- Email: [email protected]
Counterpoint: Should Positive End-Expiratory Pressure in Patients With ARDS Be Set Based on Oxygenation? No
9. Villar J, Kacmarek RM, Pérez-Méndez L, Aguirre-Jaime A. A high positive end-expiratory pressure, low tidal volume ventilatory strategy improves outcome in persistent acute respiratory distress syndrome: a randomized, controlled trial. Crit Care Med. 2006;34(5):1311-1318. 10. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359(20):2095-2104. 11. Grasso S, Stripoli T, De Michele M, et al. ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure. Am J Respir Crit Care Med. 2007; 176(8):761-767. 12. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18): 1301-1308. 13. Brower RG, Lanken PN, MacIntyre N, et al; National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327-336. 14. Stewart TE, Meade MO, Cook DJ, et al; Pressure- and Volume-Limited Ventilation Strategy Group. Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. N Engl J Med. 1998;338(6):355-361. 15. Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. The Multicenter Trail Group on Tidal Volume reduction in ARDS. Am J Respir Crit Care Med. 1998;158(6):1831-1838. 16. Brower RG, Shanholtz CB, Fessler HE, et al. Prospective, randomized, controlled clinical trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome patients. Crit Care Med. 1999;27(8): 1492-1498. 17. Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive endexpiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):637-645. 18. Mercat A, Richard JC, Vielle B, et al; Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646-655. 19. Phoenix SI, Paravastu S, Columb M, Vincent JL, Nirmalan M. Does a higher positive end expiratory pressure decrease mortality in acute respiratory distress syndrome? A systematic review and meta-analysis. Anesthesiology. 2009;110(5): 1098-1105. 20. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010;303(9):865-873. 21. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med. 2006;354(17):1775-1786. 22. Bikker IG, Preis C, Egal M, Bakker J, Gommers D. Electrical impedance tomography measured at two thoracic levels can visualize the ventilation distribution changes at the bedside during a decremental positive end-expiratory lung pressure trial. Crit Care. 2011;15(4):R193.
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Counterpoint: Should Positive End-Expiratory Pressure in Patients With ARDS Be Set Based on Oxygenation? No 40 years ago, novel animal studies laid the Nearly foundation for lung-protective ventilation. Both
lung overdistention and the absence of positive endexpiratory pressure (PEEP) were linked to gross and histologic lung injury.1 Tidal volume was shown subsequently to be clinically important: 6 mL/kg compared with 12 mL/kg predicted body weight reduced absolute mortality by 9% in patients with acute lung injury (ALI) or ARDS.2 PEEP is biologically relevant, too: Limiting tidal recruitment and derecruitment 3,4,5,6 Yet PEEP may proreduces lung inflammation. fl voke deleterious effects, so that choosing the appropriate level requires balancing benefits and costs. In addition, PEEP should be individualized—in the right amount, to those most likely to benefit. fi In most patients with ALI and ARDS, the clinician chooses a level of PEEP based on oxygenation. Typically, low oxygen saturation leads to an increase in PEEP, whereas elevated saturations prompt a reduced PEEP. One widely used approach is that devised by the ARDS Network, in which PEEP and Fio2 combinations are chosen from a table to achieve oxygenation goals.2 Basing the dose of PEEP on arterial oxygenation has multiple, serious drawbacks, however. First, the degree to which PEEP recruits lung varies dramatically from patient to patient. For example, extrapulmonary ARDS tends to respond to PEEP with higher compliance and CT scan evidence of recruitment, whereas pulmonary ARDS does not.7 Similarly, those with ARDS harbor more potential for recruitment than those with ALI, but, overall, the amount of recruitable lung is modest (13%).8 To the extent that PEEP is valuable because it prevents cyclic recruitment and derecruitment, a rational approach should base the level of PEEP on the degree of recruitability, rather than assuming all lungs behave identically. In patients with ALI and ARDS, lung units collapse largely because of compressive forces, especially in dependent lung zones. One would anticipate PEEP to be effective in keeping the lung open when it produces a positive transpulmonary pressure. Surprisingly, when patients are managed according to the ARDS Network standard of care recommendations, transpulmonary pressure is most often negative, despite PEEP.9 The reasons that pleural pressure is often so high include the weight of edematous lung, raised abdominal pressure,7 and expiratory muscle contraction.10 Thus, even when lung is recruitable, Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on June 5, 2012 © 2012 American College of Chest Physicians
