Airway Closure during Surgical Pneumoperitoneum in Obese Patients

Abstract

Background: Airway closure causes lack of communication between proximal airways and alveoli, making tidal inflation start only after a critical airway opening pressure is overcome. The authors conducted a matched cohort study to report the existence of this phenomenon among obese patients undergoing general anesthesia.Methods: Within the procedures of a clinical trial during gynecological surgery, obese patients underwent respiratory/lung mechanics and lung volume assessment both before and after pneumoperitoneum, in the supine and Trendelenburg positions, respectively. Among patients included in this study, those exhibiting airway closure were compared to a control group of subjects enrolled in the same trial and matched in 1:1 ratio according to body mass index.results: Eleven of 50 patients (22%) showed airway closure after intubation, with a median (interquartile range) airway opening pressure of 9 cm H 2 O (6 to 12). With pneumoperitoneum, airway opening pressure increased up to 21 cm H 2 O (19 to 28) and end-expiratory lung volume remained unchanged (1,294 ml [1,154 to 1,363] vs. 1,160 ml [1,118 to 1,256], P = 0.155), because end-expiratory alveolar pressure increased consistently with airway opening pressure and counterbalanced pneumoperitoneum-induced increases in end-expiratory esophageal pressure (16 cm H 2 O [15 to 19] vs. 27 cm H 2 O [23 to 30], P = 0.005). Conversely, matched control subjects experienced a statistically significant greater reduction in end-expiratory lung volume due to pneumoperitoneum (1,113 ml [1,040 to 1,577] vs. 1,000 ml [821 to 1,061], P = 0.006). With airway closure, static/dynamic mechanics failed to measure actual lung/respiratory mechanics. When patients with airway closure underwent pressure-controlled ventilation, no tidal volume was inflated until inspiratory pressure overcame airway opening pressure.conclusions: In obese patients, complete airway closure is frequent during anesthesia and is worsened by Trendelenburg pneumoperitoneum, which increases airway opening pressure and alveolar pressure: besides preventing alveolar derecruitment, this yields misinterpretation of respiratory mechanics and generates a pressure threshold to inflate the lung that can reach high values, spreading concerns on the safety of pressure-controlled modes in this setting.

Flow-controlled ventilation (FCV) improves regional ventilation in obese patients – a randomized controlled crossover trial

“…The implications of obesity on respiratory system mechanics are well known: chest wall mechanics are impaired, and respiratory system compliance is reduced. Obese patients have an increased risk for early expiratory alveolar collapse and potential consecutive atelectrauma [3,5,17,19,20] and thus for decreased functional residual capacity and expiratory reserve volume [5,13,21,22]. Values are stated as mean ± SD.…”

“…The mechanisms behind this recruiting effects may be time dependent: when the lung volume falls below the closing capacity airway closure can occur within the expiration [5,23]. In obese patients, this airway closure can be observed frequently [3]. The overall delayed expiration during FCV delays the time point at which the lung volume falls below the closing capacity.…”

“…In obese patients, the excessive adipose tissue around the thorax and the visceral organs reduce the functional residual capacity and expiratory reserve volume [1]. Obesity also leads to a low respiratory system compliance, early expiratory alveolar collapse with consecutive atelectasis, increased airway resistance [2] and increased risk for airway closure [3]. All these changes make mechanical ventilation in obese patients prone to respiratory complications [4,5].…”

A lung rescue team improves survival in obesity with acute respiratory distress syndrome

“…In both the cohorts of patients, pressure-volume curves were not performed, thus careful airway closure was not estimated; however, as shown by Grieco [31] in people with obesity, airway closure might be a common phenomenon in the obese population and could co-exist with alveolar derecruitment in our patients as well. Despite the real value of alveolar pressure, it is unknown when airway closure is detected, it was shown [31] that theoretically it could be close to the airway opening pressure; consequently, the alveolar pressure at the end of expiration is independent of the applied PEEP when its value is below the opening airway pressure.…”

Comparison of Pressure-Controlled Ventilation with Volume Guarantee and Volume-Controlled Ventilation mode in Patients under Laparoscopic Surgery: A Meta-Analysis of Randomized Controlled Trials

“…However, during laparoscopic surgery, pneumoperitoneum pressure of about 11-15mmHg would be created to facilitate surgical access. Due to the creation of pneumoperitoneum, a series of pathophysiological changes in cardiorespiratory systems would be generated in patients during the operation, such as the decline in lung compliance [4], increase in airway pressure [5], and reduction in functional residual capacity (FRC). In the severe cases, it could lead to the imbalance of ventilation/perfusion ratio, decreased arterial oxygen levels, lung collapse etc., and promote the occurrence of postoperative pulmonary complications (PPC) [6].…”