General anesthesia and mechanical ventilation cause impairment of gas exchange due to airway closure and atelectasis.1–3 Morbidly obese patients frequently develop more atelectasis which impairs gas exchange and respiratory mechanics. Therefore, these patients are a good model of lung collapse because their lungs respond very well to a recruitment maneuver (RM).4–12 A cycling lung RM is a ventilator strategy consisting of 3 distinct interventions.13–15 First, during an RM, end-inspiratory pressure is increased in a controlled and stepwise manner until the lungs’ opening pressure is reached. Second, once the lungs are open, their closing pressure is detected during a descending positive end-expiratory pressure (PEEP) trial.15–17 The closing pressure is the level of PEEP at which lung derecruitment starts. Third, after a new RM, the lungs are kept open by maintaining ventilation at a PEEP level at least 2 cm H2O above the closing pressure.15
Because the lungs’ opening and closing pressures are not easy to detect at the bedside, it is common to use predefined levels of end-inspiratory pressure and PEEP during an RM. These general values are based on findings of clinical studies.14,15,18 However, these predefined end-inspiratory pressure and PEEP values are likely to either over or underestimate the individual’s optimal pressures because these are influenced by factors such body mass index (BMI) and the presence of capnoperitoneum.7–9,15,18
The aim of this study was to determine whether pulse oximetry together with parameters derived from volumetric capnography (VCap) were able to define the lungs’ opening and closing pressures noninvasively during a cycling RM in morbidly obese patients. We hypothesized that instantaneous changes in the area of gas exchange induced by dynamic interventions can be detected noninvasively by pulse oximetric arterial saturation (SpO2) and by expired CO2 and could therefore identify the pressures at which the lungs recruit or collapse.
To provide an answer to the above question, we studied a cohort of morbidly obese patients undergoing laparoscopic bariatric surgery with capnoperitoneum.
The study was approved by the local ethics committee. After obtaining written informed patient consent, we studied morbidly obese patients undergoing laparoscopic bariatric surgery with the following characteristics: 25 to 60 years of age, ASA physical status II and III, and BMI >40 kg/m2. We excluded patients with abnormal baseline spirometry, active smoking, bronchospasm, functional New York Heart Association class ≥III, any acute arrhythmias, arterial hypotension, or acute coronary syndrome.
Anesthesia and Monitoring
Anesthesia was induced with propofol 1.5 mg/kg, vecuronium 0.08 mg/kg, and fentanyl 3 to 4 μg/kg of ideal body weight and maintained with sevoflurane 0.5 to 0.7 minimum alveolar concentration plus remifentanil 0.5 μg/kg/h. The lungs were ventilated through a cuffed endotracheal tube using a Servo 900C (Siemens-Elema, Solna, Sweden) in a volume-controlled mode: tidal volume (VT) of 6 to 7 mL/kg of ideal body weight, respiratory rate of 15 breaths per minute, PEEP of 8 cm H2O, Inspired:Expired (I:E) ratio of 1:2 without inspiratory pause, and fraction of inspired oxygen (FIO2) of 50%.
Patients were administered 500 mL of Voluven® (6% hydroxyethyl starch 130/0.4, Fresenius-Kabi, Bad Homburg, Germany) during anesthesia induction followed by a fixed infusion of 200 mL/h Ringer’s lactate solution during surgery. Any blood lost during surgery was replaced by saline solution at a ratio of 1:3.
The multiparametric monitor Cardiocap/5 and the software Datex Collect (both GE Healthcare/Datex-Ohmeda, Helsinki, Finland) recorded electrocardiogram, FIO2, and invasive mean arterial blood pressure (MAP) measured via a 20G catheter placed in the right radial artery.
The NICO monitor and the software DataColl (both Respironics, Wallingford, CT) recorded respiratory, SpO2, and VCap data. Respiratory data consisted of VT, airway pressures, dynamic respiratory compliance (Cdyn = VT/peak pressure − PEEP), and expiratory airway resistance (Raw = peak pressure − PEEP/flow).
