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GENERAL ARTICLES

The Impact of Morbid Obesity, Pneumoperitoneum, and Posture on Respiratory System Mechanics and Oxygenation During Laparoscopy

Juraj Sprung, MD PhD^*, David G. Whalley, MB ChB, Tommaso Falcone, MD, David O. Warner, MD^*, Rolf D. Hubmayr, MD, and Jeffrey Hammel, MS^||

*Department of Anesthesiology and Thoracic Diseases Research Unit, Mayo Clinic, Rochester, Minnesota; Department of Anesthesiology, Cleveland Clinic Florida, Naples, Florida; and Obstetrics and Gynecology and Minimally Invasive Surgery Section and || Department of Biostatistics and Epidemiology, The Cleveland Clinic Foundation, Cleveland, Ohio

Address correspondence and reprint requests to Juraj Sprung, MD, PhD, Associate Professor of Anesthesiology, Mayo Medical School, Department of Anesthesiology, Mayo Clinic, 200 First St. S.W., Rochester, MN 55905. Address e-mail to Sprung.juraj{at}mayo.edu

	Abstract

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We studied the effect of morbid obesity, 20 mm Hg pneumoperitoneum, and body posture (30° head down and 30° head up) on respiratory system mechanics, oxygenation, and ventilation during laparoscopy. We hypothesized that insufflation of the abdomen with CO₂ during laparoscopy would produce more impairment of respiratory system mechanics and gas exchange in the morbidly obese than in patients of normal weight. The static respiratory system compliance and inspiratory resistance were computed by using a Servo Screen pulmonary monitor. A continuous blood gas monitor was used to monitor real-time PaCO₂ and PaO₂, and the ETCO₂ was recorded by mass spectrometry. Static compliance was 30% lower and inspiratory resistance 68% higher in morbidly obese supine anesthetized patients compared with normal-weight patients. Whereas body posture (head down and head up) did not induce additional large alterations in respiratory mechanics, pneumoperitoneum caused a significant decrease in static respiratory system compliance and an increase in inspiratory resistance. These changes in the mechanics of breathing were not associated with changes in the alveolar-to-arterial oxygen tension difference, which was larger in morbidly obese patients. Before pneumoperitoneum, morbidly obese patients had a larger ventilatory requirement than the normal-weight patients to maintain normocapnia (6.3 ± 1.4 L/min versus 5.4 ± 1.9 L/min, respectively; P = 0.02). During pneumoperitoneum, morbidly obese, supine, anesthetized patients had less efficient ventilation: a 100-mL increase of tidal volume reduced PaCO₂ on average by 5.3 mm Hg in normal-weight patients and by 3.6 mm Hg in morbidly obese patients (P = 0.02). In conclusion, respiratory mechanics during laparoscopy are affected by obesity and pneumoperitoneum but vary little with body position. The PaO₂ was adversely affected only by increased body weight.

IMPLICATIONS: Morbid obesity significantly decreases respiratory system compliance and increases inspiratory resistance. Increased body weight, and not altered mechanics of breathing, was associated with worse PaO₂ during laparoscopy.

	Introduction

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Surgery and anesthesia on morbidly obese patients carry an appreciable risk (1). Laparoscopic surgery is generally associated with reduced morbidity and hospital stay, although pneumoperitoneum and systemic resorption of CO₂ may have detrimental cardiorespiratory effects (2). The effect of maneuvers accompanying laparoscopy, such as pneumoperitoneum and the Trendelenburg (head-down) and reverse Trendelenburg (head-up) position, on respiratory system mechanics and oxygenation in morbidly obese patients is incompletely characterized. Fahy et al. (3,4) studied the effects of pneumoperitoneum and body position (10° head up and 15° head down) in normal-weight patients and found a good correlation between the patient’s weight and impairment of respiratory mechanics; such changes may be exaggerated in the obese. Morbidly obese patients have markedly reduced supine functional residual capacity (FRC) (5), which should further decrease in the Trendelenburg position and with insufflation of the abdomen with CO₂. Insufflation of CO₂ into the abdomen represents an increased ventilatory load, not only because of the increased transperitoneal CO₂ absorption, but also through increased intraabdominal pressure, which opposes diaphragm descent. The purpose of this investigation was to test the hypothesis that insufflation of the abdomen with CO₂ during laparoscopic surgery will produce a larger impairment of respiratory system mechanics and gas exchange in morbidly obese patients compared with patients of normal weight. We postulated that alterations in respiratory mechanics would be reflected in both reduced PaO₂ and efficiency of CO₂ elimination.

