Collateral vessels complicating bronchopulmonary dysplasia.
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Biomedical subjects
Publications and source records attributed to I H Gessner.
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This is a revision of the 1976 report published under the auspices of the Inter-Society Commission for Heart Disease Resources. These guidelines provide a description of optimal resources, personnel, and working arrangements and should not be used to set minimal, standard, or uniform criteria or practices for all institutions. Included in the report are specifications for radiologic and physiologic equipment, description of case loads for maintaining safe and effective performance and considerations or complication rates. Also discussed are professional staff qualifications and relationships between physicians and technical and administrative services personnel. Other topics reviewed included laboratory location, electrical safety, and radiation protection as well as optimal facilities and equipment criteria for conventional x-rays. Newer imaging modalities are briefly considered, primarily to to emphasize that the field is rapidly changing. It is not possible, however to make specific recommendations concerning how these modalities will complement and/or replace more conventional techniques and approaches now considered appropriate and optimal.
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Ten anesthetized dogs, 48 h postintravenous 131I-albumin injection, had a segment of lung airspace isolated by a balloon-tipped catheter lodged in a bronchus. An isotonic saline solution containing trace amounts of Blue Dextran, 125I-albumin, and 57Co-cyanocobalamin was instilled into the lung segment. During control periods, lung saline was absorbed at a rate of 0.133% per minute as measured by indicator dilution of Blue Dextran. Only 57Co-cyanocobalamin crossed the epithelium. Acute hemodynamic pulmonary edema was produced by aortic constriction plus saline overload. In pulmonary edema the fluid volume in the airspace increased at the rate of 0.96% per minute, and there was a significant influx of 131I-albumin into the lung saline from the blood in all animals. However, neither 125I-albumin nor Blue Dextran diffused from the airspace into blood during edema; both were merely diluted by fluid influx. The rate of diffusion of 57Co-cyanocobalamin increased fivefold during edema. A small number of discrete breaks in the lung epithelium allowing bulk flow of interstitial fluid is proposed to account for the one-way movement of albumin in hemodynamic alveolar edema.
Fourteen term newborn infants have been recognized as having transient tricuspid insufficiency associated with significant perinatal stress. Five of these infants underwent cardiac catheterization for presumed congenital heart disease, but had only massive tricuspid valve insufficiency. The other nine infants were diagnosed on the basis of a murmur characteristic of tricuspid valve insufficiency and on other clinical grounds. All had a history of significant perinatal stress in the form of asphyxia with or without hypoglycemia. Frequently, congestive heart failure, persistent cyanosis, and ECG evidence of myocardial ischemia were present. Twelve of the 14 survived, and in each of them all cardiac signs and symptoms, including the murmur, spontaneously resolved. The two patients who died had histopathologic evidence of necrosis in the anterior papillary muscle of the tricuspid valve. The constant features of perinatal stress, ST-T wave abnormalities on the ECG, and spontaneous resolution of the transient tricuspid insufficiency strongly suggest that this syndrome is secondary to a reversible form of myocardial dysfunction, perhaps by affecting papillary muscle specifically. We believe that hypoxia with or without hypoglycemia precipitates the events leading to this clinical syndrome which is distinguishable from other cardiac abnormalities in the newborn by the history, distinctive murmur, and the ECG abnormalities.
The possible diagnostic value of an enlarged left atrial appendage (LAA) on the posterior-anterior or right anterior oblique chest film as a means of implicating a rheumatic etiology for mitral valve disease in children was investigated. Chest films were examined without prior knowledge of clinical or laboratory data, and the results were later correlated with this information in 113 children and adolescents. The clinical and laboratory data included application of the modified Jones criteria for the diagnosis of acute rheumatic fever, streptococcal antibody titers and clinical and cardiac catheterization findings. In children with mitral valve disease, our data suggest that as enlarged LAA, especially in the presence of pulmonary venous obstruction, is characteristic of rheumatic heart disease. This finding appears to be particularly useful, in conjunction with streptococcal antibody studies, in distinguishing rheumatic from nonrheumatic patients with mitral insufficiency.
Five cyanotic newborn infants underwent cardiac catheterization between 8 and 36 hours of age with a tentative diagnosis of cyanotic congenital heart disease. All had normal cardiovascular anatomy. Cyanosis was the result of persistence of fetal cardiopulmonary circulation with right-to-left shunting across the ductus arteriosus. In all infants, cyanosis resolved spontaneously and the infants survived without sequelae. Admission chest roentgenograms of all infants showed marked hyperinflation of the lungs. Except for severe hypoxemia, the clinical presentation, chest films, and course of illness of these infants were consistent with transient tachypnea of the newborn. It is proposed that an increase in pulmonary vascular resistance, due to hyperinflation of the lungs, was the mechanism which reopened the fetal cardiopulmonary circulatory channels and produced hypoxemia, and that these infants suffered from a rare manifestation of a usually benign newborn respiratory condition. Further, given these pathophysiologic mechanisms, the use of continuous transpulmonary pressure gradients in the management of such infants would be contraindicated.
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This report presents a new, simple and reliable method of quantitating left-to-right shunts from arterial dilution surves. When indicatior (e,g., indocyanine green) is injected centrally (right venticle or pulmonary artery) and blood is withdrawn rapidly from either the aorta or other central systemic artery, in the presence of a left-to-right shunt to recorded indicator-dilution curve usually shows two discrete peaks: p-1 of the magnitude of the shunt expressed as percent of pulmonary blood flow, Experimental and clinical data demonstrate that this method is accurate in quantitating shunts from such curves.
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