The SpO2 raw data provided by the NICO monitor delivers 1 SpO2 value every 4 seconds, which corresponds to 1 real SpO2 value per breath at 15 breaths per minute. The accuracy and time response of SpO2 readings during lung recruitment were investigated in a pilot study in 10 morbidly obese patients (see Supplemental Digital Content 1, http://links.lww.com/AA/A682).
The mainstream CO2 sensor was zeroed and placed at the airway opening. Expired CO2 concentrations and VT data were downloaded into MATLAB® (MathWorks, Natick, MA), which constructed volumetric capnograms according to the functional approximation using the Levenberg–Marquardt algorithm.19 We measured (1) VTCO2,br or tidal elimination of CO2 measured by integrating the area under the curve (AUC) of VCaps20 and (2) dead space, calculated noninvasively using Bohr’s formula21:
VDBohr/VT = (PACO2−PĒCO2)/Paco2
where PACO2 is the mean alveolar partial pressure of CO2 measured at the midpoint of the alveolar plateau and PĒCO2 is the mixed expired partial pressure of CO2.21–23
Figure 1 shows the graphical representation of the study protocol:
* (T0) Protocol start. After induction of anesthesia, patients were submitted to a capnoperitoneum of 15 mm Hg in a supine 30° anti-Trendelenburg position.
* (T1) Data collection during baseline ventilation as described in Anesthesia and Monitoring section.
* (T2) SpO2–FIO2 trial at baseline ventilation to detect potential oxygenation deficits due to lung collapse.24,25
* (T3) Ascending limb of the RM searching for the lungs’ opening pressure.
* (T4) Descending limb of the RM searching for the lungs’ closing pressure.
* (T5) Data collection during ventilation as in T1.
* (T6) Second RM using the lungs’ opening and closing pressures found during steps T3 and T4, respectively.
* (T7) Data collection during ventilation as in T1, but in an open-lung condition setting PEEP 2 cm H2O above the lungs’ closing pressure found in T4.
The effect of an RM was evaluated by comparing several different physiological variables obtained at the same ventilator settings (T1, T5, and T7). Arterial blood samples were collected at the end of each step and analyzed within 5 minutes (ABL 615, Radiometer, Copenhagen, Denmark). The difference between alveolar and arterial partial pressure of O2 (PA − aO2) was also calculated.
An RM was performed in pressure-controlled ventilation separating the intervention into 2 well-defined parts: an ascending limb (to find the lungs’ opening pressure) and a descending limb (to find the lungs’ closing pressure; T3–T4 in Fig. 1).
Finding the Lungs’ Opening Pressure
We used the SpO2 signal to detect the lungs’ opening pressure in the following way. First, we performed an SpO2–FIO2 trial according to Jones and Jones.24 FIO2 was decreased by 10% for 1 minute, starting from 100% and ending at 21% or at the lowest FIO2 at which SpO2 reached the lowest predefined cutoff value of 92% (above the hypoxemic threshold). This trial was performed to reveal occult potential gas exchange problems which would otherwise have been masked by the high FIO2 (T2). Second, once the lower levels of values SpO2 and FIO2 were determined (Fig. 1, end of T2), we proceeded with the ascending limb of the RM (T3). Making use of Fick’s law for diffusion, the lowest safe SpO2 value is then used as an indirect marker of the area of gas exchange because any effective recruitment would result in a fast increase in SpO2. With reference to the standard behavior of the oxygen–hemoglobin dissociation curve in normal lungs, a threshold SpO2 value of ≥97% at the low FIO2 was used to define an open-lung state (see Supplemental Digital Content 1, http://links.lww.com/AA/A682).
During the ascending limb of the RM (T3), the driving pressure (peak − PEEP) was set at 20 cm H2O, I:E ratio at 1:1, and respiratory rate was maintained at 15 breaths per minute. Initially, PEEP was increased from 8 to 16 cm H2O to reach an end-inspiratory pressure of 36 cm H2O, a value safely below the typical opening pressures of anesthetized patients with normal body weight.18 Thereafter, PEEP was increased every minute by 2 cm H2O (which led to a parallel increase in end-inspiratory pressure) until an SpO2 ≥97%. The peak pressure at this stage defined the lungs’ opening pressure. Maximum end-inspiratory pressure was 50 cm H2O if necessary.12,26 The maneuver was aborted if one of the following conditions occurred: MAP either decreased by >20% from baseline or decreased <55 mm Hg, SpO2 ≤90%, or appearance of cardiac arrhythmias.
