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The Effects of Abdominal Opening on Respiratory Mechanics During General Anesthesia in Normal and Morbidly Obese Patients: A Comparative Study

Auler, José O. C. Jr., MD, PhD; Miyoshi, Erika, MD; Fernandes, Cláudia R., MD; Benseñor, Fábio E., MD; Elias, Luciana, MD; Bonassa, Jorge, PhD

doi: 10.1097/00000539-200203000-00049
General Articles: Research Report
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Morbid obesity has a profound effect on respiratory mechanics and gas exchange. However, most studies were performed in morbidly obese patients before or after anesthesia. We tested the hypothesis that anesthesia and abdominal opening could modify the elastic and resistive properties of the respiratory system. Eleven morbidly obese and eight normal-weight patients scheduled for gastric binding and cancer treatment, respectively, under laparotomy were studied. Respiratory mechanics, partitioned into its lung and chest wall components, were investigated during surgery by means of the end-inspiratory inflation occlusion method and esophageal balloon at five time points. Static respiratory and lung compliance were markedly reduced in obese patients; on the contrary, static compliance of chest wall presented comparable values in both groups. Obese patients also presented higher resistances of the total respiratory system, lung and chest wall, as well as “additional” lung resistance. Mainly in obese patients, laparotomy provoked a significant increase in lung compliance and decrease in “additional” lung resistance 1 h after the peritoneum was opened, which returned to original values after the peritoneum had been closed (P < 0.005). In obese patients, low respiratory compliance and higher airway resistance were mainly determined by the lung component.

Department of Anesthesia, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

Financial support was provided by FAPESP Grant 97/11311-2.

Presented in part at the 96th International Conference of the American Thoracic Society, Toronto, Ontario, Canada, May 5–10, 2000, abstract number A693.

November 6, 2001.

Address correspondence and reprint requests to José O. C. Auler, Jr., MD, PhD, Hospital das Clínicas da FMUSP, Anesthesia Department-Incor, Avenida Dr Enéas de Carvalho Aguiar, 44, CEP 05403-000, São Paulo, Brasil. Address e-mail to auler@incor.usp.br.

Morbid obesity has a profound effect on respiratory function, decreasing lung volumes, compliance functional residual capacity, and arterial oxygenation (1). General anesthesia, upper abdominal surgery, and supine position may accentuate respiratory mechanical abnormalities, worsening gas exchange, which can be a challenge for the anesthesiologist (2). As reported in the literature, the excellent results observed with gastroplasty (3) in the treatment of refractory morbid obesity, have created a renewed interest in the anesthetic management of this group of patients (4). To better clarify the adverse effects on respiratory function observed during general anesthesia, several investigations have focused on the study of respiratory mechanics in anesthetized morbidly obese patients (5–9). However, the literature is inconsistent (10,11) because most of the studies related to respiratory mechanical properties were performed before or after surgery (11). This is the first study to investigate, during surgery, the effects of abdominal opening on respiratory mechanics, using the end-inflation occlusion method and esophageal balloon to obtain the compliance and resistance of lung and chest wall components of the total respiratory system.

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Materials and Methods

This study was approved by the Institutional Ethics Committee of our university hospital and informed consent was obtained preoperatively from each person. Patient anthropomorphic and operative data are shown in Table 1. None of the patients had clinical evidence of cardiac and/or respiratory diseases. Heavy smokers or those with smoking histories in the last 12 mo were not included in the study. Patients having upper laparotomy under general anesthesia were selected as a control group. The patients’ entrance in the study was according to the following sequence: obese, normal weight. Three normal-weight patients were excluded from the study because of technical problems in respiratory mechanics data store.

Table 1

Table 1

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Obese Patients

Eleven morbidly obese female patients scheduled for gastric binding under laparotomy were included. The criterion of morbid obesity was a body mass index (BMI) >40. Their preoperative pulmonary function tests, performed in a standard spirometer, were the following: average forced vital capacity of 85.10% ± 9.21% of that predicted by Crapo et al. (12), the forced expiratory volume in 1 s was 83.12% ± 11.08%, and the average forced expiratory flow rate measured over the middle portion of the forced vital capacity (FEF25–75), was 88.76% ± 31.22% of the predicted. Blood gas measurements during spontaneous ventilation at room air before surgical intervention included an arterial oxygen tension (Pao2) of 76.49 ± 7.64 mm Hg, arterial carbon dioxide tension (Paco2) of 37.73 ± 2.04 mm Hg, and pHa of 7.40 ± 0.02.

