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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There's no doubt that chronic obstructive lung disease can have a disastrous impact on the heart's right ventricle--often producing hypertrophy or even failure--but its effects on the left ventricle are less clear. Some researchers speculate that disease of the right ventricle leads to disease of the left, while others consider the lung disease itself to be the more likely mechanism. Ordinarily, the left ventricle holds up well, even in far-advanced emphysema and chronic bronchitis. Recognizing the cases that do occur is important, however, since only minimal left ventricular failure can seriously compromise respiratory function. Treatment is the same as for left ventricular failure of any cause, but special precautions should be observed, particularly in prescribing diuretics. If frank pulmonary edema supervenes, mechanical ventilation and supplemental oxygen are necessary.
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PMID:The left ventricle in emphysema and chronic bronchitis. 13 13

The authors report 6 cases of acute respiratory failure complicating chronic bronchial and lung disease admitted to hospital with the diagnosis of: heart disease, 3 cases, pulmonary oedema, pulmonary embolism, atrial flutter; status asthmaticus : one case; neuro-psychiatric disease : 2 cases (toxic coma and agitation). The authors emphasize the frequency of chronic bronchial disease and recall the signs of acute decompensation discussing the possible difficulties in diagnosis and the therapeutic implications.
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PMID:[Deceptive and revealing clinical forms of acute respiratory insufficience in chronic bronchopneumopathies]. 19 94

Ten infants and children with respiratory failure, receiving standard maintenance water requirements, were treated on 13 occasions with intravenously given furosemide (1 to 2 mg/kg) because of continued impairment of oxygenation despite conventional therapy. Pulmonary auscultation and radiographs were normal or typical of the primary diagnosis. After a five-fold increase in urine output the mean Po2 rose from 61 mm Hg at a mean FiO2 of 0.7 to 140 mm Hg at an FiO2 of 0.65. The Pco2 decreased from 46 to 38 mm Hg. Interstitial pulmonary edema in these patients can be related to both their lung disease and impaired water tolerance during ventilatory therapy.
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PMID:Edema of the pulmonary interstitium in infants and children. 23 52

Twenty-two adult dogs were each given a single, 30-minute injection of 1.5 ml/kg body weight of pure triolein, and their pulmonary, hepatic, renal, and cerebral morphology was observed for 1, 2, 3, 4, 5, 6, 15, 24, and 48 hours; 3,4, and 5 days; 1 and 2 weeks; and 1 month after the injection. A picture of massive capillary occlusion by lipid droplets was followed by rapidly resolvable inflammatory pneumopathy of granulomatous type, leaving a normal lung at the end of the experiment. The cleaning of the capillaries may be attributed to the mechanical action of the blood flow and to the inflammatory reaction with evacuation of necrotic cells via the bronchial route. Transient pulmonary edema is attributed to increased pulmonary arterial pressure. There was no intravacular coagulation. The few pulmonary lesions observed after the triolein injection suggest that the chemical theory of neutral fat hydrolysis by pulmonary lipase and the toxicity of free fatty acids that are released should be reconsidered.
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PMID:Pulmonary neutral fat embolism in dogs. 43 12

The chest radiographs of 25 patients with proven antiglomerular basement membrane antibody disease (Goodpasture's syndrome) were analysed. All except two of the patients had pulmonary haemorrhage at some stage of their disease. Altogether there were 39 episodes of pulmonary haemorrhage, 25 being relapses. During seven episodes the chest radiograph was normal. Relapses of pulmonary haemorrhage never occurred in isolation but were usually associated with infection (not necessarily a chest infection) or occasionally fluid overload. Conversely fluid overload or infection were always associated with pulmonary haemorrhage provided there were high or rising titres of circulating antibodies at the time. Therefore in a patient with antiglomerular basement membrane antibody disease, the presence of shadowing in the lung fields on the chest radiograph almost invariably means the patient has pulmonary haemorrhage whether or not pulmonary oedema or a chest infection are present. Limitation of shadowing by a fissure, loss of major portions of the diaphragmatic or cardiac silhouette, involvement of the lung apex or costophrenic angles suggest an underlying chest infection. Septal lines suggest fluid overload. Pleural effusions are seen with chest infections and fluid overload. The carbon monoxide uptake (KCO) was invariably high in the presence of pulmonary haemorrhage even if the chest radiograph was normal. A combined use of KCO and chest radiographs is the best method of monitoring lung disease in these patients.
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PMID:The chest X-ray in antiglomerular basement membrane antibody disease (Goodpasture's syndrome). 46 41

