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See discussions, stats, and author profiles for this publication at: http://www.researchgate.net/publication/13556557
The Effects of Body Mass on Lung Volumes,Respiratory Mechanics, and Gas Exchange
During General Anesthesia
ARTICLE in ANESTHESIA & ANALGESIA · SEPTEMBER 1998
Impact Factor: 3.47 · DOI: 10.1097/00000539-199809000-00031 · Source: PubMed
CITATIONS
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7 AUTHORS, INCLUDING:
Paolo Pelosi
Università degli Studi di Genova
508 PUBLICATIONS 13,913 CITATIONS
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Alessia Pedoto
Memorial Sloan-Kettering Cancer Center
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Luciano Gattinoni
Fondazione IRCCS Ca' Granda - Ospedale …
457 PUBLICATIONS 17,834 CITATIONS
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Available from: Luciano Gattinoni
Retrieved on: 03 October 2015
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The Effects of Body Mass on lung Volumes, Respiratory
Mechanics, and Gas Exchange During General Anesthesia
Paolo Pelosi, MD, Massimo Croci, MD, Irene Ravagnan, MD, Stefano Tredici, MD,
Alessia Pedoto,
MD,
Alfred0 Lissoni,
MD,
and Luciano Gattinoni,
MD
Istituto di Anestesia e Rianimazione, Universita’ di Milan0 and Servizio di Anestesia e Rianimazione, Ospedale Ma&ore,
Istituto di Ricovero e Cura a Carattere Scientifico, Milan, Italy
We investigated the eff ect s of body mass index (BMI) on
functional residual capacity (FRC), respiratory me-
chanics (compliance and resistance), gas exchange, and
the inspiratory mechanical work done per liter of venti-
lation during general anesthesia. We used the esopha-
geal balloon technique, together with rapid airway oc-
clusion during constant inspiratory flow, to partition
the mechanics of the respiratory system into its pul-
monary and chest wall components. FRC was meas-
ured by using the helium dilution technique. We stud-
ied 24 consecutive and unselected patients during
general anesthesia, before surgical intervention, in
the supine position (8 normal subjects with a BMI
125 kg/m’, 8 moderately obese patients with a BMI
>25 kg/m2 and ~40 kg/m’, and 8 morbidly obese pa-
tients with a BMI 240 kg/m’). We found that, with in-
creasing BMI:
1. FRC decreased exponentially
(Y
= 0.86; P < 0.01)
2. the compliance of the total respiratory system and of
the lung decreased exponentially
(Y
= 0.86; P < 0.01
and Y = 0.81; P < 0.01, respectively), whereas the
compliance of the chest wall was only minimally af-
fected
(Y
= 0.45; P < 0.05)
3. the resistance of the total respiratory system and of
the lung increased
(Y
= 0.81; P < 0.01 and Y = 0.84;
P < 0.01, respectively), whereas the chest wall resis-
tance was unaffected (r = 0.06; P = not significant)
4. the oxygenationindex (Pao,/PAo,) decreased expo-
nentially (Y = 0.81; P < 0.01) and was correlated with
FRC
(Y
= 0.62; P < O.Ol), whereas Pace, was unaf-
fected (r = 0.06; P = not significant)
5. the work of breathing of the total respiratory system
increased, mainly due to the lung component
(Y
= 0.88;
P < 0.01 and
Y
= 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 me-
chanics, and gas exchange during general anesthesia.
(Anesth Analg 1998;87:65460)
F
r patients in the supine position, general anes-
thesia induces atelectasis formation, a reduction
in lung volume, and respiratory mechanical im-
pairment 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 shift ing 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
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.
654
Anesth Analg 1998;87:654-60
dependent lung regions and is related to the oxygen-
ation impairment after the induction of anesthesia (3).
However, studies have not confirmed this hypoth-
esis, 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 oxygen-
ation 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 ventila tory system, par-
ticularly on the thoracic and abdominal component of
the chest wall, modifies lung volumes and gas ex-
change (7). Anesthesia may thus produce more ad-
verse effect s on respiratory function in obese subjects
than in normal patients (8).
01998 by the International Anesthesia Research Society
0003-2999/98/ 5.00
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ANESTH ANALG
1998;87:654-60
PELOSI ET AL. 655
BODY MASS AND RESPIRATORY FUNCTION
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 heigh? (in squared
meters). Normal subjects had a BMI 525 kg/m’, mini-
mal to moderately obese patients had a BMI
>25 kg/m* and ~40 kg/m’, and morbidly obese pa-
tients had a BMI ~40 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: vita l capacity (VC)
was 115 + 12, 104 + 11, and 97 t 7 percent of the
predicted value, whereas the forced expiratory vol-
ume in 1 s (FEVl)/VC was 101 2 3,100 + 4, and 99 ?
