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The Effects of Body Mass on Lung Volumes, Respiratory Mechanics, and Gas Exchange During General Anesthesia

Pelosi, Paolo MD; Croci, Massimo MD; Ravagnan, Irene MD; Tredici, Stefano MD; Pedoto, Alessia MD; Lissoni, Alfredo MD; Gattinoni, Luciano MD

doi: 10.1213/00000539-199809000-00031
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We investigated the effects of body mass index (BMI) on functional residual capacity (FRC), respiratory mechanics (compliance and resistance), gas exchange, and the inspiratory mechanical work done per liter of ventilation during general anesthesia.We used the esophageal balloon technique, together with rapid airway occlusion during constant inspiratory flow, to partition the mechanics of the respiratory system into its pulmonary and chest wall components. FRC was measured by using the helium dilution technique. We studied 24 consecutive and unselected patients during general anesthesia, before surgical intervention, in the supine position (8 normal subjects with a BMI <or=to25 kg/m2, 8 moderately obese patients with a BMI >25 kg/m2 and <40 kg/m2, and 8 morbidly obese patients with a BMI >or=to40 kg/m2). We found that, with increasing BMI:

1.FRC decreased exponentially (r = 0.86; P < 0.01)

2.the compliance of the total respiratory system and of the lung decreased exponentially (r = 0.86; P < 0.01 and r = 0.81; P < 0.01, respectively), whereas the compliance of the chest wall was only minimally affected (r = 0.45; P < 0.05)

3.the resistance of the total respiratory system and of the lung increased (r = 0.81; P < 0.01 and r = 0.84; P < 0.01, respectively), whereas the chest wall resistance was unaffected (r = 0.06; P = not significant)

4.the oxygenation index (PaO2/PAo2) decreased exponentially (r = 0.81; P < 0.01) and was correlated with FRC (r = 0.62; P < 0.01), whereas PaCO2 was unaffected (r = 0.06; P = not significant)

5.the work of breathing of the total respiratory system increased, mainly due to the lung component (r = 0.88; P < 0.01 and r = 0.81; P < 0.01, respectively).

In conclusion, BMI is an important determinant of lung volumes, respiratory mechanics, and oxygenation during general anesthesia with patients in the supine position.Implications: The aim of this study was to investigate the influence of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia.

(Anesth Analg 1998;87:654-60)

Istituto di Anestesia e Rianimazione, Universita' di Milano and Servizio di Anestesia e Rianimazione, Ospedale Maggiore, Istituto di Ricovero e Cura a Carattere Scientifico, Milan, Italy.

Accepted for publication May 29, 1998.

Address correspondence and reprint requests to Dr. Paolo Pelosi, Istituto di Anestesia e Rianimazione, Universita' di Milano-Ospedale Maggiore, IRCCS, via Francesco Sforza 35, 20122 Milano, Italy.

For patients in the supine position, general anesthesia induces atelectasis formation, a reduction in lung volume, and respiratory mechanical impairment that may be combined with gas exchange abnormalities [1]. The mechanisms responsible for the reduction in lung volume and atelectasis formation are unknown. It has been hypothesized that the loss of muscular tone combined with blood shifting to the abdomen due to the anesthetic procedure causes an increase in intraabdominal pressure and a consequent cephalad diaphragmatic displacement [2]. This would account for the occurrence of atelectasis in the most dependent lung regions and is related to the oxygenation impairment after the induction of anesthesia [3].

However, studies have not confirmed this hypothesis, which suggests that atelectasis is related not only to changes in the position of the diaphragm, but also to a complex interaction of several factors, including the shape of the chest wall structures (thoracic and abdominal) and the volume or distribution of blood in the thorax [4,5]. Other than lung volumes and oxygenation changes, anesthesia reduces respiratory system compliance and increases airflow resistance, mainly because of the reduction in lung volume [6].

In awake obese patients in the supine position, the increased mass loading of the ventilatory system, particularly on the thoracic and abdominal component of the chest wall, modifies lung volumes and gas exchange [7]. Anesthesia may thus produce more adverse effects on respiratory function in obese subjects than in normal patients [8].

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Methods

The investigation was approved by our institutional ethics committee, and informed consent was obtained from each subject.

