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

The pathogenesis of shock lung as well as the success of therapy in this condition was studied in 79 cases of extrathoracic trauma. The water-, hemoglobin-, and DNA contents of the lungs were measured in order to determine the extent of edema, the rate of perfusion, and proliferation. The cases were divided into two groups according to whether they had or had not received medical therapy before death. The data from these two groups were compared using statistical methods in which time of survival was especially taken into account. The fluid balance, pO2, pCO2, central venous pressure, pH of the serum, total serum protein and serum creatinine were also studied in these cases. Results of the study are as follows. Three phases of the posttraumatic syndrome of shock-lung could be distinguished: phase I (initial phase): blood perfusion is increased, edema is beginning to form, and medical treatment has not yet begun. Phase II (early phase = sydrome of early respiratory failure): pulmonary edema is developing rapidly while perfusion is decreasing. Phase III (late phase = syndrome of late respiratory failure): proliferative changes predominante and the edema is still increasing. The mean weight of the lungs was 397 g (s = 170) in phase I, 774 G (S = 361) In phase II, and 1124 g (s = 310) in phase III. The survival times correlated significantly and positively with the amount of water and DNS in the lungs and significantly and negatively to the amount of hemoglobin in the lungs. Thus, increasing pulmonary edema and increasing proliferative changes occurred with decreasing pulmonary perfusion. This correlation was even noted in groups of patients who had not received medical treatment and whose survival times were short. In treated cases, the fluid balance was significantly and negatively correlated to the total serum protein.
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PMID:[Examinations to phenomenon of shock-lung (author's transl)]. 0 60

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Histamine causes interstitial pulmonary edema, but whether this is the result of an increased permeability of the pulmonary circulation or only of the bronchial circulation remains to be determined. In order to selectively study the effect of histamine on the pulmonary circulation, we used an isolated perfused rabbit lung preparation because in this species, the bronchial circulation is poorly developed. Edema formation was assessed by continuously monitoring the weight of the lung perfused at constant pressure. These studies were supplemented by electron microscopic observations using hemoglobin as an ultrastructural tracer for microvascular permeability. We found that histamine (8.0 microgram base/100 ml of perfusate) did not cause lung weight to increase. Ultrastructural studies showed that histamine, at this dosage, did not cause a greater leakage of hemoglobin that occurred in the control lungs. Thus, we have concluded that histamine does not increase the permeability of the pulmonary microcirculation in the isolated perfused rabbit lung.
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PMID:Morphological and physiological study of the effect of histamine on the isolated perfused rabbit lung. 54 22

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.
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PMID:Effect of afterload reduction on plasma volume during acute heart failure. 70 95

A rebreathing technique was utilized to assess changes in diffusing capacity (DCO), pulmonary capillary blood volume (Vc), pulmonary parenchymal tissue volume (Vt), and cardiac output (Qc), after infusion of 2 liters of 0.9% saline intravenously in 13-25 min in five healthy subjects. Blood hemoglobin concentration decreased an average of 17%. Vc increased strikingly in all five subjects. No significant changes in Vt, or in Vt per unit lung volume were observed. Radiographic evidence of interstitial pulmonary edema was present in four of the five subjects. Radiographic total lung capacity was reduced significantly in four of the five subjects. Significant reductions in forced vital capacity (FVC), forced expiratory volume in 1.0 and 3.0 s, and mean forced expiratory flow during the middle half of the FVC occurred in three of the five subjects. No dyspnea, cough, or physical examination abnormalities of lungs or heart occurred. This noninvasive, ventilation-limited, rebreathing technique appears capable of detecting early changes in pulmonary congestion, at a time when definitive radiographic changes and changes in the physical examination are absent. It appears capable of detecting the increase in Vc associated with hypervolemia in man.
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PMID:Rebreathing pulmonary capillary and tissue volume in normals after saline infusion. 89 78

Resuscitation and volume replacement after acute blood loss is possible for a short duration by means of 6% stroma-free hemoglobin solution (SFH). Despite transcapillary loss of SFH, pulmonary edema is not provoked after massive infusion of cristalloid solution. The oxygen supply to the tissues is maintained by a compensatory rise in cardiac output and O2-extraction, mainly from the remaining red cell hemoglobin.
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PMID:[Resuscitation with stroma-free hemoglobin solution after acute blood loss]. 103 29