Acute exposure to monomethylhydrazine and dinitrogen tetroxide, the principal toxic irritants in rocket fuels, is described with particular attention to the development of pulmonary edema as a herbinger of more severe central nervous system toxicity. An acute respiratory embarrassment is documented and possible means of therapy based on animal experimental models is suggested. Early clinical and radiographic examination as a baseline for further evaluation is essential, with follow-up radiographs recommended for assessment of possible developing chronic lung disease.
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PMID:Rocket propellant inhalation in the Apollo-Soyuz astronauts. 89 71

Routine measurement of pressure-volume curves of the lungs and thorax in seven patients treated with continuous mechanical ventilation provided supportive evidence for the presence or absence of cardiogenic pulmonary edema, noncardiogenic pulmonary edema, pneumonia, bronchospasm, mucous plugging, intubation of mainstem bronchus, atelectasis, and results of subsequent therapy. Those conditions associated with predominantly airway disease altered dynamic more than static pressure-volume measurements. Those conditions associated with parenchymal lung disease or loss of lung volume generally altered both dynamic and static pressure-volume measurements. The effectiveness of treatment of these diseases could be monitored by their effect on the pressure-volume curve. The determination of pressure-volume measurements are simple, noninvasive, and can be accomplished within minutes. The routine use of these measurements should be one of the monitoring procedures performed in patients treated with mechanical ventilation.
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PMID:Compliance and dynamic characteristics curves in acute respiratory failure. 93 12

The aim of this review is to provide a critical and concise discussion of present knowledge on the role of atrial natriuretic factor (ANF) in physiological as well as pathological pulmonary conditions. The lung contributes only to a small extent to the production of circulating ANF; on the other hand, the lung represents the major degrading site of the protein. Plasmatic ANF concentration increment during lung disease may therefore be due to a reduction in ANF plasma removal enzyme rather than to increased ANF production. Lung tissue shows more ANF receptor sites than any other organ. The effect of ANF on bronchial and pulmonary artery muscle lining is particularly evident. In fact ANF administration in asthmatic patients leads to bronchodilation comparable to dilation induced by salbutamol. Furthermore, elevated levels of circulating ANF seem to influence fluid redistribution through alveolar-capillary membrane leading to protein mobilization through the alveolar space. On the contrary, in the cardiomyopathic hamster ANF induces relevant guanylate cyclase activation before the animal has developed hemodynamic changes. Guanylate-cyclase activation may protect the lung through counteracting pulmonary edema formation, as shown by fluid reduction in alveolar spaces following pneumotoxic agents administration. This effect seems independent of natriuretic and hypotensive ANF effects.
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PMID:[Atrial natriuretic factor and pulmonary function]. 129 35

Surfactant is now available for general clinical use in infants with RDS. While surfactant is effective, it does not prevent lung disease in many preterm infants because of other aspects of lung immaturity. In experimental models, corticosteroids alter the fetal lung by improving compliances, increasing lung volumes, decreasing pulmonary edema, and altering surfactant-compliance dose response curves. These effects are independent of changes in surfactant pools but augment the responses of the lungs to surfactant treatment. Optimal outcomes for the preterm require the combined use of fetal maturation strategies and postnatal surfactant.
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PMID:Surfactant in the perinatal period. 139 80

One hundred consecutive low birth weight (LBW) infants (less than 1751 g) were randomized into a study group having a restricted fluid intake until 4 weeks of age and a control group following the fluid regimen conventionally used in the hospital. Chest X-ray films were examined on admission, at the ages of 3 days, 7 days, 2 weeks and 4 weeks and at 2-monthly visits to the outpatient clinic up to 1 year of age or until the chest examinations were normal. The severity of hyaline membrane disease (HMD) and typical radiological abnormalities of bronchopulmonary dysplasia (BPD) were assessed. Twelve patients succumbed, one in the study group and 11 in the control group. The study group seemed experience less severe HMD than the controls. Fifty-four percent of the former and 32% of the latter were alive and had no radiological signs of BPD at 4 weeks of age (P less than 0.05). The difference between the groups in the cumulative number of normal chest X-ray examinations during the follow up was even more significant. The percentage of normal X-ray films at 1 year of age was 92% in the study group and 72% in the control group. These results suggest that fluid restriction for the first 4 weeks of life can lower the incidence of radiological abnormalities typical of BPD obtained during the 1st year of life in LBW infants. Pulmonary oedema seems to be a significant aetiological factor causing HMD to develop into chronic lung disease.
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PMID:The relationship of fluid restriction during the 1st month of life to the occurrence and severity of bronchopulmonary dysplasia in low birth weight infants: a 1-year radiological follow up. 139 93


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