Finding the Lungs’ Closing Pressure
The descending limb of the RM sought to find the lungs’ closing pressure and the PEEP at which the lungs started to recollapse (T4). Starting at a PEEP of 22 cm H2O, driving pressure was reduced to and fixed at 10 cm H2O and decreased sequentially until 10 cm H2O in steps of 2 cm H2O every 2 minutes. In these healthy lungs, the PEEP at which Cdyn reached its maximum was considered the open-lung condition while the PEEP 1 step lower defined the lungs’ closing pressure.27
Statistical analysis was performed with MATLAB. A nonnormal distribution of some variables was found with the Lilliefors test.a Wilcoxon test was used for comparisons between variables. Results are expressed as median and interquartile range (IQR). A P value <0.05 was considered statistically significant.
The role of SpO2, VTCO2,br, and VDBohr/VT to detect lung collapse were evaluated by discrete receiver operating characteristic (ROC) analysis.28 Taking Cdyn as the reference method to detect the lungs’ closing pressure, we assigned a binary classification of “1” to the open-lung condition (maximum Cdyn) or “0” to the onset of lung collapse (the first decrement in Cdyn from its maximum value).27 Similarly, a value of 1 was assigned to the maximum elimination of CO2 per breath (VTCO2,br), the minimum dead space (VDBohr/VT), and pulse oximetry (SpO2) values ≥97%. On the contrary, a value of 0 was assigned whenever VTCO2,br started to decrease, VDBohr/VT started to increase, and SpO2 decreased <97%. These assignments determine true and false positive or negative conditions in a 2 × 2 table from which sensitivity and specificity were calculated. The AUC of a discrete ROC is equivalent to the Wilcoxon test of ranks.29 The SE of AUC was calculated from the Wilcoxon statistic.30
We studied 20 morbidly obese patients all of whom completed the protocol successfully without complications. Patient characteristics are summarized in Table 1.
Lungs’ opening pressures ranged between 42 and 48 cm H2O with a median value of 44 (IQR 4) cm H2O (Fig. 2). While Cdyn and the elimination of CO2 increased directly and in proportion to the end-inspiratory pressure, dead space remained rather stable along the ascending limb (Fig. 3).
The lungs’ closing pressure was found to be 14 (IQR 2) cm H2O (Fig. 3). Subsequently, the level of PEEP that kept the lungs from collapsing was 16 (IQR 3) cm H2O. This level of PEEP was related to the highest VTCO2,br and the lowest dead space at SpO2 ≥97% (Figs. 3 and 4). ROC analysis showed that these variables were adequate to detect the lungs’ closing pressure referencing Cdyn (Table 2).
Figure 4 shows the behavior of SpO2 and Cdyn during T2, T3, and T4 in patient #11.
Table 3 describes the physiological variables recorded during the fixed ventilator settings at baseline (T1), when the lungs derecruited after the first RM (T5) and at the open-lung condition after the second RM (T7). In general, the physiological condition shown by an improvement in gas exchange and lung mechanics at T7 was better than the physiological condition during the other 2 studied periods. Dead space was similar during all study periods despite higher PEEP values at T7. MAP and heart rate of all patients are depicted in Figure 5. These variables remained stable throughout the study.
After decreasing FIO2, SpO2 turned into a real-time marker of the area of gas exchange that was able to identify the lungs’ opening pressure. The values of the area under the ROC curve found in VTCO2,br, VDBohr/VT, and SpO2 determined that such variables were useful for detecting the closing pressure at the bedside.
Lung Opening and Closing Pressures in Morbidly Obese Patients
Obese patients develop airway closure and extensive atelectasis during laparoscopic bariatric surgery.4–10 Even though RMs are highly effective to counteract lung collapse, the exact pressures to reexpand the collapsed lungs of morbidly obese patients are largely unknown and difficult to determine.