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Normal-Weight Subjects

Eight patients (five male patients) scheduled for gastric surgery (seven patients to treat cancer) and one for colon resection under laparotomy were included in the study. Patients presented with normal thoracic radiograph and history, and physical examination was negative for cardiac and respiratory diseases.

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Protocol Design

Anesthesia.

Electrocardiogram, direct radial arterial and central venous pressure, capnography, and arterial oxygen saturation were monitored continuously. Inspired and expired oxygen and inhaled anesthetic (sevoflurane) concentration were monitored continuously by using a Capnomac Ultima (Datex Instrumentarium, Helsinki, Finland) respiratory monitor. All anesthetic dosages for obese patients were based on their ideal weight in kilograms (for the calculation of ideal body weight, subtract 100 from the patient’s height in centimeters for males, and 105 for females). Patients were premedicated with midazolam 0.1 mg/kg IM. Standard general anesthesia was induced with etomidate 0.3 mg/kg, and fentanyl 5 μg/kg. Oral endotracheal intubation (tubes ranged from 7.5 to 8.5 mm inside diameter; Portex, Kent, UK) was facilitated by paralysis induced by pancuronium (0.08 mg/kg). They were ventilated with air-oxygen 50%, and sevoflurane 2%–4% (Ohmeda calibrated vaporizer, model Sevotec 5, Madison, WI). Fentanyl and propofol were used for the maintenance of anesthesia. The lungs were ventilated via a standard anesthesia machine with a constant flow, mode of ventilation volume controlled and open circuit. The ventilator variables (tidal volume and respiratory rate) were adjusted initially to maintain normocarbia. During airway occlusion, necessary to obtain the respiratory mechanical data, ventilatory variables were kept the same for both groups (inspiratory flow of 0.60 L/s and tidal volume of 0.6 L). To avoid the effect of the time of anesthesia on the history of the lung, preceding the airway occlusion, a recruitment maneuver (inspiratory inflation to a maximal capacity repeated three times and holding for a few seconds) was performed before each measurement. The effect of gas compression on respiratory circuits was calculated and considered during the calculations of respiratory mechanics, and positive end-expiratory pressure (PEEP) was not used. Laparotomy was performed via a midline incision extending from the xiphoid notch to the umbilicus. Open gastroplasty consisted of a reduction of the stomach, with the creation of a small pouch. All measurements (gas exchange, blood sampling, elastic and flow-resistive properties of the respiratory system, lung and chest wall) were performed with the patient in the supine position at five time points. The first time point (AI: anesthetic induction) was considered at approximately 15 min after tracheal intubation and before laparotomy; the second time point (OP: opened peritoneum), immediately after abdominal wall opening; the third time point (OP1h), 1 h after abdominal opening; the fourth time point, immediately after the peritoneum was closed (CP); the fifth and last time point (AC: abdomen closed), 30 min after abdominal wall closing. Muscle relaxation during measurements was assured by a peripheral neuromuscular monitor (TOF-GUARD®; Organon Teknika NV, Turnhout, Belgium). During the measurement procedures, surgery was stopped, and all retractors were removed.

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Respiratory Mechanics.

The end-inflation occlusion method was used to measure the resistive and elastic properties of the respiratory system (9). This method consists of inflating the relaxed respiratory system with a constant square wave flow provided by a ventilator, followed by a rapid airway occlusion at end-inspiration, which is maintained until a plateau in tracheal pressure is achieved. A rapid airway occlusion was performed during 5 s of inspiratory pause by pressing the end-inspiratory hold button of the ventilator and decreasing fresh gas flow from the flow meters to zero. This maneuver was applied three times, with a brief interval of normal ventilation between each one. An average of three measurements was used to calculate a posteriori the elastic and resistive values of the respiratory system. The contribution in pressures because of volume loss by continuing gas exchange should be considered insignificant.

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Inspiratory Flow, Airway Pressure, and Esophageal Pressure.

Airway opening pressure (Pao and inspiratory airflow were measured by using a variable area pneumotachograph inserted between the proximal tip of the endotracheal tube and the “Y” circuit of the ventilator. The response of the Bicore monitor (Allied Healthcare Products, Irvine, CA), which was calibrated with the gas mixture in use during measurements, was linear over the proposed range of flows. Esophageal pressure (Pes) was obtained from an esophageal balloon introduced orally, inflated with 0.5–1.0 mL, and positioned at the lower third of the esophagus. The correct positioning of esophageal balloon and Pes data in the anesthetized, paralyzed patient were verified according to data from the literature (13). Analog output signals from the Bicore monitor were recorded in an IBM personal computer by means of an analog-to-digital at a sample rate of 200 Hz and processed in a specific software calibration analyzer (Timeter RT-200; Allied, St. Louis, MO). Volume was obtained by digital integration of the flow signal, and was directly correlated with the average tidal volume displayed by the ventilator. Data processed in the specific software were stored in a computer program (Excel for Windows 97), and the results presented herein were calculated with conventional formulae for respiratory data mechanics described in the section below.

