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

Proposed since 1938 as a treatment for pulmonary edema, continuous positive pressure ventilation (PPP) still called teleexpiratory positive pressure in France (PPTE) and "Positive End Expiratory Pressure" (PEEP) or even "Continuous Pressure Breathing" (CPPB) in Anglo-Saxon countries, has taken a place in the first line of therapy in refractory hypoxia and particulary when the latter originate from lesional pulmonary edema. The aim of PPP is to open up the alveolar territories by calling on their elastic properties, to fight against micro-atelectasis and bronchial collapse, to diminish the closing volume, to increase the FRC, thereby improve VA/Qc, decrease Qs/Qt and increase PaO2. Furthermore, in the particular case of pulmonary edema, PPP acts against the hydrostatic pressure by increasing the external component of the transmural pressure and by evening out pulmonary capillary blood flow.
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PMID:[Justification, methods and indications for positive-pressure respiration in controlled and spontaneous ventilation in lesional pulmonary edeman]. 0 66

A case of pulmonary edema following reexpansion of a collapsed lung due to pneumothorax is described and illustrated. The importance of recognizing this relatively uncommon phenomenon is stressed. The development of such edema can be prevented by avoiding application of sudden and excessive negative pleural pressures during the evacuation of a pneumothorax or a pleural effusion. The edema generally occurs in a lung that has been collapsed for more than three days. The importance of the duration of pulmonary collapse in the causation of edema is demonstrated in this patient.
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PMID:Reexpansion pulmonary edema. 42 56

A 13-year-old hypertensive girl with a history of severe headaches following exercise developed circulatory collapse after "squat jumps." Pulmonary edema was present without evidence of a cerebral mass. The patient died with increased intracranial pressure despite decompressive craniectomy. Neuropathological evaluation revealed diffuse cerebral edema and a pheochromocytoma in the right adrenal gland. Examination of urine revealed elevation of vanillylmandelic acid levels.
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PMID:Pheochromocytoma causing exercise-related headache and pulmonary edema. 42 71

The effects of the mode of reinflation and of the duration of prior collapse on the development of unilateral pulmonary edema following reexpansion of collapsed lung were studied in a rabbit model simulating the human syndrome of "reexpansion pulmonary edema." The right lungs of rabbits were maintained in an atelectatic state for 0.5 h to 8 days, by injection of air into the pleural space. Reexpansion was achieved in 2 h by application of positive pressure to the airway while a chest tube was connected to underwater seal, or by application of negative pressure (-20 to -100 Torr) to a screened window in the partietal pleura. The lung surface pressures we actually applied by the two methods are not known. Animals were then killed and pulmonary edema was determined by wet-to-dry weight ratios. The incidence of unilateral pulmonary edema increased as the duration of prior collapse was increased (85% after 7--8 days; 17% after 3 days; and 0% after 0,5 h) when reinflated with -100 Torr applied to the pleural window. Although the incidence was less, it also occurred following the use of pleural window pressure less negative than -100 Torr, and after reinflation by positive airway pressure.
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PMID:Unilateral pulmonary edema in rabbits after reexpansion of collapsed lung. 45 26

Intraruminal administration of 0.25 g of 3-methylindole (3MI; skatole/kg of body weight) to seven young calves generally caused mild respiratory signs and lesions, accompanied by only slight changes in cardiopulmonary function. Moderate depression, trembling, and irregular respiratory rate were observed between postadministration hours (PAH) 6 and 12. By PAH 24 at this dosage, abnormal clinical signs were not present. Statistically significant (P less than or equal to 0.05) changes observed in blood gas data from the seven calves were a decrease in aortic oxygen tension at PAH 12, increases in free-flowing venous oxygen tension in the intervals between PAH 6 and 12 and between PAH 6 and 24, and an increase in occluded venous oxygen tension at PAH 24. All calves had increases (although generally not statistically significant) in heart rate, cardiac output, cardiac index, stroke volume, and stroke index after 3MI administration. Mean aortic and pulmonary arterial pressure changes were generally small and variable. At necropsy, the lungs of the calves did not collapse when the thorax was opened. Patchy areas of consolidation (0.5 cm in diameter) were scattered throughout the parenchyma. Pulmonary edema or emphysema was not observed grossly. Microscopically, the alveolar septae were irregularly thickened because of edema, infiltration by polymorphonuclear and mononuclear cells, and vascular congestion. Interstitial lesions were patchy in distribution and severity and corresponded to the areas of consolidation observed grossly. Alveolar epithelial hypertrophy and hyperplasia were present, and an occasional focus of alevoli contained fluid of edema. Degeneration of individual hepatocytes was observed in scattered areas of the liver, especially in the periportal areas. It was concluded that differences in 3MI dosage response may exist between young calves and adult cattle in which calves are more resistant to the pulmonary cytotoxicity of 3MI.
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PMID:Pathophysiologic studies of calves given 3-methylindole intraruminally. 51 32

