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

Inhalation injuries occur in approximately one-third of all major burns and account for a significant number of deaths in those burn patients each year. Victims die as a result of carbon monoxide poisoning, hypoxia, and smoke inhalation. These deaths can occur without thermal wounds as well as with burn injuries. There are three distinct problems with inhalation injuries: thermal burns of the upper airway, carbon monoxide poisoning, and smoke inhalation. Each has different symptoms and signs, different treatment, and different prognosis. Thermal burns occurring in the upper airway are usually manifested within 48 hours of injury. Diagnosis is made by direct visualization of the upper airway, looking for signs of thermal injury. Admission for observation with humidified oxygen, attentive pulmonary toilet, bronchodilators as needed, and prophylactic endotracheal intubation as indicated are the mainstays of treatment. Resolution of the injury usually occurs within days. Carbon monoxide poisoning, the most common cause of death in inhalation injury, is a result of combustion. Symptoms and signs correlate with blood levels, but arterial blood gases are used to determine the degree of carbon monoxide intoxication. Treatment is based on the principle that carbon monoxide dissociation occurs much faster if the patient is placed on 100% oxygen. Occasionally the patient's symptoms may persist or get worse despite adequate treatment. Smoke inhalation significantly damages normal respiratory physiology, resulting in injury progressing from acute pulmonary insufficiency to pulmonary edema to bronchopneumonia, depending on the severity of exposure. Diagnosis is based on history, but clinical findings, arterial blood gases, and fiberoptic bronchoscopy are helpful. Treatment is supportive with careful attention paid to fluid resuscitation in the patient with burns.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhalation injuries. 261 27

Croup and epiglottitis, which cause greater than normal negative inspiratory intrathoracic pressure (NIIP), have been associated with pulmonary edema. To examine the effects of increased NIIP per se on blood gases, hemodynamics, and lung water content, we carried out 2 types of experiments in 18 anesthetized dogs. Short-term, low-pressure experiments (6 control dogs and 6 dogs that generated intratracheal pressures of -12 cm H2O during inspiration for 3 h) and long-term, high-pressure experiments (6 dogs that generated -20 cm H2O during inspiration for 6 h). In the short-term, low-pressure experiments, animals made to generate negative inspiratory pressure differed from control dogs by demonstrating decreased pleural pressure (p less than 0.01), increased arterial PCO2 (p less than 0.05), and decreased minute volume (p less than 0.05); no differences occurred in hemodynamic data (pulmonary arterial, left atrial, and aortic pressures and cardiac index) and in extravascular lung water (indicator dilution and gravimetric analyses). Similarly, in the long-term, high-pressure dogs, arterial PCO2 increased (p less than 0.05) and lung water was normal by gravimetric analysis. We conclude that both 3 and 6 h of increased NIIP cause CO2 retention but have minimal effects on hemodynamics and lung fluid exchange.
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PMID:Pulmonary and systemic effects of increased negative inspiratory intrathoracic pressure in dogs. 307 77

Intravenous infusion of free fatty acid (FFA) produces an increase in the alveolar surfactant pool of the rabbit and pulmonary edema, hyperventilation, hypoxemia and hypocapnia. Previous studies suggested that alveolar PCO2 would be a regulator of intracellular storages of surfactant. In order to study the role of hypocapnia in the increase of lung surfactant in our experiments we administered 20 mg FFA X kg-1 X min-1 i.v. to rabbits breathing room air (n = 10) or 5% CO2, 21% O2, 74% N2 (n = 7). Disaturated phosphatidylcholine (DSPC) was determined in bronchial-alveolar lavage fluid as index of alveolar surfactant content, 5% CO2 in the inspired air prevented the hypocapnia and blocked the increase in DSPC induced by FFA (p less than 0.01). Pulmonary edema post-FFA was not changed by 5% CO2 administration. We conclude that hypocapnia produced by hyperventilation during FFA infusion would be an important factor in the increase of DSPC observed after FFA infusion.
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PMID:Role of hypocapnia in the alveolar surfactant increase induced by free fatty acid intravenous infusion in the rabbit. 308 86