	Methods

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With IRB approval and written, informed consent, we studied eight normal-weight (control; body mass index = 22.8 ± 2.6 kg/m²) and nine morbidly obese (body mass index = 46.6 ± 6.9 kg/m²) patients scheduled for elective laparoscopic gynecological surgery. The mean age of the normal-weight and obese patients was 43 ± 7 yr and 35 ± 12 yr, respectively. All patients were nonsmokers and were free of cardiac, pulmonary, renal, or neuromuscular disease (ASA classes I and II).

All patients received premedication with IV midazolam (2–4 mg). After preoxygenation, anesthesia was induced with 2 mg/kg of propofol and 10 µg/kg of alfentanil. Tracheal intubation (8.0-mm-inner-diameter endotracheal tube) was facilitated by the administration of succinylcholine 1–2 mg/kg IV. Total IV anesthesia was maintained with 150 µg · kg^-1 · min^-1 of propofol and 2 µg · kg^-1 · min^-1 of alfentanil, with the dose adjusted to deep hypnotic effect as assessed by automated encephalogram analysis (bispectral index monitor; Aspect Medical Systems, Inc., Natick, MA). Rocuronium was used to ensure complete muscle relaxation throughout the surgery, such that during measurements of respiratory system mechanics, the patients demonstrated no train-of-four response to stimulation of the ulnar nerve. The patient’s lungs were ventilated with air and oxygen (fraction of inspired oxygen [FIO₂], 0.5) with volume-controlled ventilation, and the initial ventilator setting was set at a frequency of 10 breaths/min and a tidal volume of 800 mL (Servo-Siemens 300 ventilator; Siemens-Elma AB, Solna, Sweden). In addition to standard anesthesia monitors, arterial blood pressure was directly measured from a radial artery catheter.

We measured static respiratory system compliance (Cst,rs) and inspiratory resistance (RI,rs) by using a Servo Screen 390 V2.0 (Siemens-Elma AB) pulmonary monitor. All measurements of Cst,rs and RI,rs were performed before the surgery was initiated, and all manipulations of the patient were halted during the measurement. The patients were studied in supine, Trendelenburg (30° head-down), and reverse Trendelenburg (30° head-up) body positions before and after insufflation of the abdomen with CO₂ to a pressure of 20 mm Hg (Electronic Endoflator, Model 26012; Storz, Charlton, MA). Cst,rs was calculated by dividing the expiratory tidal volume by the difference between the end-inspiratory plateau pressure and end-expiratory pressure. RI,rs was calculated as the difference between peak inspiratory pressure and end-inspiratory plateau pressure divided by end-inspiratory flow. A Paratrend 7^® (Diametrics Medical Inc., St. Paul, MN) continuous blood gas monitor was used to monitor on-line PaO₂ and PaCO₂. To perform this measurement, an ultrathin sensor, a part of the Paratrend 7 monitoring system, was inserted through the standard 20-gauge arterial line catheter. Pulmonary oxygenation was assessed by the alveolar-to-arterial oxygen tension difference according to the following equation:

equation

where PB is actual barometric pressure, PH₂O is the water vapor tension at 37°C, and RQ is a respiratory quotient of 0.8.

To test the ventilatory requirements for maintaining normocarbia in the supine body position without pneumoperitoneum, the respiratory rate was kept at 10 breaths/min, and the tidal volume was adjusted to maintain the PaCO₂ at 40 mm Hg. We achieved normocapnia with conventional ratio ventilation, with an inspiratory/expiratory ratio of 1:2.5 and a positive end-expiratory pressure of 5 cm H₂O. The resulting minute ventilation was recorded.