the pressure required to keep it open varies widely, and it would be surprising if a table based solely on oxygenation could cater to this. If PEEP-induced lung recruitment produced predictable changes in oxygenation, perhaps oxygenbased metrics would suffice. The fly in this ointment is the variable impact of PEEP on the circulation: Falling cardiac output both lowers shunt directly11 and reduces the venous blood saturation (Fick principle). Because arterial oxygenation reflects a complex interplay of shunt and mixed venous oxyhemoglobin saturation, recruitment and oxygenation are related only poorly, as has been shown with CT scanning.12 Something better is needed. Three clinical trials addressed the potential role of higher levels of PEEP than required for acceptable oxygenation. Although each failed to demonstrate that higher PEEP enhances survival, all showed a trend in that direction (after adjustment for differences in baseline covariates),13,14,15 and meta-analyses have shown this benefit fi to be statistically signifi ficant.16,177 This is a remarkable result, especially when considering that subjects were treated with higher or lower PEEP without regard to whether the lung was recruitable. Presumably, many were treated with PEEP even when this had little prospect of biologic benefit. fi Further, because raising PEEP leads to more distention at end-inspiration, all else being equal, one might expect higher PEEP in these trials to have produced benefit for some (by reducing tidal derecruitment), harm for others (no recruitment, more overdistention), and a mixture for the rest (less derecruitment but also more overdistention). Perhaps a better trial design would apply higher PEEP only to those subjects with the potential for meaningful recruitment, while also seeking to limit overdistention. In the meantime, what tools are available to the clinician to identify recruitment while avoiding the pitfalls of oxygen-based PEEP dosing? CT scanning may be the most accurate tool, but it is simply not practical. Some have advocated analyzing the pressure-volume curve for evidence of the inflation limb lower inflecfl tion point (Pflex) fl , defl flation limb upper Pfl flex, maximal compliance, true inflection point of the deflation fl limb, or the degree of hysteresis. In an ovine model of ARDS, 10 different means (gas exchange- and mechanical-based) of calculation led to rather similar PEEP levels for most.18 Disadvantages of using the pressure-volume curve include the requirement for paralysis or, at least, deep sedation; inability to discern an inflation-limb fl Pfl flex in many patients; and confounding by the effects of the chest wall. A simpler means to identify the presence of tidal derecruitment, which also warns of overdistention, is to assess the rise in pressure during constantwww.chestpubs.org
flow, volume-preset ventilation (the so-called “stress index”).19 Normally, the airway opening pressure rises linearly because respiratory system mechanical properties (compliance and resistance) do not vary much over the tidal range. If compliance increases during tidal inflation (suggesting that lung is being recruited), the pressure-time display will be convex upward (stress index , 1): More PEEP is likely to be helpful. If the pressure-time display is concave upward, compliance is falling as the lung inflates, fl possibly signaling overdistention: Tidal volume or PEEP should be lowered. Several novel means of choosing PEEP have been advocated. One uses esophageal pressure as a surrogate for pleural pressure; then PEEP is augmented until end-expiratory transpulmonary pressure is positive in the range of 0 to 10 cm H2O.9 This approach led to substantially higher PEEP in the esophageal pressure group (17 vs 10 cm H2O), higher values for oxygenation and compliance, and better adjusted 28-day survival. Another method is to use an investigational forced oscillation technique that applies lowamplitude but rapid pressure changes to estimate compliance during conventional ventilation and without need for a paralytic.20 In sum, an individualized approach to PEEP identifies fi patients whose lungs can be recruited, then applies a sufficient amount to prevent tidal recruitment and derecruitment (an amount that is often higher than PEEP tables or oxygen-based protocols would prescribe). In those who have little recruitable lung, PEEP