We studied the effects of neutrophil activation on collateral ventilation and peripheral lung reactivity in anesthetized dogs. A fiberoptic bronchoscope was wedged into a segmental airway under direct vision. Ventilation beyond the obstruction thus occurred only through collateral channels. Through one lumen of a double-lumen catheter threaded through the suction port of a bronchoscope, 5% CO2 in air was infused at a known constant rate (V coll). Through the other lumen, pressure at the tip of the bronchoscope was monitored (Pb). For measurements of resistance to flow through the collateral system (Rcs), the ventilation was stopped at functional residual capacity (FRC). Histamine was delivered through the bronchoscope to the obstructed lung segment in the form of an aerosol mist generated by an ultrasonic nebulizer. Measurements of Rcs were used as a parameter of the peripheral lung reactivity to histamine challenge. Within one hour after intravenous infusion of phorbol myristate acetate (PMA), a neutrophil activator, the reactivity to histamine significantly increased. After this, Rcs increased even without histamine challenge. This increase may have been due to an edematous injury of lung caused by PMA. The nature of the injury was confirmed by wet to dry weight ratios. In the other group, the white cell count dropped below 1000 per cu. mm. after intravenous infusion of nitrogen mustard. The same experimental protocols were followed. The Rcs did not increase even with histamine challenge. Our results suggested that substances such as oxygen radicals and arachidonic acid metabolites, which can be released by activated neutrophils, may not not only increase peripheral lung reactivity, but may also induce pulmonary edema.
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PMID:Effects of neutrophils on collateral ventilation and peripheral lung reactivity in dogs. 342 42

Male Hartley guinea pigs were exposed either to filtered air or to 1 ppm ozone (O3) for 1 hr. At 2, 8, 24, or 48 hr after exposure we measured ventilation, respiratory mechanics, lung volumes, diffusing capacity for carbon monoxide (DLCO), and alveolar volume (VA) in anesthetized, tracheotomized animals. Respiratory frequency and tidal volume were unchanged in all groups. Pulmonary resistance was increased 2 hr after O3 but returned to control at 8 hr and thereafter. Prolonged reductions in lung volumes (total lung capacity, vital capacity, functional residual capacity, and residual volume) as well as in DLCO and VA occurred after O3, with maximum decreases at 8 and 24 hr postexposure. Increased ratios of wet lung weight to body weight were seen at 2, 8, and 24 hr. In separate groups of animals, also exposed either to filtered air or to 1 ppm O3, plasma eicosanoid (EC) concentrations were measured at 2, 8, 24, 48, or 72 hr after exposure. Significant increases in thromboxane B2 concentrations were seen at 2, 24, and 48 hr after exposure. Plasma concentrations of 6-keto prostaglandin F1 alpha (PGF1 alpha) and prostaglandin E1 (PGE1) were increased at 24 hr and at 24, 48, and 72 hr, respectively. The nature of this long-term pulmonary response to a short-term exposure to O3 suggests alveolar involvement, including probable alveolar duct constriction and localized pulmonary edema. Although changes in plasma EC concentrations were observed concurrent with impaired lung functions, no simple causal relationship was apparent from these studies.
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PMID:Effect of ozone exposure on lung functions and plasma prostaglandin and thromboxane concentrations in guinea pigs. 347 Sep 78

We studied the effects of regional hypoxic pulmonary vasoconstriction (HPV) on lobar flow diversion in the presence of hydrostatic pulmonary edema. Ten anesthetized dogs with the left lower lobe (LLL) suspended in a net for continuous weighing were ventilated with a bronchial divider so the LLL could be ventilated with either 100% O2 or a hypoxic gas mixture (90% N2-5% CO2-5% O2). A balloon was inflated in the left atrium until hydrostatic pulmonary edema occurred, as evidenced by a continuous increase in LLL weight. Left lower lobe flow (QLLL) was measured by electromagnetic flow meter and cardiac output (QT) by thermal dilution. At a left atrial pressure of 30 +/- 5 mmHg, ventilation of the LLL with the hypoxic gas mixture caused QLLL/QT to decrease from 17 +/- 4 to 11 +/- 3% (P less than 0.05), pulmonary arterial pressure to increase from 35 +/- 5 to 37 +/- 6 mmHg (P less than 0.05), and no significant change in rate of LLL weight gain. Gravimetric confirmation of our results was provided by experiments in four animals where the LLL was ventilated with an hypoxic gas mixture for 2 h while the right lung was ventilated with 100% O2. In these animals there was no difference in bloodless lung water between the LLL and right lower lobe. We conclude that in the presence of left atrial pressures high enough to cause hydrostatic pulmonary edema, HPV causes significant flow diversion from an hypoxic lobe but the decrease in flow does not affect edema formation.
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PMID:Hypoxic pulmonary vasoconstriction does not affect hydrostatic pulmonary edema formation. 355 36