Rothen et al.18 described the lungs’ opening pressures to be close to 40 cm H2O in healthy anesthetized patients using computed tomography scan imaging. They showed that the amount of atelectasis was correlated with their patient’s BMI. As a result of the large decrement in transpulmonary pressure in morbidly obese patients undergoing bariatric surgery,9,10 it can be assumed that their opening pressures should be approximately 40 to 50 cm H2O.12,26 Our SpO2 results support this assumption (Fig. 2). At the highest end-inspiratory pressure, Cdyn and the elimination of CO2 improved while dead space remained constant (Fig. 3). These findings suggested the absence of alveolar overdistension in our patients during the ascending limb of the RM despite the high airway pressures.
It has been demonstrated that the use of PEEP without an RM has limited effects on lung function irrespective of the patient’s BMI or lung condition.14,15 However, once effectively recruited, PEEP plays a key role in maintaining the lungs open.29 PEEP applied after an RM improved gas exchange and lung mechanics in morbidly obese patients, and this effect depended on the level of PEEP applied and was better at 10 cm H2O than at 5 cm H2O.11 In another study, we found that PEEP 15 cm H2O was even better than 10 cm H2O to improve lung function in morbidly obese patients during anesthesia with and without capnoperitoneum.12 Using electric impedance tomography, Erlandsson et al.31 showed that 15 cm H2O of PEEP after an RM maintained functional residual capacity and minimized shunt in anesthetized morbidly obese patients.31 These findings support the concept of using high PEEPs in obese patients to prevent the lungs from collapsing once the lungs have been reexpanded by an RM.
Based on the behavior of Cdyn, we found a median closing pressure of 14 (IQR 2) cm H2O27 while a PEEP value 2 cm H2O above the respective individual closing pressure of each morbidly obese patient was enough to keep the lungs open (Table 2). The PEEP of 16 cm H2O in our study was similar to the optimal PEEP of 15 cm H2O described by Böhm et al.12 and by Erlandsson et al.31
Rationale for Using SpO2 to Detect Changes in the Area of Gas Exchange During an RM
The use of high inspiratory fractions of oxygen has been historically recommended to avoid or treat hypoxemic episodes during anesthesia. One disadvantage of high FIO2 is that it may disguise even large impairments of gas exchange as long as hemoglobin saturation remains >97%, thereby rendering SpO2 useless for assessing many pulmonary problems of mechanically ventilated patients. Decreasing FIO2 forces SpO2 to operate on the steepest part of the oxygen–hemoglobin dissociation curve. This is the rationale behind the SpO2–FIO2 diagram described by Jones and Jones,24 which helps clinicians characterize lung function at the bedside without blood gas analysis.
The novelty of the present study is that we used the same principle but this time to detect changes in the area of alveolar–capillary membrane during a noninvasive RM. By decreasing FIO2, we also forced SpO2 values to move along the steepest part of the oxygen–hemoglobin curve (<97%) always keeping it above the hypoxemic threshold (≥92%). This intervention reveals the presence of previously occult deficiencies of gas exchange such as the ones due to lung collapse. Based on Fick’s law of diffusion, we could then use SpO2 as a real-time marker of changes in the area of gas exchange during an RM:
Dg/dt = λ × A × (P1−P2)/T
where the amount of O2 that passes through the alveolar–capillary membrane per unit of time (Dg/dt) is directly proportional to the coefficient of diffusion for O2 (λ), and the area of gas exchange (A) and partial pressure difference of O2 at both sides of the membrane (P1 − P2) are inversely proportional to the thickness of the membrane. Provided that λ, (P1 − P2), and T are constant, any change in the diffusion of O2, which instantaneously affects hemoglobin O2 saturation, could only be explained by an instantaneous change in A.
To define an open-lung condition, we arbitrarily selected a cutoff value for SpO2 of ≥97% based on the typical characteristics of the oxygen–hemoglobin dissociation curve during ambient air breathing.24 Following this reasoning, in healthy lungs, an end-inspiratory pressure that yields an SpO2 ≥97% during the ascending limb of an RM can be defined as the opening pressure (see Supplemental Digital Content 1, http://links.lww.com/AA/A682). In contrast, during the descending limb, a PEEP that results in a decrease of SpO2 <97% can be defined as the lungs’ closing pressure.
