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

To investigate the hypotheses that activated coagulation, catecholamine release, or arginine vasopressin release are involved in the pathogenesis of high-altitude pulmonary edema (HAPE), we measured these variables in seven subjects susceptible to HAPE and in nine control subjects at an altitude of 1,600 m, and after 6 and 12 h at a simulated altitude of 4,150 m. Each subject was studied twice, once after 3 days of placebo medication and once after 3 days of premedication with aspirin and dipyridamole. At high altitude, HAPE-susceptible subjects showed significantly exaggerated hypoxemia and a slightly higher end-tidal carbon dioxide partial pressure that did not account fully for the hypoxemia. Fibrinolytic activity was significantly accelerated in both groups at high altitude, whereas other coagulation measurements, catecholamines and arginine vasopressin levels, and pulmonary function tests were not significantly changed. Similar findings were obtained after both placebo and platelet-inhibitor premedication. The results indicate that none of the three hypothesized mechanisms, i.e., activated coagulation, excessive catecholamine release, or antidiuresis, would account for HAPE susceptibility. Instead, HAPE-susceptible subjects exhibited exaggerated hypoxemia associated with relative hypoventilation and a widened alveolar-arterial gas pressure difference.
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PMID:Accentuated hypoxemia at high altitude in subjects susceptible to high-altitude pulmonary edema. 45 28

The passage of different-sized marker molecules over the lower respiratory tract into the blood circulation during pulmonary inflammation induced by dextran, endotoxin [i.e., lipopolysaccharide from Escherichia coli (LPS)], or ferritin was assessed in the rat. Bovine immunoglobulin G (BIgG, mol wt = 150,000 Da), bovine serum albumin (BSA, mol wt = 67,000 Da), and the nonapeptide 1-deaminocysteine-8-D-arginine vasopressin (dDAVP, mol wt = 1,067 Da) were used as permeability markers after intratracheal instillation. The pathophysiological indexes of a proceeding lung inflammation were increased total cell number, changed leukocyte proportions and increased total protein content obtained in bronchoalveolar lavage, and lung edema formation shown as an increased lung wet-dry weight difference. Intratracheal instillation of dextran induced a moderate neutrophil invasion into the lungs but had no effect on the passage of the different markers over the lungs (BIgG 1.8 +/- 0.6%, BSA 3.5 +/- 1.2%, dDAVP 26.1 +/- 20.7%) compared with control rats instilled with the markers alone (1.8 +/- 0.4%, 4.1 +/- 1.3%, 20.0 +/- 3.8%, respectively). Endotoxin administration resulted in markedly higher lavage cell counts and lung edema concomitantly with an increased lung passage of the markers (3.2 +/- 0.9%, 22.0 +/- 6.1%, 33.3 +/- 12.0%, respectively; P less than 0.01-P less than 0.001). The highest marker passage was obtained when the inflammation was most severe, i.e., after ferritin administration (17.6 +/- 2.3%, 60.0 +/- 6.7%, 41.6 +/- 6.9%, respectively; P less than 0.001), which resulted in markedly elevated lavage cell numbers and protein content as well as edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lung to blood passage of different-sized molecules during lung inflammation in the rat. 172 3

A diagnosis of acute high-altitude pulmonary edema was made in five male skiers (age, 35.0 +/- 1.8 years) by history and physical examination and was confirmed by a characteristic chest radiogram showing alveolar infiltrates associated with a normal cardiac silhouette. Five healthy age- and sex-matched subjects with similar physical activity at the same altitude served as controls. Plasma sodium was 135.0 +/- 1.5 mmol/L in the acutely ill patients compared with 144.0 +/- 3.3 mmol/L in the controls (P less than 0.025). Mean plasma atrial natriuretic factor immunoreactivity averaged 17.6 +/- 5.6 pmol/L in patients with high-altitude pulmonary edema compared with 6.8 +/- 0.7 pmol/L in the controls at the same altitude (P less than 0.05). Elevated atrial natriuretic factor levels normalized to 7.5 +/- 1.9 pmol/L (P less than 0.05) during recovery in Denver (altitude, 1600 meters) 24 hours later. Plasma arginine vasopressin levels were 1.8 +/- 0.37 pmol/L in patients with high-altitude pulmonary edema at diagnosis compared with 0.92 +/- 0.28 pmol/L in controls (P = 0.07). The inappropriately elevated arginine vasopressin levels decreased to 1.29 +/- 0.37 pmol/L during recovery (P less than 0.025), but the lowered plasma sodium concentration had not normalized by discharge within 24-hours of transfer to Denver and averaged 135.8 +/- 1.2 mmol/L. The pathophysiologic implications of these findings are discussed.
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PMID:Elevated plasma atrial natriuretic factor and vasopressin in high-altitude pulmonary edema. 297 74