Healthy adult baboons exposed to 100% oxygen for 5 to 7 days maintained on continuous mechanical ventilation develop severe bilateral noncardiogenic pulmonary edema that resembles in many aspects the human adult respiratory distress syndrome (ARDS). In the present study, we evaluated the effects of hyperoxia for 5 to 6 days in 8 baboons to compare changes in abnormalities in bronchoalveolar lavage fluid (BALF) biochemical markers, hemodynamic measurements, and pulmonary function tests in order to find early predictors of lung injury. All animals had bilateral alveolar infiltrates, severe hypoxemia, and progressive deterioration of pulmonary function tests. Diffuse alveolar damage and mild-moderate pneumonias were found and were associated with low-grade bacterial infection. Total lung capacity, diffusing capacity for carbon monoxide, pulmonary static compliance, and oxygenation were significantly impaired after Day 5; BALF proteins, elastase, and total polymorphonuclear leukocytes increased significantly at least 24 h before (Day 4) any abnormalities in chest radiographs, pulmonary function tests, and hemodynamic measurements were detected. We conclude that exposure to 100% oxygen in this model causes marked gas exchange, hemodynamic, biochemical, cytologic, radiographic, and pathologic changes similar to those noted in patients with ARDS. Bronchoalveolar lavage abnormalities precede hemodynamic and gas exchange abnormalities.
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PMID:One hundred percent oxygen lung injury in adult baboons. 363 38

A study of the blood oxygenation in pulmonary capillaries is made by considering the transport mechanisms of molecular diffusion, convection and the facilitated diffusion due to the presence of haemoglobin. The resistance offered by the pulmonary membrane on the transport of gases has been incorporated. The resulting system of coupled, non-linear partial differential equations is solved numerically. It is found that, in the immediate neighbourhood of the entry, the amount of dissolved O2 decreases. This decreases further as the resistance offered by the pulmonary membrane increases. The rate of oxygenation of blood increases as the permeability coefficient for O2 (PO) increases. It is shown that the ideally permeable case for both O2 and CO2 can be approximated by taking PO approximately 10 cm/s. Further, it is shown that the oxygen takes longest and CO2 is the fastest to attain equilibration. The equilibration length increases as the resistance offered by the membrane increases. Finally, some of the pulmonary diseases such as pulmonary oedema and fibrosis have been analyzed.
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PMID:A numerical model for blood oxygenation in the pulmonary capillaries--effect of pulmonary membrane resistance. 365 68

A case of paint remover inhalation causing pulmonary edema and pleural effusions is described. Methylene chloride, an ingredient of paint removers, can cause pulmonary edema and carbon monoxide poisoning. The expanding interest in home projects involving furniture refinishing and paint removal puts a large segment of the population at risk. The implications of such exposure need to be recognized by the medical community.
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PMID:Diffuse pulmonary injury following paint remover exposure. 376 99

This study was undertaken to determine the site of initial pulmonary injury in smoke inhalation. A hotel fire in Houston, Texas, resulted in the on-site deaths of 10 white people (2 to 62 years of age). All underwent autopsy examinations which included measurement of carbon monoxide (CO) and cyanide (CN) levels, as well as electron microscopy of lung samples. Average CO levels of 40% and CN levels of 0.6 ppm were obtained. In all cases, the lungs were heavy, hyperemic, and edematous with soot staining the tracheobronchial mucosa. Light microscopy showed soot, pulmonary congestion, and edema. Electron microscopy confirmed the presence of interstitial and intraalveolar congestion and edema. Carbon particles were also present, and occasionally were seen undergoing phagocytosis by alveolar macrophages. Intracellular edema with focal bleb and vesicle formation was prominent within Type I pneumocytes in 9 of 10 cases. Endothelial cells showed similar but much less severe changes, lacking the distinct blebs seen in the Type I cells. This investigation reveals that smoke, like ammonia inhalation and nitric acid instillation, appears to cause pulmonary edema by initial injury to the Type I pneumocyte.
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PMID:Smoke inhalation: an ultrastructural study of reaction to injury in the human alveolar wall. 378 Jun 43


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