Low Respiratory Rate Plus Minimally Invasive Extracorporeal Co2 Removal Decreases Systemic and Pulmonary Inflammatory Mediators in Experimental Acute Respiratory Distress Syndrome*
Authors:
- Salvatore GrassoSGSalvatore Grasso
- Tania StripoliTSTania Stripoli
- Palma MazzonePMPalma Mazzone
- Marco PezzutoMPMarco Pezzuto
- Luca LacitignolaLLLuca Lacitignola
- Paola CentonzePCPaola Centonze
- Alessandro GuarracinoAGAlessandro Guarracino
- Cosimo EspositoCECosimo Esposito
- Peter HerrmannPHPeter Herrmann
- Michael QuintelMQMichael Quintel
- Paolo TrerotoliPTPaolo Trerotoli
- Francesco BrunoFBFrancesco Bruno
- 1 June 2014
- journal article
- research article
- Published by Wolters Kluwer Health in Critical Care Medicine
- Vol. 42 (6) , e451-e460
Abstract
The Acute Respiratory Distress Syndrome Network protocol recommends limiting tidal volume and plateau pressure; it also recommends increasing respiratory rate to prevent hypercapnia. We tested a strategy that combines the low tidal volume with lower respiratory rates and minimally invasive CO2 removal. Ten lung-damaged pigs (instilled hydrochloride). Two conditions randomly applied in a crossover fashion: the Acute Respiratory Distress Syndrome Network protocol and the Acute Respiratory Distress Syndrome Network protocol plus lower respiratory rate plus minimally invasive Co2 removal. A similar arterial Co2 partial pressure was targeted in the two conditions. Physiological parameters, computed tomography scans, plasma and bronchoalveolar lavage concentrations of interleukin-1β, interleukin-6, interleukin-8, interleukin-10, interleukin-18, and tumor necrosis factor-α. During the lower respiratory rate condition, respiratory rate was reduced from 30.5 ± 3.8 to 14.2 ± 3.5 (p < 0.01) breaths/min and minute ventilation from 10.4 ± 1.6 to 4.9 ± 1.7 L/min (p < 0.01). The extracorporeal device removed 38.9% ± 6.1% (79.9 ± 18.4 mL/min) of CO2 production. During the lower respiratory rate condition, interleukin-6, interleukin-8, and tumor necrosis factor-α concentrations were significantly lower in plasma; interleukin-6 and tumor necrosis factor-α concentrations were lower in bronchoalveolar lavage, whereas the concentrations of the other cytokines remained unchanged. The strategy of lower respiratory rate plus minimally invasive extracorporeal CO2 removal was feasible and safe and, as compared with the Acute Respiratory Distress Syndrome Network protocol, reduced the concentrations of some, but not all, of the tested cytokines without affecting respiratory mechanics, gas exchange, and hemodynamics.Keywords
This publication has 49 references indexed in Scilit:
- Effects of respiratory rate on ventilator-induced lung injury at a constant Paco2 in a mouse model of normal lungCritical Care Medicine, 2008
- ARDSnet Ventilatory Protocol and Alveolar HyperinflationAmerican Journal of Respiratory and Critical Care Medicine, 2007
- Tidal Hyperinflation during Low Tidal Volume Ventilation in Acute Respiratory Distress SyndromeAmerican Journal of Respiratory and Critical Care Medicine, 2007
- Tidal Volume Reduction in Patients with Acute Lung Injury When Plateau Pressures Are Not HighAmerican Journal of Respiratory and Critical Care Medicine, 2005
- Protective effects of low respiratory frequency in experimental ventilator-associated lung injury*Critical Care Medicine, 2005
- Effect of ventilatory rate on airway cytokine levels and lung injuryJournal of Surgical Research, 2003
- Kinetic and reversibility of mechanical ventilation-associated pulmonary and systemic inflammatory response in patients with acute lung injuryIntensive Care Medicine, 2002
- Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress SyndromeNew England Journal of Medicine, 2000
- Effects of Decreased Respiratory Frequency on Ventilator-induced Lung InjuryAmerican Journal of Respiratory and Critical Care Medicine, 2000
- Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndromeIntensive Care Medicine, 1990