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

Although the physiological effects of positive pressure ventilation are numerous, sometimes undesirable and have varying degrees of significance, positive pressure ventilation still plays a major role in the resuscitation and treatment of critically ill patients. Advances in the various methods of delivering positive pressure, especially when incorporating spontaneous breathing, have reduced the severity of complications. Despite serious complications, mechanical ventilation has advantages. When it is instituted for ventilatory and hypoxaemic respiratory failure, the benefits can be viewed in the context of the work of breathing. Spontaneous breathing normally requires 5% of total oxygen delivery to meet its demands. In lung disease, the ratio of oxygen consumption by the respiratory muscles to whole body oxygen consumption can increase to 25-30% (Henning 1986, Pinksy 1990). Mechanical ventilation reduces the energy demand of respiratory muscles and increases the oxygen delivery to other vital organs. When mechanical ventilation improves hypoxaemia and/or hypercarbia, or significantly decreases the work of breathing, it may also normalize associated changes in heart rate (Perel & Pizov 1991 p53). When cardiac output is increased in response to the increased work of breathing and associated stress, the institution of mechanical ventilation may beneficially lower the cardiac output simply due to the decrease in oxygen demand; thus the physiological reduction in cardiac output may not necessarily be regarded as a complication. The effects of raised intrathoracic pressure during mechanical ventilation may be beneficial when used to prevent or reduce pulmonary oedema, though problematic in some other situations. Mechanical ventilation is a life-saving treatment which has many associated complications; nurses have to accept the unavoidable hazards and adapt their nursing care to minimize their effects.
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PMID:Physiological changes occurring with positive pressure ventilation: Part Two. 956 54

Metaplastic pulmonary ossification is usually described as dendriform or nodular in patients with chronic inflammatory lung disease or long-standing pulmonary edema. We present a case of dendriform pulmonary ossification found accidentally at autopsy in a 66-year old man. In addition, some of the theories relating to the development of this rare phenomenon are discussed.
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PMID:[Disseminated pulmonary ossification. Case report]. 965 79

The present article reviews the basic principles of a new approach to the characterization of pulmonary disease. This approach is based on the unique nuclear magnetic resonance (NMR) properties of the lung and combines experimental measurements (using specially developed NMR techniques) with theoretical simulations. The NMR signal from inflated lungs decays very rapidly compared with the signal from completely collapsed (airless) lungs. This phenomenon is due to the presence of internal magnetic field inhomogeneity produced by the alveolar air-tissue interface (because air and water have different magnetic susceptibilities). The air-tissue interface effects can be detected and quantified by magnetic resonance imaging (MRI) techniques using temporally symmetric and asymmetric spin-echo sequences. Theoretical models developed to explain the internal (tissue-induced) magnetic field inhomogeneity in aerated lungs predict the NMR lung behavior as a function of various technical and physiological factors (e.g., the level of lung inflation) and simulate the effects of various lung disorders (in particular, pulmonary edema) on this behavior. Good agreement has been observed between the predictions obtained from the mathematical models and the results of experimental NMR measurements in normal and diseased lungs. Our theoretical and experimental data have important pathophysiological and clinical implications, especially with respect to the characterization of acute lung disease (e.g., pulmonary edema) and the management of critically ill patients.
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PMID:Modeling the nuclear magnetic resonance behavior of lung: from electrical engineering to critical care medicine. 1033 20

Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.
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PMID:Pulmonary surfactant in health and human lung diseases: state of the art. 1044 27

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

Physiological respiratory and hormonal changes occurring during pregnancy result in increased oxygen consumption related to fetal growth. The increase in the maternal basal metabolism leads to hyperventilation and increased cardiac output. This explains why pathological respiratory or cardiovascular conditions existing prior to pregnancy can rapidly worsen during the course of the pregnancy. However, even if no cardiorespiratory disease exists prior to pregnancy, an inhalation lung disease, pre-eclampsia or sepsis can lead to pulmonary edema due to the increased plasma volume in the pregnant woman. These different pathological situations as well as infectious lung diseases are discussed here. We examine the evolution of respiratory function during the course of labor, delivery and the post-partum period. In addition, pregnancy also has an effect on chronic respiratory disease, particularly asthma.
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PMID:[Development of acute and chronic respiratory diseases during pregnancy]. 1063 1

