| Background ARDS is a common severe disease with high mortality and is always paid attention by the class of critical care medicine. There is a general belief that ARDS is the extreme form of a spectrum of lung injury caused by a uniform inflammatory mechanism that is independent of the primary disease, so is the respiratory mechanics of ARDS. But, it is only a deduction. Most of the studies report late or terminal events, and pathological features of early phases of ARDS such as interstitial edema and alveolar collapse are not easily recognized. Now more and more studies report different pathological features in the early phase of ARDS caused by different mechanisms.The American-European consensus conference on ARDS in 1992 categorized risk factors for ARDS into two types. direct(primary or pulmonary) injury whichimpaired lung tissue directly and indirect(secondary or extrapulmonary) injury which impaired lung tissue indirectly. The latter accompanied with acute systemic inflammatory response syndrome. The difference in two risk factors is clear.Some reports overseas pointed that there are different pathological features in the early phase between ARDS caused by direct injury (pulmonary ARDS) and ARDS caused by indirect injury(extrapulmonary ARDS). But no reports correlated in our country. Different pathological features in two types of insult had been proved in animal models. Prevalent consolidation is noted in direct injury type ARDS and prevalent interstitial edema and alveolar collapse in indirect injury type ARDS. Objective In the early phase of pulmonary ARDS and extrapulmonary ARDS, we will observe the differences in static compliance of the total respiratory system, static compliance of the chest wall and static lung compliance. We will also examine the different responses of respiratory mechanics and work of breath to various PEEP levels in two types ARDS.Methods ARDSp group and ARDSexp group of about ten patients each were assigned that were based on history, clinical presentation and microbiological results. Before the investigation, the patients were sedated with midazolam and paralyzed with vecuronium bromide. All the patients were ventilated in the volume control mode with constant inspiratory flow. Airway pressure and gas flow were measuredand recorded by Bicore CP-100 Pulmonary Monitor at the endotracheal tube opening. Esophageal pressure was determined from an esophageal balloon inflated with 0.5-1 ml air, positioned at the lower third of the esophagus. We measured the elastic properties of the lung and chest wall (in triplicate) and work of breath at four different PEEP levels(0, 5, 10, and 15 cm HjO) applied in elevated order. Static compliance of the total respiratory system (Cst,rs) was computed as VT/ A Pao, where A Pes is the difference between end-inspiratory and end-expiratory airway pressure. Static compliance of the chest wall (Cst,w) was computed as VT/ A Pes, where A Pes is the difference between end-inspiratory and end-expiratory esophageal pressure. Static lung compliance (Cst,L) was calculated as [l/Cst,L =(1/ Cst,rs) - (l/Cst,w)]. Results1. The low values of Cst,rs, Cst,L and Cst,w are typical in the total population of ARDS. When PEEP was increased from 0 to 15 cm H2O, Cst^s and Cst,L did not change significantly, Cst,w increased slightly.2. When PEEP was increased from 0 to 15 cm H2O, increasing PEEP caused an decrease of Cst,rs in ARDSp, whereas PEEP resulted in a increase in Cst,rs in ARDSexp. There was significant change in Cst,rs at 15 cm H2O PEEP comparing with ZEEP.3. When PEEP was increased from 0 to 15 cm H2O, increasing PEEP caused andecrease of Cst,L in ARDSp, whereas PEEP resulted in a increase in Cst,L in ARDSexp. There were no significant change in Cst,L at all levels of PEEP.4. At the same level of PEEP, Cst,rs in ARDSp had no significant difference with that in ARDSexp, except for 15 cm H2O PEEP, Cst,L and Cst,w in two type ARDS had significant differences. Cst,L in ARDSp was lower than in ARDSexp, but C... |
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