Perioperative Protective Ventilatory Strategies in Patients without Acute Lung Injuries

We enjoyed reading the recent editorial and review article about optimal tidal volume (V^T) in patients without acute lung injury.1,2Overstretching healthy lungs with “traditional” V^Tin the range of 10–15 ml/kg predicted body weight has been shown to trigger inflammatory and procoagulant alveolar responses. Furthermore, synergism rather than additivity between ventilator-induced alveolar stress and other injurious pulmonary factors (sepsis, ischemia–reperfusion, hypoxia–reoxygenation, major trauma and surgery) has been incriminated in damaging the alveolocapillary barrier. Ultimately, a multiple hit concept has emerged to explain the pathophysiologic mechanisms of acute lung injury.

We fully agree that protective ventilatory strategies (V^Tof 6 ml/kg predicted body weight, inspiratory plateau pressure <20 cm H²O, positive end-expiratory pressure [PEEP] levels >5 cm H²O) currently applied in the intensive care unit should also be adopted to manage surgical patients with “vulnerable” lungs (e.g. , ongoing inflammatory/infectious disease, lung resection, major trauma and surgery). Unfortunately, in the majority of surgical patients with “healthy” lungs and no acute lung injury risk factors, the proposed ventilatory guidelines (V^T<10 ml/kg predicted body weight, inspiratory plateau pressure <20 cm H²O, PEEP ≥5 cm H²O) will little influence the incidence and severity of postoperative respiratory complications. Indeed, in this large population group, postoperative atelectasis is the commonest problem and the major cause of hypoxemia and nosocomial pneumonia. Accordingly, preventing atelectasis should be considered as an important objective in perioperative management.3 

After anesthesia induction in the supine position, functional residual capacity is markedly reduced (approximately 0.7–1.3 l), and atelectasis develops in the dependent part of the lungs as a result of the loss of inspiratory muscle tone, cephalad diaphragm displacement, intrathoracic shift of blood volume, and oxygen resorption.4Starting from a lower functional residual capacity, the inspiratory–expiratory cycles are completed on a lesser compliant part of the pressure–volume curve, and the repetitive opening–closing of small airways and unstable alveoli initiate proinflammatory responses. Accordingly, the mechanical breath (V^T) is delivered to a nonhomogenous lung with a continuum ranging from variable degree of alveolar collapse (dependent areas) to a variable degree of overdistension (nondependent areas) that translates into ventilation–perfusion mismatch with impaired oxygenation.

Besides limiting alveolar trauma with low V^T, attenuating the loss of functional residual capacity and preventing the formation of atelectasis should be attempted by a stepwise approach (fig. 1): (1) application of continuous positive airway pressure and PEEP during the induction of anesthesia5,6; (2) titration of low to moderate PEEP levels according to physiologic indices (lower inflection point of the pressure–volume curve, oxygenation indices, hemodynamics) and/or lung imaging techniques (e.g. , electrical thoracic impedance)7; (3) intraoperative lung recruitment maneuvers (manual inflation up to the vital capacity, “ramp” PEEP elevation up to 20 cm H²O)8; (4) use of inspiratory oxygen concentration less than 80%; and (5) postoperative lung expansion strategies, including postural changes, early mobilization, and deep breathing exercises, as well as noninvasive ventilatory support.

Whenever possible, partial ventilatory modes (assist-controlled, pressure-support, bilevel positive airway pressure) through facial or laryngeal masks should be considered to avoid tracheal (re)intubation, to reduce the duration of mechanical ventilation, and to promote active displacement of the dependent part of the diaphragm. Intraoperatively, bilevel positive airway pressure ventilation has been shown to improve oxygenation indices by decreasing ventilation–perfusion mismatch.9Likewise, reversal of atelectasis and hypoxemia after major thoracic and abdominal surgery has been successfully achieved with noninvasive ventilatory techniques that resulted in a reduced need for reintubation and a lower incidence of pneumonia and sepsis.10 

To date, further randomized controlled trials are needed to question whether a multimodal lung approach effectively prevents the formation of lung atelectasis and reduces the incidence of other pulmonary complications (pneumonia, respiratory failure, hypoxemia necessitating oxygen therapy) after various types of surgical procedures.

*University Hospital of Geneva, Geneva, Switzerland. marc-joseph.licker@hcuge.ch