Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47-year-old man with a history of industrial exposure and interstitial lung disease was admitted for acute pulmonary decompensation. Clinical course was characterized by severe dyspnea at rest, fever, hypoxemia, and elevated pulmonary arterial pressures. At autopsy, pulmonary problems were explained by a selective veno-occlusive process. Associated with pulmonary phlebitis was cerebral vasculitis and lymph node enlargement with erythrophagocytosis suggesting underlying viral infection. Pulmonary veno-occlusive disease should be considered in cases of pulmonary fibrosis, pulmonary hypertension with cor pulmonale, and pulmonary edema and congestion with normal left atrial pressures.
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PMID:Pulmonary veno-occlusive disease. Morphological changes suggesting a viral cause. 725 18

The pharmacodynamic effects (changes of systolic time intervals, STI, reaction of pulmonary arterial pressure) of digitoxin were studied in 7 patients with severe congestive heart failure in comparison with the corresponding plasma level. STI indicated glycoside-dependent changes, i.e. shortening of LVETc and QS2c and normalization of prolonged PEPc, while ICT shortening was less observed. In 2 patients with cor pulmonale a pulmonary oedema occurred accompanied with prolonged LVETc. During the early period of glycoside-dependent recompensation no significant correlation between STI shortening and glycoside plasma level was observed. Because of the retarded normalization of the haemodynamics of the pulmonary circulation and because of possible side-effects, rapid digitalization has to be reconsidered.
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PMID:Problems of rapid digitalization in severe congestive heart failure. 736 26

Respiratory insufficiency is one of the most common and most serious complications of the postoperative period. Preexisting risk factors include cardiopulmonary disease, significant smoking history, obesity and advanced age. The risk of postoperative respiratory insufficiency is increased in emergency surgical procedures (particularly those related to trauma), procedures involving the chest or upper abdomen and procedures requiring prolonged anesthesia. Postoperatively, prolonged sedation or neuromuscular blockade, cardiovascular instability, respiratory problems and immobilization are important risk factors. Common clinical causes of respiratory insufficiency are atelectasis, aspiration, pulmonary edema and pulmonary embolism. Management strategies are directed at treatment of the cause of the insufficiency and restoration of pulmonary function. All surgical patients should be carefully assessed before surgery, monitored closely during and after the procedure, and aggressively treated to prevent or correct respiratory insufficiency.
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PMID:Postoperative respiratory insufficiency. 773 49

Pulmonary hypertension may occur in the antiphospholipid syndrome as a result of recurrent pulmonary embolism or microthrombosis of pulmonary vessels. We describe 3 cases of primary antiphospholipid syndrome (APS) and cor pulmonale that fulfilled the criteria for chronic major vessel thromboembolic pulmonary hypertension. Pulmonary thromboendarterectomy was performed in all 3 patients and it was successful in 2. One patient died in the immediate postoperative period from hemorrhagic pulmonary edema. Chronic thromboembolic pulmonary hypertension should be added to the list of pulmonary vascular complications of primary APS. Despite its risk, pulmonary thromboendarterectomy represents a treatment option for this otherwise lethal condition.
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PMID:Primary antiphospholipid syndrome presenting as chronic thromboembolic pulmonary hypertension. Treatment with thromboendarterectomy. 873 Jan 45

The purpose of the present study is twofold: to evaluate alterations in total phospholipid content and individual phospholipid classes of the surfactant, and to detect markers of inflammatory reaction in bronchoalveolar lavage (BAL) from patients with hydrostatic pulmonary edema (HPE). Mechanically ventilated patients with HPE (Group 1) were compared with mechanically ventilated patients without cardiopulmonary disease (Group 2), considered as the control group. Group 3, including patients with high-permeability pulmonary edema, was used for further comparison. BAL was obtained and immediately cooled at 4 degrees C. Total proteins, albumin, and platelet-activating factor--acetylhydrolase (PAF-AcH) were measured. Total lipids were extracted and analyzed after thin-layer chromatographic separation. PAF was determined with bioassay. Total BAL proteins and albumin were found significantly higher in patients with HPE compared with control, but were lower compared with adult respiratory distress syndrome (ARDS). PAF was elevated in patients with HPE and ARDS, whereas in the control group it was actually in nondetectable levels. PAF was significantly higher in ARDS than in HPE patients. BAL neutrophils concentration was higher in HPE compared with control, but lower compared with ARDS. There was an inverse correlation between PAF-AcH and PAF. Quantitative reduction of total BAL phospholipids (PL) and qualititative deficiency was observed in both patients with HPE and ARDS. The findings of this study suggest that there is evidence of inflammation in the airspaces of patients with HPE.
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PMID:Proteins and phospholipids in BAL from patients with hydrostatic pulmonary edema. 911 30

