Effect of Mechanical Ventilation on Inflammatory Mediators in Patients With Acute Respiratory Distress Syndrome: A Randomized Controlled Trial

• Published in: JAMA : the journal of the American Medical Association 1999-07, Vol.282 (1), p.54-61
• Main Authors: Ranieri, V. Marco, Suter, Peter M, Tortorella, Cosimo, De Tullio, Renato, Dayer, Jean Michel, Brienza, Antonio, Bruno, Francesco, Slutsky, Arthur S
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Cytokines - metabolism; Emergency and intensive respiratory care; Female; Humans; Inflammation Mediators - metabolism; Intensive care medicine; Male; Medical sciences; Middle Aged; Positive-Pressure Respiration; Respiration, Artificial - adverse effects; Respiratory Distress Syndrome, Adult - immunology; Respiratory Distress Syndrome, Adult - therapy; Respiratory Function Tests
• ISSN: 0098-7484; 1538-3598
• DOI: 10.1001/jama.282.1.54

CONTEXT Studies have shown that an inflammatory response may be elicited by mechanical ventilation used for recruitment or derecruitment of collapsed lung units or to overdistend alveolar regions, and that a lung-protective strategy may reduce this response. OBJECTIVE To test the hypothesis that mechanical ventilation induces a pulmonary and systemic cytokine response that can be minimized by limiting recruitment or derecruitment and overdistention. DESIGN AND SETTING Randomized controlled trial in the intensive care units of 2 European hospitals from November 1995 to February 1998, with a 28-day follow-up. PATIENTS Forty-four patients (mean [SD] age, 50 [18] years) with acute respiratory distress syndrome were enrolled, 7 of whom were withdrawn due to adverse events. INTERVENTIONS After admission, volume-pressure curves were measured and bronchoalveolar lavage and blood samples were obtained. Patients were randomized to either the control group (n=19): tidal volume to obtain normal values of arterial carbon dioxide tension (35-40 mm Hg) and positive end-expiratory pressure (PEEP) producing the greatest improvement in arterial oxygen saturation without worsening hemodynamics; or the lung-protective strategy group (n=18): tidal volume and PEEP based on the volume-pressure curve. Measurements were repeated 24 to 30 and 36 to 40 hours after randomization. MAIN OUTCOME MEASURES Pulmonary and systemic concentrations of inflammatory mediators approximately 36 hours after randomization. RESULTS Physiological characteristics and cytokine concentrations were similar in both groups at randomization. There were significant differences (mean [SD]) between the control and lung-protective strategy groups in tidal volume (11.1 [1.3] vs 7.6 [1.1] mL/kg), end-inspiratory plateau pressures (31.0 [4.5] vs 24.6 [2.4] cm H2O), and PEEP (6.5 [1.7] vs 14.8 [2.7] cm H2O) (P