Objective: 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. Subjects: Ten lung-damaged pigs (instilled hydrochloride). Interventions: 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. Measurements and Main Results: Physiological parameters, computed tomography scans, plasma and bronchoalveolar lavage concentrations of interleukin-1[beta], interleukin-6, interleukin-8, interleukin-10, interleukin-18, and tumor necrosis factor-[alpha]. 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-[alpha] concentrations were significantly lower in plasma; interleukin-6 and tumor necrosis factor-[alpha] concentrations were lower in bronchoalveolar lavage, whereas the concentrations of the other cytokines remained unchanged. Conclusion: 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.

Low respiratory rate plus minimally invasive extracorporeal CO2 removal decreases systemic and pulmonary inflammatory mediators in experimental Acute Respiratory Distress Syndrome

GRASSO, Salvatore;LACITIGNOLA, Luca;TREROTOLI, Paolo;BRUNO, Francesco;CROVACE, Antonio;
2014-01-01

Abstract

Objective: 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. Subjects: Ten lung-damaged pigs (instilled hydrochloride). Interventions: 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. Measurements and Main Results: Physiological parameters, computed tomography scans, plasma and bronchoalveolar lavage concentrations of interleukin-1[beta], interleukin-6, interleukin-8, interleukin-10, interleukin-18, and tumor necrosis factor-[alpha]. 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-[alpha] concentrations were significantly lower in plasma; interleukin-6 and tumor necrosis factor-[alpha] concentrations were lower in bronchoalveolar lavage, whereas the concentrations of the other cytokines remained unchanged. Conclusion: 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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/129271
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