Editorial Views  |   June 2007
Tidal Volumes in Patients with Normal Lungs: One for All or the Less, the Better?
Author Notes
  • Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany.
Article Information
Editorial / Respiratory System
Editorial Views   |   June 2007
Tidal Volumes in Patients with Normal Lungs: One for All or the Less, the Better?
Anesthesiology 6 2007, Vol.106, 1085-1087. doi:
Anesthesiology 6 2007, Vol.106, 1085-1087. doi:
MECHANICAL ventilation (MV) using tidal volumes (VT) of not more than 6 ml/kg predicted body weight (PBW) has been shown to result in reduction of systemic inflammatory markers, increased ventilator-free days, and reduction in mortality when compared with VTof 12 ml/kg PBW in patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) (table 1).1,2 In the low VTgroup, VTwas reduced further to 5 or 4 ml/kg PBW if necessary to maintain plateau pressure (Pplat) at less than 30 cm H2O.1 However, decreasing VTdid not improve outcome in three other controlled trials investing VTin ALI and ARDS patients, which was explained by differences in study design (table 1).3–5 Using VTof not more than 6 ml/kg PBW comparing a high positive end-expiratory pressure (PEEP)–low inspiratory oxygen fraction (Fio2) with a low PEEP–high Fio2strategy to prevent hypoxemia did not demonstrate advantageous of higher PEEP levels in ALI and ARDS patients.6 The lack of effect of higher PEEP levels was partially explained by the resulting higher Pplat. A secondary analysis of the ARDS Network database showed a beneficial effect of VTreduction from 12 ml/kg to 6 ml/kg PBW even in patients with low Pplatranging between 16 and 26 cm H2O before VTreduction.7 In this issue of Anesthesiology, Schultz et al.  8 suggest the use of low VTventilation with PEEP levels above 5 cm H2O in patients without ALI or ARDS in absence of large-scale prospective randomized trials.
Table 1. Randomized and Controlled Trials Comparing High  versus  Low Tidal Volume Ventilation in Patients with Acute Lung Injury and Acute Respiratory Distress Syndrome 
Image not available
Table 1. Randomized and Controlled Trials Comparing High  versus  Low Tidal Volume Ventilation in Patients with Acute Lung Injury and Acute Respiratory Distress Syndrome 
Schultz et al.  argue that in critically ill patients requiring MV for pulmonary edema, chronic obstructive pulmonary disease, congestive heart failure, aspiration, pneumonia, and trauma and after surgery not fulfilling ARDS criteria, mortality is associated with application of high VTand Pplat.8,9 Two retrospective analyses identified high airway pressures and VTas independent risk factors for development of ALI and ARDS in patients requiring MV for acute respiratory failure.10,11 It is of importance that these analyses included patients who were critically ill and had obviously either cardiopulmonary disease or ventilatory dysfunction and had thus per se  a certain risk to develop ALI or ARDS. In an international cohort of unselected ARDS patients, neither Pplatnor VTbut use of low or no PEEP was associated with adjusted mortality.12 Recent surveys demonstrated that VTin critically ill patients is on average approximately 7–8 ml/kg BW but that still VTbetween 12 and 18 ml/kg BW are used with low or nil PEEP.13 Based on these data, it seems justified to request protective ventilator strategies in risk patients routinely and not to wait until the ALI or ARDS criteria are fulfilled. Although we do not have evidence that the ventilator settings suggested by Schultz et al.  , which are essentially based on the ARDS Network protocol, are the best way to ventilate patients at risk for ALI or ARDS, they may prevent harm from the use of too-high VTand low or nil PEEP levels.
Potential adverse effects of protective MV should be considered in all critically ill patients. Hypercapnia may cause increased intracranial pressure, pulmonary hypertension, decreased myocardial contractility, decreased renal blood flow, and release of endogenous catecholamines. Moreover, MV with low VTand Pplatmay promote atelectasis formation and increase requirements for higher Fio2and PEEP. To counteract cardiovascular depression caused by higher PEEP levels, fluid loading frequently associated with a positive fluid balance and/or catecholamines may be required. Therefore, all of these variables must be carefully considered and balanced when reducing VTin individual patients.
