New horizons (Baltimore, Md.)
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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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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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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.
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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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In 1987, nitric oxide was reported to be an endothelium-dependent relaxing factor. When inhaled as a gas at low levels, nitric oxide selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because nitric oxide is inactivated by rapidly binding to hemoglobin. ⋯ Tachyphylaxis to nitric oxide inhalation has not been observed. While additional chronic toxicology studies need to be performed, significant pulmonary toxicity has not been observed at low inhaled concentrations (< 80 parts per million by volume). Potentially, inhaled nitric oxide may be a valuable therapy in patients with adult respiratory distress syndrome.