can do little good and should be minimized. Notice how this differs from an algorithm directed at oxygenation by imagining a patient with ARDS with an unrecruitable lesion. If the arterial saturation is low, oxygen-based treatment prescribes more PEEP. This will be ineffective and may prompt overdistention. Moreover, if the saturation is still low, yet more PEEP may be prescribed. In contrast, a mechanical approach identifies the absence of tidal recruitment immediately (such as a stress index 5 1), focusing treatment away from PEEP. Current evidence points to a survival advantage to higher PEEP, but this should be targeted to those who will benefit fi and used in a way that minimizes the risk of overdistention. Gregory A. Schmidt, MD, FCCP Iowa City, IA Affiliations: fi From the Division of Pulmonaryy Diseases, Critical Care, and Occupational p Medicine, Department of Internal Medicine, Universityy of Iowa. Financial/nonfi financial disclosures: The author has reported p to CHEST T that no p potential conflicts of interest exist with anyy companies/organizations p g whose products or services may be discussed in this article. Correspondence p to: Gregory g y A. Schmidt, MD, FCCP, Division of Pulmonary Diseases, Critical Care, and Occupational CHEST / 141 / 6 / JUNE, 2012
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on June 5, 2012 © 2012 American College of Chest Physicians
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Medicine, Department p of Internal Medicine, Universityy of Iowa, 200 Hawkins Dr, C304-GH, Iowa City, IA 52246; e-mail: [email protected] © 2012 American College g of Chest Physicians. y Reproduction p of this article is p prohibited without written p permission from the American College g of Chest Physicians. y See online for more details. DOI: 10.1378/chest.12-0157
References 1. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflafl tion pressures. Protection by positive end-expiratory pressure. Am Rev Respir Dis. 1974;110(5):556-565. 2. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18): 1301-1308. 3. Tremblay L, Valenza F, Ribeiro SP, Li J, Slutsky AS. Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model. J Clin Invest. 1997; 99(5):944-952. 4. Fanelli V, Mascia L, Puntorieri V, et al. Pulmonary atelectasis during low stretch ventilation: “open lung” versus “lung rest” strategy. Crit Care Med. 2009;37(3):1046-1053. 5. Farias LL, Faffe DS, Xisto DG, et al. Positive end-expiratory pressure prevents lung mechanical stress caused by recruitment/derecruitment. J Appl Physiol. 2005;98(1):53-61. 6. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation fl pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis. 1988;137(5):1159-1164. 7. Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissonii A. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med. 1998;158(1):3-11. 8. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med. 2006;354(17):1775-1786. 9. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359(20):2095-2104. 10. Coggeshall JW, Marini JJ, Newman JH. Improved oxygenation after muscle relaxation in adult respiratory distress syndrome. Arch Intern Med. 1985;145(9):1718-1720. 11. Dantzker DR, Lynch JP, Weg JG. Depression of cardiac output is a mechanism of shunt reduction in the therapy of acute respiratory failure. Chest. 1980;77(5):636-642. 12. Cressoni M, Caironi P, Polli F, et al. Anatomical and functional intrapulmonary shunt in acute respiratory distress syndrome. Crit Care Med. 2008;36(3):669-675. 13. Brower RG, Lanken PN, MacIntyre N, et al; National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327-336. 14. Mercat A, Richard J-CM, Vielle B, et al; Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646-655. 15. Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive endexpiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008; 299(6):637-645. 1384
16. Phoenix SI, Paravastu S, Columb M, Vincent JL, Nirmalan M. Does a higher positive end expiratory pressure decrease mortality in acute respiratory distress syndrome? A systematic review and meta-analysis. Anesthesiology. 2009;110(5):1098-1105. 17. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010;303(9):865-873. 18. Caramez MP, Kacmarek RM, Helmy M, et al. A comparison d of methods to identify open-lung PEEP. Intensive Care Med. 2009;35(4):740-747. 19. Grasso S, Stripoli T, De Michele M, et al. ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure. Am J Respir Crit Care Med. 2007;176(8):761-767. 20. Dellacà RL, Zannin E, Kostic P, et al. Optimisation of positive end-expiratory pressure by forced oscillation technique in a lavage model of acute lung injury. Intensive Care Med. 2011;37(6):1021-1030.
