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

The side effects of a beta 2-mimetic tocolytic therapy are of importance for anaesthesiologists who administer anaesthesia for obstetric operations, as our case report illustrates. In a healthy 28 year old pregnant woman during the 32nd week of pregnancy i.v. fenoterol was started because of premature labor. After two days severe respiratory failure developed and cesarean section was performed. The patient needed mechanical ventilation with positive endexpiratory pressure and high inspiratory oxygen concentrations (F1O2 greater than 0.7) for 5 days thereafter. The chest x-ray revealed a fluid lung. With artificial respiration and a consequent diuretic therapy with dopamine and furosemide (10 mg . h-1 continuously, negative water balance--5,000 ml on the 4th day) gas exchange improved and extubation was possible on the 6th postoperative day. After exclusion of cardiac or renal disease as well as aspiration of gastric content, the diagnosis of a fenoterol-associated pulmonary edema was thought probable. From the literature it is known that beta 2-mimetics can aggravate the increased water and sodium retention during pregnancy and cause pulmonary edema by an additional increase in pulmonary artery pressure. Therapy consists of adequate oxygenation and induction of diuresis with continuous furosemide and dopamine to achieve negative water balance. When administering anaesthesia to patients on tocolytic therapy positive water balance has to be avoided and great care must be directed to the postoperative gas exchange.
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PMID:[Fenoterol (Partusisten)-associated lung edema. A case report]. 371 43

In a prospective study of lung function of 34 patients taking amiodarone, 24 showed no functional changes but 10 developed a sustained fall in CO transfer factor (TLCO) exceeding 15 per cent. These patients had on average received a higher dose of drug in the first three months of treatment. Seven showed no clinical or radiographic changes and TLCO improved with reduction in drug dose. The other three patients developed florid clinical and radiographic features of amiodarone pulmonary toxicity. All three had impaired TLCO before receiving amiodarone. During the course of the prospective study amiodarone pulmonary toxicity was diagnosed in four other patients. Lung tissue was examined in five of the seven patients with clinical toxicity and showed alveolar wall thickening, exudation and interstitial and intra-alveolar fibrosis with prominent 'foamy' macrophages. Electron microscopy of macrophages showed numerous lysosomal multilamellar bodies, which were demonstrated by energy dispersive X-ray analysis to contain iodine, a constituent of the amiodarone molecule. Two of the patients with clinical toxicity died of respiratory failure; the other five showed gradual improvement on withdrawal of the drug and treatment with corticosteroids. Subsequent withdrawal of steroids was associated with clinical and/or functional deterioration in five patients. A separate autopsy study of the lungs of eight patients dying during treatment with amiodarone, but without clinically-recognised toxicity, showed that an alveolitis had been present in two and prominent 'foamy' macrophages were seen in the lungs of six patients. We conclude that clinical and subclinical effects of amiodarone on the lung are common. The clinical syndrome may be easily misdiagnosed as pulmonary oedema. Subclinical changes in lung function are usually reversible, but whether they herald clinical toxicity if treatment is continued without modification is not established. The presence of 'foamy' macrophages may simply reflect exposure to the drug rather than clinically-important toxicity.
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PMID:Amiodarone pulmonary toxicity: clinical and subclinical features. 376 11

Diffuse pulmonary opacification is commonly seen on chest radiographs from infants with severe respiratory failure treated with extracorporeal membrane oxygenation (ECMO). The chest radiographs and clinical records of 18 such infants were reviewed to determine the correlation among degree of abnormality on chest radiograph (as determined by a radiographic score), clinical severity of disease (as measured by ECMO requirements [ECMO flow rate]), and dynamic lung compliance determinations. Increasing lung compliance and decreasing ECMO flow rates correlated well with decreasing (improving) radiographic score. Pathologic changes were mainly those associated with intensive respiratory support and the underlying pulmonary condition. One patient had diffuse pulmonary hemorrhage. Other than bleeding, no distinctive pathologic features could be attributed to therapy with ECMO. We conclude that the degree of pulmonary opacification seen in infants undergoing ECMO therapy is an accurate reflection of markedly decreased lung compliance and lung volumes caused by hyaline membrane formation, pulmonary edema, and atelectasis associated with the various causes of severe respiratory failure.
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PMID:Diffuse pulmonary opacification in infants undergoing extracorporeal membrane oxygenation: clinical and pathologic correlation. 376 98

