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

Pulmonary artery wedge and plasma colloid osmotic pressures and their relationship to pulmonary edema were investigated in 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema. In the absence of pulmonary edema, both the pulmonary artery wedge pressure and plasma colloid osmotic pressure were in normal range; after onset pulmonary edema, a moderate increase in pulmonary wedge pressure and reduction in plasma colloid osmotic pressure were observed. When the gradient between the plasma colloid osmotic pressure and the pulmonary artery wedge pressure was calculated, highly significant differences were demonstrated (P less than 0.002). In the absence of pulmonary edema, this gradient averaged 9.7 (plus or minus 1.7 SEM) torr; following appearance of pulmonary edema, it was reduced to 1.2 (plus or minus 1.3) torr. During therapy with digoxin and furosemide, reversal of pulmonary edema was closely related to a concomitant change in the colloid osmotic-hydrostatic pressure gradient. These observations indicate that both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure may follow the onset of pulmonary edema. Such decline in colloid osmotic pressure and especially the reduction in colloid osmotic-hydrostatic capillary pressure gradient may favor transudation of fluid into the lungs.
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PMID:Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction. 23 2

The effect of 10 cm H2O of positive end-expiratory pressure (PEEP) on pulmonary extravascular water volume (PEWV) was measured in an animal model of noncardiogenic pulmonary edema. Three groups of animals were studied: (1) controls, (2) those given a saline infusion plus alloxan, and (3) those which received saline infusion plus alloxan and PEEP. All animals were ventilated with a constant volume ventilator. Mean PEWV (+/- SEM) in milliliters per gram of dry lung weight was 4.00 +/- 0.21 for group 1, 6.01 +/- 0.70 for group 2, and 5.77 +/- 0.83 for group 3. Mean PEWV increased significantly in both alloxan groups (groups 2 and 3) as compared to the control group (for both, p less than 0.05); however, PEWV did not differ significantly in the group that received PEEP, as compared to the group ventilated without PEEP. Arterial PO2 and airway pressure required to deliver a constant tidal volume did not change significantly in the experimental groups as compared to the control group. It was concluded that PEEP does not decrease lung water content in pulmonary edema caused by damage to fluid-exchanging vessels.
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PMID:Failure of positive end-expiratory pressure to decrease lung water content in alloxan-induced pulmonary edema. 38 15

Noncardiogenic pulmonary edema has been reported to follow the intravenous use of ethchlorvynol (Placidyl) in both human clinical and animal experimental situations. In a further attempt to define ethchlorvynol-pulmonary tissue inter-relations, we measured ethchlorvynol concentrations in venous and arterial blood and lung and liver tissue of dogs after intravenous injection of 15 to 25 mg of the drug per kg of body weight. In 10 dogs, the mean +/- SEM lung concentrations 1, 3, and 5 min after injection were 70 +/- 20, 50 +/- 13, and 24 +/- 9 mug per g of tissue, respectively. Simultaneous mean +/- SEM venous contrations were 75 +/- 40, 29+/-5, and 22 +/- 5 mug per ml of blood, respectively. During minutes 1 and 3, the liver concentrations were lower than those found in the lung. In an additional 3 dogs, injection of ethchlorvynol into the portal vein led to higher concentrations (at all sample times) in the liver when compared to the lung. In vitro lung slice studies using ethchlorvynol labeled with iodine-131 revealed no active energy-dependent uptake. Intravenously administered ethchlorvynol rapidly fluxes into and out of lung tissue, apparently following the laws of diffusion.
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PMID:Pulmonary tissue concentrations of ethchlorvynol after intravenous injection. 83 95

The relationship of colloid osmotic pressure (COP) to pulmonary edema and mortality in 128 critically ill patients was investigated in our critical care unit, and confirms previously reported observations. The COP in the 86 survivors was 22.0 (+/- 0.4 SEM) mm Hg versus 17.2 (+/- 0.6 SEM) mm Hg in the 42 who died (P less than 0.001). The patients were divided into three groups: 71 with no pulmonary edema, COP of 21.5 (+/- 0.5 SEM) mm Hg; 40 with cardiogenic pulmonary edema, COP of 21.4 (+/- 0.4 SEM) mm Hg; and 17 with noncardiogenic pulmonary edema, COP OF 13.6 (+/- 0.8 SEM) mm Hg. Colloid osmotic pressure was significantly lower in patients with noncardiogenic pulmonary edema (P less than 0.001). In 36 patients in whom pulmonary artery wedge pressures (PWP) were available, a COP-PWP gradient of 4.0 mm Hg or less was always associated with pulmonary edema, while a COP-PWP gradient greater than 4.0 mm Hg was never associated with pulmonary edema. Colloid osmotic pressure is a useful prognostic indicator of pulmonary edema and mortality in the critically ill.
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PMID:Colloid osmotic pressure as a prognostic indicator of pulmonary edema and mortality in the critically ill. 92 5