In children, pulmonary sequelae contribute to early and late morbidity after bone marrow transplantation (BMT). Between 1975-1999, we performed 152 BMTs in 138 pediatric patients with malignant and nonmalignant diseases. Allogenic bone marrow was used from 99 HLA identical siblings and from 23 other related or unrelated donors. Autologous marrow was used in 30 transplantations. Median age was 8. 6 years (range, 1.1-22.4) at time of BMT. The median survival was 42%, the survival time was 6.5 years (range, 0.8-23.1), and the median follow-up time was 6.8 years (range, 0.8-23.2). Seventeen patients had severe respiratory complications. Early severe respiratory complications leading to death within the first 4 months after BMT were due to pulmonary edema (n = 1), or fungal (n = 3), bacterial (n = 1), or viral (n = 2) pneumonia. Late severe respiratory sequelae were defined as persistent respiratory symptoms for more than 4 months despite treatment, and these occurred in 10 patients, of whom 5 died. Underlying diagnoses covered a wide spectrum, including bronchiolitis obliterans (n = 3), severe restrictive lung disease (n = 2), idiopathic pneumonia syndrome (n = 3), chronic bronchitis (n = 1), and hepatopulmonary syndrome (n = 1). The overall probability for death was 0.58, and for death from severe respiratory complications, 0.16. With improved HLA matching, fewer BMTs after relapsed or primary progressive disease, and improved supportive care, including the usage of CMV negative blood products, after 1990 the probability of death from severe respiratory complications was only 0.04, whereas before 1990 it was 0.23 (P = 0.029; in each time period, n = 69). The disease spectrum has changed from initially more infectious complications to bronchiolitis obliterans and idiopathic pneumonia syndrome. Lung function measurements performed in 85 of 138 patients usually showed a mild restrictive pattern. To identify those children as early as possible who are at risk for severe respiratory complications, a close longitudinal follow-up after BMT by pediatric pulmonologists is necessary.
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PMID:Pulmonary complications after bone marrow transplantation in children: twenty-four years of experience in a single pediatric center. 1106 30

Fourteen of 400 consecutive patients having high-resolution computed tomography (HRCT) with expiratory images showed findings of infiltrative lung disease on inspiratory HRCT and air trapping on expiratory CT. Diagnoses included hypersensitivity pneumonitis, sarcoidosis, atypical infection, and pulmonary edema. The extent of infiltrative abnormalities and air trapping were correlated with pulmonary function tests (PFT) in 11 patients. PFT indicated a mixed pattern in five, an obstructive pattern in three, and a restrictive pattern in three. Forced expiratory volume (FEV) in 1 second/forced vital capacity (FVC) correlated significantly with the extent of air-trapping (r = 0.60; p = 0.05). The extent of infiltrative abnormalities correlated significantly and negatively with forced vital capacity (r = -0.82, p = 0.002), FEV1 (r = -0.59, p = 0.05), total lung capacity (TLC) (r = -0.67, p = 0.05), and DLCO (r = -0.75, p = 0.02). Findings of lung infiltration on inspiratory HRCT scans and air trapping on expiratory CT correlated respectively with PFT measures of restrictive and obstructive lung disease.
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PMID:Mixed infiltrative and obstructive disease on high-resolution CT: differential diagnosis and functional correlates in a consecutive series. 1129 7

In patients with chronic renal failure, mechanical and hemodynamic changes could occur in the lungs without obvious pulmonary symptoms and findings and their effects could pave the way to pulmonary functional disorders. In this study, pulmonary functional disorders and especially alveolocapillary defects, which are frequently seen in uremia, were determined in renal transplanted patients. Pulmonary functions and diffusion capacity were assessed in uremic patients (n = 20) and in successfully transplanted patients (n = 20) without any lung disease or pulmonary edema symptoms and findings. Patients were selected randomly among outpatients who were followed up in a Nephrology and Transplantation Unit. Forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and peak expiratory flow (PEF25-75) were measured. Single breath carbon monoxide diffusion test and diffusion lung capacity adjusted for hemoglobin concentration (DLAdj) were done. The means of the spirometric values such as FVC, FEV1 and FEV1/FVC were normal in the nondialyzed uremic group, but the PEF25-75 value (68.7%) and diffusion capacity (DLAdj 72.7%) were found to be slightly low. There were 2 patients with normal values and 18 patients with some functional abnormalities in this nondialyzed uremic group. The means of all spirometric parameters and diffusion capacities were found to be normal in the transplanted group. There were 7 patients with normal function and 13 patients with some functional abnormalities in this transplanted group. When the nondialyzed uremic group and the transplanted group were compared statistically, significant differences were found between their spirometric values (except for FVC) and their diffusion capacities. Even though the uremic patients did not show any symptoms, their pulmonary function tests, especially diffusion capacity, were found to be disturbed. Although the transplanted patients as a group had normal mean spirometric values and diffusion capacity there were nevertheless many individual transplanted patients with defective diffusion capacity and abnormal spirometric values.
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PMID:The effect of renal transplantation on pulmonary function. 1174 8

Application of positive end-expiratory pressure (PEEP) in acute lung injury patients under mechanical ventilation improves oxygenation and increases lung volume. The effect of PEEP is to recruit lung tissue in patients with diffuse lung edema. This effect is particularly important in patients ventilated with low tidal volumes. Measurement of respiratory system mechanics in patients with acute respiratory distress syndrome is important to assess the status of the disease and to choose appropriate ventilator settings that provide maximum alveolar recruitment while avoiding overdistention. In patients with acute respiratory distress syndrome in whom the lungs have been near-optimally recruited by PEEP and tidal volume, the use of recruitment maneuvers as adjuncts to mechanical ventilation remains controversial. The application of PEEP in patients with unilateral lung disease may be detrimental if PEEP hyperinflates normal lung regions, thus directing blood flow to diseased lung regions. In patients with air flow limitation and lung hyperinflation, the application of additional external PEEP to compensate for intrinsic PEEP and flow limitation frequently decreases the inspiratory effort to initiate an assisted breath, thus decreasing breathing work load.
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PMID:How to set positive end-expiratory pressure. 1187 7


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