Controversies in the pathophysiology and fluid management of postoperative adult respiratory distress syndrome.
Physiologic changes that lead to the development of ARDS begin with the precipitating shock syndrome. Hypovolemia, pulmonary vasoconstriction, reduced myocardial performance, and diminished O2 transport typically precede the development of clinical ARDS after hemorrhage, trauma, postoperative conditions, and sepsis. Since shock lung is a complication of shock, it is not surprising that the antecedent clinical and physiologic events that characterize the shock state may be determinants of both the genesis and the outcome of ARDS. Postoperative ARDS follows unrecognized or inadequately treated hypovolemia and hypoxia during an antecedent period of preoperative or intraoperative shock. Hypovolemia and hypoxia increase cardiac and ventilatory drive and stimulate neurohumoral mechanisms to increase pulmonary vasoconstriction. The last-named, when extensive and uneven, produces maldistribution of flow and reduces DO2 and VO2. Subsequently, mediator-induced pulmonary vasoconstriction increases the problem. When sufficiently extensive, these antecedent physiologic alterations culminate in ARDS. With impaired flow and O2 transport, pathogenic mechanisms of ARDS and acute renal failure may be set in motion; further, the naturally occurring immune mechanisms may be impaired and may lead to associated infection. There are at least six redistributions that are major pathophysiologic influences in ARDS. They are uneven ventilation throughout the lung; redistribution of regional pulmonary blood flow between zones due to gravity; nonuniform pulmonary blood flow between individual metarteriolar-capillary networks because of local vasoconstriction; uneven systemic blood flow between organs; irregular systemic blood flow at the microcirculatory level, producing inadequate nutritional flow to the tissues; and redistribution of body water, leading particularly to fluid accumulation in the extracellular compartment, with expanded interstitial space and contracted plasma volume (hypovolemia). Pathogenic roles have been implicated for capillary leak, surfactant synthesis, erythrocyte and platelet aggregation, leukocyte margination in the pulmonary circulation, complement and kinin cascades, neurohumoral responses, histamine, serotonin, vasoactive peptides, and the metabolic products of arachidonic acid breakdown in pulmonary vessels. However, these potential pathogenic influences have yet to be described in terms of their temporal relationships to the natural physiologic history of ARDS; nor have their roles been evaluated in terms of mechanistic interrelationships.(ABSTRACT TRUNCATED AT 400 WORDS)
D001804:Blood Transfusion, Autologous; D001810:Blood Volume; D003102:Colloids / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D005440:Fluid Therapy; D006439:Hemodynamics; D006470:Hemorrhage / Q000401:mortality; D006801:Humans; D007022:Hypotension / Q000209:etiology; D007385:Intermittent Positive-Pressure Ventilation / Q000379:methods; D011183:Postoperative Complications; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000401:mortality / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D012771:Shock, Hemorrhagic / Q000150:complications; D014692:Ventilation-Perfusion Ratio; D014883:Water-Electrolyte Imbalance / Q000150:complications
D003102:Colloids; D004232:Diuretics