Preventing intraoperative ventilator-induced lung injury is an important and evolving clinical goal in the practice of anesthesia. Lung protective ventilation (LPV) strategies have been studied for more than 2 decades, both in the critical care setting and, more recently, in the intraoperative period.1–6 Mechanical ventilation can lead to lung injury through several mechanisms including elevated tidal volumes (TVs; volutrauma), pressures (barotrauma), or shear stress from repeated cycles of opening and closing of atelectatic alveoli (atelectrauma).7 These processes can result in inflammation that may lead to increased risk of pulmonary complications. While minimizing both intraoperative volutrauma and barotrauma seems to be largely validated, the importance of appropriate positive end-expiratory pressure (PEEP) selection to prevent atelectrauma remains less clear.5 Unique scenarios encountered solely in the intraoperative period, such as steep Trendelenburg positioning and laparoscopic abdominal insufflation, make identification of mechanical ventilation parameters that minimize lung trauma especially challenging.
In this issue of Anesthesia & Analgesia, Gali et al8 present their retrospective study of perioperative complications in subjects undergoing robotic hysterectomy. Their hypothesis was that subjects undergoing robotic hysterectomy would experience increased peak inspiratory pressures (PIPs) leading to more frequent postoperative pulmonary complications compared to standard open abdominal hysterectomy, and that obesity would be associated with more complications due to higher PIP. They found no increase in pulmonary complications in subjects undergoing robotic hysterectomy despite higher observed PIP. Not surprisingly, they also found higher PIP in obese patients undergoing robotic hysterectomy when compared to nonobese patients, but this was not associated with increased pulmonary complications in the obese group. Their conclusion was that clinicians could or should deprioritize their goal of minimizing PIP in this patient population. The authors note that PIP does not accurately reflect the pressure transmitted to the alveoli due to changes in transpulmonary pressure (TPP) induced by peritoneal insufflation and steep Trendelenburg positioning.
Unfortunately, the authors were unable to report the TVs and PEEP for this retrospective study. We have only partial insight into the intraoperative ventilation strategy experienced by these patients. As the intraoperative LPV literature has blossomed, clinicians now are more likely to use smaller TV and increased levels of PEEP.9 Thus, as this study compared open hysterectomies from 2004 to 2006 with robotic hysterectomies from 2009 to 2012, it is possible that these 2 groups received different TV and PEEP strategies, introducing unmeasured confounding into their comparison. Also, the degree of inflammation resulting from surgical stress may vary when comparing an open versus minimally invasive surgical technique. Further, this is a relatively small study. The propensity matched study population with ventilator data was composed of only 138 subjects (69 in each group: open versus robotic hysterectomy). To demonstrate a significant reduction in pulmonary complications after abdominal surgery, other studies have required a significantly larger number of study subjects.1,4,10
We suggest deconstructing the approach to LPV into inspiratory and expiratory strategies. Following abdominal insufflation and Trendelenburg positioning, increased PIP in the setting of unchanged TV would be expected. These surgical conditions, along with other potential patient factors, such as obesity or increased chest wall mass, contribute to a change in pulmonary dynamics consistent with external restrictive lung disease. This reduction in pulmonary compliance leads to an uncoupling of what we would normally consider acceptable TV and PIP. Meaning, even if PIP is increased, volutrauma may still be absent if administered TV is appropriate for predicted body weight. As the authors note, in this clinical setting, PIP does not accurately reflect the TPP transmitted across the alveoli. TPP is defined as airway opening pressure minus pleural pressure (TPP = Pao − Ppl). Hence, any process that increases Ppl (obesity, chest wall mass, Trendelenburg positioning, insufflation) renders Pao measured by the ventilator less reflective of the pressure the alveoli are truly experiencing. Intuitively, if both the Pao and Ppl are increased in this scenario, alveolar TPP may remain unchanged, and barotrauma not induced. Also, the data from this study are presented as PIP, as opposed to plateau pressures (Pplat) measured during an inspiratory hold. PIP is influenced not only by compliance but also by airway resistance. Without documentation of the study population’s endotracheal tube size, history of reactive airway disease, or other confounders that may influence airway resistance, it may be unwise to extrapolate significance from the provided PIP. Additional literature has intimated the importance of inspiratory driving pressures (driving pressure = Pplat − PEEP) in the development of perioperative lung injury.4 Data on PEEP and Pplat would be needed for accurate evaluation of driving pressures in this study. Ultimately, many experts maintain the focus of LPV should be more on volume and not pressure.11 We agree. Even with the expected increase in PIP in these surgical conditions, this should not induce excessive TV or volutrauma.