Rebuttal From Dr Miller et al of positive end-expiratory pressure Application (PEEP) in ARDS is evolving. Higher PEEP may
prove beneficial in some patients with ARDS.1 We propose combining PEEP and Fio2 using a table. Dr Schmidt2 has appropriately pointed out several limitations of this method and suggested alternative strategies to management of PEEP. However, we remain unconvinced that these have been tested sufficiently to prove their reliability, safety, or overall clinical effectiveness. We recognize that the ability of PEEP to recruit lung units varies from patient to patient and mayy3 or may not4 vary by etiology of ARDS. How should this information be used? Might paired titration of PEEP and Fio2 be acceptable in extrapulmonary ARDS but not in pulmonary ARDS? Moreover, is injury among various pulmonary etiologies uniform or might hemorrhagic alveolitis respond differently than pneumococcal pneumonia after progression to ARDS? While it is important to raise the suggestion of splitting rather than lumping treatment of ARDS, answers to these questions do not presently exist. ARDS is characterized by hypoxemia because poorly aerated lung units remain perfused, creating low ventilation/perfusion regions and absolute right-to-left shunt. This hypoxemia is usually managed with supplemental oxygen delivery and/or attempts at lung unit recruitment with positive airway pressure. Both of these strategies have the potential for harm—oxygen toxicity and lung overdistention, respectively. In our opinion, Dr Schmidt overestimates the ability of current clinical tools to assess recruitment and provide a reliable guide to PEEP application. Indeed, lung recruitment correlates poorly with oxygenation. For instance, recruitment may not improve oxygenation Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on June 5, 2012 © 2012 American College of Chest Physicians
1382
Counterpoint: Should Positive End-Expiratory Pressure in Patients With ARDS Be Set Based on Oxygenation? No 40 years ago, novel animal studies laid the Nearly foundation for lung-protective ventilation. Both
lung overdistention and the absence of positive endexpiratory pressure (PEEP) were linked to gross and histologic lung injury.1 Tidal volume was shown subsequently to be clinically important: 6 mL/kg compared with 12 mL/kg predicted body weight reduced absolute mortality by 9% in patients with acute lung injury (ALI) or ARDS.2 PEEP is biologically relevant, too: Limiting tidal recruitment and derecruitment 3,4,5,6 Yet PEEP may proreduces lung inflammation. fl voke deleterious effects, so that choosing the appropriate level requires balancing benefits and costs. In addition, PEEP should be individualized—in the right amount, to those most likely to benefit. fi In most patients with ALI and ARDS, the clinician chooses a level of PEEP based on oxygenation. Typically, low oxygen saturation leads to an increase in PEEP, whereas elevated saturations prompt a reduced PEEP. One widely used approach is that devised by the ARDS Network, in which PEEP and Fio2 combinations are chosen from a table to achieve oxygenation goals.2 Basing the dose of PEEP on arterial oxygenation has multiple, serious drawbacks, however. First, the degree to which PEEP recruits lung varies dramatically from patient to patient. For example, extrapulmonary ARDS tends to respond to PEEP with higher compliance and CT scan evidence of recruitment, whereas pulmonary ARDS does not.7 Similarly, those with ARDS harbor more potential for recruitment than those with ALI, but, overall, the amount of recruitable lung is modest (13%).8 To the extent that PEEP is valuable because it prevents cyclic recruitment and derecruitment, a rational approach should base the level of PEEP on the degree of recruitability, rather than assuming all lungs behave identically. In patients with ALI and ARDS, lung units collapse largely because of compressive forces, especially in dependent lung zones. One would anticipate PEEP to be effective in keeping the lung open when it produces a positive transpulmonary pressure. Surprisingly, when patients are managed according to the ARDS Network standard of care recommendations, transpulmonary pressure is most often negative, despite PEEP.9 The reasons that pleural pressure is often so high include the weight of edematous lung, raised abdominal pressure,7 and expiratory muscle contraction.10 Thus, even when lung is recruitable, Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on June 5, 2012 © 2012 American College of Chest Physicians