Another question is whether protective ventilation is beneficial in patients with healthy lungs requiring short-term MV during anesthesia. Besides airway closure and reduced lung volumes in the supine position, distortion of rib cage (and lung), cephalad shift of the diaphragm, surfactant alteration, blood shift from abdomen to thorax, or a combination of these contribute to atelectasis formation in 90% of the patients during anesthesia.14 In the 1960s, use of large VTof approximately 15 ml/kg BW was advocated to reopen collapsed lung tissue and prevent impaired oxygenation during anesthesia.15 Cyclic opening and closing caused by recruitment and derecruitment of small airways or lung units may lead to increased local shear stress (atelectrauma), which has been suggested to contribute to lung damage even in the absence of high Pplat.16 However, for identical VTand PEEP, reducing respiratory frequency attenuates or delays damage, provided that tidal ventilatory stress is sufficiently high.17 This indicates that the doses of stress will matter. Whereas a ventilator cycle is repeated 20,000–40,000 times per day for a longer period in critically ill patients, probably not more than 900 cycles are commonly applied per 1 h of anesthesia. PEEP levels up to 10 cm H2O are necessary in healthy patients during anesthesia to keep open those units that are most likely to close. However, any lung-protective benefit of PEEP is expected to be unimpressive when Pplatis modest or when the lung contains few recruitable units. Atelectatic area on computed tomography slice near the diaphragm is generally approximately 5–6% of the total lung area but can exceed 15–20% during uneventful anesthesia.14 This may explain why in patients with healthy lungs undergoing elective major thoracic or abdominal surgery, MV with VTof 12–15 ml/kg PBW and nil PEEP did not result in different pulmonary or systemic levels of inflammatory markers when compared with VTof 6 ml/kg PBW and PEEP of 10 cm H2O.18 
Individual factors such as obesity, pneumoperitoneum, preexisting disease, and some surgical interventions may aggravate atelectasis formation. In addition, a variety of cofactors apart from ventilator settings such as positioning; systemic inflammatory response depending, for example, on the amount of surgical trauma; and higher precapillary19 and lower postcapillary20 pulmonary vascular pressures are important for generation or prevention of ventilator-induced lung injury. As highlighted by Schultz et al.  , smaller randomized controlled trials of perioperative ventilatory strategies during major surgery revealed nonuniform results.8 The impression is that ventilatory strategy is more relevant during surgery that triggers a higher inflammatory response, such as esophagectomy or cardiac surgery. However, these studies where not designed or powered to draw clinically relevant conclusions on clinical outcome measures, but studied inflammatory markers that are likely to but not proven to be surrogate markers of clinical outcome. To avoid high plateau pressures during one-lung ventilation, it has been suggested to use VTof 5–6 ml/kg BW with PEEP in the absence of auto PEEP and to limit Pplatto less than 25 cm H2O during one-lung ventilation.21 However, application of PEEP in the dependent ventilated lung may increase pulmonary vascular resistance in this lung, diverting blood flow to the nonventilated lung, and thereby increasing intrapulmonary shunt and hypoxemia.
Although VTof more that 10 ml/kg PBW are probably seldom used during anesthesia, there is no sound scientific basis to consider further VTreduction necessary when Pplatis not higher than 16 cm H2O to prevent lung injury.8 Hypercapnia and its side effects can be generally prevented by moderate increased respiratory rates due to reduced carbon dioxide production during anesthesia. To counteract atelectasis formation during MV with low VTand Pplat, higher Fio2and PEEP may be required. Especially in the presence of hypovolemia or shock, already moderate PEEP levels require fluid loading resulting in a positive fluid balance, which is a significant risk factor for major and minor morbidity and gastrointestinal paralysis after colorectal and major surgery.22 To what extent postoperative complications are caused by respiratory dysfunction and ventilator settings during anesthesia is not yet clear.
Therefore, it is essential to tailor ventilator settings during anesthesia to the specific physiologic changes caused by surgery and preexisting disease of the patient, while treating the lungs gently. It may be concluded so far that the more ill the patient is, the more relevant the ventilatory strategy may be.
Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany.
