Effects of Recruitment Maneuver and Positive End-expiratory Pressure on Respiratory Mechanics and Transpulmonary Pressure during Laparoscopic Surgery

Laparoscopy is a well-established procedure for pelvic gynecologic surgery often performed in Trendelenburg position.1,2To facilitate laparoscopic surgical manipulation, a pneumoperitoneum is usually induced through carbon dioxide inflation. Both the increase in abdominal pressure as a result of carbon dioxide inflation and the head down body position have been shown to impair the respiratory function during the procedure, mainly inducing atelectasis formation in the dependent lung regions.1,3–6The resulting decrease in functional residual capacity poses patients at risk of perioperative complications, particularly if they are obese and/or submitted to intricate surgical procedures.4,7In fact, ventilation at low lung volumes may generate tidal alveolar recruiting (i.e. , some alveolar units that are collapsed at end-expiration are cyclically reopened during tidal inflation), a mechanism generating an alveolar shear stress known as “atelectrauma”.8Furthermore, in presence of atelectasis, delivering the tidal volume to the limited amount of patient lung parenchyma may induce alveolar stress and strain.9Both stress, strain and atelectrauma are main mechanisms underlying ventilator-induced lung injury.9,10Despite definitive evidences that ventilator-induced lung injury may play a role when ventilating normal lungs (as generally done during anesthesia) are lacking,11the hypothesis that a lung-protective ventilatory strategy should be applied during general anesthesia is sound and widely debated.1,6,7,12–14Several ventilatory strategies aiming at improving arterial oxygenation and respiratory mechanics during laparoscopic surgery have been investigated: the application of positive end-expiratory pressure (PEEP) has been shown to counterbalance the diaphragm cranial shift increasing functional residual capacity and decreasing respiratory system elastance (ERS).12,13,15–17Recently, translating the concept of lung-protective ventilatory strategy from the adult respiratory distress syndrome context,9,14,18–20the application of an “open lung” strategy consisting in a recruiting maneuver (RM) followed by the subsequent application of PEEP has been suggested to effectively reexpand pneumoperitoneum-induced atelectasis and improve oxygenation during laparoscopic surgery.21–25However, to our knowledge, the effects of the open lung strategy on respiratory mechanics partitioned between its chest wall and lung components (i.e. , the relative effect exerted by the open lung strategy on lung and chest wall mechanics) have not been thoroughly investigated.26–28This is of particular interest because classical physiologic concepts29and recent experimental and clinical data clearly show that chest wall mechanical impairment has a deep impact on the response to any open lung strategy.9,16,20,30In fact, during controlled positive pressure ventilation, the real lung-distending pressure is the transpulmonary pressure (PL), that is, the difference between airways opening pressure (PAO) and the pressure required to expand the chest wall,28,29,31clinically estimated by measuring esophageal pressure (PES) as a surrogate of pleural pressure.32The hypothesis of the current study is that during laparoscopic gynecologic surgery, both the Trendelenburg position and pneumoperitoneum worsen chest wall elastance (ECW), concomitantly decreasing PL, and that an open lung strategy consisting of an RM followed by ventilation with PEEP applied after pneumoperitoneum induction, by increasing PL, would result in alveolar recruitment and improvement in respiratory mechanics and gas exchange.After approval of the Policlinico Riuniti, Foggia, Italy, ethics committee and written informed consent from each patient, the study was performed in consecutive patients scheduled to undergo elective gynecologic laparoscopic surgery from January to July 2011. Inclusion criteria were age more than 18 yr and American Society of Anesthesiology physical status I and II. Patients with preexisting lung or cardiac disease, pathologic lung function, or obesity (body mass index ≥ 30 Kg/m2) were excluded from the study.On their arrival in the operating room, patients were premedicated with midazolam 0.03–0.04 mg/kg. After applying standard monitoring device (electrocardiogram and pulse oximeter [Intellivue MP40 monitor, Philips, Boeblingen, Germany]), the radial artery was cannulated (Radial Artery Catheterization Set, Arrow International, Reading, PA) for continuous monitoring of blood pressure. The arterial line was connected to the FloTrac sensor and the Vigileo monitor (Edwards Life Sciences LLC, Irwine, CA, software version 03.10), which allows cardiac output and stroke volume estimation from the arterial pressure waveform and computes the stroke volume variation (SVV) in response to positive pressure mechanical ventilation as an index of cardiac preload and fluid responsiveness.33Patients were given 8 ml/kg of normal saline intravenously before the induction of anesthesia and were then maintained with 5 ml·kg–1·h–1of normal saline solution. Anesthesia was induced with propofol 2 mg/kg, fentanyl 3 ng/kg, and succinylcholine 1 mg/kg. After induction, the trachea was intubated with an endotracheal tube of appropriate size (Rushelit Rush AG Lab, Waiblingen, Germany). Anesthesia was maintained with an infusion of propofol 150–200 γ·kg–1·min–1, remifentanil 0.1–0.2 γ·kg–1·min–1, and cisatracurium 1.5 γ·kg–1·min–1. The level of anesthesia was assessed through bispectral index monitoring (Aspect A-2000®; Aspect Medical System, Newton, MA). The infusion rate of propofol was varied to target a bispectral index value between 50 and 60. The lungs were ventilated through a Servo Ventilator 900C (Siemens-Elema AB, Berlin, Germany) with a square flow waveform with a tidal volume (Vt) of 8 ml/kg ideal body weight, respiratory rate of 12 breath/min, inspiratory time of 33%, and an inspiratory pause of 20%. Patients were ventilated using oxygen in air with an inspiratory oxygen fraction set at 40% as needed to maintain the SaO2≥ 95%. No PEEP was initially added.An esophageal thin latex balloon-tipped catheter (Compliance catheter, Microtek Medical B.V. Zutphen, The Netherlands) was inserted through the mouth, advanced into the esophagus and connected by means of a polyethylene catheter to a pressure transducer (Digima-Clic, Nordlingen, Germany), to measure PES. The esophageal balloon was filled with 1–1.5 ml of air, and its correct positioning in the lower third of the esophagus was verified according to literature, by allowing a brief period of spontaneous breathing after the induction of anesthesia and comparing the esophageal and the airway opening pressure traces.32In addition, the correct balloon position in the lower third of the esophagus was confirmed by the presence of appropriate esophageal pressure deflections induced by mechanical ventilation and moderate push on the abdomen. All the data were controlled on the computer software of recording and analysis (ICU Lab, KleisTEK Engineering, Bari, Italy) through an optimal waveform.A standardized protocol for hemodynamic management was applied to ensure fluid volume optimization. In brief, if SVV was lower than 13%, no additional fluids were given, whereas if SVV was higher than 13%, additional boluses of 250 ml of artificial colloid were infused over 15–20 min. After each bolus, SVV was re-evaluated, and a further bolus was administered if stroke volume increased by more than 10%, until reaching an SVV lower than 13%.33About 15 min after pneumoperitoneum induction, if the patients were hemodynamically stable, that is, with mean blood pressure ≥ 80 mmHg, heart rate ≥ 60 beats/min, and SVV < 13%, the open lung strategy was applied as already described.34In brief, the ventilator was switched to pressure-control ventilation, inspiratory time was increased to 50%, the peak inspiratory pressure gradient (above PEEP) was set at 20 cm H2O, and PEEP was progressively increased to obtain a stepwise increase of peak inspiratory to 30, 35, and 40 cm H2O every three breaths. The final recruiting pressure of 40 cm H2O was applied for six breaths. After ward, the ventilator switched again to the volume-control ventilation with baseline settings but with a PEEP level of 5 cm H2O that was maintained after abdominal deflation until the end of surgery. Overall, the RM procedure lasted approximately 1 min. Measurements were obtained (1) 15 min after anesthesia induction in supine position before inducing the pneumoperitoneum (TBSL); (2) 15 min after pneumoperitoneum induction (abdominal carbon dioxide inflation to obtain and intra-abdominal pressure of 10 mmHg) with the patient positioned at 20° head down (TpreOLS); (3) 20 min after the application