Lung RMs performed at low FIO2 force SpO2 to move along the steepest part of the oxygen–hemoglobin dissociation curve, and thus SpO2 behaves in a similar way as invasive intra-arterial online PaO2 measurements32 (Fig. 4). The comparable behavior of SpO2 and PaO2 over the selected saturation range suggests that SpO2 is a simple and good surrogate of arterial oxygenation that can efficiently monitor RM in this well-defined context.
The Role of VCap-Derived Parameters to Monitor RMs
The elimination of CO2 per breath can be used as a marker of alveolar ventilation and the efficiency of gas exchange during nonsteady-state conditions like RMs.33,34 Lung recruitment is characterized by an increment in Cdyn and the area of gas exchange. Thus, when using a fixed driving pressure, VTCO2,br increases in proportion to the augmentation in alveolar VT and the area of gas exchange during the ascending limb of an RM, assuming stable hemodynamics and metabolism. The opposite effect will be seen when the lungs recollapse during the descending limb of an RM. Figure 3 and Table 2 illustrate the similarities between Cdyn and VTCO2,br during the complete RM sequence and how VTCO2,br could detect the lungs’ closing pressure according to the above rationale.
It has been demonstrated that “dead space” measured invasively using Enghoff’s modification of Bohr’s equation was useful to detect lung collapse in lung-lavaged animals.35 Because this formula, however, includes shunt in its dead space calculation, it was reasoned that during PEEP titration in collapse-prone experimental models this index primarily represents changes in shunt and not in dead space. In the present study, we therefore applied Bohr’s original formula to calculate dead space, a value that is not contaminated by shunt.21,22 We found that the lowest VDBohr/VT value occurred at the PEEP level that keeps the lungs open, and when the lungs became collapsed, the VDBohr/VT value predictably increased again. Our data resemble those of the classical publication of Suter et al.,36 in which the “best PEEP” was defined, among other variables, by the lowest dead space.
This study shows that pulse oximetry and VCap can effectively monitor the dynamic changes in the area of gas exchange which are induced by RMs. They can be used to determine a lung’s opening and closing pressures and may thus guide clinicians during the implementation of an open-lung ventilation strategy.
Name: Gerardo Tusman, MD.
Contribution: This author helped in study design, conduct of the study, data collection, data analysis, and manuscript preparation.
Attestation: Gerardo Tusman reviewed the original study data and data analysis and is the archival author.
Name: Iván Groisman, MD.
Contribution: This author helped in data collection and data analysis.
Attestation: Iván Groisman collected and analyzed the data.
Name: Felipe E. Fiolo, MD, FACS.
Contribution: This author helped in study design and data collection.
Attestation: Felipe E. Fiolo reviewed the original study and collected the data.
Name: Adriana Scandurra, Eng, PhD.
Contribution: This author helped in data analysis.
Attestation: Adriana Scandurra analyzed the data.
Name: Jorge Martinez Arca, Eng.
Contribution: This author helped in data analysis.
Attestation: Jorge Martinez Arca analyzed the data.
Name: Gustavo Krumrick, MD.
Contribution: This author helped in data collection.
Attestation: Gustavo Krumrick collected the data.
Name: Stephan H. Bohm, MD.
Contribution: This author helped in study design and manuscript preparation.
Attestation: Stephan H. Bohm reviewed the original study data and data analysis.
Name: Fernando Suarez Sipmann, MD, PhD.
Contribution: This author helped in study design and manuscript preparation.
Attestation: Fernando Suarez Sipmann reviewed the original study data and data analysis.
This manuscript was handled by: Maxime Cannesson, MD, PhD.
a Sample size was not calculated because (1) this is a preliminary pilot and descriptive study without control group and (2) all morbidly obese patients developed large atelectasis1–7 and all responded to lung recruitment maneuvers, increasing respiratory compliance exaggeratedly.11,12,30 Using this information, calculated sample side formula gave <5 patients. Thus, we arbitrarily decided to study 20 patients. Cited Here...
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