We studied 24 consecutive subjects characterized by different body mass (8 normal patients, 8 moderately obese patients, and 8 morbidly obese patients). Body mass was evaluated using the body mass index (BMI), i.e., weight (in kilograms) x height2 (in squared meters). Normal subjects had a BMI <or=to25 kg/m2, minimal to moderately obese patients had a BMI >25 kg/m2 and <40 kg/m2, and morbidly obese patients had a BMI >or=to40 kg/m2[9]. Inclusion criteria were age 40-75 yr, height 1.60-1.80 m, no history of smoking, and no previous cardiopulmonary disease. The preoperative pulmonary function data for each of the three groups are as follows: vital capacity (VC) was 115 +/- 12, 104 +/- 11, and 97 +/- 7 percent of the predicted value, whereas the forced expiratory volume in 1 s (FEV1)/VC was 101 +/- 3, 100 +/- 4, and 99 +/- 6 percent of the predicted value, respectively. All the patients were scheduled for elective surgery (herniated disc or gastric binding) and were studied before surgical intervention. Anesthesia was induced with IV propofol (1-3 mg/kg of ideal body weight). Muscle relaxation to facilitate endotracheal intubation was provided with succinylcholine (1 mg/kg of ideal body weight), and paralysis was maintained with pancuronium bromide. Patients' tracheas were intubated with a Portex cuffed endotracheal tube (7-7.5 mm inner diameter) and mechanically ventilated. Anesthesia was maintained with a continuous infusion of propofol (6-12 mg [center dot] kg-1 [center dot] h-1). The ventilatory settings were as follows: tidal volume 10 mL/kg of ideal body weight [10], respiratory rate 14 breaths/min, inspiratory time 33%, inspiratory oxygen concentration 40%. No positive end-expiratory pressure was used.

After 15 min of stabilization and before surgical intervention, measurements of gas exchange, respiratory mechanics, and lung volumes were collected with patients in the supine position.

Functional residual capacity (FRC) was measured at end-expiration using a simplified closed-circuit helium dilution method. Possible limitations of the procedure have been fully discussed elsewhere [11].

Briefly, an anesthesia bag filled with 2 L of a known gas mixture (13% helium in oxygen) was connected to the airway opening at end-expiration and 10 deep (inflation of the entire bag volume) manual breaths were performed. The helium concentration in the anesthesia bag was measured by using a helium analyzer (PK Morgan Ltd., Chatham, Kent, England), and the FRC was computed according to the following formula: Equation 1 where Vi is the initial gas volume in the anesthesia bag and [He]i and [He]fin are the initial and final helium concentrations, respectively, in the anesthesia bag.

Airway pressure (PaO2) was measured proximal to the endotracheal tube by using polyethylene tubing (2 mm inner diameter, 120 cm long), connected to a Bentley Trantec pressure transducer (Irvine, CA). Esophageal pressure (Pes) was measured by using an esophageal balloon (Bicore, Irvine, CA) modified to allow connection to the transducer. During measurements, the balloon was inflated with 0.5-1 mL of air. The validity of Pes was verified using the occlusion test method of Baydur et al. [12], and the balloon was fixed in that position. In obese subjects in the supine position, mediastinal organs may compress the esophagus and invalidate the translation of Pes into pleural pressure. However, no alternative methods are available, and this technique was adopted to partition respiratory mechanics in both awake [13] and paralyzed supine obese subjects [13,14]. Gas flow was recorded by using a heated pneumotachograph connected to a Validyne MP 45-1 differential pressure transducer (Northridge, CA). Volume was obtained by digital integration of the flow signal. Both flow and pressure signals were recorded on a four-channel recorder (Battaglia Rangoni, Bologna, Italy) and processed via an analog to digital converter (100 samples per second per channel) by a portable personal computer for storage and calculations. The pressure-flow relationships of endotracheal tubes were determined after each experiment by using the experimental gas mixture. These relationships were used to determine the resistive pressure drop caused by the endotracheal tubes for any given flow.