the pressure required to keep it open varies widely, and it would be surprising if a table based solely on oxygenation could cater to this. If PEEP-induced lung recruitment produced predictable changes in oxygenation, perhaps oxygenbased metrics would suffice. The fly in this ointment is the variable impact of PEEP on the circulation: Falling cardiac output both lowers shunt directly11 and reduces the venous blood saturation (Fick principle). Because arterial oxygenation reflects a complex interplay of shunt and mixed venous oxyhemoglobin saturation, recruitment and oxygenation are related only poorly, as has been shown with CT scanning.12 Something better is needed. Three clinical trials addressed the potential role of higher levels of PEEP than required for acceptable oxygenation. Although each failed to demonstrate that higher PEEP enhances survival, all showed a trend in that direction (after adjustment for differences in baseline covariates),13,14,15 and meta-analyses have shown this benefit fi to be statistically signifi ficant.16,177 This is a remarkable result, especially when considering that subjects were treated with higher or lower PEEP without regard to whether the lung was recruitable. Presumably, many were treated with PEEP even when this had little prospect of biologic benefit. fi Further, because raising PEEP leads to more distention at end-inspiration, all else being equal, one might expect higher PEEP in these trials to have produced benefit for some (by reducing tidal derecruitment), harm for others (no recruitment, more overdistention), and a mixture for the rest (less derecruitment but also more overdistention). Perhaps a better trial design would apply higher PEEP only to those subjects with the potential for meaningful recruitment, while also seeking to limit overdistention. In the meantime, what tools are available to the clinician to identify recruitment while avoiding the pitfalls of oxygen-based PEEP dosing? CT scanning may be the most accurate tool, but it is simply not practical. Some have advocated analyzing the pressure-volume curve for evidence of the inflation limb lower inflecfl tion point (Pflex) fl , defl flation limb upper Pfl flex, maximal compliance, true inflection point of the deflation fl limb, or the degree of hysteresis. In an ovine model of ARDS, 10 different means (gas exchange- and mechanical-based) of calculation led to rather similar PEEP levels for most.18 Disadvantages of using the pressure-volume curve include the requirement for paralysis or, at least, deep sedation; inability to discern an inflation-limb fl Pfl flex in many patients; and confounding by the effects of the chest wall. A simpler means to identify the presence of tidal derecruitment, which also warns of overdistention, is to assess the rise in pressure during constantwww.chestpubs.org
flow, volume-preset ventilation (the so-called “stress index”).19 Normally, the airway opening pressure rises linearly because respiratory system mechanical properties (compliance and resistance) do not vary much over the tidal range. If compliance increases during tidal inflation (suggesting that lung is being recruited), the pressure-time display will be convex upward (stress index , 1): More PEEP is likely to be helpful. If the pressure-time display is concave upward, compliance is falling as the lung inflates, fl possibly signaling overdistention: Tidal volume or PEEP should be lowered. Several novel means of choosing PEEP have been advocated. One uses esophageal pressure as a surrogate for pleural pressure; then PEEP is augmented until end-expiratory transpulmonary pressure is positive in the range of 0 to 10 cm H2O.9 This approach led to substantially higher PEEP in the esophageal pressure group (17 vs 10 cm H2O), higher values for oxygenation and compliance, and better adjusted 28-day survival. Another method is to use an investigational forced oscillation technique that applies lowamplitude but rapid pressure changes to estimate compliance during conventional ventilation and without need for a paralytic.20 In sum, an individualized approach to PEEP identifies fi patients whose lungs can be recruited, then applies a sufficient amount to prevent tidal recruitment and derecruitment (an amount that is often higher than PEEP tables or oxygen-based protocols would prescribe). In those who have little recruitable lung, PEEP can do little good and should be minimized. Notice how this differs from an algorithm directed at oxygenation by imagining a patient with ARDS with an unrecruitable lesion. If the arterial saturation is low, oxygen-based treatment prescribes more PEEP. This will be ineffective and may prompt overdistention. Moreover, if the saturation is still low, yet more PEEP may be prescribed. In contrast, a mechanical approach identifies the absence of tidal recruitment immediately (such as a stress index 5 1), focusing treatment away from PEEP. Current evidence points to a survival advantage to higher PEEP, but this should be targeted to those who will benefit fi and used in a way that minimizes the risk of overdistention. Gregory A. Schmidt, MD, FCCP Iowa City, IA Affiliations: fi From the Division of Pulmonaryy Diseases, Critical Care, and Occupational p Medicine, Department of Internal Medicine, Universityy of Iowa. Financial/nonfi financial disclosures: The author has reported p to CHEST T that no p potential conflicts of interest exist with anyy companies/organizations p g whose products or services may be discussed in this article. Correspondence p to: Gregory g y A. Schmidt, MD, FCCP, Division of Pulmonary Diseases, Critical Care, and Occupational CHEST / 141 / 6 / JUNE, 2012
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on June 5, 2012 © 2012 American College of Chest Physicians
1383