To see whether antihistamines could prevent and reverse histamine-induced pulmonary edema and increased lung vascular permeability, we compared the effects of a 4-h intravenous infusion of 4 mug/kg per min histamine phosphate on pulmonary hemodynamics, lung lymph flow, lymph and plasma protein content, arterial blood gases, hematocrit, and lung water with the effects of an identical histamine infusion given during an infusion of diphenhydramine or metiamide on the same variables in unanesthetized sheep. Histamine caused lymph flow to increase from 6.0+/-0.5 to 27.0+/-5.5 (SEM) ml/h (P less than 0.05), lymph; plasma globulin concentration ratio to increase from 0.62+/-0.01 to 0.67+/-0.02 (P less than 0.05), left atrial pressure to fall from 1+/-1 to -3+/-1 cm H2O (P less than 0.05), and lung lymph clearance of eight protein fractions ranging from 36 to 96 A molecular radius to increase significantly. Histamine also caused increases in lung water, pulmonary vascular resistance, arterial PCO2, pH, and hematocrit, and decreases in cardiac output and arterial PO2. Diphenhydramine (3 mg/kg before histamine followed by 1.5 mg/kg per h intravenous infusion) completely prevented the histamine effect on hematocrit, lung lymph flow, lymph protein clearance, and lung water content, and reduced histamine effects on arterial blood gases and pH. 6 mg/kg diphenhydramine given at the peak histamine response caused lymph flow and lymph: plasma protein concentration ratios to fall. Metiamide (10 mg/kg per h) did not affect the histamine lymph response. We conclude that diphenhydramine can prevent histamine-induced pulmonary edema and can prevent and reverse increased lung vascular permeability caused by histamine, and that histamine effects on lung vascular permeability are H1 actions.
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PMID:Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability. 95 73

We have previously demonstrated that reperfusion of a rabbit lung in vivo after 24 h of unilateral pulmonary artery occlusion results in edema, transient leukopenia, and intravascular leukocyte aggregation. We hypothesized that complement was activated by reperfusion and that this in turn contributed to lung injury. In the preliminary phase of the study, we found that ischemia followed by reperfusion resulted in a drop in C3 to 15 +/- 10% (mean +/- SEM) of the prereperfusion value as compared with no change in a group of control animals that had undergone an identical thoracotomy but without pulmonary artery occlusion and reperfusion (p less than 0.05). We then studied three groups of animals to determine if complement depletion with cobra venom factor (CVF) prior to ischemia and reperfusion would prevent the injury. Rabbits treated with CVF but without occlusion and reperfusion did not develop significant lung edema, with left and right lung wet/dry ratios of 5.32 +/- 0.11 and 5.26 +/- 0.12, respectively. For rabbits that were not treated with CVF but underwent ischemia and reperfusion, the comparable numbers were 6.15 +/- 0.36 and 5.19 +/- 0.32 (p less than 0.05 for right versus left). For CVF-treated rabbits that underwent ischemia and reperfusion, the right/left difference persisted (6.77 +/- 0.48 versus 5.35 +/- 0.14, p less than 0.01). Immunocytochemistry documented C3 deposition in non-CVF rabbits that underwent ischemia and reperfusion but not in CVF-treated rabbits. We conclude that ischemia/reperfusion of the lung results in complement activation, but it is not a complement-dependent injury.
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PMID:Complement activation is a secondary rather than a causative factor in rabbit pulmonary artery ischemia/reperfusion injury. 199 Sep 58

Reduced oxygen tension is regarded as the primary physiologic signal for the production of erythropoietin (EPO). There is little information available about early changes of EPO production in man due to severe hypoxia. The purpose of the present study was to examine the time course of EPO in serum of patients with acute cardiogenic pulmonary edema (ACPE). In 29 patients (seventy-five +/- six years, mean age +/- SEM) who were hospitalized within two hours after onset of symptoms of ACPE, serum EPO concentrations were monitored for up to seventy-two hours. At the moment of admission all patients showed significantly increased EPO concentrations of 121 +/- 64 mU/mL (mean +/- SEM) compared with a healthy population (15-35 mU/mL). Twenty-three patients who recovered within thirty minutes (group A) exhibited a quick return of their EPO serum levels to normal. The remaining 6 patients (group B) had a protracted clinical course and their EPO concentration showed a further increase up to the end of the observation period. The comparative monitoring of concentrations of alpha-1-proteinase inhibitor, antithrombin III, C-reactive protein, fibronectin, hapotoglobin, and transerrin in serum and plasma revealed no significant changes. Thus a major contribution of fluid shifts into or from the intravascular compartment to the observed changes in EPO concentration seems to be unlikely. The data suggest that the production and release of EPO in the kidneys due to altered oxygen delivery is a fast-responding mechanism.
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PMID:Serum-erythropoietin concentration during acute cardiogenic pulmonary edema. 201 19