of the open lung strategy (TpostOLS); and (4) at the end of surgery, after abdominal deflation and in supine position with a PEEP level of 5 cm H2O.Hemodynamic and respiratory mechanics parameters were recorded, digitized, and collected on a personal computer through a 12-bit analog-to digital converter board (DAQCard 700; National Instrument, Austin, TX) at a sample rate of 200 Hz (ICU Lab, KleisTEK Engineering).Blood pressure was measured through a radial catheter connected to the pressure transducer of the MP40 monitor. Hemodynamic parameters obtained through the Vigileo monitor included stroke volume, cardiac output, and SVV, whereas stroke volume index and cardiac index were calculated using standard formulae. All intravascular pressure measurements were zeroed to the mid-axillary line. Analysis of arterial blood gases was performed (ABL 330; Radiometer, Copenhagen, Denmark).Flow was measured with a heated pneumotachograph (Fleisch no. 2; Fleisch, Lausanne, Switzerland), connected to a differential pressure transducer (Diff-Cap, ±1 cm H2O; Special Instruments, Nordlingen, Germany) inserted between the Y-piece of the ventilator circuit and the endotracheal tube. The pneumotachograph was linear over the experimental range of flow. Volume was obtained by numerical integration of the flow signal. PAOwas measured proximal to the endotracheal tube with a pressure transducer (Special Instruments Digima-Clic ± 100 cm H2O; Nordlingen, Germany). The difference between the level of the PEEP set on the ventilator (read as the PAOvalue at the end of a regular breath) (PEEPexternal) and the pressure in PAOduring a 3- to 5-s end-expiratory occlusion (PEEPtotRS) was measured and regarded as the static intrinsic PEEP of the respiratory system according to Pepe.35The end-expiratory occlusion was performed through the expiratory hold on the Servo 900C ventilator.Static ERSwas calculated using:ERS= PplatRS–PEEPtotRS/Vt(1)where PplatRSis the value of PAOobtained by adding an end-inspiratory pause of 2–3 s through the inspiratory hold of the ventilator.Static ECWwas calculated as:ECW= (PplatCW− PEEPtotCW)/Vt, (2)where PplatCWis the value of PESobtained contemporaneously to PplatRSduring the end-inspiratory pause. Lung static elastance (EL) was calculated as:EL= ERS– ECW(3)Transpulmonary end-inspiratory pressure (PplatL) was computed, according to Gattinoni et al .9,29as:PplatL= PplatRS× EL/(EL+ ECW) (4)Transpulmonary end-expiratory pressure (PEEPtotL) was computed during the end-expiratory pause as:PEEPtotL= PEEPtotRS× EL/(EL+ ECW) (5)Alveolar recruitment was measured though a physiologic method originally described by Ranieri et al .,36subsequently applied in several physiologic clinical studies18,28,34,37–39and recently validated by Dellamonica et al .40In brief, for each experimental condition, we first measured the quasistatic volume–pressure curves of the respiratory system through the low-flow inflation technique as originally described by Lu et al .41and subsequently measured the delta end-expiratory lung volume as the difference between the end-expiratory lung volume during mechanical ventilation and the elastic equilibrium volume of the respiratory system at zero end-expiratory pressure, or relaxation volume (Vr) or functional residual capacity. The delta end-expiratory lung volume was measured by disconnecting the patient from the ventilator circuit distally from the pneumotachograph and allowing a prolonged expiration (15–20 s; fig. 1). Of note, this method does not measure Vrper se but assumes that any alveolar recruitment obtained by applying RM or PEEP does not modify Vrand that therefore Vrremains the same in all the experimental conditions.36Knowing the respective delta end-expiratory lung volume, the quasistatic volume–pressure curves obtained before and after the RM were plotted on the same volume–pressure axis and referred to Vr(fig. 2). To do so, each volume–pressure curve started at a point corresponding to PEEPTOT(referred to the X axis) and to the end-expiratory lung volume (referred to the Y axis) (fig. 2). The recruited volume (the gas volume of collapsed or fluid-filled alveolar units eventually reaerated by the open lung strategy) was computed as the difference in lung volume at the same static PAOread on the two pressure–volume curves (fig. 2).Total airways resistances were calculated as the difference between PpeakRSand PplatRSdivided by the inspiratory airflow.37,41A