It’s worth to go back in history and see the evolution of proposed ventilator strategies for anesthesia and mechanical ventilation. There are two interesting studies, which should be mentioned here. More than 50 years ago, at the beginning of modern mechanical ventilation, in 1963, Bendixen et al. found a relation between the degree of ventilation and the magnitude of fall in arterial oxygen tension [3]. Large tidal volumes (VTs) appeared to protect against falls in oxygen tension, presumably by providing continuous hyperinflation, while shallow VTs lead to atelectasis and increased shunting, with impaired oxygenation. The second study [4], at the beginning of this century, a multicenter, randomized study, compared two methods of mechanical ventilation in patients with ALI and ARDS. Traditional ventilation method with VT of 12 ml/kg of predicted body weight (PBW) and an end-inspiratory airway pressure (plateau pressure) of 50 cmH₂O or less was compared with ventilation with an initial VT of 6 ml/kg of PBW and a plateau pressure of 30 cmH₂O or less. In patients with ALI and ARDS, mechanical ventilation with a lower VT than was traditionally used at that time resulted in decreased mortality and increased the number of postoperative days without a need for mechanical ventilation. Interesting to mention, too, is that the trial was stopped before the initially proposed number of patients was reached, because the results were very satisfactory.

Better understanding of the pathophysiology of ARDS has led to the proposal that airway pressures and tidal volumes should be limited in ventilator management of these patients [5]. This means that sometimes a rise in the arterial partial pressure of carbon dioxide (PaCO₂) should be accepted. Severe hypercapnia and acidosis can have adverse effects, including increased intracranial pressure, depressed myocardial contractility, pulmonary hypertension, and depressed renal blood flow. The view that these risks are preferable to the higher plateau pressure required to achieve normocapnia has represented a substantial shift in ventilatory management. Cyclic inflation-deflation of injured lung units or alveoli can exacerbate lung injury, and medium to high levels of positive end-expiration pressure (PEEP) should be used to keep alveoli open throughout the ventilatory cycle. Overall, this type of approach has been termed lung-protective ventilation strategy. Ventilation with lower VT was also associated with lower levels of systemic inflammatory mediators [6].

In a retrospective cohort study of patients with normal lungs at the onset of mechanical ventilation in ICU, three different VTs were used for mechanical ventilation (either <9, 9–12, or >12 ml/kg PBW). The study showed the occurrence of ventilator-associated lung injury in these patients; however, their incidence was significantly lower in those who were ventilated with lower VT [7].

A preventive, randomized controlled trial, also in ICU settings, compared 6 vs 10 ml/kg PBW VTs in mechanically ventilated patients without ALI at the start of mechanical ventilation. The percentage of occurrence of ALI/ARDS in the group ventilated with 6 ml/kg was 2.6 % as compared to 13.5 % in the second group [8].

These presented studies have identified the use of large VTs as a major risk factor for development of lung injury in mechanically ventilated patients without acute lung injury.

A multicenter observational study of intraoperative ventilatory management during GA and TLV showed that according to ideal body weight, approximately 30 % of patients are still ventilated with VTs higher than 10 ml/kg [9].

A recent meta-analysis [10] assessed whether incidence, morbidity, and in-hospital mortality associated with postoperative lung injury are affected by type of surgery and whether outcomes are dependent on type of ventilation. The total incidence of postoperative lung injury was similar for abdominal and thoracic surgery. Patients who developed postoperative lung injury were older, with higher ASA scores and prevalence of sepsis or pneumonia, more frequently received blood transfusions during surgery, and were ventilated with higher tidal volumes, lower PEEP, or both, than patients who did not. ICU and hospital stay were longer, and in-hospital mortality was higher in the patients with lung injury than in those without injury and also higher in the patients who underwent thoracic interventions as compared to abdominal surgery. Lung-protective ventilatory strategies reduced the incidence of postoperative lung injury but did not improve mortality.

