34.02 Impaired Respiratory Mechanics and Repetitive Atelectasis during Laparoscopic Abdominal Surgery

S. Murphy1, C. Love4, M. W. Breidenstein2, M. Rafferty4, A. Friend2, J. Bates3, G. Tharp2, P. Bender2  4University Of Vermont College Of Medicine / Fletcher Allen Health Care,College Of Medicine,Burlington, VT, USA 3University Of Vermont College Of Medicine / Fletcher Allen Health Care,College Of Engineering And Mathematical Sciences,Burlington, VT, USA 1University Of Vermont College Of Medicine / Fletcher Allen Health Care,General Surgery,Burlington, VT, USA 2University Of Vermont College Of Medicine / Fletcher Allen Health Care,Department Of Anesthesia,Burlington, VT, USA

Introduction:

Laparoscopic abdominal surgery and general anesthesia alter respiratory mechanics, which can lead to postoperative pulmonary complications (PPC). PPC mechanisms are not understood but may partly depend on ventilation technique.  Lung protective ventilation strategies pioneered in the ICU have had some success in the OR but are not yet standardized.  One component of intraoperative ventilation that may reduce lung trauma is individualization of positive end expiratory pressures (PEEP) to maintain a positive transpulmonary pressure (TPP). The TPP is a summation of forces experienced by the alveoli and is the difference between airway pressure (Pao) and intrapleural pressure (Ppl). When TPP is positive, the alveoli open; when TPP is negative, the alveoli close.  TPP can be estimated using esophageal manometry, which approximates Ppl, by the equation PTPP=Pao–Pes, where Pes is the esophageal pressure. We hypothesized that subjects undergoing robotic abdominal laparoscopic surgery (RALS) would have negative TPP at end-expiration (TPPexp), positive TPP at end-inspiration (TPPins), and that TPP would decrease with insufflation and Trendelenberg positioning (Tberg).

Methods:

We conducted a cross-sectional study of pulmonary mechanics in subjects having RALS at the University of Vermont Medical Center. Using a flow meter and esophageal manometry we calculated TPPexp and TPPins after subjects were intubated and supine, then supine with abdominal insufflation, insufflated and in Tberg, and finally, supine and desufflated.  TPP data were extracted from 2–3 minutes of stable ventilation using a single compartment model of pulmonary mechanics. Data were analyzed using repeated measures ANOVA. A p <0.05 was considered significant. Data are presented as mean±s.d cmH2O.

Results:

We recruited 28 subjects undergoing RALS.  Not all positions had reliable data for 2–3 minutes.  We found mean TPPexp following intubation to be –3.9±5.2 with mean TPPins of 3.2±4.1 (n=28). Once insufflated with pressures ranging from 12–16mmHg, TPPexp fell to–6.9±6.1 with TPPins of 2.7±3.4 (n=27). With Tberg between 13–30?, mean TPPexp was –7.7±6.0 with TPPins of 3.3±3.4 (n=27). After returning to supine and desufflated, TPPexp averaged –3.8±5.1 with TPPins of 4.0±3.8 (n=20). Repeated measures ANOVA showed insufflation and Tberg significantly decreased TPPexp (p<0.001) compared to the initial supine position.

Conclusions:

Even without abdominal pressure from insufflation and Tberg, the changes in TPP show cycling of the alveolar units, concerning for atelectatic trauma. Abdominal insufflation and head-down positioning contributed significantly to atelectatic cycling. Our results suggest that PPC may be related to repeated atelectasis from ventilation parameters and imply individualized changes in PEEP could improve respiratory dynamics in the surgical patient.