Individuals with preexisting cardiopulmonary disease are thought to be more susceptible to acute episodes of particulate pollution resulting in increased morbidity and mortality. Our study was designed to evaluate particle fate and macrophage function in an animal model of monocrotaline (MCT)-induced pulmonary hypertension. Two weeks following a single MCT injection, Sprague-Dawley rats were exposed sequentially to two different colored fluorescent microspheres 1.0 micron in diameter by aerosolization. Morphometric evaluation of lung sections was performed 0 and 24 h following the final particle exposure to determine the intrapulmonary location of inhaled microspheres. A decrease in the number of particles phagocytized by alveolar macrophages and an increase of free particles overlying the epithelium were found in MCT-treated animals compared with control. Pulmonary macrophages recovered by bronchoalveolar lavage were evaluated for chemotactic and phagocytic ability. Macrophage chemotaxis was significantly impaired following MCT treatment compared with controls, whereas phagocytic activity of macrophages lavaged from MCT and control treatment groups was similar. Macrophages were stained for filamentous (F) and globular (G) actin using Texas-Red-labeled phalloidin and Oregon-green-labeled DNase I, respectively. The area of microfilament staining for F and G actin increased, but the ratio of F/G actin was significantly decreased in animals with MCT treatment compared with control. While the responses observed with MCT treatment, such as pulmonary edema, polymorphonuclear leukocytes influx, and unique macrophage morphology may contribute to impaired macrophage function, the change in microfilament arrangement suggests that MCT may inhibit macrophage chemotaxis and impair particle clearance from the lungs.
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PMID:Alteration in lung particle translocation, macrophage function, and microfilament arrangement in monocrotaline-treated rats. 987 97

Compared with open procedures, laparoscopic surgery is safe with a low incidence of complications. In rare circumstances, however, intraoperative complications such as acute pulmonary edema have been reported. The patient described herein is a 59-year-old woman with obesity, gastroesophageal reflux disease, and chronic obstructive pulmonary disease who developed acute congestive heart failure (CHF) and cardiomegaly immediately following laparoscopic cholecystectomy. She required emergent reintubation, diuresis, and admission to the intensive care unit for postoperative mechanical ventilation. Potential causes of pulmonary edema associated with laparoscopic surgery (extreme Trendelenburg position, venous carbon dioxide embolism, absorption of crystalloid irrigation fluid, cardiopulmonary disease, adverse drug reactions, negative pressure [postobstructive pulmonary edema]) were considered. A process of exclusion revealed that the hemodynamic changes induced by insufflation with an intra-abdominal pressure of 20 mm Hg were the most likely causes of the CHF. Suggestions to prevent occurrence of CHF are tight control of hemodynamics with use of invasive monitoring in high-risk patients and gentle, slow insufflation of the abdomen to an intra-abdominal pressure of 15 mm Hg or less. Intraoperative and/or postoperative CHF should be treated with diuretics, intravenous nitroglycerin, arterial vasodilators, and/or inotropic agents as needed.
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PMID:Acute congestive heart failure after laparoscopic cholecystectomy: a case report. 1277 45

In pulmonary hypertension right ventricular pressure overload leads to abnormal left ventricular (LV) diastolic function. Acute high-altitude exposure is associated with hypoxia-induced elevation of pulmonary artery pressure particularly in the setting of high-altitude pulmonary edema. Tissue Doppler imaging (TDI) allows assessment of LV diastolic function by direct measurements of myocardial velocities independently of cardiac preload. We hypothesized that in healthy mountaineers, hypoxia-induced pulmonary artery hypertension at high altitude is quantitatively related to LV diastolic function as assessed by conventional and TDI Doppler methods. Forty-one healthy subjects (30 men and 11 women; mean age 41 +/- 12 yr) underwent transthoracic echocardiography at low altitude (550 m) and after a rapid ascent to high altitude (4,559 m). Measurements included the right ventricular to right atrial pressure gradient (DeltaP(RV-RA)), transmitral early (E) and late (A) diastolic flow velocities and mitral annular early (E(m)) and late (A(m)) diastolic velocities obtained by TDI at four locations: septal, inferior, lateral, and anterior. At a high altitude, DeltaP(RV-RA) increased from 16 +/- 7 to 44 +/- 15 mmHg (P < 0.0001), whereas the transmitral E-to-A ratio (E/A ratio) was significantly lower (1.11 +/- 0.27 vs. 1.41 +/- 0.35; P < 0.0001) due to a significant increase of A from 52 +/- 15 to 65 +/- 16 cm/s (P = 0.0001). DeltaP(RV-RA) and transmitral E/A ratio were inversely correlated (r(2) = 0.16; P = 0.0002) for the whole spectrum of measured values (low and high altitude). Diastolic mitral annular motion interrogation showed similar findings for spatially averaged (four locations) as well as for the inferior and septal locations: A(m) increased from low to high altitude (all P < 0.01); consequently, E(m)/A(m) ratio was lower at high versus low altitude (all P < 0.01). These intraindividual changes were reflected interindividually by an inverse correlation between DeltaP(RV-RA) and E(m)/A(m) (all P < 0.006) and a positive association between DeltaP(RV-RA) and A(m) (all P < 0.0009). In conclusion, high-altitude exposure led to a two- to threefold increase in pulmonary artery pressure in healthy mountaineers. This acute increase in pulmonary artery pressure led to a change in LV diastolic function that was directly correlated with the severity of pulmonary hypertension. However, in contrast to patients suffering from some form of cardiopulmonary disease and pulmonary hypertension, in these healthy subjects, overt LV diastolic dysfunction was not observed because it was prevented by augmented atrial contraction. We propose the new concept of compensated diastolic (dys)function.
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PMID:Impact of acute hypoxic pulmonary hypertension on LV diastolic function in healthy mountaineers at high altitude. 1460 53