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; 342:1301–8
Amato MB, Barbas CS, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, Kairalla RA, Deheinzelin D, Munoz C, Oliveira R, Takagaki TY, Carvalho CR: Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998; 338:347–54Amato, MB Barbas, CS Medeiros, DM Magaldi, RB Schettino, GP Lorenzi-Filho, G Kairalla, RA Deheinzelin, D Munoz, C Oliveira, R Takagaki, TY Carvalho, CR
Stewart TE, Meade MO, Cook DJ, Granton JT, Hodder RV, Lapinsky SE, Mazer CD, McLean RF, Rogovein TS, Schouten BD, Todd TR, Slutsky AS: Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. Pressure- and Volume-Limited Ventilation Strategy Group. N Engl J Med 1998; 338:355–61Stewart, TE Meade, MO Cook, DJ Granton, JT Hodder, RV Lapinsky, SE Mazer, CD McLean, RF Rogovein, TS Schouten, BD Todd, TR Slutsky, AS
Brochard L, Roudot-Thoraval F, Roupie E, Delclaux C, Chastre J, Fernandez-Mondejar E, Clementi E, Mancebo J, Factor P, Matamis D, Ranieri M, Blanch L, Rodi G, Mentec H, Dreyfuss D, Ferrer M, Brun-Buisson C, Tobin M, Lemaire F: Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. The Multicenter Trial Group on Tidal Volume Reduction in ARDS. Am J Respir Crit Care Med 1998; 158:1831–8Brochard, L Roudot-Thoraval, F Roupie, E Delclaux, C Chastre, J Fernandez-Mondejar, E Clementi, E Mancebo, J Factor, P Matamis, D Ranieri, M Blanch, L Rodi, G Mentec, H Dreyfuss, D Ferrer, M Brun-Buisson, C Tobin, M Lemaire, F
Brower RG, Shanholtz CB, Fessler HE, Shade DM, White P Jr, Wiener CM, Teeter JG, Dodd-o JM, Almog Y, Piantadosi S: Prospective, randomized, controlled clinical trial comparing traditional versus  reduced tidal volume ventilation in acute respiratory distress syndrome patients. Crit Care Med 1999; 27:1492–8Brower, RG Shanholtz, CB Fessler, HE Shade, DM White, P Wiener, CM Teeter, JG Dodd-o, JM Almog, Y Piantadosi, S
Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz M, Schoenfeld D, Thompson BT: Higher versus  lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004; 351:327–36Brower, RG Lanken, PN MacIntyre, N Matthay, MA Morris, A Ancukiewicz, M Schoenfeld, D Thompson, BT
Hager DN, Krishnan JA, Hayden DL, Brower RG: Tidal volume reduction in patients with acute lung injury when plateau pressures are not high. Am J Respir Crit Care Med 2005; 172:1241–5Hager, DN Krishnan, JA Hayden, DL Brower, RG
Schultz MJ, Haitsma JJ, Slutsky AS, Gajic O: What tidal volumes should be used in patients without acute lung injury? Anesthesiology 2007; 106:1226–31Schultz, MJ Haitsma, JJ Slutsky, AS Gajic, O
Esteban A, Anzueto A, Frutos F, Alia I, Brochard L, Stewart TE, Benito S, Epstein SK, Apezteguia C, Nightingale P, Arroliga AC, Tobin MJ: Characteristics and outcomes in adult patients receiving mechanical ventilation: A 28-day international study. JAMA 2002; 287:345–55Esteban, A Anzueto, A Frutos, F Alia, I Brochard, L Stewart, TE Benito, S Epstein, SK Apezteguia, C Nightingale, P Arroliga, AC Tobin, MJ
Gajic O, Dara SI, Mendez JL, Adesanya AO, Festic E, Caples SM, Rana R, St Sauver JL, Lymp JF, Afessa B, Hubmayr RD: Ventilator-associated lung injury in patients without acute lung injury at the onset of mechanical ventilation. Crit Care Med 2004; 32:1817–24Gajic, O Dara, SI Mendez, JL Adesanya, AO Festic, E Caples, SM Rana, R St Sauver, JL Lymp, JF Afessa, B Hubmayr, RD