sample size calculation was performed using data from the study by Grasso et al .18on the effects of RMs in patients with adult respiratory distress syndrome ventilated with protective ventilatory strategy. On the basis of these data, the significant recruitment was designated as a 100-ml increase in end-expiratory lung volume with an SD of 116.7. By using a one-sample, one-sided test, the sample size calculated was of 23 patients; this number was increased to 31 to allow for an expected dropout of around one third of patients and was used for patient enrolment. The α and β errors for the sample size were chosen as 0.05 and 90%, respectively. Because only two patients dropped out from the analysis (fig. 3), the study power was 99%.Statistical comparison of respiratory mechanics, hemodynamic, and gas exchange data was performed between the four study steps: data were tested for normal distribution by the Kolmogorov–Smirnov goodness-of-fit test and are presented as mean ± SD. Data analysis was performed using repeated-measures one-way ANOVA; if significant, the test of Tukey was applied for post hoc comparison between the different experimental conditions. A P value of less than 0.05 was considered statistically significant. Statistical analysis was performed using Statistica 8.0 (Statsoft Italia srl 2008, Vigonza Padova, Italy).Twenty-nine of 35 patients initially candidate for enrolment were included in the study. The enrolment flow diagram is reported in figure 3. Demographic characteristics of the population studied are presented in table 1. The study was completed successfully in every patient without complications or adverse events as a result of the study protocol. Data are presented as mean ± SD).Compared with the baseline (table 2), the induction of pneumoperitoneum and the Trendelenburg position worsened ECWand ELresulting in an overall increase of ERS(P = 0.00015 on TpreOLSvs. TBSL, respectively). The open lung strategy decreased both ECWand EL(P = 0.0007 on TpostOLSvs . TpreOLS, for both parameters). Both end-inspiratory and end-expiratory transpulmonary pressure (PplatLand PEEPtotL, respectively) decreased at TpreOLScompared with TBSL(P = 0.008) and both increased on TpostOLS(P = 0.008 vs. TpreOLS).Figure 4shows the quasistatic volume–pressure curves of the respiratory system measured immediately before and 20 min after the application of open lung strategy and plotted on the same volume–pressure axis (see Materials and Methods), in a representative patient. Of note, the curve obtained during the open lung strategy is shifted upward on the volume axis, clearly indicating the occurrence of alveolar recruitment. Overall, the open lung strategy resulted in a significant alveolar recruitment in all patients (194 + 80 ml, range 65–323 ml).The PaO2/inspiratory oxygen fraction ratio (table 2) worsened at TpreOLScompared with TBSL(P = 0.008) and returned to baseline values at TpostOLS(P = 0.008 vs. TpreOLS). Despite alveolar minute ventilation remained unchanged, PaCO2increased at TpreOLScompared with TBSL(P = 0.008) and returned to baseline value after the application of the open lung strategy.During the RM (table 3), cardiac index decreased by approximately 20% compared with TpreOLS(P = 0.0007), returned to TpreOLSvalues immediately after the RM and remained stable thereafter. SVV was 8.10 ± 2.37% on TBSLand remained stable throughout all the experimental conditions. Mean blood pressure and heart rate remained stable throughout the study.Our data show that in patients submitted to pelvic laparoscopic surgery in Trendelenburg position under general anesthesia, the application of an RM followed by PEEP after pneumoperitoneum induction leads to alveolar recruitment and improvement of chest wall and lung elastance.Because the diaphragm is mechanically coupled to the abdominal wall, any increase in abdominal pressure may decrease functional residual capacity.28,42During laparoscopy, the raised abdominal pressure distends the abdominal wall, increases its elastance, shifts cranially the diaphragm, and moves a large part of the ventilation-related volume changes through the rib cage.7,26,27The Trendelenburg position often needed to perform pelvic surgery facilitates the transmission of the abdominal weight to the lung data the pneumoperitoneum and Trendelenburg of respiratory by whereas by and static intrinsic PEEP of the respiratory system and airways resistances increased compared