Medicine, Department p of Internal Medicine, Universityy of Iowa, 200 Hawkins Dr, C304-GH, Iowa City, IA 52246; e-mail: [email protected] © 2012 American College g of Chest Physicians. y Reproduction p of this article is p prohibited without written p permission from the American College g of Chest Physicians. y See online for more details. DOI: 10.1378/chest.12-0157
References 1. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflafl tion pressures. Protection by positive end-expiratory pressure. Am Rev Respir Dis. 1974;110(5):556-565. 2. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18): 1301-1308. 3. Tremblay L, Valenza F, Ribeiro SP, Li J, Slutsky AS. Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model. J Clin Invest. 1997; 99(5):944-952. 4. Fanelli V, Mascia L, Puntorieri V, et al. Pulmonary atelectasis during low stretch ventilation: “open lung” versus “lung rest” strategy. Crit Care Med. 2009;37(3):1046-1053. 5. Farias LL, Faffe DS, Xisto DG, et al. Positive end-expiratory pressure prevents lung mechanical stress caused by recruitment/derecruitment. J Appl Physiol. 2005;98(1):53-61. 6. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation fl pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis. 1988;137(5):1159-1164. 7. Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissonii A. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med. 1998;158(1):3-11. 8. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med. 2006;354(17):1775-1786. 9. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359(20):2095-2104. 10. Coggeshall JW, Marini JJ, Newman JH. Improved oxygenation after muscle relaxation in adult respiratory distress syndrome. Arch Intern Med. 1985;145(9):1718-1720. 11. Dantzker DR, Lynch JP, Weg JG. Depression of cardiac output is a mechanism of shunt reduction in the therapy of acute respiratory failure. Chest. 1980;77(5):636-642. 12. Cressoni M, Caironi P, Polli F, et al. Anatomical and functional intrapulmonary shunt in acute respiratory distress syndrome. Crit Care Med. 2008;36(3):669-675. 13. Brower RG, Lanken PN, MacIntyre N, et al; National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327-336. 14. Mercat A, Richard J-CM, Vielle B, et al; Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646-655. 15. Meade MO, Cook DJ, Guyatt GH, et al; Lung Open Ventilation Study Investigators. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive endexpiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008; 299(6):637-645. 1384
16. Phoenix SI, Paravastu S, Columb M, Vincent JL, Nirmalan M. Does a higher positive end expiratory pressure decrease mortality in acute respiratory distress syndrome? A systematic review and meta-analysis. Anesthesiology. 2009;110(5):1098-1105. 17. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010;303(9):865-873. 18. Caramez MP, Kacmarek RM, Helmy M, et al. A comparison d of methods to identify open-lung PEEP. Intensive Care Med. 2009;35(4):740-747. 19. Grasso S, Stripoli T, De Michele M, et al. ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure. Am J Respir Crit Care Med. 2007;176(8):761-767. 20. Dellacà RL, Zannin E, Kostic P, et al. Optimisation of positive end-expiratory pressure by forced oscillation technique in a lavage model of acute lung injury. Intensive Care Med. 2011;37(6):1021-1030.
Rebuttal From Dr Miller et al of positive end-expiratory pressure Application (PEEP) in ARDS is evolving. Higher PEEP may
prove beneficial in some patients with ARDS.1 We propose combining PEEP and Fio2 using a table. Dr Schmidt2 has appropriately pointed out several limitations of this method and suggested alternative strategies to management of PEEP. However, we remain unconvinced that these have been tested sufficiently to prove their reliability, safety, or overall clinical effectiveness. We recognize that the ability of PEEP to recruit lung units varies from patient to patient and mayy3 or may not4 vary by etiology of ARDS. How should this information be used? Might paired titration of PEEP and Fio2 be acceptable in extrapulmonary ARDS but not in pulmonary ARDS? Moreover, is injury among various pulmonary etiologies uniform or might hemorrhagic alveolitis respond differently than pneumococcal pneumonia after progression to ARDS? While it is important to raise the suggestion of splitting rather than lumping treatment of ARDS, answers to these questions do not presently exist. ARDS is characterized by hypoxemia because poorly aerated lung units remain perfused, creating low ventilation/perfusion regions and absolute right-to-left shunt. This hypoxemia is usually managed with supplemental oxygen delivery and/or attempts at lung unit recruitment with positive airway pressure. Both of these strategies have the potential for harm—oxygen toxicity and lung overdistention, respectively. In our opinion, Dr Schmidt overestimates the ability of current clinical tools to assess recruitment and provide a reliable guide to PEEP application. Indeed, lung recruitment correlates poorly with oxygenation. For instance, recruitment may not improve oxygenation Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on June 5, 2012 © 2012 American College of Chest Physicians