Positive end expiratory pressure (PEEP) is an accepted treatment for children with acute respiratory failure secondary to restrictive lung diseases. Using a simple technique based on open circuit nitrogen washout, we determined the functional residual capacity (FRC) in 25 ventilated children (age 3 wk-10 y) with acute respiratory failure secondary to restrictive lung disease (pulmonary edema, bilateral pneumonia). FRC measured at a physiologic level of PEEP (2-4 cm H2O) was 45.0 +/- 3.6% (mean +/- SEM; range 12-80%) lower than normal predicted values. At the PEEP level chosen clinically (4-10 cm H2O, mean = 6.0), the FRC was below normal predicted values for nonintubated children by a mean of 31.8% (range 0-73%) (p = 0.0001) and only seven patients (28%) had FRC within 20% below predicted normal values. FRC normalized at PEEP levels of 6-18 cm H2O (mean = 11.6), which was up to 200% above the clinically chosen PEEP level. In six children without lung disease who were ventilated at a PEEP level of 2-4 cm H2O, the FRC was within normal range in two, but significantly higher (by 45%) in the other four. We conclude that FRC in ventilated children with acute restrictive lung disease is significantly lower than normal and the clinically chosen PEEP fails to normalize the FRC in most of the cases.
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PMID:Functional residual capacity in ventilated infants and children. 225 67

The Extra Vascular Lung Water (EVLW) was measured using the thermal sodium double indicator dilution technique in 21 patients undergoing surgery for esophageal cancer. This measurement is an important parameter in the control of the respiratory function. In the 16 cases without pulmonary complications, the preoperative EVLW was 5.3 +/- 0.2 (mean +/- SEM) ml/kg and the immediate postoperative EVLW was 4.8 +/- 0.4 ml/kg. This change was significant (p less than 0.05), but within 24 hours the EVLW returned to almost the same levels as those recorded before surgery. In only 3 cases, the EVLW were elevated beyond 7.5 ml/kg, but these high EVLW levels did not continue for more than 12 hours. Of the 5 patients with pulmonary complications, only two experienced pulmonary edema. Their preoperative EVLW levels were normal, but the immediate postoperative EVLW levels were significantly elevated beyond 10 ml/kg. These elevated levels were observed before the PaO2, the portable chest roentgenograms and the other test results changed following surgery. The high EVLW levels beyond 7.5 ml/kg continued for 72 hours after surgery. We found no correlation between the EVLW and measureable hemodynamic parameters (Cardiac Index, Pulmonary Wedge Pressure, Colloid Osmotic Pressure-Pulmonary Wedge Pressure gradient) during the observation period. In the other cases with pulmonary complications (2 cases were pneumonia, one was atelectasis with pneumonia), the changes in the EVLW levels were the same as for the cases without pulmonary complications. These results indicate that the EVLW is the optimum parameter for the control of the respiratory function and early diagnosis of pulmonary edema after surgery for esophageal cancer.
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PMID:[The measurement of extra vascular lung water using a thermal-sodium double indicator dilution technique in patients undergoing surgery for esophageal cancer]. 228 95

Amiodarone (ADR), a new antiarrhythmic drug for life-threatening cardiac arrhythmias, causes pneumonitis or lung fibrosis in a sizeable minority of patients. The cause of lung damage is not known. We have shown that infusion of 10 mg amiodarone into the inflow circuit of ventilated and perfused rabbit lungs causes immediate increase in pulmonary artery pressure (mean +/- SEM) (from 13.6 +/- 1.2 to 40.6 +/- 9.5 mm Hg, p less than 0.01) and pulmonary edema with marked increase in the pulmonary generation of thromboxane and leukotrienes C4 and/or D4. Albumin (2 g%) in the perfusate prevents any increase in lung perfusion pressure or edema formation. When lung perfusion pressure increase is blocked with the combined cyclooxygenase and lipoxygenase inhibitor enolicam sodium (CG5391B, 35 microM in perfusate), significant lung edema still occurs after amiodarone, indicating that amiodarone causes increased alveolar-capillary membrane permeability. Addition of catalase (100 U/ml) or superoxide dismutase and catalase (100 U/ml each) to perfusate fails to protect from amiodarone lung injury. Immediate infusion of amiodarone (10 mg) into lungs ventilated with room air (ADR + RA) causes an increase in lung weight gain from baseline (delta W) of 5.7 +/- 1.5 g/min. Compared with ADR + RA, ventilation of lungs with 4% O2 (delta W = 0.7 +/- 0.3 g/min, p less than 0.05), pretreatment of rabbits for 3 days with butylated hydroxyanisole (BHA, 100 mg/kg/day i.p., delta W = 0.05 +/- 0.02 g/min, p less than 0.01), pretreatment of rabbits for 3 days with vitamin E (Vit E, 300 U/day orally, delta W = 0.6 +/- 0.2 g/min, p less than 0.05), or addition of N-acetylcysteine to the lung perfusate (NAC, 5 mM, delta W = 0.1 +/- 0.08 g/min, p less than 0.01) all protect from lung edema formation after amiodarone. Amiodarone (100 mg) also caused a marked increase in luminol-enhanced lung chemiluminescence, lung production of superoxide anion (O2-), and tissue levels of lung glutathione disulfide. These results suggest that amiodarone causes lung injury by an oxidant mechanism.
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PMID:Amiodarone causes acute oxidant lung injury in ventilated and perfused rabbit lungs. 245 31


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