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Anesthesiology:
doi: 10.1097/01.anes.0000265424.07486.8c
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Tidal Volumes in Patients with Normal Lungs: One for All or the Less, the Better?

Putensen, Christian M.D.; Wrigge, Hermann M.D.

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Table 1
Table 1
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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 VT of 12 ml/kg PBW in patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) (table 1).1,2 In the low VT group, VT was 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 VT did not improve outcome in three other controlled trials investing VT in ALI and ARDS patients, which was explained by differences in study design (table 1).3–5 Using VT of 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 Fio2 strategy 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 VT reduction from 12 ml/kg to 6 ml/kg PBW even in patients with low Pplat ranging between 16 and 26 cm H2O before VT reduction.7 In this issue of Anesthesiology, Schultz et al.8 suggest the use of low VT ventilation with PEEP levels above 5 cm H2O in patients without ALI or ARDS in absence of large-scale prospective randomized trials.
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 VT and Pplat.8,9 Two retrospective analyses identified high airway pressures and VT as 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 Pplat nor VT but use of low or no PEEP was associated with adjusted mortality.12 Recent surveys demonstrated that VT in critically ill patients is on average approximately 7–8 ml/kg BW but that still VT between 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 VT and 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 VT and Pplat may promote atelectasis formation and increase requirements for higher Fio2 and 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 VT in 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 VT of 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 VT and 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 Pplat is 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 VT of 12–15 ml/kg PBW and nil PEEP did not result in different pulmonary or systemic levels of inflammatory markers when compared with VT of 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 VT of 5–6 ml/kg BW with PEEP in the absence of auto PEEP and to limit Pplat to 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 VT of more that 10 ml/kg PBW are probably seldom used during anesthesia, there is no sound scientific basis to consider further VT reduction necessary when Pplat is 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 VT and Pplat, higher Fio2 and 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.
Christian Putensen, M.D.
Hermann Wrigge, M.D.
Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany. putensen@uni-bonn.de
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References

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