Congestive heart failure (CHF) from ischemic cardiomyopathy has emerged as an epidemic health problem. The pathogenesis of CHF is characterized by heightened activity of many neuroendocrine factors, including norepinephrine, angiotensin II, and arginine vasopressin, which lead to heightened systemic vascular resistance and further impedance of left ventricular ejection. Once CHF reaches New York Heart Association (NYHA) class III or IV with heightened activity of the many neurohumoral factors, it tends to be refractory to conventional therapy of vasodilators, inotropic agents, and diuretics. Treatment of refractory CHF appears to require a break in the neurohumoral hemodynamic vicious cycle, and ultrafiltration appears able to produce this interruption. Ultrafiltration has been shown to be successful in patients with NYHA class III to VI CHF and urine output less than 1,000 mL/d. It relieves pulmonary edema, reduces ascites and peripheral edema, and enhances the response to subsequent diuretic therapy. In patients with refractory CHF, the ability to provide adequate volume removal, thus improving overall volume status, normalizing filling pressures, and reducing clinical symptoms, offers an improvement in overall quality of life. Early results have shown that ongoing therapy actually may be associated with decreased hospital readmissions or, at the very least, shortened intensive care unit length of stay.
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PMID:Refractory congestive heart failure: overview and application of extracorporeal ultrafiltration. 881 23

Exercise-associated hyponatremia (EAH) has emerged in recent years as a life-threatening complication of endurance sports that may lead to fatal cerebral and pulmonary edema. Defined as a serum sodium concentration <135 mEq/L (1 mEq/L = 1 mmol/L), symptomatic EAH is a dilutional hyponatremia with abnormal fluid retention mediated by decreased urine production, which is a variant of the syndrome of inappropriate antidiuretic hormone secretion. Strategies for prevention and treatment must take into account the pathophysiology underlying this dominant clinical paradigm. Beyond educating runners to drink moderately, monitoring changes in body weight during endurance sports may facilitate the early detection of positive fluid balance characteristic of symptomatic cases. Rapid diagnosis by point-of-care testing indicates the need for fluid restriction in mild cases and emergent treatment with hypertonic (3%) NaCl to reverse acute hypotonic encephalopathy. The efficacy of arginine vasopressin V(2) receptor antagonists warrants study as an alternative treatment to loop diuretics for volume overload in these patients. Nonosmotic stimulation of arginine vasopressin secretion may be mediated in part by enhanced release of muscle-derived interleukin-6 during glycogen depletion, linking exertional rhabdomyolysis to the pathogenesis of EAH.
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PMID:Exercise-associated hyponatremia: role of cytokines. 1684 89

Disorders of serum sodium occur commonly in athletes participating in endurance sports. The most life-threatening of these is hyponatremia, which can occur in as many as 2% to 7% of participants. Exercise-associated hyponatremia (EAH) is caused by a combination of excessive water or hypotonic fluid intake as well as high levels of arginine vasopressin, which limits the ability of the kidney to excrete water. Other factors in the pathogenesis of EAH include sweat sodium loss, inability to mobilize exchangeable sodium stores, metabolic water production, and impaired renal blood flow and glomerular filtration rate. Most cases of EAH lead to minimal or absent complications and do not require specific therapy other than close monitoring and fluid restriction. However, a small number of athletes may present with severe and life-threatening hyponatremia associated with cerebral edema and possibly noncardiogenic pulmonary edema. Rapid diagnosis and appropriate therapy of these athletes with hypertonic saline is required to prevent severe complications or death.
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PMID:Exercise-associated hyponatremia. 1952 74