We used the model of bilateral cervical vagotomy of adult rabbits to cause respiratory failure characterized by pulmonary edema, decreased lung compliance, and atelectasis. We documented an 18-fold increase in radiolabeled albumin leak from the vascular space into alveolar washes of vagotomy vs. sham-operated rabbits (P less than 0.01). Despite a twofold increase in percent of prelabeled saturated phosphatidylcholine secreted (P less than 0.01), the alveolar wash saturated phosphatidylcholine pool sizes were not different. The minimum surface tensions were 19.6 +/- 2.5 vs. 9.4 +/- 2.2 dyn/cm for alveolar washes from vagotomy and control rabbits, respectively (P less than 0.01). The soluble proteins from alveolar washes inhibited the surface tension lowering properties of natural surfactant, whereas those from the control rabbits did not (P less than 0.01). When vagotomy rabbits in respiratory failure were treated with 50 mg natural surfactant lipid per kilogram arterial blood gas values and compliances improved relative to control rabbits. Vagotomy results in alveolar pulmonary edema, and surfactant dysfunction despite normal surfactant pool sizes and respiratory failure. A surfactant treatment can improve the respiratory failure.
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PMID:Respiratory distress and surfactant inhibition following vagotomy in rabbits. 378 84

The perfluorochemical O2-transport fluid, Fluosol-DA 20 percent (PFC), is being clinically evaluated as a volume expander in patients who are unable to receive blood products. Since patients treated with Fluosol-DA may be at risk of developing adult respiratory distress syndrome (ARDS) as a complication of the original disorder for which they were transfused, we examined central hemodynamics and gas exchange in anesthetized O2-ventilated dogs with oleic-acid induced pulmonary edema before and after transfusion with 400 ml of either PFC (n = 5) or whole blood (n = 5). Transfusion produced similar increases in cardiac output, pulmonary and systemic vascular pressures and intrapulmonary shunt in the two groups. Arterial O2 tension, however, fell from 209 +/- 117 to 172 +/- 81 mmHg in the blood transfused group but increased from 219 +/- 145 to 302 +/- 138 mmHg in the PFC group. Arterial O2 content, on the other hand, increased in the blood transfused group due to an increase in hematocrit, but fell with PFC because of hemodilution. This lower total arterial O2 content in the PFC group was, however, compensated for by more efficient O2 transport by the PFC in that the PFC arteriovenous O2 content difference accounted for 26 percent of the total arteriovenous O2 content difference, making it about four times as efficient as hemoglobin in tissue O2 delivery. Fluosol DA, 20 percent, is an effective volume expander in this model of hypoxemic respiratory failure, and it can transport significant amounts of O2 even in the presence of a substantial intrapulmonary shunt.
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PMID:Perfluorochemical artificial blood as a volume expander in hypoxemic respiratory failure in dogs. 381 21

In the present study we investigated the phospholipid composition of small-volume (up to 20 ml) in vivo bronchoalveolar lavage and that of quantitative ex vivo bronchoalveolar lavage. Furthermore, the accuracy of the small-volume lavage in predicting lung disease was evaluated. There was a positive linear correlation (r approximately equal to 0.87-0.91) between the amount of saturated phosphatidylcholine and the saturated phosphatidylcholine/sphingomyelin ratio in quantitative bronchoalveolar lavage. The phospholipid distributions in the small-volume lavage and the quantitative lavage were similar (r approximately equal to 0.78-0.94, n = 14). The overall accuracy of phosphatidylcholine/sphingomyelin ratio and phosphatidylglycerol/total phospholipid ratio in predicting the presence or absence of respiratory failure was 85-87% in newborns, children, and adults. In respiratory diseases without respiratory failure, the abnormalities in the phospholipids were frequent, although less distinct. According to animal experiments the surfactant system is inhibited at the onset of high permeability lung edema. Soon thereafter, the lavageable surfactant pool is decreased. Present findings support the view that surfactant defects are of importance in the pathogenesis of respiratory disease, and that surfactant-oriented therapy may be effective in the treatment and prevention of respiratory failure.
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PMID:Endobronchial surface active phospholipids in various pulmonary diseases. 386 Mar 95

