Marini, John

Richard, Jean-Christophe

RERO DOC Digital Library

Jean-Christophe M. RichardJohn J. MariniTranspulmonary pressure as a surrogateof plateau pressure for lung protectivestrategy: not perfect but more physiologicReceived: 11 December 2011Accepted: 9 January 2012Published online: 10 February 2012 Copyright jointly held by Springer and ESICM 2012This editorial refers to the article available at:doi:10.1007/s00134-012-2490-7.J.-C. M. Richard ())Intensive Care Department, University Hospital of Geneva,Geneva, Switzerlande-mail: jcm.richard@hcuge.chJ. J. MariniPulmonary and Critical Care,University of Minnesota and Regions Hospital,St. Paul, MN, USADuring the last pandemic, experience in the managementof the most severely affected patients with influenza A(H1N1)-related acute respiratory distress syndrome(ARDS) included increased use of extracorporeal mem-brane oxygenation (ECMO) [1, 2]. Growing interest inthis technique has been spurred by the results of a largecohort study in which transfer to an ECMO center wasassociated with lower hospital mortality than matchednon-ECMO-referred patients [3]. To date, it has beendifficult to establish recommendations for ECMO referral,since neither the type of patients who benefit from thistechnique nor the exact timing of the switch from con-ventional treatment to ECMO have been systematicallyinvestigated [4].In this issue of Intensive Care Medicine, Grasso et al.[5] evaluate whether the use of transpulmonary pressure(PTP) [as opposed to airway pressure (Paw) alone] as asurrogate of the true lung distending pressure might leadto safely increased positive end-expiratory pressure(PEEP) and improved oxygenation, thereby avoidingunnecessary ECMO. In fact, whereas Paw is influencedby chest wall properties and respiratory muscle activity,the PTP (Paw – pleural pressure) enables estimation ofpassive lung’s actual distending pressure, unencumberedby the influence of the chest wall and patient effort onrecorded airway pressures. To assess PTP, an esophagealballoon catheter was used to estimate global pleuralpressure, a venerable laboratory technique that hasrecently been deployed in the clinical setting of lungprotective ventilation [6]. Grasso and colleagues hypoth-esized that, despite high Paw, the actual PTP observed insome very severe patients with ARDS might be lowenough to allow safe increases of PEEP and improvedlung recruitment when a relatively large proportion ofPaw dissipates against a stiff chest wall. In the currentstudy, the authors nicely demonstrated that PTP, asopposed to unadjusted Paw, effectively guided theselection of PEEP while keeping end-inspiratory PTP in atheoretically safe range. Many of the studied patients hadabnormal chest wall elastance related to obesity. Becausethe chest wall may account for an unexpectedly highfraction of total respiratory system elastance even in lunginjured patients, relying on Paw to estimate distension andguide recruitment may be misleading [7]. Using PTP tooptimize PEEP and tidal volume (Vt) is a particularlyattractive option for influenza A (H1N1) patients withdiffuse ARDS which appears to have occurred dispro-portionately often in the obese.Clinical findings have supported the idea that end-expiratory collapse, inspiratory recruitment, and potentialregional overdistension are continuous and interdepen-dent phenomena [8]. Nevertheless, the complexrelationship between PTP, recruitment, and the risk ofoverdistension has frustrated most attempts to establishreliable rules with which to govern clinical choicesamong options for selecting PEEP and Vt [9].Intensive Care Med (2012) 38:339–341DOI 10.1007/s00134-012-2492-5 EDITORIALFindings reported in this current case series may beviewed as a partial ‘‘proof of concept,’’ but severalmethodological limitations relating to the design and thereliability of esophageal pressure (Pes) measurement maylimit broader clinical application of this approach toeveryday practice.First, the authors postulated that 27 cmH2O couldrationally be considered the safe upper limit target forPTP. Clinical observations supporting this statement arerelatively scarce. In a large group of patients with andwithout ARDS, Chuimello et al. investigated the rela-tionship between stress (i.e., transpulmonary pressure)and strain defined as the ratio between Vt and end-expi-ratory lung volume [10]. With imaging data used as thecriterion, the authors demonstrated that plateau pressure(Pplat) and Vt are imprecise surrogates for lung tissuestress and strain. The poor relationship they observedbetween Pplat and lung distension was related to theheterogeneous influence of the chest wall. Interestingly,the stress to strain ratio (i.e., specific