Exercise-associated hyponatremia is hyponatremia occurring during or up to 24 hours after prolonged exertion. In its more severe form, it manifests as cerebral and pulmonary edema. There have now been multiple reports of its occurring in a wilderness setting. It can now be considered the most important medical problem of endurance exercise. The Second International Exercise-Associated Hyponatremia Consensus Conference gives an up-to-date account of the nature and management of this disease. This article reviews key information from this conference and its statement. There is clear evidence that the primary cause of exercise-associated hyponatremia is fluid consumption in excess of that required to replace insensible losses. This is usually further complicated by the presence of inappropriate arginine vasopressin secretion, which decreases the ability to renally excrete the excess fluid consumed. Women, those of low body weight, and those taking nonsteroidal anti-inflammatory drugs are particularly at risk. When able to be biochemically diagnosed, severe exercise-associated hyponatremia is treated with hypertonic saline. In a wilderness setting, the key preventative intervention is moderate fluid consumption based on perceived need ("ad libitum") and not on a rigid rule. (Editor's Note: This paper was written at my request in an effort to increase awareness of this important clinical entity among members of the wilderness community, many of whom are involved in activities that place them at risk of its development. I thank the authors for their diligent efforts.)
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PMID:Exercise-associated hyponatremia: overzealous fluid consumption. 2083 13

The term ''adrenergic'' originates from ''adrenaline'' and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ''fight-flight response'' is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.
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PMID:Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress. 2750 1

Exercise-associated hyponatremia (EAH) is hyponatremia that occurs <or= 24 hours after prolonged physical activity. It is a potentially serious complication of marathons, triathlons, and ultradistance events, and can occur in hot and cold environments. Clear evidence indicates that EAH is a dilutional hyponatremia caused by excessive fluid consumption and the inappropriate release of arginine vasopressin. Cerebral and pulmonary edema can cause serious signs and symptoms, including altered mental status, respiratory distress, seizures, coma, and death. Rapid diagnosis and urgent treatment with hypertonic saline is necessary to prevent severe complications or death. Prevention is based on educating athletes to avoid excessive drinking before, during, and after exercise.
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PMID:Exercise-associated hyponatremia during winter sports. 2042 7

A 20-year-old female presented with confusion, generalized tonic-clonic seizures, and severe hyponatremia after ingesting 3,4-methylenedioxymethamphetamine (MDMA). Brain computed tomography (CT) demonstrated cerebral edema. Her hospital course was rapidly complicated by respiratory failure and shock requiring intubation and vasopressors. Refractory acute respiratory distress syndrome (ARDS) was diagnosed which was unresponsive to conventional and salvage therapies, requiring initiation of extracorporeal membrane oxygenation (ECMO), leading to normalization of oxygenation parameters. Hyponatremia was corrected and the encephalopathy resolved. The patient was decannulated and extubated after three days. MDMA-induced hyponatremia is hypothesized to result from enhanced serotonergic activity and arginine vasopressin (AVP) release in the brain leading to hyperthermia-induced polydipsia and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. A common but often unrecognized complication of severe hyponatremia is the Ayus-Arieff syndrome where cerebral edema causes neurogenic pulmonary edema via centrally mediated increases in catecholamine release and capillary injury. For our patient, ECMO was required for three days while the hyponatremia was corrected which led to rapid clearing of the cerebral edema and neurogenic pulmonary edema. This case illustrates that, in selecting patients with refractory ARDS from MDMA-associated cerebral and pulmonary edema, ECMO may be a temporizing and life-saving modality of treatment.
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PMID:A Case of MDMA-Associated Cerebral and Pulmonary Edema Requiring ECMO. 2927 Mar 22


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