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Analysis of Respiratory Mechanics.

After airway occlusion, both the Pao and Pes decreased from a maximal value (Pmax) to an evident plateau (P2) (Fig. 1). Initially, there was a fast decrease in tracheal pressure (ΔP1), from the peak airway pressure and esophageal pressure to a deflection in the pressure curve (P1), followed by a slower decay (ΔP2) until an apparent plateau was reached; this decay was observed in Pao but not in Pes. ΔP2 of Pao and Pes represented the static end-inspiratory recoil pressure of the respiratory system (Pst,rs) and chest wall (Pst,w), respectively (14).

Figure 1

Figure 1

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Compliance.

Static respiratory compliance (Cst,rs) (mL/cm H2O) was computed by dividing the correspondent tidal volume (Vt) by the difference between Pst,rs − Pao at end-expiration (8). Static compliance of chest wall (Cst,w) was obtained by dividing Vt by the difference between Pst,w − Pes at end-expiration. The static lung compliance (Cst,L) was acquired from the Cst,rs and Cst,w by conventional formulae: Cst,L = Cst,rs × Cst,w/Cst,w − Cst,rs(11). To avoid auto-PEEP, each maneuver was accomplished by allowing a complete expiration to zero end-expiratory pressure and observing the P-V curve in the monitor (Capnomac Ultima, Datex Instrumentarium).

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Resistance.

The maximal and minimal resistance (cm H2O.L−1.s−1) of the total respiratory system (Rmax,rs and Rmin,rs, respectively), lung (RL,max and RL,min), and chest wall (Rw,max and Rw,min) were computed by dividing peak airway pressure minus plateau pressure (P′max − P2) and peak pressure minus initial pressure (P′max − P1) from the airway, transpulmonary, and esophageal pressure tracings, respectively, by the flow immediately preceding the occlusion (14). The additional resistance of the respiratory system (DRrs), lung (DRL), and chest wall (DRw), were calculated as maximal minus minimal resistance of the respiratory system (DRrs = Rmax,rs − Rmin,rs), lung (DRL = Rmax,L − Rmin,L), and chest wall (DRw = Rmax,rw − Rmin,rw). Minimal resistance (Rmin) reflects true airway resistance, whereas additional resistance (DR) reflects both the viscoelastic properties and time constant inhomogeneities within the respiratory tissues (9). ΔP1 corresponds to pressure loss across the airways, with some contribution of rapid resistive components of the chest wall, where ΔP2 represents pressure dissipation attributed to lung and chest wall viscoelastic properties. (ΔP1 + ΔP2) divided by the antecedent inspiratory flow gives the Rrmax,rs. ΔP1 divided by the preceding flow gives Rmin,rs which is attributed mainly to airway resistive properties. ΔP2 divided by the inspiratory flow immediately preceding airway occlusion indicates tissue viscance (DR). However, there was no considerable decrease in Pes, in most of the tracings, so P1 in the Pes was not detectable immediately after the occlusion. As a consequence, Rmin,rs reflects true airway resistance (9), whereas Rmin,L and Rmin,w may be considered irrelevant. Consequently, Rmax,w represents the result of the viscoelastic properties of the chest wall tissues, according to this concept (Rmax,w = DRw). The flow resistive properties of the equipment (endotracheal tube plus connectors and circuits) were experimentally calculated and subtracted from the obtained resistance (9).

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Gas Exchange Variables.

Arterial samples were collected at each time point of the study for pH, Paco2, and Pao2 measurements (i-Stat portable clinical analyzer; i-Stat Corporation, East Windsor, NJ).

Values were expressed as mean ± sd. The average value of three end-inspiration pause maneuvers was considered for each variable calculation. Anthropomorphic data comparisons among normal subjects and obese patients, as well as the surgical times, were performed by using the unpaired Student’s t-test (P < 0.05). Analysis of variance for repeated measures was used to verify the presence of differences in the values of respiratory mechanics and gas exchange during the five established time points, followed by the Tukey test to evaluate the differences between the established study points within the groups. For this purpose, a statistical software (SAS, release 6.11; SAS Institute, Inc., Cary, NC) was used, with a 5% significance level.

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Results

All patients had a normal postoperative evolution and were discharged from the hospital at the expected times for their physical conditions, according to primary disease and surgical magnitude. Normal-weight and obese patients did not present any significant differences in age, height, and surgical time; however, the groups significantly differed in weight, BMI (P < 0.05), and gender distribution (100% of women in the obese group), P < 0.001 (Table 1).