elastance) wasremarkably constant (around 13 cmH2O) whatever thedisease severity and combination of PEEP and Vt. Basedon animal studies [11, 12] which suggest that tidal ven-tilation at strain ratio above 2 (which corresponds to anend-inspiratory lung volume approaching total lungcapacity) may prove rapidly lethal, the authors proposedto set the harmful threshold arbitrarily at 27 cmH2O(2 9 13.5 cmH2O). While this proposal would appearconceptually sound, the designated criterion value forPTP is based on animal observations rather than clinicalstudies. Moreover, in a clinical study investigating thechest wall’s contribution to the inspiratory pressure–vol-ume relationship of the respiratory system during ARDS,Owens et al. [13] observed relatively little influence. Thismay have been due to the fact that most of these patientssuffered from ARDS related to medical illnesses. How-ever, in patient with ARDS related to intra-abdominaldisease and in those exhibiting high BMI, the chest wallmay account for a much higher proportion of total elas-tance [14, 15]. In accordance with those observations,Grasso et al. [5] suggested that targeting Pplat of30 cmH2O may be excessively prudent in some patientsand may lead to unjustified recommendations for ECMOmanagement. On the other hand, Terragni et al. [16]showed in 30 patients managed according to the ARDSnetwork strategy that one-third experienced tidal hyper-inflation [assessed by CT scan systematic analysis]despite a Vt of 6 ml/kg PBW and a Pplat limited at30 cmH2O. In that study, patients exhibiting Pplat below28 cmH2O were significantly less prone to hyperinflation.How to reconcile these contrasting observations suggest-ing that a 30 cmH2O Pplat may both overestimatedistension and underestimate the true hyperinflation ischallenging without invoking important differences inlung disease severity and/or chest wall distensibility.Predicting mechanical properties from traditional obser-vations of physical examination or airway pressuremeasurements is difficult in clinical practice, especiallywhen disease is unevenly distributed and spontaneousbreathing efforts are permitted or encouraged. In thiscontext, Pes measurement and transpulmonary pressureestimation may be essential in differentiating patientswho may benefit from a PEEP increase because ofincreased chest wall elastance from those at risk of hy-perdistension despite relatively low Paw. Yet, the truetension experienced in the alveolar micro-environmentmay only be crudely represented by the PTP, howeveraccurate the latter might be measured.The second point that merits discussion concerns thepotential impact of higher PEEP levels on hemodynamics.The physiological rationale of the study reported byGrasso et al. relied on the fact that ECMO is a rescuetherapy that should be avoided whenever possible. Sup-posing that this statement is correct, the consequence ofavoiding ECMO according to their strategy (consideredsafe as regards to end-inspiratory PTP) will be a poten-tially major increase of PEEP. Therefore, one price to paythat should be considered in avoiding ECMO’s drawbacksis the possible impact of greater lung distension andhigher pleural pressure on hemodynamic status. The samegroup of authors have shown several years ago thatrecruitment maneuvers were significantly less efficient(and potentially harmful) in patient exhibiting high chestwall elastance compared with ARDS in which the chestwall was not altered [17]. Predictably, the authorsobserved in this study a significantly larger impact of Pawon cardiac output in the group of patients with higherchest wall elastance. This harmful hemodynamic effect(which in addition did not result in oxygenationimprovement) expected in patients with high chest wallelastance should be considered as a possible price to payfor a strategy based on PTP measurement to increasePEEP in order to avoid ECMO requirement.Finally, before we can embrace Pes as an accuratesurrogate for the pressure that surrounds the lung, wemust understand that the esophageal balloon cathetermeasures the least pressure in its local environment, andthat this pressure may vary considerably from that exist-ing elsewhere. Even locally, the sensitivity of Pes tochanges in abdominal pressure and lung volume is suspectat end exhalation [18].Despite numerous shortcomings, the option to sensepleural pressure at the bedside by an esophageal balloonrepresents the next logical step in a more physiologicaland individually tailored approach to lung protectiveventilation.340References1. Davies A, Jones D, Bailey M, Beca J,Bellomo R, Blackwell N, Forrest P,Gattas D, Granger E, Herkes R, JacksonA, McGuinness S, Nair P, Pellegrino V,Pettila