The main differences between mechanical ventilation in ICU patients and patients in OR settings are the duration of ventilation (short term, rarely exceeding 6–8 h in OR, with in most cases an easy weaning, while in ICU ventilation is most of times lasting for more than 24 h, with sometimes difficult weaning). However, even short-term ventilation can produce lung damage, and injurious mechanical ventilation may lead to epithelial cell apoptosis (far from the lungs, including kidneys and the small intestine) [11].

As anesthesiologists and physicians first of all, we are striving to improve quality of care in medicine and of course in mechanical ventilation too. There is enough evidence in the literature with physiological rationale, meta-analyses, or just small studies which suggest the low-VT option as a valuable one.

The main determinants of ventilator-induced lung injury were proposed to be the end-inspiratory transpulmonary pressure and the regional overdistension – mainly determined by the high VT – which would not occur during “normal” spontaneous breathing. There are other causes which even during very short-term mechanical ventilation may cause injury to the lungs, surfactant deactivation by mechanical ventilation causing problems in surfactant adsorption and desorption, or elevated tissue stress between lung structures with different mechanical properties. The second main mechanism is the low end-expiratory lung volume injury, in other words the atelectasis-induced lung injury, the so-called silent killer of peripheral airways [12].

Normally, in a healthy, erect subject, ventilation occurs above closing capacity (CC) (the resting volume in the lungs at which peripheral airway closure occurs, with inhomogeneity of distribution of ventilation and impaired gas exchange and consequent risk of peripheral airway injury). Airway closure, which can occur when the CC exceeds the end-expiratory lung volume (FRC), is commonly observed in diseases characterized by increased CC (e.g., chronic obstructive pulmonary disease, asthma, aging) and/or decreased FRC (e.g., obesity, chronic heart failure). Airway closure is a commonly observed phenomenon during GA and not only in obese patients, where FRC is already decreased.

Applying high VT with high inspiratory pressures, during mechanical ventilation, will lead to barotrauma or volutrauma, with release of inflammatory cytokines interleukin (IL)-1 beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha leading to biotrauma. On the other hand, if low VT is used without PEEP, atelectrauma will occur with the same consequences [13].

Atelectasis and pulmonary gas exchange were studied in supine patients without lung disease. Positive end-expiratory pressure reduced the atelectasis in all patients but did not change the degree of shunt. It was concluded that the development of atelectasis in dependent lung regions is a major cause of gas exchange impairment during GA, during both spontaneous breathing and mechanical ventilation, and that PEEP diminishes the atelectasis, but not necessarily the shunt [14]. Even if a PEEP is associated with low-VT ventilation, prolonged impaired lung function after major surgery is not ameliorated [15].

Some minutes after induction of general anesthesia, in healthy patients, FRC decreases by almost 20 % [16]. All anesthetic drugs (but ketamine), even with spontaneous breathing, decrease FRC after induction of anesthesia. During sleep, FRC is reduced during rapid eye movement (REM) sleep at the same level as after induction of GA. Reduced respiratory muscle tone and airway closure are likely causative factors. However, during sleep, atelectasis does not develop, because the FiO₂ is low [17]. At the induction of GA, preoxygenation with FiO₂ of 80 % instead of 100 % may be sufficient in most patients with no anticipated difficulty in managing the airway, but time to hypoxemia during apnea decreases. Continuous positive airway pressure (CPAP)/PEEP was proposed to prevent fall in FRC. Inspired oxygen concentration of 30–40 %, or even less, should suffice if the lung is kept open [18].

