ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure.
BACKGROUND
In patients with acute respiratory distress syndrome (ARDS), a focal distribution of loss of aeration in lung computed tomography predicts low potential for alveolar recruitment and susceptibility to alveolar hyperinflation with high levels of positive end-expiratory pressure (PEEP).


OBJECTIVE
We tested the hypothesis that, in this cohort of patients, the table-based PEEP setting criteria of the National Heart, Lung, and Blood Institute's ARDS Network (ARDSnet) low tidal volume ventilatory protocol could induce tidal alveolar hyperinflation.


METHODS
In 15 patients, physiologic parameters and plasma inflammatory mediators were measured during two ventilatory strategies, applied randomly: the ARDSnet and the stress index strategy. The latter used the same ARDSnet ventilatory pattern except for the PEEP level, which was adjusted based on the stress index, a monitoring tool intended to quantify tidal alveolar hyperinflation and/or recruiting/derecruiting that occurs during constant-flow ventilation, on a breath-by-breath basis.


RESULTS
In all patients, the stress index revealed alveolar hyperinflation during application of the ARDSnet strategy, and consequently, PEEP was significantly decreased (P < 0.01) to normalize the stress index value. Static lung elastance (P = 0.01), plasma concentrations of interleukin-6 (P < 0.01), interleukin-8 (P = 0.031), and soluble tumor necrosis factor receptor I (P = 0.013) were significantly lower during the stress index as compared with the ARDSnet strategy-guided ventilation.


CONCLUSIONS
Alveolar hyperinflation in patients with focal ARDS ventilated with the ARDSnet protocol is attenuated by a physiologic approach to PEEP setting based on the stress index measurement.
Università di Bari, Dipartimento dell'Emergenza e Trapianti d'Organo (DETO), Sezione di Anestesiologia e Rianimazione, Ospedale Policlinico, Piazza Giulio Cesare 11, Bari 70124, Italy. grassos@libero.it
Salvatore
S
Grasso
Tania
T
Stripoli
Michele
M
De Michele
Francesco
F
Bruno
Marco
M
Moschetta
Giuseppe
G
Angelelli
Irene
I
Munno
Vincenzo
V
Ruggiero
Roberto
R
Anaclerio
Aldo
A
Cafarelli
Bernd
B
Driessen
Tommaso
T
Fiore
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002302:Cardiac Output / Q000502:physiology; D015331:Cohort Studies; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011175:Positive-Pressure Respiration / Q000379:methods*; D011650:Pulmonary Alveoli / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange / Q000502:physiology; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D012128:Respiratory Distress Syndrome / Q000503:physiopathology* / Q000628:therapy; D015656:Respiratory Mechanics / Q000502:physiology; D013990:Tidal Volume / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology
D015850:Interleukin-6; D016209:Interleukin-8; D047888:Receptors, Tumor Necrosis Factor, Type I