Lung protective ventilation in Cardiac Surgery.

Multicenter, randomized, controlled trials and meta-analyses have demonstrated that, during abdominal surgery, protective ventilation, based on low tidal volumes, positive end-expiratory pressure, and recruitment maneuvers improves postoperative outcomes [1]. Protective ventilation strategies are aimed at preventing alveolar over-distension, cyclic opening and closure of peripheral airways, trans-pulmonary pressure related lung stress, recruitment and de-recruitment of lung units, and local and systemic release of inflammatory mediators. Barotrauma, volutrama, and atelectrauma are all involved in ventilator induced lung injury, and it is generally accepted that protective ventilation, delivered in patients with injured lungs (acute respiratory distress syndrome), increases patients’ survival [2, 3]. It is also of note that non-injured lungs (e.g. those undergoing elective surgery) may suffer from ventilator induced lung injury independently of an underlying pulmonary or extra-pulmonary disease. General anesthesia reduces muscular tone and alters diaphragmatic position promoting reduction in lung volume, alteration in ventilation/perfusion ratio, and the onset of lung atelectasis, all of which are strong predictors of pulmonary complications. Hence, mechanical ventilation is an injurious procedure. Its effects depend on intensity, duration and underlying predisposing factors. In light of this, patients undergoing cardiac surgery are particularly sensitive to lung damage for several reasons: mechanical ventilation may be long lasting, co-morbidities are frequently present, and pro-inflammatory co-factors (cardiopulmonary bypass, transfusions, ischemia/reperfusion) negatively affect the lungs. In fact, respiratory dysfunction is a very common complication after cardiac surgery, with an incidence of about 25% [4]. Approximately 2-5% of these patients are at risk of developing severe postoperative lung dysfunction, which contributes to perioperative mortality. Cardiopulmonary bypass related systemic inflammatory response syndrome represents an important first hit for lung injury, and injurious (or non-protective) ventilation may act as a second hit that worsens the lung damage. In addition, during cardiopulmonary bypass, the lungs are under-perfused, non-ventilated (lung function is carried out by an extracorporeal gas-exchanger, and the absence of lung movement clearly facilitates surgery) or under low-continuous positive airway pressure, depending on center protocols. Recently, beneficial effects of protective ventilation in cardiac surgery patients have been published. However, there is still insufficient evidence supporting specific ventilation strategies in cardiac surgery patients. In addition, the role of inspired oxygen fraction has been poorly evaluated. Oxygenation targets in intensive care units are established in order to limit oxygen toxicity [5]. In spite of this, recent trials on protective ventilation in patients undergoing surgery have not included oxygenation targets, and clear indications about the optimal oxygen inspiratory fraction during mechanical ventilation are missing. Depending on the concentration and duration of oxygen exposure, excessive production of reactive oxygen species may lead to the development of oxidative stress, damaging the lungs and distal organs. Increase in vascular resistance, reduction in cardiac output, carotid and downstream cerebral arteries vasoconstriction and decrease in coronary blood flow have all been demonstrated in healthy people, during cardiac surgery and medical emergencies involving the routine use of supplemental oxygen. In conclusion, although the protective ventilation strategy may be beneficial in a broader population with and without lung injury, the use of high tidal volume without positive end-expiratory pressure is still common during general anesthesia. The pathogenesis of postoperative pulmonary dysfunction after cardiac surgery is clearly multifactorial, and multiple strategies should be applied for its prevention. Among them, the implementation of protective ventilation strategies in these patients may play a crucial role but further trials (NCT02090205, NCT02081274) are clearly necessary since evidence is still too weak.