2), which was not significantly different from the value of control patients. However, in 6 patients with ventricular septal defect, PA hypertension, normal left atrial pressure and an equivalent left-to-right shunt to ASD patients, EVLW was 15.9 +/- 3.8 ml/kg (270 +/- 60 ml/m2). This was significantly different from values in both control and ASD patients (p less than 0.01). It is concluded that in the face of normal pulmonary vascular resistance, PA pressure is transmitted to the microvasculature, causing hydrostatic pulmonary edema. Other factors that may be implicated in the pathogenesis of pulmonary edema, such as increased pulmonary blood flow and relative lymphatic insufficiency in infants, cannot be excluded.
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PMID:Extravascular lung water in children immediately after operative closure of either isolated atrial septal defect or ventricular septal defect. 403 40

The effect of ergotamine and ergometrine on the venous compliance of the forearm has been studied in normal persons. Ergotamine tartrate (0.25 mg. intravenously) led to a fall in venous compliance amounting to 49% on average, while ergometrine maleate (0.25 mg. intravenously) caused a reduction of 41%; these changes were statistically significant. The potent veno-constrictor action of these ergot alkaloids appears to be a major component of the circulatory response to small doses and may be important in provoking the harmfull cardiovascular side-effects (such as angina and pulmonary oedema) that are sometimes observed in patients with pre-existing heart disease.
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PMID:Effect of ergotamine and ergometrine on forearm venous compliance in man. 541 50

Six patients received heart-lung transplants between March, 1981, and January, 1982. There were four women and two men between 26 and 45 years of age, three with primary pulmonary hypertension and three with congenital heart disease and pulmonary hypertension (Eisenmenger's syndrome). Immunosuppression was primarily with cyclosporin-A, with additional corticosteroid, azathioprine, and rabbit antihuman thymocyte globulin. Six episodes of allograft rejection in four patients (10, 11, 21, 24, 53, and 86 days after transplantation) were detected by means of transvenous endomyocardial biopsy. All patients experienced pulmonary edema early after transplantation (reimplantation response), and two patients required mechanical ventilatory support for allograft rejection at 10 and 11 days. Treatment of rejection consisted of intravenous methylprednisolone (four episodes) or augmented oral prednisone (two episodes), with resolution. No episode thought to be pulmonary rejection has occurred in the absence of cardiac findings. Four patients are alive from 6 to 15 months after transplantation and are functionally normal. Early experience with heart-lung transplantation suggests (1) that allograft rejection can be detected by cardiac findings and successfully treated by augmented corticosteroids, (2) that lung rejection does not occur in the absence of cardiac findings, (3) that the frequency and severity of rejection episodes are not greater than with standard cardiac transplantation, and (4) that the frequency of rejection episodes is highest within the first 60 days after transplantation.
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PMID:Diagnosis and treatment of allograft rejection in heart-lung transplant recipients. 640 22

A 34-year-old woman without heart disease had an acute pulmonary edema after a grand mal seizure. Neurogenic pulmonary edema is characterized by the primary role played by the central nervous system in its pathogenesis, usually in the absence of cardiopulmonary disease. We believe that the initiating mechanism was a marked, although brief, generalized vasoconstriction, followed by a shift of blood from the peripheral vascular bed to the pulmonary vascular bed. We stress the need of treating the underlying neurologic disease as the only regional way of preventing the recurrence of pulmonary edema.
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PMID:[Neurogenic pulmonary edema. Description of a case occurring after an epileptic crisis]. 643 96

Fluid movement from the pulmonary capillaries into the interstitial space occurs continuously and is drained by the lymphatics. With increased leakage or decreased clearance, excessive extravascular lung water accumulates, initially as interstitial edema and subsequently as alveolar edema. The most common cause of pulmonary edema is an increase in microvascular hydrostatic pressure. An increased permeability of the capillaries is the other mechanism of production of pulmonary edema. An acute, critical reduction in colloid osmotic pressure may play a contributory role in pulmonary edema even at normal hydrostatic pressures. Dyspnea, diaphoresis, and anxiety characterize the clinical picture. A history of heart disease and congestive heart failure may be present in CPE, whereas evidence of an inciting event or disease process suggests NCPE. Hypoxia, decreased lung compliance, and increased shunt fraction are seen in both types of pulmonary edema, but the duration of pulmonary edema tends to be more severe and prolonged in NCPE. Evidence of increased permeability in NCPE distinguishes it from CPE. Clinically, this is assumed when pulmonary edema is demonstrated at normal PCWP and when edema fluid protein concentration and COP are close to those of plasma. The management of pulmonary edema consists of the improvement of gas exchange by methods that range from supplemental oxygen administration to mechanical ventilatory support with PEEP, depending on the severity of the disturbance in lung function. Improvement in myocardial function and a decrease in pulmonary congestion are accomplished with diuretics and morphine; in those patients who do not respond to this therapy, manipulation of preload, afterload, and myocardial contractility by vasodilators and inotropic agents may be required. In acute pulmonary edema, intravenously administered agents with a short half-life and rapid onset of action are preferred. The role of colloids in the treatment of pulmonary edema is controversial. The indications for the use of corticosteroids in ARDS are controversial, and an optimum dose has not been determined. Many clinicians tend to choose steroids to treat these patients, but the value of these agents in this setting awaits the results of controlled trials now under way.
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PMID:Acute pulmonary edema. 644 44

Extreme variations of heart rate caused clinical and radiographic findings of heart failure in six neonates in the absence of structural heart disease. Two infants had heart block with heart rates below 50/min and four had paroxysmal atrial tachycardia with rates approaching 300/min. Each infant had interstitial or alveolar pulmonary edema and most had cardiomegaly. After restoration of a normal heart rate, there was rapid and dramatic resolution of pulmonary edema and reduction in cardiac size.
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PMID:Heart failure in the neonate due to extreme abnormalities of heart rate: clinical and radiographic features. 644 42

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.
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PMID:Hypertropic cardiomyopathy and hyperthyroidism in the cat. 654 Feb 56

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Sudden onset of pulmonary edema after administration of intravenous propranolol hydrochloride developed in a patient with pheochromocytoma but without clinical or histological evidence of heart disease. Previous cases of pulmonary edema have been reported in association with oral propranolol therapy but have failed to document histological absence of cardiac pathology. The mechanism for the development of pulmonary edema may have been a propranolol-induced beta 1- and beta 2-blockade that led to unopposed alpha effects and sudden elevation of afterload. This case underlines the caution that should be used in the administration of propranolol when the diagnosis of pheochromocytoma is considered.
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PMID:Propranolol-induced pulmonary edema and shock in a patient with pheochromocytoma. 669 55


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