To study the relationship between the changes in ETCO₂ and PaCO₂, we recorded these variables in supine, anesthetized patients by changing the tidal volume in 100-mL steps at 20 mm Hg pneumoperitoneum; i.e., in each patient, the tidal volume was decreased in 100-mL steps from the initially set tidal volume of 800–1000 mL down to the tidal volume of 100 mL. For each step (i.e., each change in tidal volume), we allowed 5 min of equilibration before we recorded the respective PaCO₂ (Paratrend) and ETCO₂ (mass spectrometer, Solar 9500 Monitor; Marquette Corp., Milwaukee, WI) values. This 5-min period may not permit full equilibration, but it was chosen to avoid extensive prolongation of the anesthesia time.

Respiratory mechanics variables were measured in triplicate and averaged for each patient, such that each patient’s data were used as a single observation and contributed only once to each overall data set. Data are presented as means ± SD. Effects of body position, weight, and abdominal insufflation were analyzed by repeated-measures analysis of variance, because multiple observations per patient were included in these analyses. The MIXED procedure in SAS version 8 (SAS, Inc., Cary, NC) was used to perform these analyses, and a compound symmetric error structure was assumed for all models on the basis of the repeated measurements. These models assumed that each of the two groups (obese and normal weight) had a linear trend (in the measured range) describing an average population trend between the outcome (changes in PaCO₂ and ETCO₂) and tidal volume. With the inclusion of an interaction between obesity and tidal volume in each model, we tested whether the slopes of the linear trends were different for the obese and normal-weight patients at a P < 0.05 significance level. Graphical representations were also produced to assist in describing the relationships.

	Results

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Figure 1 (upper panel) shows the effect of weight, body position, and abdominal insufflation on Cst,rs. In the supine body position, Cst,rs was lower in the morbidly obese patients compared with the normal-weight patients (62 vs 44 mL/cm H₂O, respectively; P < 0.001). Changing the position from supine to Trendelenburg or reverse Trendelenburg did not significantly affect Cst,rs in either normal-weight (P = 0.77) or obese (P = 0.20) patients, but the difference between normal-weight and morbidly obese patients remained (from P < 0.01 to P < 0.001). Pneumoperitoneum induced a significant decrease in Cst,rs in both patient groups (from P < 0.01 to P < 0.001). Again, changing the body position during pneumoperitoneum did not cause significant additional changes in Cst,rs in either group, but contrary to before pneumoperitoneum, the difference between Cst,rs in the two groups was not significant, despite the trend for Cst,rs to remain lower in morbidly obese patients. Figure 1 (lower panel) shows effects of weight, body position, and abdominal insufflation on RI,rs. In the supine position before insufflation, RI,rs was 68% higher in the obese compared with normal-weight patients (17.1 vs 10.2 cm H₂O · L^-1 · s^-1; P = 0.01). Changing the position from supine to Trendelenburg or reverse Trendelenburg did not significantly affect RI,rs in either patient group, but the RI,rs remained higher in morbidly obese patients at all body positions (from P < 0.01 to P < 0.001). After insufflation, RI,rs increased and reached the maximum in the Trendelenburg position, more in obese (from 17.1 to 27.8 cm H₂O · L^-1 · s^-1, a 63% increase) than in normal-weight patients (from 10.2 to 15.2 cm H₂O · L^-1 · s^-1, a 49% increase). During pneumoperitoneum, repositioning the patients from the supine position to either the Trendelenburg or reverse Trendelenburg position did not induce any further significant changes in RI,rs, but the RI,rs remained higher in morbidly obese patients at both body positions (from P < 0.01 to P < 0.001).

View larger version (34K): [in this window] [in a new window]   Figure 1. Effects of weight, body position, and abdominal insufflation on static respiratory system compliance and on inspiratory resistance. Rev = reverse; Trend = Trendelenburg. Data are means ± SD. P from <0.01 to <0.001 versus the same body position in morbidly obese patients; *P from <0.01 to <0.001 versus the same group in supine and reverse Trendelenburg positions before pneumoperitoneum.

