New horizons (Baltimore, Md.)
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The justification for restricting fluid administration, or more directly, for actively trying to lower pulmonary capillary pressures during pulmonary edema, is embodied in the familiar "Starling equation." This model predicts that pulmonary edema will develop if lymph flow or changes in other so-called "safety factors" cannot compensate for increases in pulmonary capillary pressures. Numerous experimental studies support the logical extension of this paradigm, namely that reduced capillary pressures and/or reduced perfusion to acutely injured lung units will result in reduced extravascular lung water accumulation. ⋯ Furthermore, although a strategy of fluid restriction/diuresis could potentially increase the risk of either cardiac or renal dysfunction, currently available data suggest that this management strategy in euvolemic (and certainly in hypervolemic) ARDS patients can be pursued without clinically important deterioration in either type of organ function. Thus, on balance, a strategy of fluid restriction/diuresis should be pursued during the first few days of ARDS, while carefully monitoring and supporting the perfusion of vital organs.
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Time relationships of physiologic patterns that are relevant to the pathogenesis of adult respiratory distress syndrome (ARDS) have not been well studied. The purpose of this review is to summarize the temporal relationship of blood volume, hemodynamics, and oxygen transport patterns occurring in postoperative patients before and after ARDS in order to develop a more complete mechanistic evaluation of its pathophysiology and to propose more rational therapeutic strategies. The data indicate that hypovolemia, reduced or uneven blood flow, inadequate delivery of oxygen, and insufficient consumption of oxygen precede the appearance of ARDS and are the primary precipitating physiologic events. ⋯ The conventional approach also ignores events antecedent to ARDS that produce hypoxia of the lung tissue, result in pulmonary vasoconstriction, and increased pulmonary venous admixture (shunt). Therapy to prevent or rapidly treat these antecedent events has been shown to prevent or attenuate postoperative and posttraumatic ARDS. Various mediators such as interleukin (IL)-1, IL-6, and IL-8 and tumor necrosis factor as measured by plasma concentrations do not precede diagnostic criteria of ARDS, but may accelerate and augment the disorder as it is occurring.
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Long-term extracorporeal support for acute lung failure was introduced in 1972. In the 1970s, much effort was concentrated on technical improvements. However, a multicenter study comparing continuous positive-pressure ventilation and continuous positive-pressure ventilation plus extracorporeal circulation failed to show improvement in survival rates. ⋯ The main complication of the technique was bleeding due to systemic heparinization. However, the technology used in that period was the same as in the 1970s. Recently, technological improvement--such as percutaneous cannulation and surface-heparinized artificial lungs--has allowed clinical performances to improve substantially. "Lung rest" philosophy, coupled with safe technology, may provide a rational basis to test this technique in a randomized fashion for widespread use.
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Protocol control of severely ill ICU patients seems feasible. A satisfactory computer infrastructure makes protocol control practical. A reported four-fold survival rate increase associated with protocol control of ventilatory management of adult respiratory distress syndrome patients suggests that it is not harmful. ⋯ Such a consortium could rapidly complete large, randomized, clinical trials under computerized protocol control. This arrangement could provide much more definitive results than are currently possible. Interpretation of outcomes research results should thereby be made easier and conclusions should be more credible and more likely to contribute to medical policy formulation.
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The traditional practice of using high inflation pressures to maintain normal tidal volumes and arterial blood gases has been encouraged by the perception of uniformly distributed damage in acute lung injury. Although the frontal chest radiograph often suggests uniformity, recent work highlights the heterogeneous pathoanatomy and lung mechanics that actually characterize the adult (acute) respiratory distress syndrome. This heterogeneity is important to consider when applying mechanical ventilation, because impressive experimental evidence strongly indicates the potential for traditional selections for volume and pressure to impede lung healing or extend damage to previously unaffected areas. ⋯ Pathologic, physiologic, and theoretical arguments favor a strategy that attempts to avoid tidal alveolar collapse and to keep transalveolar pressure (not PaCO2) within normal physiologic limits. CO2 retention may be an unavoidable consequence of such a lung-protection strategy. Although the traditional paradigm for ventilation appears in need of revision, it must be recognized that few prospective, controlled trials of alternative ventilation modes have been undertaken to prove their superiority.