Perioperative Lung Protective Strategies

The traditional intraoperative ventilatory settings (tidal volume > 10 ml/kg ideal body weight) can be harmful even in patients with healthy lungs. In the operating theatre, safe anesthesia and optimization of oxygen delivery should be achieved while minimizing the deleterious effects of surgical trauma and avoiding iatrogenic complications. This review examines the mechanisms of perioperative lung injuries and particularly the injurious effects of mechanical ventilation. Protective lung strategies are discussed using a physiological approach, being mainly focused on the surgical patients with “healthy” lungs. *Corresponding author: Marc J Licker MD, Department of Anesthesiology, Pharmacology and Intensive Care, University Hospital of Geneva, rue GabriellePerret-Gentil, CH-1205 Geneva, Switzerland, E-mail: Marc-joseph.licker@hcuge.ch Received November 11, 2011; Accepted December 19, 2011; Published January 12, 2012 Citation: Licker MJ, Tschopp J, Diaper J (2012) Perioperative Lung Protective Strategies. J Pulmonar Respirat Med S2:002. doi:10.4172/2161-105X.S2-002 Copyright: © 2012 Licker MJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Introduction Currently, the incidence of postoperative pulmonary complications (PPC) far outnumbers cardiovascular complications [1]. They vary from 10% to 70%, depending on their definition, study design (retrospective or prospective), the heterogeneity of patient populations and the type of procedure [2]. In thoracic surgery, the main causes of perioperative deaths have now shifted from cardiovascular to infectious and pulmonary complications [3,4]. Pulmonary morbidity has also been associated with increasing health care costs and poor outcome as reflected by prolonged hospital stay, (re-)admission in intensive care units and reduced long-term survival [5,6]. Transient and self-limiting impairments in gas exchange should be considered as part of the anesthesia emergence period and as the physiological response to surgery. Most of the patients undergoing cardiothoracic or abdominal operations present some degree of hypoxemia and diffuse micro-atelectasis that will barely impact on the postoperative clinical course. In contrast, pleural effusions, sustained bronchospasm, lobar atelectasis or hypoxemia unresponsive to supplemental oxygen may forecast serious adverse events such as bronchopleural fistula, pneumonia, acute lung injury (ALI) or respiratory failure [7]. Predictive factors of PPCs include patient-related factors (e.g., chronic obstructive pulmonary disease [COPD], advanced age, poor nutritional status, decreased exercise tolerance, heart failure) and intraoperative related factors (i.e., emergency surgery, upper abdominal and intra-thoracic procedures, duration of anesthesia, presence of a nasogastric tube, ventilatory settings, fluid balance) [2,8]. These procedure-related factors are much more amenable to modification than preexisting chronic diseases. In an effort to standardize the reporting of adverse perioperative events, Dindo and coll. [9] have validated a 5-grade scoring system based on the therapeutic consequences and residual disabilities in relation to surgical operations. Grade I complications entail any deviation from the normal postoperative course with no need for medical interventions (except a slight increase in inspiratory oxygen fraction [FIO2] or lung recruitment maneuvers). Grades II and III complications require non-invasive ventilatory support, pharmacological treatment (e.g., bronchodilators, diuretics) or specific interventions (e.g., fiberoptic bronchoscopy, thoracic drainage). Grade IV includes life-threatening complications (single-or multiple organ failure) requiring ICU admission and/or mechanical ventilation. Mechanisms of Perioperative Pulmonary Injuries Atelectasis Collapsed lung areas or atelectasis develop in about 90% anaesthetized patients, irrespective of ventilatory control (spontaneous or mechanically supported) and of anesthesia type (intravenous agent, volatile anaesthetics or, combined general anesthesia and regional block) [10]. Atelectasis formation predominantly results from the reduction of lung volumes and from deficient or abnormal synthesis of surfactants that occur during anesthesia and could persist or even worsen after completion of the surgical procedure. By changing from upright to supine position, the functional respiratory capacity (FRC) is decreased by 0.8-1.0 L and a further reduction of 0.4-0.5 L occurs after the induction of anesthesia owing to the relaxation of the respiratory muscles and the decrease in thoracic elastic recoil [11,12]. Ventilation with enriched oxygen mixture (FIO2 > 80%) promotes the development of atelectasis as a result of complete absorption of O2 in poorly ventilated lung regions. Depending on the duration of mechanical ventilation, 3% to 40% of the total lung volume collapses in the dependent zone resulting in impaired gas exchange intraoperatively [13]. Moreover, atelectasis impairs the clearing of bronchial secretions, it impedes lymphatic flow and may become a focus of infection in the postoperative period. In obese patients, the healthy lungs are compressed by the “heavy” weight of the chest/abdominal wall, resulting in further aggravation of the restrictive pulmonary syndrome associated with anesthesia and surgery. Likewise, in acute lung diseases and heart failure, ongoing inflammation and fluid accumulation within the lung interstitium and the alveolar space, tissue tend to expel air/gas out of the alveoli and thereby promote the development of atelectasis. Ventilator-induced lung injuries (VILI) During spontaneous ventilation (at rest), tidal volume (VT) and transpulmonary pressure (Ptp) in healthy subjects vary within tight limits of 4 to 6 ml per kg of ideal body weight (IBW) and 4 to 8 mmHg, respectively. Surprisingly and for decades, anaesthetists have been taught to apply “unphysiological” large tidal volume (10 to 15 ml/kg) to prevent the development of atelectasis. Citation: Licker MJ, Tschopp J, Diaper J (2012) Perioperative Lung Protective Strategies. J Pulmonar Respirat Med S2:002. doi:10.4172/2161-105X. S2-002