View larger version (26K): [in this window] [in a new window]   Figure 2. Effect of weight, body position, and abdominal insufflation on alveolar-to-arterial oxygen tension difference (A-aDO2) in normal-weight and morbidly obese patients. Morbidly obese patients had higher A-aDO2. Data are means ± SD. Statistical significance compares A-aDO2 between normal-weight and morbidly obese patients: *P < 0.03; P < 0.02; ¥P < 0.05 at same body position. Rev = reverse; Trend = Trendelenburg.

View larger version (20K): [in this window] [in a new window]   Figure 3. Relationship among weight, PaCO2/ETCO2 gradient, and tidal volume. The linear trends for change in PaCO2/ETCO2 gradients in obese and normal-weight patients were different (P = 0.009 by mixed analysis of variance). Tidal volumes were averaged for the following ranges (in mL): 300, 301–399, 400–499, 500–599, 600–699, 700–799, and 800. All data are means ± SD. The polynomial curves fitted through the mean PaCO2/ETCO2 gradients serve only as a descriptive tool.

	Discussion

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We examined the effects of body weight and pneumoperitoneum on changes in pulmonary mechanics and gas exchange in different body positions during laparoscopy. We found that morbidly obese, anesthetized, supine patients in the absence of pneumoperitoneum have lower Cst,rs and higher RI,rs compared with their normal-weight counterparts. A standard 20 mm Hg CO₂ pneumoperitoneum in normal-weight patients induces a decrease in Cst,rs and an increase in RI,rs equivalent to, or greater than, those seen in anesthetized morbidly obese patients. Whereas the PaO₂ was lower in morbidly obese than in normal-weight patients, neither changes in position nor pneumoperitoneum further affected oxygenation in either population.

Respiratory mechanics in healthy, normal-weight, nonanesthetized patients change minimally over a wide range of postures, including both 30° head-up and head-down positions (6). Fahy et al. (3) demonstrated that respiratory system impedances (elastance and resistance) increase with pneumoperitoneum, more in the head-down than in the head-up position, and that these changes may be attributed to alteration in the lung rather to the chest wall properties (4). In healthy, nonobese patients, abdominal insufflation in the head-down position only moderately decreases respiratory system compliance (7). Morbid obesity itself may cause significant respiratory system alteration (8,9). For example, Pelosi et al. (10) demonstrated that respiratory system compliance exponentially decreases as a function of increased body mass index. In the obese, changes in pulmonary mechanics accompanying the transition from the upright to supine position are exaggerated, and the FRC may decrease within or below closing capacity in the supine position (8,11,12). The reduced lung volume can explain, at least in part, the alterations of respiratory system mechanics (decreased compliance and increased resistance) in supine, anesthetized, morbidly obese individuals (5,13).

Consistent with these results, we found that in anesthetized, supine, morbidly obese patients, Cst,rs before pneumoperitoneum was 30% less than that in normal-weight patients. Positioning of these patients in either the Trendelenburg or the reverse Trendelenburg posture did not have a major effect on compliance. The induction of 20 mm Hg CO₂ pneumoperitoneum further reduced respiratory compliance in both patient groups. Our findings are similar to those of Dumont et al. (13), who described a 31% decrease in respiratory system compliance with CO₂ insufflation in morbidly obese patients undergoing laparoscopic gastroplasty. In our study, before pneumoperitoneum, RI,rs was substantially more (70%) in morbidly obese patients compared with normal-weight patients and was further increased after pneumoperitoneum, more in obese than in normal-weight patients (63% vs 49%). This finding, also shown by Pelosi et al. (5), is consistent with the smaller FRC in morbidly obese patients that causes intrinsic narrowing of the airways.