Respiratory rate, Paco2, and Pao2 at the five time points during the study are presented in Table 2. Oxygenation expressed as Pao2 was significantly lower, but within acceptable physiologic levels in obese patients (P < 0.008) compared with normal-weight patients at all time points of the study. Paco2 and respiratory rate were not significantly different between obese and normal-weight patients.

Table 2

Table 2

Pst,rs was clearly higher in obese patients compared with normal-weight ones at all time points (P < 0.0001). In obese patients, 1 h after the peritoneum cavity had been opened, there was a significant decrease in Pst,rs (P < 0.001). After closing the abdominal cavity, the value of Pst,rs increased again and became significantly higher (P < 0.0152) compared with the values obtained after anesthetic induction (Table 3).

Table 3

Table 3

Pst,w was higher in obese patients (P < 0.0033) compared with normal-weight subjects. For both groups, we observed a significant increase in Pst,w in the last established measurement, abdomen closed (P < 0.0013), compared with the initial values.

Cst,rs was significantly reduced in obese compared with normal-weight patients at all studied time points (P < 0.0001). Cst,w presented straight and comparable values and was consequently not significant in both groups (Fig. 2). As predicted, the mean values of Cst,L were significantly less in obese patients compared with normal-weight patients (P < 0.05) at all time points of the study. Only in obese patients did Cst,L increase significantly 1 h after the peritoneum was opened (P < 0.0001), and it decreased again to the original values after the peritoneum had been closed (P < 0.0004) (Fig. 3).

Figure 2

Figure 2

Figure 3

Figure 3

Rmax,rs and Rmin,rs were higher in obese patients at all time points; in the last part of the study, it was observed to increase in normal-weight patients (P < 0.0009).

Rmax,L was higher in obese patients compared with normal-weight patients during the entire study; however, there was a significant difference between the groups at AI (P < 0.0015); OP (P < 0.02). In normal-weight patients, Rmax,L remained unchanged during the whole study. In contrast with obese patients, Rmax,L was higher after anesthetic induction and decreased significantly until 1 h after the peritoneum had been opened; after that, it remained unaltered until the end of the study (Fig. 4).

Figure 4

Figure 4

Maximum chest wall resistance (Rmax,w) may be interpreted as DRw, and is presented in Table 3. No difference was observed in this variable when comparing normal-weight and obese patients.

DRrs and DRL were significantly higher in obese patients compared with normal-weight patients (P < 0.0012 and P < 0.013, respectively). Considering the Obese group, a significant decrease of DRL after peritoneum opening was observed (P < 0.0028), a tendency that was maintained while the abdominal cavity was still open.

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Discussion

Morbidly obese patients, compared with normal-weight patients, presented significantly lower levels of oxygenation, and a marked reduction of static lung compliance. Static compliance of chest wall presented straight and comparable values in both groups during the study. Obese patients also presented higher resistance of the total respiratory system, lung, airways, as well as “additional” lung resistance, but chest wall resistance was comparable in both groups. Mainly in obese patients, the abdominal opening seemed to increase lung compliance.

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Compliance of the Total Respiratory System, Lung, and Chest Wall

Several studies suggest an increase in respiratory system elastic recoil pressure after anesthesia in recumbent humans (8,15). As shown in Table 3, Pst,rs is significantly higher in obese patients compared with normal-weight subjects, probably because of the reduced functional residual capacity (FRC) seen in obesity (5,8). Anesthesia also seems to decrease FRC 0.5 L or 18% in normal-weight patients (15). In obese patients, this reduction is more pronounced (5,8), correlated to the increased BMI (5,8). Damia et al. (15) showed that the onset of anesthesia in morbidly obese patients was associated with a 51% reduction in FRC, explained by a cranial shift of the diaphragm muscle, and a partial recovery of FRC after laparotomy by a probable back movement of the diaphragm into the abdomen. In our study, Pst,rs decreased significantly in obese patients one hour after the peritoneum cavity opening (P < 0.001), and increased again after its closure (P < 0.0152). Compared with the values obtained after anesthetic induction, Pst,w was higher in obese patients than in normal-weight subjects, different from Pst,rs, which did not vary with laparotomy. Pelosi et al. (5) described that abdominal pressure was twice as much in obese patients compared with normal-weight patients.