with at after the induction of anesthesia in supine On the we a in PaO2/inspiratory oxygen fraction ratio that significant was (table 2). is not an of pneumoperitoneum-induced of respiratory function during in and oxygenation has been shown to be a of the of pneumoperitoneum-induced lung strategies have been to counterbalance the in respiratory mechanics induced by pneumoperitoneum during laparoscopic surgery. PEEP has been shown to have but whereas recently et al that the of position and PEEP in obese patients during pneumoperitoneum is not in surgical settings in which are et al that an RM applied after pneumoperitoneum induction and followed by the application of PEEP significant in oxygenation both in and obese the of a recruiting strategy to induce alveolar recruitment by a improvement of respiratory mechanics in patients laparoscopic surgery in Trendelenburg in respiratory mechanics between lung and chest wall that the amount of pressure applied to the airway opening that was to the chest wall increased after the induction of pneumoperitoneum in Trendelenburg resulting in a decrease in both end-inspiratory and end-expiratory the RM reopened collapsed lung units and subsequently PEEP by increasing we point out that the physiologic method used in the current study to alveolar been shown to alveolar recruitment in some (see for the we that the open lung strategy decreased To this we that applied after the at the diaphragm cranial shift induced by pneumoperitoneum and Trendelenburg position and that the corresponding lung to a more physiologic chest wall to the in has recently been in patients with adult respiratory distress to PEEP and RM for in lung and chest wall mechanics, to target an end-expiratory lung and In patients with adult respiratory distress a and 10 cm H2O and or a of cm H2O has been shown to oxygenation without inducing on patients submitted to general anesthesia for laparoscopic surgery are show that monitoring time would be to the between respiratory mechanics, anesthesia, and Trendelenburg hypothesis is that basis during laparoscopic surgery would be a sound strategy to obtain alveolar recruitment and respiratory mechanics we point out that our study was not to test this and we applied a standardized open lung strategy successfully tested in a different are required to the end-expiratory and end-inspiratory and to test a ventilatory strategy in this the increase in pressure induced by the open lung hemodynamic status remained output was only by the RM decreased by 20% during the maneuver and returned to its baseline values immediately the application of table to our is by in our patients cardiac preload was before the open lung strategy (see Materials and current study has some (1) our patients were elective surgery and therefore more are required to study the effects of the open lung strategy on partitioned respiratory mechanics in patients with (2) some in the surgical our patients be into when our (3) we after the RM and the subsequent PEEP the position of the esophageal balloon in the esophagus remained the at to our knowledge, in all the clinical after the correct balloon position was at the esophageal balloon position was not because was that the application of RM and/or different PEEP not in our according to the not on the but we used the positive tidal to ECWand subsequently calculated on the between ECWand for the same our is less than the be by different of lung (4) in our we applied a standardized open lung strategy consisting in an RM followed by PEEP 5 cm our data show that strategy resulted in significant alveolar recruitment and improvement in lung mechanics, we point out that the PEEP level applied in our study was to alveolar recruitment. we PEEP to alveolar recruitment is an that further to open lung alveolar we used the method originally by Ranieri et al point out that this method is to that recruitment may to the amount of alveolar recruitment in some as recently shown by et al this as a of our and the has not been thoroughly validated in the surgical and is validated to monitor the of cardiac output than its we the physiologic effects of a ventilatory strategy aiming at pneumoperitoneum-induced alveolar in patients with normal lung function laparoscopic surgery in Trendelenburg should be that this was a physiologic study not to the impact of the tested open lung strategy on parameters and therefore any of our to the clinical be with