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Anesthesiology:
doi: 10.1097/01.anes.0000300053.91799.27
Correspondence

Perioperative Protective Ventilatory Strategies in Patients without Acute Lung Injuries

Licker, Marc M.D.*; Diaper, John R.A.; Ellenberger, Christoph M.D.

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To the Editor:—

We enjoyed reading the recent editorial and review article about optimal tidal volume (VT) in patients without acute lung injury.1,2 Overstretching healthy lungs with “traditional” VT in 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 (VT of 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 (VT <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.4 Starting 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 (VT) 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.
Fig. 1
Fig. 1
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Besides limiting alveolar trauma with low VT, 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.9 Likewise, 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.
Marc Licker, M.D.,*
John Diaper, R.A.,
Christoph Ellenberger, M.D.
*University Hospital of Geneva, Geneva, Switzerland. marc-joseph.licker@hcuge.ch
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References

1. Schultz MJ, Haitsma JJ, Slutsky AS, Gajic O: What tidal volumes should be used in patients without acute lung injury? Anesthesiology 2007; 106:1226–31

2. Putensen C, Wrigge H: Tidal volumes in patients with normal lungs: One for all or the less, the better? Anesthesiology 2007; 106:1085–7

3. Turrentine FE, Wang H, Simpson VB, Jones RS: Surgical risk factors, morbidity, and mortality in elderly patients. J Am Coll Surg 2006; 203:865–77

4. Hedensternia G, Edmark L: The effects of anesthesia and muscle paralysis on the respiratory system. Intensive Care Med 2005; 31:1327–35

5. Rusca M, Proietti S, Schnyder P, Frascarolo P, Hedenstierna G, Spahn DR, Magnusson L: Prevention of atelectasis formation during induction of general anesthesia. Anesth Analg 2003; 97:1835–9

6. von Ungern-Sternberg BS, Regli A, Schibler A, Hammer J, Frei FJ, Erb TO: The impact of positive end-expiratory pressure on functional residual capacity and ventilation homogeneity impairment in anesthetized children exposed to high levels of inspired oxygen. Anesth Analg 2007; 104:1364–8

7. Erlandsson K, Odenstedt H, Lundin S, Stenqvist O: Positive end-expiratory pressure optimization using electric impedance tomography in morbidly obese patients during laparoscopic gastric bypass surgery. Acta Anaesthesiol Scand 2006; 50:833–9

8. Whalen FX, Gajic O, Thompson GB, Kendrick ML, Que FL, Williams BA, Joyner MJ, Hubmayr RD, Warner DO, Sprung J: The effects of the alveolar recruitment maneuver and positive end-expiratory pressure on arterial oxygenation during laparoscopic bariatric surgery. Anesth Analg 2006; 102:298–305

9. Yu G, Yang K, Baker AB, Young I: The effect of bi-level positive airway pressure mechanical ventilation on gas exchange during general anaesthesia. Br J Anaesth 2006; 96:522–32

10. Squadrone V, Coha M, Cerutti E, Schellino MM, Biolino P, Occella P, Belloni G, Vilianis G, Fiore G, Cavallo F, Ranieri VM, Piedmont Intensive Care Units Network (PICUN): Continuous positive airway pressure for treatment of postoperative hypoxemia: A randomized controlled trial. JAMA 2005; 293:589–95

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Current Opinion in Anesthesiology
Update on one-lung ventilation: the use of continuous positive airway pressure ventilation and positive end-expiratory pressure ventilation – clinical application
Grichnik, KP; Shaw, A
Current Opinion in Anesthesiology, 22(1): 23-30.
10.1097/ACO.0b013e32831d7b41
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