Acute pulmonary edema.
Fluid movement from the pulmonary capillaries into the interstitial space occurs continuously and is drained by the lymphatics. With increased leakage or decreased clearance, excessive extravascular lung water accumulates, initially as interstitial edema and subsequently as alveolar edema. The most common cause of pulmonary edema is an increase in microvascular hydrostatic pressure. An increased permeability of the capillaries is the other mechanism of production of pulmonary edema. An acute, critical reduction in colloid osmotic pressure may play a contributory role in pulmonary edema even at normal hydrostatic pressures. Dyspnea, diaphoresis, and anxiety characterize the clinical picture. A history of heart disease and congestive heart failure may be present in CPE, whereas evidence of an inciting event or disease process suggests NCPE. Hypoxia, decreased lung compliance, and increased shunt fraction are seen in both types of pulmonary edema, but the duration of pulmonary edema tends to be more severe and prolonged in NCPE. Evidence of increased permeability in NCPE distinguishes it from CPE. Clinically, this is assumed when pulmonary edema is demonstrated at normal PCWP and when edema fluid protein concentration and COP are close to those of plasma. The management of pulmonary edema consists of the improvement of gas exchange by methods that range from supplemental oxygen administration to mechanical ventilatory support with PEEP, depending on the severity of the disturbance in lung function. Improvement in myocardial function and a decrease in pulmonary congestion are accomplished with diuretics and morphine; in those patients who do not respond to this therapy, manipulation of preload, afterload, and myocardial contractility by vasodilators and inotropic agents may be required. In acute pulmonary edema, intravenously administered agents with a short half-life and rapid onset of action are preferred. The role of colloids in the treatment of pulmonary edema is controversial. The indications for the use of corticosteroids in ARDS are controversial, and an optimum dose has not been determined. Many clinicians tend to choose steroids to treat these patients, but the value of these agents in this setting awaits the results of controlled trials now under way.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D001815:Bloodletting; D002199:Capillary Permeability; D004077:Digoxin / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D004280:Dobutamine / Q000627:therapeutic use; D004298:Dopamine / Q000627:therapeutic use; D004630:Emergencies; D006331:Heart Diseases / Q000150:complications; D006801:Humans; D006874:Hydrostatic Pressure; D008168:Lung / Q000503:physiopathology; D009020:Morphine / Q000627:therapeutic use; D005996:Nitroglycerin / Q000627:therapeutic use; D009599:Nitroprusside / Q000627:therapeutic use; D009997:Osmotic Pressure; D010956:Plasmapheresis; D011187:Posture; D011654:Pulmonary Edema / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D012121:Respiration, Artificial; D014111:Tourniquets; D014665:Vasodilator Agents / Q000627:therapeutic use
D000305:Adrenal Cortex Hormones; D004232:Diuretics; D014665:Vasodilator Agents; D009599:Nitroprusside; D004280:Dobutamine; D004077:Digoxin; D009020:Morphine; D005996:Nitroglycerin; D004298:Dopamine