Gajic O, Frutos-Vivar F, Esteban A, Hubmayr RD, Anzueto A: Ventilator settings as a risk factor for acute respiratory distress syndrome in mechanically ventilated patients. Intensive Care Med 2005; 31:922–6Gajic, O Frutos-Vivar, F Esteban, A Hubmayr, RD Anzueto, A
Ferguson ND, Frutos-Vivar F, Esteban A, Anzueto A, Alia I, Brower RG, Stewart TE, Apezteguia C, Gonzalez M, Soto L, Abroug F, Brochard L: Airway pressures, tidal volumes, and mortality in patients with acute respiratory distress syndrome. Crit Care Med 2005; 33:21–30Ferguson, ND Frutos-Vivar, F Esteban, A Anzueto, A Alia, I Brower, RG Stewart, TE Apezteguia, C Gonzalez, M Soto, L Abroug, F Brochard, L
Sakr Y, Vincent JL, Reinhart K, Groeneveld J, Michalopoulos A, Sprung CL, Artigas A, Ranieri VM: High tidal volume and positive fluid balance are associated with worse outcome in acute lung injury. Chest 2005; 128:3098–108Sakr, Y Vincent, JL Reinhart, K Groeneveld, J Michalopoulos, A Sprung, CL Artigas, A Ranieri, VM
Hedenstierna G, Edmark L: The effects of anesthesia and muscle paralysis on the respiratory system. Intensive Care Med 2005; 31:1327–35Hedenstierna, G Edmark, L
Bendixen HH, Hedley-Whyte J, Laver MB: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation: A concept of atelectasis. N Engl J Med 1963; 269:991–6Bendixen, HH Hedley-Whyte, J Laver, MB
Mols G, Priebe HJ, Guttmann J: Alveolar recruitment in acute lung injury. Br J Anaesth 2006; 96:156–66Mols, G Priebe, HJ Guttmann, J
Moloney ED, Griffiths MJ: Protective ventilation of patients with acute respiratory distress syndrome. Br J Anaesth 2004; 92:261–70Moloney, ED Griffiths, MJ
Wrigge H, Uhlig U, Zinserling J, Behrends-Callsen E, Ottersbach G, Fischer M, Uhlig S, Putensen C: The effects of different ventilatory settings on pulmonary and systemic inflammatory responses during major surgery. Anesth Analg 2004; 98:775–81Wrigge, H Uhlig, U Zinserling, J Behrends-Callsen, E Ottersbach, G Fischer, M Uhlig, S Putensen, C
Hotchkiss JR Jr, Blanch L, Naveira A, Adams AB, Carter C, Olson DA, Leo PH, Marini JJ: Relative roles of vascular and airspace pressures in ventilator-induced lung injury. Crit Care Med 2001; 29:1593–8Hotchkiss, JR Blanch, L Naveira, A Adams, AB Carter, C Olson, DA Leo, PH Marini, JJ
Broccard AF, Vannay C, Feihl F, Schaller MD: Impact of low pulmonary vascular pressure on ventilator-induced lung injury. Crit Care Med 2002; 30:2183–90Broccard, AF Vannay, C Feihl, F Schaller, MD
Michelet P, D'Journo XB, Roch A, Doddoli C, Marin V, Papazian L, Decamps I, Bregeon F, Thomas P, Auffray JP: Protective ventilation influences systemic inflammation after esophagectomy: A randomized controlled study. Anesthesiology 2006; 105:911–9Michelet, P D'Journo, XB Roch, A Doddoli, C Marin, V Papazian, L Decamps, I Bregeon, F Thomas, P Auffray, JP
Soop M, Nygren J, Ljungqvist O: Optimizing perioperative management of patients undergoing colorectal surgery: What is new? Curr Opin Crit Care 2006; 12:166–70Soop, M Nygren, J Ljungqvist, O
Table 1. Randomized and Controlled Trials Comparing High  versus  Low Tidal Volume Ventilation in Patients with Acute Lung Injury and Acute Respiratory Distress Syndrome 
Image not available
Table 1. Randomized and Controlled Trials Comparing High  versus  Low Tidal Volume Ventilation in Patients with Acute Lung Injury and Acute Respiratory Distress Syndrome