The first phase of accidental drowning begins with asphyxia, due to either laryngospasm (10-15 percent of cases) or water aspiration. The second phase is characterized by water and electrolyte changes in the blood. The physiopathological modifications caused by drowning in fresh water differ from those of drowning in sea water. The hypotonic fresh water quickly diffuses in the bloodstream. The consequences are, in many cases, hypervolemia with pulmonary edema, hemolysis, hyperkalemia with risk of ventricular fibrillation, diminution of hemoglobin, and a relative decrease in plasma concentration of Na, Cl, Ca, and albumin. Further, inactivation and washing out of the anti-atelectasis factor from the alveoli by fresh water facilitate the formation of atelectasis. In cases of accidental drowing in sea water the osmotic gradient is in inverse: the electrolytes of aspirated salt water diffuse in the circulation, whereas the blood serum and the plasma albumin pass into the alveoli. Acute pulmonary edema often follows these pathological changes. Hypovolemia with circulatory collapse, hemoconcentration with rise in hemoglobin, hematocrit, sodium, potassium and albumin, and, finally, an elevated risk of thromboembolism due to increased blood viscosity, represent further complications. On the other hand, ventricular fibrillation is rare, hemolysis is absent and atelectasis usually does not occur.
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PMID:[Physiopathology of accidental drowning]. 112 62

A Thai female patient infected with P. falciparum had 80 per cent P. falciparum infected red cells at ring stage in the peripheral blood smear. The complications included anemia, thrombocytopenia, acute renal failure and pulmonary edema. A marked decrease in platelets number, low hemoglobin, low hematocrit and decreased red blood cell count were detected. More than 70 per cent of total platelets detected in the blood smear were binding to parasitized red blood cells. The number of binding platelets declined with decreasing per cent parasitized red cells. It was also noted that some platelets (10-20%) adhered to nonparasitized red cells. An increased number of large lymphocytes was shown by increased numbers of large unstained cells (LUC) by H* 1 automated analyzer. The peripheral blood smear showed abnormal binding of platelets to the infected red cells more frequently than to non infected red cells and free platelets on the day of high parasitemia. This abnormal phenomena was related to the number of platelets in the circulation. When the parasitized red cells were not detected in the blood smear, the number of platelets in the circulation had returned to normal.
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PMID:An unusual adhesion between red-cells and platelets in falciparum malaria. 140 64

A 12-year-old girl was injured in a traffic accident and suffered fractures of all the long bones of both legs. During the operation she received 10 l of lactated Ringer's solution, 3 l of 0.9% NaCl, and 2 l of 5% glucose, until blood was available, because of difficulty in its cross-matching. Her hemoglobin dropped to 4.9 g%. After the operation a distension of the abdomen was noted. An abdominal tap confirmed ascites. A simultaneous intravenous pyelogram and retrograde cystogram revealed no leakage from the urinary tract. An over-transfusion ascites was diagnosed combined with pulmonary edema. The patient was treated for 2 days in the ICU, until she was transferred to the orthopedic department with no signs of ascites.
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PMID:Over-transfusion ascites. 165 30

Conscious rats were given either 14 g/dl bis(3,5-dibromosalicyl) fumarate cross-linked hemoglobin (DBBF-Hb) in lactated Ringer's (LR) as an intravenous bolus (40, 50, or 60% of blood volume), 12.5 g/dl human serum albumin (HSA) in LR as a control for oncotic effects, or LR as a control for injection volume. The high dose HSA and DBBF-Hb rats experienced pulmonary edema after injection; one rat in each of these groups died soon after dosing. Rats were killed after 48 hours for histopathology. Only the 60% HSA and the 50% and 60% DBBF-Hb rats had treatment-related lesions. In the liver, randomly distributed mononuclear cell aggregates occasionally surrounded a necrotic hepatocyte. Liver lesions in 60% DBBF-Hb rats were the largest and most numerous, but in all groups were qualitatively similar. Hearts from HSA and DBBF-Hb rats had similar mild inflammatory lesions. We conclude that bolus administration of DBBF-Hb causes morphologic lesions in rats only at volumes sufficient to cause pulmonary edema. Hepatic and cardiac changes with high volumes of DBBF-Hb resembled those in rats given a corresponding bolus of HSA, suggesting that vascular overload with a hyperoncotic solution, rather than cytotoxicity of DBBF-Hb, caused the injury.
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PMID:Morphologic effects of hypervolemic administration of DBBF hemoglobin in the rat. 236 54


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