Following a case of mannitol-induced respiratory and circulatory collapse, the effects of hyperosmolar injections on pulmonary arterial pressure, systemic blood pressure, and cardiac output were studied in dogs. The injection of 20 ml of 10% NaCl into the pulmonary artery increased pulmonary arterial pressure and decreased systemic blood pressure by approximately 50% of control values. Injections of solutions of equal hyperosmolar strength, 50 ml of 25% mannitol or 50 ml of 4% NaCl into the pulmonary artery produced no significant elevation of pulmonary arterial pressure, but were associated with comparable decreases in systemic blood pressure. When allowed to vary, cardiac output increased with injections of all three hyperosmolar solutions, yet was still accompanied by falls in systemic blood pressure as large as when cardiac output was held constant. Vagotomy did not prevent these changes in systemic and pulmonary arterial pressure, nor the increase in cardiac output. After five to 10 injections, the decreases in system blood pressure with any of the solutions and the increases in pulmonary arterial pressure with 10% NaCl disappeared and further injections were without effect. It is concluded that adminstration of mannitol probably does not cause pulmonary edema due to fluid overload, nor does it cause heart failure as evidenced by increases in pulmonary arterial pressure. However, rapid injection may cause a fall in blood pressure and may on occasion be accompanied by bronchospasm, especially in sensitive subjects.
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PMID:Hypotension and respiratory distress caused by rapid infusion of mannitol or hypertonic saline. 57 Dec 22

Dogs and cats killed by intravenous injection of either 0.3 ml/kg body weight T-61 or 100 mg/kg body weight pentoarbital and necropsied at less than 5 minutes or at 15 minutes after injection did not have gross or microscopic pathological changes. However, dogs and cats killed with T-61 at a dose of 1.0--1.5 ml/kg body weight and necropsied at 15 minutes after injection had significant gross and microscopic pathological lesions. Grossly, the lungs were severely edematous, did not collapse, and were deep red. Microscopically, the lungs had severe pulmonary edema and endothelial necrosis. Endothelial swelling of glomerular tuft vessels was also present. These lung and kidney lesions are classified as an euthanasia artefact.
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PMID:Pathologic changes induced by an euthanasia agent. 70 53

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

Unilateral pulmonary oedema is a rare complication in the routine management of spontaneous pneumothorax. Previous reports have emphasized excessive negative intrapleural pressure, rapid re-expansion of the lungs and bronchial obstruction as major factors in the pathogenesis. We have encountered four cases, and at least one of these factors have been absent in each case. Review of the literature, and our own experience suggests that the major factor is chronic and total lung collapse resulting in hypoxia and increased alveolar-capillary membrane permeability. Other factors which may be contributory are discussed.
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PMID:Unilateral pulmonary oedema following re-expansion of pneumothorax. 113 Jun 42

Twenty-four dogs underwent in vivo left pulmonary hilar occlusion with the lung continuously expanded at 10 centimeters or 25 centimeters of water pressure to determine the period of pulmonary ischemia that may be tolerated before consistent pulmonary edema and congestion develop after lung revascularization. Consistent and prolonged pulmonary edema and congestion that caused death of the dog occurred in at least one-half of the dogs when the period of hilar occlusion was extended beyond six hours. Elevation of the left pulmonary artery pressure was only a rough measurement of the severity of the anoxic pulmonary injury. Expansion of the lung at 10 centimeters of water continuous pressure was more beneficial than was expansion at 25 centimeters of pressure. Cyclic ventilation with slight negative-expiratory pressure provided less support to the lung than did continuous expansion at either pressure tested. Intial decreases in both ventilation and perfusion isotope uptake and the percentage of the total volume of oxygen uptake per minute by the ischemic lung returned to near normal levels in three weeks in dogs that survived. Lung expansion during periods of ischemia appears to prevent alveolar collapse and to facilitate oxygenation.
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PMID:Evaluation of pulmonary function in the ischemic expanded canine lung. 125 71


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