Low respiratory rate plus minimally invasive extracorporeal Co2 removal decreases systemic and pulmonary inflammatory mediators in experimental Acute Respiratory Distress Syndrome.
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.


METHODS
Ten lung-damaged pigs (instilled hydrochloride).


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
1Dipartimento dell'Emergenza e Trapianti d'Organo, Sezione di Anestesiologia e Rianimazione, Università degli Studi Aldo Moro, Bari, Italy. 2Intensive Care, Ospedale Di venere, Bari, Italy. 3Dipartimento dell'Emergenza e Trapianti d'Organo, Sezione di Chirurgia Veterinaria, Università degli Studi Aldo Moro, Bari, Italy. 4Dottorato in Scienze Chirurgiche Sperimentali e Terapie Cellulari, Università degli Studi Aldo Moro, Bari, Italy. 5Center for Anesthesiology, Emergency and Intensive Care Medicine, University Medical Center Göttingen, Göttingen, Germany. 6Dipartimento di Scienze Biomediche ed Oncologia Umana, Cattedra di Statistica Medica, Università degli Studi Aldo Moro, Bari, Italy.
Salvatore
S
Grasso
Tania
T
Stripoli
Palma
P
Mazzone
Marco
M
Pezzuto
Luca
L
Lacitignola
Paola
P
Centonze
Alessandro
A
Guarracino
Cosimo
C
Esposito
Peter
P
Herrmann
Michael
M
Quintel
Paolo
P
Trerotoli
Francesco
F
Bruno
Antonio
A
Crovace
Francesco
F
Staffieri
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D016207:Cytokines / Q000032:analysis*; D004195:Disease Models, Animal; D015199:Extracorporeal Membrane Oxygenation / Q000295:instrumentation / Q000379:methods*; D005240:Feasibility Studies; D005260:Female; D006439:Hemodynamics; D008168:Lung / Q000378:metabolism / Q000503:physiopathology*; D011175:Positive-Pressure Respiration / Q000009:adverse effects / Q000379:methods* / Q000592:standards; D017410:Practice Guidelines as Topic; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000378:metabolism / Q000628:therapy*; D015656:Respiratory Mechanics; D056152:Respiratory Rate; D013552:Swine; D013990:Tidal Volume; D055397:Ventilator-Induced Lung Injury / Q000517:prevention & control*
D016207:Cytokines