Which of these components, chest wall, lung, or both, is responsible for the decrease in total respiratory compliance? This is another important question that is not totally elucidated in the literature. In awake obese patients, investigators using different methods found decreased chest compliance (8,16,17). In contrast, Suratt et al. (18) found no correlation between BMI and Cst,w when comparing normal-weight and obese awake subjects. Interestingly, Pelosi et al. (5), in another group of anesthetized obese patients, demonstrated that the reduction in respiratory compliance was caused mostly by the lung component. Our data showed that the main responsibility for Cst decrease in anesthetized obese patients should be attributed to the lung component, because Cst,w was comparable to that of the normal-weight patients. We also demonstrated that lung compliance increased significantly during the period of abdomen opening, almost 60%, decreasing again after the abdomen had been closed. Cst,w in both groups decreased progressively during the study until the final time point. This effect may be caused by a probable stiffening of the superior part of the abdomen enclosing the inferior part of the chest wall, because of the surgical trauma involving the abdominal wall (19). As a consequence, the low levels of Cst,L in obese patients, partly dependent on increased abdominal pressure, may explain the necessity of high transpulmonary pressures and/or PEEP recommended to maintain adequate oxygenation during anesthesia and in the postoperative period.

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Resistance of the Respiratory System, Lung, and Chest Wall

According to our results, obese patients present higher respiratory resistance, mostly dependent on the lung component. A high resistive component implies that obese patients may sometimes require higher inspiratory flows during anesthesia to assure adequate ventilation. One critique of our study is related to the measurement of lung volume. We encountered problems using the helium technique to measure FRC during anesthesia. In fact, airway conductance is linearly related to lung volume (20). Zerah et al. (21) showed a significant decrease in FRC and total lung capacity in obese awake patients and a significantly increased respiratory and airway resistance, whereas chest wall resistance remained unaltered. Low lung volume may explain in part the higher values in Rmax,rs and its subcomponents (Rmin,rs, Rmax,L) reported in the study by Pelosi et al. (5,8), and in ours. However, it should not be assumed that a decrease in FRC caused by anesthesia in the obese is the only mechanism responsible for the significant increases in Rmax,rs. The partitioned components, including the tissue component of resistance, DRL, from the obtained Rmax,L, must also be considered, because general anesthesia in humans increases, decreases, or does not change airway resistance (22). There are experimental data (23) showing that, during stimulation of the airway smooth muscle, halothane attenuates airway resistance along with reductions of lung volume, but that it may increase the tissue component of resistance (24). It is possible to speculate that our results related to resistive properties were dependent on the interaction of lung volume reduction and a progressive alveolar recruitment after tracheal intubation. This effect seems to be predominant in obese patients and was more pronounced in Rmax,rs after anesthetic induction. The increased lung resistance herein represented by DRL verified in our study and reported in the literature (8,11), implies that obese patients presented an increase of viscoelastic/inhomogeneous and elastic pressures applied to the lung, reflecting stiffening of lung tissues that explain, in part, the necessity of high volume and inspiratory flow to obtain adequate alveolar ventilation. Perhaps these stiffened tissues could not be totally recruited during ventilatory maneuvers which may contribute to low lung compliance and a high tissue-resistive component.

Most of the studies related to anesthesia in obese patients recommend high transpulmonary inspiratory pressure and/or PEEP to maintain end-expiratory volume, together with high Fio2, to preserve blood oxygenation (2). But few studies made any correlation between respiratory mechanics and implications of ventilation during anesthesia as well as changes that may occur during laparotomy. Although in our study obese patients presented significantly lower levels of arterial oxygen (P < 0.008) compared with the normal-weight ones, the mean values of Pao2 remained higher than 100 mm Hg at all time points, without PEEP. Vt guided by the normal levels of end-tidal CO26, high Vt (15–20 mL/kg) adjusted according to the calculated ideal weight, or simplistically high levels of Vt without any mention of the exact values (4) have been reported in different studies to preserve arterial oxygenation. The mean values of Vt used during our study was close to 0.60L or approximately 11 mL/kg of ideal weight. Compared with the higher Vt values (sometimes of >15 mL/kg) (10) recommended in the literature, those we used were relatively low. Pelosi et al. (8,11) have been using Vt values similar to ours. We found that laparotomy significantly alters lung compliance, which should be taken into account during the use of higher Vt. The increased resistive component of obese patients may be accentuated during anesthesia and may require flow or volume adjustment to maintain alveolar ventilation, mostly during variations of intraabdominal pressure. Some questions remain open to discussion, especially those involving respiratory mechanical particularities of obese patients and the setting of ventilation variables.

The authors gratefully acknowledge the support and generous assistance during the study of the technician Anderson Silva, BS, and of Karine Savalli Redigolo and Lilian Natis (Department of Statistics, Instituto do Coração-Incor HC-FMUSP) for the statistical analysis.

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