We expected that the reverse Trendelenburg position would reverse gravitational effects on abdominal contents and improve respiratory mechanics altered by pneumoperitoneum. However, positioning the patients in the reverse Trendelenburg position did not have any effect on either respiratory mechanics or PaO₂. Perilli et al. (8) studied the effects of the reverse Trendelenburg position on respiratory mechanics in morbidly obese patients during open bariatric surgery and found that the respiratory system compliance was significantly higher in the reverse Trendelenburg position, but this situation is clearly different from that of our laparoscopic patients with closed abdomen and pneumoperitoneum. We believe that the absence of an expected increase in compliance in the reverse Trendelenburg position may be attributed to the mechanical effects of pneumoperitoneum, which opposed the gravitational shift of abdominal contents. Our finding is in agreement with another recent study, which reported that the 25° reverse Trendelenburg position had no beneficial effect on respiratory variables in morbidly obese patients undergoing laparoscopic gastric banding (14).

We have demonstrated that during anesthesia and laparoscopy, the PaO₂ and alveolar-to-arterial oxygen tension gradient were determined exclusively by body weight and were not associated with changes in respiratory mechanics. These findings agree with those of Pelosi et al. (15).

Typically, normal-weight patients require a 20%–30% increase in minute ventilation to maintain normocarbia during pelvic laparoscopy in the Trendelenburg position (16). Because morbid obesity creates detrimental changes in respiratory mechanics, it may be expected that these patients may require even higher minute ventilation to maintain the same level of ventilation compared with normal-weight patients. During anesthesia and before pneumoperitoneum, our morbidly obese supine patients required 15% higher minute ventilation to maintain normocarbia compared with the normal-weight patients. Of note, this increased ventilation requirement was not in proportion to increased patient weight. Furthermore, over a wide range of tidal volumes during pneumoperitoneum, morbidly obese supine patients had less efficient ventilation; i.e., tidal volume increased in increments of 100 mL of decreased PaCO₂ in normal-weight patients on average 5.3 mm Hg, and in morbidly obese patients, 3.6 mm Hg. Therefore, ventilation/perfusion inequalities in morbidly obese patients during laparoscopy may impair the efficiency of CO₂ elimination, and larger volumes of ventilation are required to achieve a certain PaCO₂.

Monitoring of ETCO₂ is a simple and noninvasive technique that accurately estimates PaCO₂, but its reliability under conditions in which there is increased ventilation/perfusion mismatching may be questioned. In this study, we demonstrated that the PaCO₂/ETCO₂ gradient was similar for the morbidly obese and normal weight-patients over a large range of tidal volumes. However, the PaCO₂/ETCO₂ gradient was increased in morbidly obese patients at low tidal volumes (<300 mL); this may be explained by an increase in dead-space ventilation. Conversely, small tidal volume may have failed to wash out the alveolar dead space. Increasing the tidal volume results in lung volume recruitment and, therefore, improvement of alveolar ventilation, resulting in decreases in the PaCO₂/ETCO₂ gradient. At the same time, a large difference in PaCO₂/ETCO₂ was found in normal-weight patients at high tidal volumes (>800 mL). We can only postulate that higher peak inspiratory pressures compressed the pulmonary blood flow (normal-weight patients have more compliant lungs), thus causing a decrease in the CO₂ transfer from the circulation to the alveolar space. Our results suggest that during laparoscopy, ETCO₂ less accurately reflects PaCO₂ in morbidly obese patients at low tidal volumes and in normal-weight patients at high tidal volumes.

In conclusion, morbid obesity and pneumoperitoneum have significant effects on respiratory mechanics, whereas PaO₂ was adversely affected only by increased body weight. Repositioning the patient from the supine position into the Trendelenburg or reverse Trendelenburg position had no effect on PaO₂ either before or after abdominal insufflation. Morbidly obese, anesthetized, supine patients had only a 15% higher ventilatory requirement to maintain normocapnia before pneumoperitoneum. Despite less favorable mechanical and ventilatory characteristics during anesthesia for laparoscopy, it appears that morbid obesity-associated alterations in the mechanics of breathing are of little clinical significance.

	Acknowledgments

 
We acknowledge Fanny Shutway, RN, and William Wilks, Respiratory Therapist, The Cleveland Clinic Foundation, Cleveland, OH.

	References

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999