V, Plunkett B, Pye R, Torzillo P,Webb S, Wilson M, Ziegenfuss M(2009) Extracorporeal membraneoxygenation for 2009 influenzaA(H1N1) acute respiratory distresssyndrome. JAMA 302:1888–18952. Fuhrman C, Bonmarin I, Bitar D,Cardoso T, Duport N, Herida M, IsnardH, Guidet B, Mimoz O, Richard JC,Brun-Buisson C, Brochard L, MaillesA, Paty AC, Saura C, Levy-Bruhl D(2011) Adult intensive-care patientswith 2009 pandemic influenza A(H1N1)infection. Epidemiol Infect139:1202–12093. Noah MA, Peek GJ, Finney SJ, GriffithsMJ, Harrison DA, Grieve R, SadiqueMZ, Sekhon JS, McAuley DF, FirminRK, Harvey C, Cordingley JJ, Price S,Vuylsteke A, Jenkins DP, Noble DW,Bloomfield R, Walsh TS, Perkins GD,Menon D, Taylor BL, Rowan KM(2011) Referral to an extracorporealmembrane oxygenation center andmortality among patients with severe2009 influenza A (H1N1). JAMA306:1659–16684. Checkley W (2011) Extracorporealmembrane oxygenation as a first-linetreatment strategy for ARDS: is theevidence sufficiently strong? JAMA306:1703–17045. Grasso Salvatore, Terragni Pierpaolo,Birocco Alberto, Urbino Rosario, DelSorbo Lorenzo, Filippini Claudia,Mascia Luciana, Pesenti Antonio,Zangrillo Alberto, Gattinoni Luciano,Marco Ranieri V (2012) ECMO criteriafor influenza A (H1N1)-associatedARDS: role of transpulmonary pressure.Intensive Care Med. doi:10.1007/s00134-012-2490-76. Talmor D, Sarge T, Malhotra A,O’Donnell CR, Ritz R, Lisbon A,Novack V, Loring SH (2008)Mechanical ventilation guided byesophageal pressure in acute lunginjury. N Engl J Med 359:2095–21047. Gattinoni L, Pelosi P, Suter PM, PedotoA, Vercesi P, Lissoni A (1998) Acuterespiratory distress syndrome caused bypulmonary and extrapulmonary disease.Different syndromes? Am J Respir CritCare Med 158:3–118. Jonson B, Richard JC, Straus C,Mancebo J, Lemaire F, Brochard L(1999) Pressure-volume curves andcompliance in acute lung injury:evidence of recruitment above the lowerinflection point. Am J Respir Crit CareMed 159:1172–11789. Pelosi P, Goldner M, McKibben A,Adams A, Eccher G, Caironi P,Losappio S, Gattinoni L, Marini JJ(2001) Recruitment and derecruitmentduring acute respiratory failure: anexperimental study. Am J Respir CritCare Med 164:122–13010. Chiumello D, Carlesso E, Cadringher P,Caironi P, Valenza F, Polli F, TallariniF, Cozzi P, Cressoni M, Colombo A,Marini JJ, Gattinoni L (2008) Lungstress and strain during mechanicalventilation for acute respiratory distresssyndrome. Am J Respir Crit Care Med178:346–35511. Mandava S, Kolobow T, Vitale G, FotiG, Aprigliano M, Jones M, Muller E(2003) Lethal systemic capillary leaksyndrome associated with severeventilator-induced lung injury: anexperimental study. Crit Care Med31:885–89212. Kolobow T, Moretti MP, Fumagalli R,Mascheroni D, Prato P, Chen V, Joris M(1987) Severe impairment in lungfunction induced by high peak airwaypressure during mechanical ventilation.An experimental study. Am Rev RespirDis 135:312–31513. Owens RL, Hess DR, Malhotra A,Venegas JG, Harris RS (2008) Effect ofthe chest wall on pressure-volume curveanalysis of acute respiratory distresssyndrome lungs. Crit Care Med36:2980–298514. Ranieri VM, Brienza N, Santostasi S,Puntillo F, Mascia L, Vitale N, GiulianiR, Memeo V, Bruno F, Fiore T, BrienzaA, Slutsky AS (1997) Impairment oflung and chest wall mechanics inpatients with acute respiratory distresssyndrome: role of abdominal distension.Am J Respir Crit Care Med156:1082–109115. Gattinoni L, Chiumello D, Carlesso E,Valenza F (2004) Bench-to-bedsidereview: chest wall elastance in acutelung injury/acute respiratory distresssyndrome patients. Crit Care 8:350–35516. Terragni PP, Rosboch G, Tealdi A,Corno E, Menaldo E, Davini O,Gandini G, Herrmann P, Mascia L,Quintel M, Slutsky AS, Gattinoni L,Ranieri VM (2007) Tidal hyperinflationduring low tidal volume ventilation inacute respiratory distress syndrome. AmJ Respir Crit Care Med 175:160–16617. Grasso S, Mascia L, Del Turco M,Malacarne P, Giunta F, Brochard L,Slutsky AS, Marco Ranieri V (2002)Effects of recruiting maneuvers inpatients with acute respiratory distresssyndrome ventilated with protectiveventilatory strategy. Anesthesiology96:795–80218. Valenza F, Chevallard G, Porro GA,Gattinoni L (2007) Static and dynamiccomponents of esophageal and centralvenous pressure during intra-abdominalhypertension. Crit Care Med35:1575–1581341

Transpulmonary pressure as a surrogate of plateau pressure for lung protective strategy: not perfect but more physiologic

http://doc.rero.ch/record/317172/files/134_2012_Article_2492.pdf

Transpulmonary pressure as a surrogate of plateau pressure for lung protective strategy: not perfect but more physiologic

Abstract

Similar works

Full text

Available Versions

RERO DOC Digital Library