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ARDS发病机制的新见解

New Insights Into the Pathogenesis of the Acute Respiratory Distress Syndrome
Disclosures
Arthur S. Slutsky, MD
Introduction
　　Professor Luciano Gattinoni, MD,[1] of Universita Degli Studi Milano, Milano, Italy, presented a plenary lecture at the recent Society for Critical Care Medicine symposium that was held in San Antonio, Texas. He discussed new insights into the pathogenesis of acute respiratory distress syndrome (ARDS), with a focus on mechanisms and potential implications for improving ventilatory strategies for patients with ARDS.
　　There is no question that our approach to mechanical ventilation has changed over the past 30 years. In 1972, Henning Pontoppidan, a pioneer in mechanical ventilation, commented in The New England Journal of Medicine on the fact that patients were often ventilated with tidal volumes of 12 to 15 mL/kg with a positive end-expiratory pressure (PEEP) of 5 to 10 cm H2O: "We ventilated thousands of patients in this way and the only side effect was hypocapnia."[2-4] Today, in ventilating patients with ARDS, the recommendations are to use tidal volumes that are substantially less than those considered by Pontoppidan to be standard. What have we learned over the past 30 years that has changed clinical practice in this way?
　　We have learned a great deal from computed tomography (CT) studies in patients with ARDS. When ARDS was originally described in 1967 and for decades after its initial description, it was thought that ARDS was acute lung injury that was relatively uniformly distributed in the lung. This concept was obtained by analysis of routine chest x-rays of the lung. However, over the past 15 years, a number of studies using CT scans have taught us that, in fact, the distribution of opacities in the lung is quite heterogeneous with a strong tendency for the dependent regions of the lung to be fluid filled/atelectatic, and the nondependent regions to appear relatively normal. This often leaves a relatively small region of the lung available for ventilation -- so called "baby lung." If one tries to ventilate this "baby lung" with adult-size tidal volumes, this can lead to further lung injury induced by the ventilatory process.
　　Force, Strain, and Stress of Ventilator-Induced Lung Injury
　　Clinical Application
Conclusion
VILI is caused by excessive global/regional stresses and strains that affect healthy lung regions. These stresses/strains can lead to mechanical failure of the lung, with cellular stresses and strains leading to release of various cytokines/chemokines, which in turn lead to neutrophil accumulation and subsequent lung injury. At the bedside, these detrimental effects of ventilation can be (at least partially) overcome by ventilatory strategies that use low transpulmonary pressures; the prone position, which leads to more even distribution of transpulmonary pressure; and the use of PEEP, which decreases stress/strain maldistribution in recruitable lungs.
References
1. Gattinoni L. Plenary: ARDS physiopathology: an update. Program and abstracts of the 32nd Critical Care Congress; January 28-February 2, 2003; San Antonio, Texas.
2. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the adult. 3. N Engl J Med. 1972;287:799-806.
3. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the adult. 2. N Engl J Med. 1972;287:743-752.
4. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the adult. 1. N Engl J Med. 1972;287:690-698.
5. Mead J, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol. 1970;28:596-608.
6. Belperio JA, Keane MP, Burdick MD, et al. Critical role for CXCR2 and CXCR2 ligands during the pathogenesis of ventilator-induced lung injury. J Clin Invest. 2002;110:1703-1716.
7. Broccard A, Shapiro RS, Schmitz LL, Adams AB, Nahum A, Marini JJ. Prone positioning attenuates and redistributes ventilator-induced lung injury in dogs. Crit Care Med. 2000;28:295-303. t
8. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301-1308.