The causes of obstruction to airflow in the pediatric upper airway include craniofacial disorders, subglottic stenosis, choanal atresia, syndromes associated with neuromuscular weakness, and the most common, hypertrophy of the tonsils and adenoids. Abnormal breathing can adversely affect craniofacial growth, and abnormal craniofacial development can promote upper airway obstruction. Chronic upper airway obstruction often presents with evidence of obstructive sleep apnea syndrome; in severe cases these children also present with pulmonary hypertension and cor pulmonale. The development of pulmonary hypertension and right heart dysfunction from chronic upper airway obstruction is complex. Hypoxemia and hypercarbia-induced respiratory acidosis are potent mediators of pulmonary vasoconstriction that can lead to reversible and irreversible chronic changes in the pulmonary vasculature. It is likely that production of various neurohumoral factors in response to hypoxemia and respiratory distress may further promote pulmonary hypertension, right ventricular dysfunction, and consequent impairment of systemic cardiac output. The anesthetic considerations for children undergoing adenotonsillectomy for chronic airway obstruction are significant. These children are at high risk for complications such as laryngospasm, desaturation, stimulation of pulmonary hypertension and cardiac dysfunction, pulmonary edema, postoperative upper airway obstruction, and respiratory arrest. Because of underlying condition(s) (facial abnormalities, neuromuscular disease, etc.), successful adenotonsillar surgery may not improve upper airway obstruction significantly, especially in the immediate postoperative period when edema, bleeding and the effects of anesthetics and analgesics are present.
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PMID:Chronic upper airway obstruction and cardiac dysfunction: anatomy, pathophysiology and anesthetic implications. 1471 77

Humans encounter hypoxia throughout their lives. This occurs by destiny in utero, through disease, and by desire, in our quest for altitude. Hypoxic pulmonary vasoconstriction (HPV) is a widely conserved, homeostatic, vasomotor response of resistance pulmonary arteries to alveolar hypoxia. HPV mediates ventilation-perfusion matching and, by reducing shunt fraction, optimizes systemic Po(2). HPV is intrinsic to the lung, and, although modulated by the endothelium, the core mechanism is in the smooth muscle cell (SMC). The Redox Theory for the mechanism of HPV proposes the coordinated action of a redox sensor (the proximal mitochondrial electron transport chain) that generates a diffusible mediator [a reactive O(2) species (ROS)] that regulates an effector protein [voltage-gated potassium (K(v)) and calcium channels]. A similar mechanism for regulating O(2) uptake/distribution is partially recapitulated in simpler organisms and in the other specialized mammalian O(2)-sensitive tissues, including the carotid body and ductus arteriosus. Inhibition of O(2)-sensitive K(v) channels, particularly K(v)1.5 and K(v)2.1, depolarizes pulmonary artery SMCs, activating voltage-gated Ca(2+) channels and causing Ca(2+) influx and vasoconstriction. Downstream of this pathway, there is important regulation of the contractile apparatus' sensitivity to calcium by rho kinase. Controversy remains as to whether hypoxia decreases or increases ROS and which electron transport chain complex generates the ROS (I and/or III). Possible roles for cyclic adenosine diphosphate ribose and an unidentified endothelial constricting factor are also proposed by some groups. Modulation of HPV has therapeutic relevance to cor pulmonale, high-altitude pulmonary edema, and sleep apnea. HPV is clinically exploited in single-lung anesthesia, and its mechanisms intersect with those of pulmonary arterial hypertension.
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PMID:Hypoxic pulmonary vasoconstriction. 1559 9


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