The focus of the expiratory phase should be adequate PEEP administration to minimize atelectrauma. In fact, TV reduction without adequate PEEP could lead to more atelectasis and cyclic shear stress, potentially leading to harm. Ideally, measuring Ppl would be the optimal way to quantify TPP at both inspiration and expiration. An end-expiratory TPP greater than zero should maintain an open alveolus and minimize atelectasis.6 Thus, any scenarios that increase Ppl (Trendelenburg position, abdominal insufflation, obesity, etc) should be accompanied by an increase in PEEP sufficient to overcome the increase in Ppl. Direct measurement of Ppl by placement of an intrapleural manometer is invasive and rife with potential complication ranging from infection to pneumothorax. However, esophageal manometry can approximate Ppl, has been well validated in human and animal models, and may be used to guide ventilator settings to maintain lung-protective and open lung ventilation.6,12–14 As elegantly described by Talmor et al,6 a strategy using esophageal manometry in patients with known lung injury to guide ventilator settings by targeting TPP led to improved oxygenation when compared to the ARDSNet PEEP/FIO2 protocol.
With a goal of promoting open lung ventilation, several trials have attempted to identify the optimal PEEP settings, with contradictory results. Some studies have demonstrated that the use of adequate PEEP can lead to decreased postoperative complications in certain surgical patients.1,3,15 Others found no difference between high and low PEEP with identical TV in patients undergoing abdominal surgery.2 These studies point to the importance of PEEP for some patients and surgical conditions, but simple application of high versus low PEEP is painting with a broad brush. Patients with varying medical complexity, body habitus, and undergoing the wide range of potential intraoperative surgical conditions should not be thought of as equal. Appropriate PEEP may be a moving target, just as clinicians may tolerate higher PIP in certain situations. Individual titration of PEEP via measured or estimated Ppl would allow clinicians to minimize the risks and potential complications of atelectrauma and inflammation. Our current practice is to make an educated guess as to which patients may benefit from higher PEEP. We often empirically administer higher PEEP, and tolerate higher PIP, during steep Trendelenburg, abdominal insufflation, obesity, or significant chest wall mass, knowing that the pressure measured by the ventilator is less likely to reflect alveolar TPP.
In summary, we agree with the authors that PIP measured by the ventilator in this patient population may not meaningfully reflect forces experienced by the alveoli. However, we urge all clinicians to not prematurely discount the potential importance of LPV in these patients and others. We should strive for an improved understanding of the true TPP experienced during both inspiration and expiration in various patient and surgical populations and become less reliant on ventilator-measured PIP as a surrogate for TPP. Esophageal manometry may provide an easy method for approximating Ppl and guiding TPP-based ventilation strategies. Further refinement of our knowledge of intraoperative TPP could aid in identification of optimal ventilation strategies aimed at reducing postoperative pulmonary complications based on patient-specific comorbidities and surgical conditions. For now, we should maintain our focus on the administration of appropriate TV and PEEP, as opposed to readily measured ventilator pressures.
Name: S. Patrick Bender, MD.
Contribution: This author helped review the original article and contributed to writing and revision of the editorial.
Name: William G. Tharp, MD, PhD.
Contribution: This author helped review the original article and contributed to writing and revision of the editorial.
This manuscript was handled by: Richard C. Prielipp, MD.
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