To partition the mechanics of the respiratory system into its pulmonary and chest wall components, we used the esophageal balloon technique, together with rapid airway occlusions during constant flow inflation [15]. The end-inspiratory hold button of the mechanical ventilator was pressed for brief (3-4 s) airway occlusions. During this period, the contribution in pressures due to volume loss by continuing gas exchange should be considered negligible. Occlusion was maintained until both Pao and Pes decreased from a maximal value (Pmax) to an apparent plateau (P2). After the occlusion, an immediate drop from Pmax to a smaller value (P1) at flow 0 was appreciable in Pao, but not in Pes. The P2 values of Pao and Pes were taken to represent the static end-inspiratory recoil pressures of the respiratory system (Pst,rs) and chest wall (Pst,w), respectively. Similarly, the end-expiratory airway pressure (PEst,rs) and the end-expiratory esophageal pressure (PEst,w) were recorded during an end-expiratory occlusion. The static respiratory system (Cst,rs) and chest wall (Cst,w) compliances were obtained by dividing the tidal volume by the difference of Pst,rs - PEst,rs and Pst,w - PEst,w, respectively. The static lung compliance (Cst,L) was obtained from Cst,rs and Cst,w according to the following equation: Equation 2 With the ventilator settings in use, the end-expiratory volume corresponded to the elastic equilibrium volume in each patient, as evidenced by an expiratory pause (zero flow) and by the absence of changes in PaO2 after airway occlusion at end-expiration.

Maximal (Rmax,rs) and minimal (Rmin,rs) resistance of the respiratory system were computed from PaO2 as Equation 3 where Pmax' represents the new Pmax value obtained correcting PaO2 for tube resistance (see above) and Vi' is the flow immediately preceding the occlusion.

Rmin,rs represents the "ohmic" (flow-dependent) resistive component of the respiratory system, and Rmax,rs includes Rmin,rs plus the additional respiratory resistance caused by stress relaxation and/or time constant inequalities within the respiratory system tissues. The difference between Rmax,rs and Rmin,rs was termed DR,rs. Because there was no appreciable decrease in Pes (i.e., P1 was not identifiable in the esophageal tracings) immediately after the occlusion, Rmin,rs essentially reflects airway resistance (Rmin,L), and minimal chest wall resistance (Rmin,w) can be considered negligible. As a consequence, maximal chest wall resistance (Rmax,w) is caused entirely by the viscoelastic properties of the chest wall tissues (i.e., Rmax,w = DR,w). Additional resistance of the lung (DR,L) was obtained as DR,rs - DR,w, whereas the sum of Rmin,L + DR,L gives the maximal lung resistance (Rmax,L). DR,L and DR,w (i.e., Rmax,w) are caused by stress relaxation and/or time constant inequalities within the lung and chest wall, respectively.

Arterial blood samples were analyzed for pH, PO2, and PCO2. Pulmonary oxygenation was assessed by the arterial to alveolar oxygen tension ratio (PaO2/PAO2) and the alveolar to arterial difference [D(A-a)O2]. The PaO2/PAO2 ratio was calculated as: Equation 4 whereas the D(A-a)O2 value was calculated as: Equation 5 where PiO2 is the partial pressure of inspired O2 and 0.8 is the respiratory quotient. PIO2 was calculated by the formula: PiO2 = FIO2 (Pb-47), where FIO2 is the fraction of inspired oxygen.

Measurement of the work of ventilation during passive inflation was obtained using a previously described and validated method [14], as briefly summarized below.

The mechanical work performed by the ventilator to inflate the respiratory system (Wtot,rs), excluding the endotracheal tube, was computed integrating the area of PaO2 (corrected for the resistive components of the endotracheal tube) during inspiration over the inflation volume. The mechanical work performed by the ventilator to inflate the chest wall (Wtot,w) was computed, integrating the area subtended by Pes and volume. Subtracting Wtot,w from the corresponding work of the total respiratory system, we obtained the total work of the lung (Wtot,L).

Values are expressed as mean +/- SD. The mean value of three breaths was used for each variable and for each experimental condition. To perform different fittings, we used GraphPad Prism[trade mark sign] version 2.0 software (GraphPad Software, Inc, San Diego, CA). Different equations were used: linear regression, hyperbola, one-phase exponential decay, one-phase exponential association. Analysis between groups was performed by using analysis of variance.