Alveolar recruitment maneuvers (ARMs) were proposed to ameliorate oxygenation before applying a PEEP [19]. Different methods of ARM were described. But very simply explained, it consists of inflation to an airway pressure of 40 cmH₂O for 10 s and to higher airway pressures in patients with reduced abdominal compliance (obese and patients with abdominal disorders), while respecting a driving pressure of maximum 15 cmH₂O and increasing PEEP. A low and constant driving pressure during all the procedure allows an increased safety margin when a higher PEEP is employed during ARM. Alveolar recruitment maneuvers followed by PEEP reduce atelectasis and improve oxygenation in morbidly obese patients, whereas either PEEP or ARM alone does not [20]. The effect of ARMs on patient outcome in the postoperative period is, however, not yet known.

There is large evidence that during GA, lung-protective ventilation should be used. Ideally it should be a combination of low VT (how low is low?) and ARM (early and repeated) before applying PEEP. A study comparing standard mechanical ventilation lasting more than 2 h (VT 9 ml/kg, without PEEP or ARM) versus lung-protective ventilation (VT 7 ml/kg with PEEP 10 cmH₂O and ARM) obtained better inflammatory responses and better chest X-ray postoperatively in the group with protective ventilation [21]. The IMPROVE study (n = 400) [22] compared ventilation with VTs of 10–12 ml/kg, without PEEP or ARM, to ventilation with VT of 8 ml/kg, with PEEP 6–8 cmH₂O and ARM after intubation and repeated every 30–40 min. As compared with a practice of non-protective mechanical ventilation, the use of a lung-protective ventilation strategy in intermediate-risk and high-risk patients undergoing major abdominal surgery was associated with improved clinical outcomes.

The PROVHILO international study (n = 900) [23] compared two groups during abdominal surgery too, using the same VT of 8 ml/kg for both groups, but in the conventional ventilation group with a PEEP <2 cmH₂O and in the protective ventilation group with a PEEP of 12 cmH₂O and ARM after intubation, after any disconnection of ventilator, and before extubation. Compared with patients in the lower PEEP group, those in the higher PEEP group developed intraoperative hypotension and needed more vasoactive drugs. The high level of PEEP and ARM during open abdominal surgery did not protect against postoperative pulmonary complications. Their recommendations were that an intraoperative protective ventilation strategy should include a low tidal volume and low PEEP (not the 12 cmH₂O used), without ARM.

After all these large, international studies, with different and sometimes contradictory findings, the question, if they are of real help or more confusing, may be justified [24].

There are benefits for both of them; however, the incidence of perioperative complications is not different. The best mode depends on the patient and the anesthesiologists should apply the mode that they best know and master. Even in obese patients, no real benefits could be demonstrated when using these two types of mechanical ventilation, which remains rather physician dependent, than really goal oriented.

Mechanical ventilation should no longer be considered only as a way to supply gas exchange during GA. Inadequate ventilatory settings can produce lung damage even in patients with healthy lungs, even for short periods of mechanical ventilation, not only in ICU, but in OR too. Lung-protective ventilation is the standard of care in most ARDS patients and it should become in OR too.

The relative contribution of low VT, low pressures, and PEEP in prevention of ventilator-induced lung injury is uncertain. Driving pressure (VT/compliance of respiratory system (CRS)), in which VT is intrinsically normalized to functional lung size (instead of predicted lung size in healthy persons), was suggested to be a better parameter associated with survival than VT or PEEP in patients who are not actively breathing [25].

The “baby lung” concept was described by Gattinoni et al., to characterize the normally aerated lung tissue in ARDS/ALI patients, which was comparable to the lung dimensions of a young child. They suggested that in these patients, the CRS is linearly related to the dimensions of the aerated lung regions, which is not at all stiff, but with normal elasticity; thus, for ventilator-induced lung injury, what is important is the ratio of VT to aerated lung volume and to body weight; the smaller the “baby lung,” the greater is the potential for unsafe mechanical ventilation [26]. This principle may be extrapolated for OLV also.

One-lung ventilation is a technique that adds supplementary difficulties to the complexity of anesthesia management per se (generally combined sometimes with epidural technique) and to the management of patients which present in most of cases with compromised pulmonary (and other organ system) functions.