Neurogenic pulmonary edema.
Neurogenic pulmonary edema is an anomaly because it cannot be categorized into either of the two major types of pulmonary edema. Both high-pressure and increased-permeability abnormalities may be involved in the pathogenesis of neurogenic pulmonary edema. Furthermore, the mechanisms responsible for these abnormalities appear quite complex. The high-pressure insult appears to be a function of systemic hypertension, pulmonary venoconstriction, negative and positive inotropic factors, and intrinsic myocardial function. Mediators of the pulmonary endothelial permeability defect have not been defined. Although the high-pressure and increased-permeability abnormalities seem to develop through separate mechanisms, their combined effect is probably synergistic on the accumulation of extravascular lung water. The neurologic pathways responsible for initiating neurogenic pulmonary edema remains a mystery. Despite the questions and uncertainties still surrounding neurogenic pulmonary edema, the substantial progress made in understanding the clinical expression, incidence, and pathogenesis of this syndrome does provide a framework for a reasonable approach to its clinical management.
D000328:Adult; D001285:Atropine / Q000494:pharmacology; D001919:Bradycardia / Q000209:etiology; D001921:Brain / Q000502:physiology; D001927:Brain Diseases / Q000150:complications*; D002199:Capillary Permeability; D002395:Catecholamines / Q000502:physiology; D005260:Female; D006801:Humans; D008875:Middle Aged; D011654:Pulmonary Edema / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D011669:Pulmonary Wedge Pressure; D013577:Syndrome; D014661:Vasoconstriction
D002395:Catecholamines; D001285:Atropine