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Results

The general characteristics of the patients are presented in Table 1. Patients in all three groups were comparable in gender distribution, age, and height (P = not significant) and significantly differed in weight (P < 0.01) and BMI (P < 0.01). The average tidal volume and inspiratory flow were 0.619 +/- 0.062 L and 0.470 +/- 0.090 L/s, 0.702 +/- 0.100 L and 0.490 +/- 0.070 L/s, and 0.681 +/- 0.069 L and 0.470 +/- 0.090 L/s for normal patients, moderately obese patients, and morbidly obese patients, respectively.

Table 1

Table 1

The FRC decreased with BMI (Figure 1). There was a major decrease in FRC with a moderate increase in body mass (FRC = 11.97 x exp[-0.096 x BMI] + 0.46; r = 0.86; P < 0.01).

Figure 1

Figure 1

As shown in Figure 2, respiratory compliance decreased with BMI, and decreases were evident with small increases in body mass (Cst,rs = 233.3 x exp[-0.086 x BMI] + 40; r = 0.86; P < 0.01). The reduction in respiratory compliance with BMI was caused by a reduction in both lung compliance (Cst,L = 7198 x exp[-0.230 x BMI] + 71.5; r = 0.81; P < 0.01) and chest wall compliance (Cst,w = 257.7 -2.078 x Cst,w; r= 0.45; P < 0.05).

Figure 2

Figure 2

As shown in Figure 3, total respiratory resistance markedly increased with BMI (Rmax,rs = 2.55 x exp[0.03 x BMI]; r = 0.81, P < 0.01), and this increase was caused mainly by an increase in the resistance of the lung (Rmax,L = 1.78 x exp[0.03 x BMI]; r = 0.84, P < 0.01). Chest wall resistance was not significantly correlated with BMI (r = 0.06). The increase in the resistance of the lung with BMI was caused mainly by the increase in airway resistance (Rmin,L = -3.6 + 0.23 x BMI; r = 0.84) because the relationships of both DR,rs and DR,L with BMI were extremely weak (r = 0.44; P < 0.05 and r = 0.46; P < 0.05, respectively).

Figure 3

Figure 3

As shown in Figure 4, oxygenation (PaO2/PAO2) exponentially decreased with increasing BMI (PaO2/PAO2 = 1.23 x exp[-0.037 x BMI] + 0.196; r = 0.81; P < 0.01). Consequently, D(A-a)O2 was linearly correlated with BMI (D[A-a]O2 = -7.15 + 3.37 x BMI; r = 0.84; P < 0.01). PaCO2 was not significantly related to BMI (r = 0.06).

Figure 4

Figure 4

As shown in Figure 5, the work of breathing performed by the ventilator on the respiratory system linearly increased with increasing BMI (Wtot,rs = 0.10 + 0.02 x BMI; r = 0.88; P < 0.01), and it was related both to the lung component (Wtot,L = 0.23 x exp[0.026 x BMI]; r = 0.81; P < 0.01) and to the chest wall component (Wtot,w = 0.58 x BMI/[51.0 + BMI]; r = 0.47; P < 0.01).

Figure 5

Figure 5

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Discussion

During general anesthesia with patients in the supine position, 1) body mass is an important determinant of lung volumes, oxygenation and respiratory mechanics, mainly affecting the lung component; 2) alterations in respiratory mechanics are present not only in patients with severe obesity, but also in patients with moderate obesity; 3) the work of breathing increases with body mass and was quite near or even greater than the commonly reported limits of muscle fatigue in most of the overweight patients [16].

We found a linear relationship between the increase in BMI and the reduction in FRC. The FRC is reduced in recumbent adult humans after the induction of anesthesia, and the magnitude of its reduction-with consequent atelectasis formation-has been related to age, weight, and height [1]. However, the mechanisms of FRC reduction and atelectasis formation during anesthesia are not completely understood.