The therapeutic efficacy of continuous positive airway pressure (CPAP) administered by face mask was studied in 40 patients with acute cardiogenic pulmonary edema and respiratory failure. Arterial blood gas values and pH, systemic arterial pressure, heart rate and respiratory rate were measured during administration of 30% oxygen with a high-flow face mask apparatus at ambient airway pressure. Twenty patients were then randomly chosen to continue ambient airway pressure breathing and 20 received 10 cm H2O of CPAP. The measurements were repeated 10, 60 and 180 minutes after therapy was initiated. During the first 10 minutes of CPAP treatment, arterial blood oxygen partial pressure increased 8 +/- 9 mm Hg (mean +/- 1 standard deviation), (p less than 0.01) and respiratory rate decreased 5 +/- 5 breaths/min (p less than 0.001). Systolic arterial pressure decreased 12 +/- 21 mm Hg (p less than 0.05), and heart rate by 10 +/- 11 beats/min (p less than 0.001). A decrease in respiratory rate by 2 +/- 5 breaths/min (p less than 0.05) was the only change that occurred in the control group. The improvement in arterial blood oxygenation persisted throughout the investigation period (p less than 0.05). Thirteen patients (65%) in the control group and 7 patients (35%) in the CPAP group met our criteria for treatment failure during the study (p = 0.068). Thus, CPAP administered by face mask improves gas exchange, decreases respiratory work, unloads circulatory stress, and may reduce the need for ventilator treatment in acute cardiogenic pulmonary edema.
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PMID:Continuous positive airway pressure by face mask in acute cardiogenic pulmonary edema. 388 20

We did two studies to see if severe neutropenia might reduce the severity or delay development of O2-induced lung microvascular injury. First, we treated 11 rabbits with nitrogen mustard until their circulating neurophil count decreased to less than 50/microliters of blood, after which the rabbits breathed pure O2 until death; nine other rabbits received no nitrogen mustard and had normal numbers of circulating neutrophils during O2 breathing. All rabbits died of respiratory failure with pulmonary edema, and although chemotherapy decreased the number of neutrophils in the lungs by greater than 90%, it did not influence survival time or extravascular lung water content. To see if severe neutropenia might slow the development of O2-induced lung microvascular injury, we assessed the effects of sustained hyperoxia on lung fluid balance in unanesthetized lambs treated with hydroxyurea, so that their absolute neutrophil count was less than 50/microliters of blood. We measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma during a 2- to 4-h control period and then daily for 2 to 4 h as the lambs continuously breathed pure O2. After 3 days of hyperoxia, lymph flow doubled and the concentration of protein in lymph increased from 3.3 +/- 0.5 to 4.2 +/- 0.3 g/dl. Tracer studies with 125I-albumin before and 3 days after the start of O2 breathing confirmed the development of increased lung vascular permeability to protein. All lambs died of respiratory failure with pulmonary edema after 3-5 days in O2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen-induced lung microvascular injury in neutropenic rabbits and lambs. 398 Mar 93

Acute respiratory failure caused by infection with Coccidioides immitis is a rare, usually fatal, event. We report 2 patients who survived acute respiratory failure caused by primary pulmonary coccidioidomycosis. We attribute the severity of illness to a large inoculum of organisms. Their treatment included antifungal therapy with amphotericin B and diuresis to decrease noncardiogenic pulmonary edema. Coccidioidomycosis causing respiratory failure may be more frequent than currently clinically appreciated and may result from primary pulmonary coccidioidomycosis, miliary pulmonary disease, or as part of the multisystem organ failure seen in fungemic patients.
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PMID:Acute respiratory failure caused by primary pulmonary coccidioidomycosis. Two case reports and a review of the literature. 400 23

A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported. A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior communicating artery aneurysm on the right side. She showed respiratory failure due to pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of inferolateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypothalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn discharged endogenic catecholamine. This was probably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Furthermore, myocardial oxygen consumption could have been increased by the increase in catecholamine. Finally, it gave rise to neurogenic pulmonary edema and extensive diffuse myocytolysis of the heart occurred.
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PMID:[Myocardial damage (myocytolysis) caused by subarachnoid hemorrhage]. 409 85


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