The formation of atelectasis has been ascribed to a decreased distribution of ventilation in the dependent lung zones during anesthesia and mechanical ventilation. The loss of the diaphragmatic tone induced by anesthetics makes the movement of the diaphragm passively dependent on the relative pressures present at its thoracic and abdominal slices [2]. Because there is a gravitational pressure gradient in the abdomen due to the presence of abdominal viscera, the distribution of ventilation is preferentially directed toward the nondependent lung regions. With increasing BMI, an increase in abdominal mass and intraabdominal pressure is expected [11]. Consequently, the gravitational intraabdominal pressure gradient is likely increased, with an increased load particularly on the most dependent lung regions and a consequent, and more important, cephalad displacement and reduction in the passive movements of the dependent part of the diaphragm. This preferential alteration of the diaphragm likely favors the development of more atelectasis in the dependent lung regions [17,18]. However, studies performed in normal subjects using a three-dimensional fast computed tomography scan questioned the role of the diaphragm alone in determining atelectasis formation and reducing FRC [4,5]. It is likely that the interaction of several potentially significant factors, such as the thoracic spine, rib cage, and diaphragm, leads to a reduction in FRC and atelectasis formation.

We found that the reduction in respiratory compliance with increasing BMI was caused mainly by the lung component, with chest wall compliance only weakly dependent on the BMI. Similar results were obtained by Hedenstierna and Santesson [13] and Van Lith et al. [19], who found approximately normal values of chest wall compliance in anesthetized and paralyzed obese subjects. The most likely cause of the reduction in lung compliance with BMI is simply the reduction in FRC, with the intrinsic mechanical characteristics of the lung being approximately normal.

From our data, it is quite clear that chest wall compliance is only weakly influenced by the increase in BMI. Several factors may, however, explain the slight influence of BMI on chest wall compliance: the presence of the pressure-volume curve of the chest wall on a flatter section of the elastic recoil of the chest wall, due to a greater reduction in the total thoracic volume in overweight patients; or the presence of a progressively increased mass added to the chest wall and/or abdomen in patients with an increased BMI. Both of these factors explain the reduction in chest wall compliance in obese subjects [20].

We found that respiratory system resistance increased with increasing BMI, mainly because of an increase in lung resistance, whereas chest wall resistance seemed unaffected. The increase in lung resistance was caused mainly by the airway resistance component, whereas the viscoelastic component was only weakly dependent on BMI.

Using body plethysmography, Zerah et al. [21] found airway resistance values comparable to ours in awake seated patients with different severity of obesity. Moreover, they also observed that airway resistance was approximately twice as high in patients with severe obesity compared with those with minimal obesity. One hypothesis to explain the increase in airway resistance with BMI is that the large decrease in FRC and/or an intrinsic narrowing of the airways in obesity are responsible for these abnormalities. Indeed, Briscoe and Dubois [22] showed that airway conductance, i.e., the reciprocal of airway resistance, was linearly related to lung volume, in normal awake subjects. We found that DR,rs and DR,L were only weakly associated with BMI. This is in line with the results of Zerah et al. [21], who found that the difference between the resistance of the total respiratory system and airway resistance (equivalent to DR,rs in our study) was little affected by increasing BMI.

We found that oxygenation, expressed as PaO2/PAO2 ratio, decreased with increasing BMI. The major cause of this decrease is likely related to the reduction in FRC. Moderate to severe hypoxemia has been reported in supine obese subjects during both spontaneous breathing and anesthesia and paralysis [8,17,13]. Moreover ventilation-perfusion mismatch has been reported even in awake, seated, obese subjects [23]. The lung bases are well perfused, but they are underventilated because of airway closure and alveolar collapse. This effect is likely more pronounced and enhanced in obese subjects in the supine position during anesthesia and paralysis.

In contrast, PCO2 was not correlated to BMI, as previously reported in awake and anesthetized obese subjects without obesity hypoventilation syndrome [13].

We found that the work of breathing of the total respiratory system increased with BMI. The increase was due to both the lung and chest wall components, but the former was more significant.

Measurements of the work performed by the ventilator during passive inflation may be an index of the actual work performed by the respiratory muscles during spontaneous breathing [14]. Our results are in line with those of Suratt et al. [24], who hypothesized a predominant effect of the lung, not the chest wall, in determining the work of breathing in awake, obese, upright subjects. On the contrary, other authors found a prevalent increase in the respiratory work of breathing due to the chest wall component [25], and others did not find any increase in the work of breathing with increasing BMI [26]. However, in these latter studies, no attempt was made to assure complete relaxation of the respiratory muscles. Thus, the role of the chest wall in determining the work of breathing may have been overestimated.

In conclusion, we found that the BMI is an important determinant of lung volumes, respiratory mechanics, and oxygenation in anesthetized patients in the supine position.

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