6 percent of the predicted value, respectively. All the
patients were scheduled for elective surgery (herniat-
ed disc or gastric binding) and were studied before
surgical intervention. Anesthesia was induced with IV
propofol (l-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 pancuro-
nium 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 propo-
fol (6-12 mg * kg-’ * h-l). The ventilatory settings
were as follows: tidal volume 10 mL/kg of ideal body
weight (lo), respiratory rate 14 breaths/min, inspira-
tory time 33%, inspiratory oxygen concentration 40%.
No posit ive end-expiratory pressure was used.
After 15 min of stabilization and before surgical
intervention, measurements of gas exchange, respira-
tory 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 he-
lium dilution method. Possible limitations of the pro-
cedure have been fully discussed elsewhere (11).
Briefly, an anesthesia bag fil led with 2 L of a known
gas mixture (13% hel ium 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 an-
esthesia bag was measured by using a hel ium analyzer
(PK Morgan Ltd., Chatham, Kent, England), and the
FRC was computed according to the following
formula:
FRC = Vi X ([He]i - [He]fin)/[He]i
where Vi is the ini tia l gas volume in the anesthesia bag
and [He]i and [Helfin are the init ial and final helium
concentrations, respectively, in the anesthesia bag.
Airway pressure (Pao,) 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 measure-
ments, the balloon was in flated with 0.5-l mL of air.
The valid ity of Pes was verified using the occlusion
test method of Baydur et al. (12), and the bal loon was
fixed in that position. In obese subjects in the supine
position, mediastinal organs may compress the esoph-
agus and invalidate the translation of Pes into pleural
pressure. However, no alternative methods are avail-
able , and this technique was adopted to part ition re-
spiratory 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 MI’ 45-l different ial pressure transducer
(Northridge, CA). Volume was obtained by dig ital
integration of the flow signal. Both flow and pressure
signals were recorded on a four-channel recorder (Bat-
taglia Rangoni, Bologna, Italy) and processed via an
analog to dig ita l converter (100 samples per second
per channel) by a portable personal computer for stor-
age and calculations. The pressure-flow relationships
of endotracheal tubes were determined after each ex-
periment by using the experimental gas mixture.
These relationships were used to determine the resis-
tive pressure drop caused by the endotracheal tubes
for any given flow.
To part ition 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 inf lation
(15). The end-inspiratory hold button of the mechan-
ica l ventilator was pressed for brief (3-4 s) airway
occlusions. During this period, the contribution in
pressures due to volume loss by cont inuing gas ex-
change 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 (Pl) at flow 0 was appreciable
in Pao, but not in Pes. The I’2 values of Pao and Pes
were taken to represent the static end-inspiratory re-
coil pressures of the respiratory system (Pst,rs) and
chest wall (Pst,w), respectively. Simi larly , the end-
expiratory airway pressure (PEst,rs) and the end-
expiratory esophageal pressure (PEst,w) were re-
corded 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
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656
PELOSI ET AL.
BODY MASS AND RESPIRATORY FUNCTION
ANESTH ANALG
1998;87:654dO
Table 1. Patients’ Characteristics
n Gender M/F)
Age yr)
Height m) Weight kg) BMI kg/m’)
Normal patients
8 l/7 52 t 13 1.64 + 0.05 58.6 + 5.8 21.9 + 0.5
Moderately obesepatients 8 l/7 54 2 15 1.62 + 0.05 87.9 + 10 33.6 -c 2.8
Morbidly obesepatients
8 l/7 50 k 10 1.65 + 0.09 130.8 I 18 48.2 + 8
P NS NS NS co.01 co.01
Data are expressed as mean 2 SD.
NS = not significant.
Pst,w - PEst,w, respectively. The static lung compli-
ance Cst,L) was obtained from Cst,rs and Cst,w ac-
cording to the following equation:
tidal volume
Cst,L =
[ Pst,rs - Pst,w) - IJEst,rs - PESt,W)]’
With the ventilator settings in use, the end-expiratory
volume corresponded to the elastic equilibrium vol-
ume in each patient, as evidenced by an expiratory
pause zero flow) and by the absence of changes in
Pao, after airway occlusion at end-expiration.
Maximal Rmax,rs) and minimal Rmin,rs) resis-
tance of the respiratory system were computed from
Pao, as
Pmax’ - P2)/Vi’ and Pmax’ - Pl)/Vi’
where Pmax’ represents the new Pmax value obtained
correcting Pao, 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 respira-
tory resistance caused by stress relaxation and/or time
constant inequalities within the respiratory system tis-
sues. The difference between Rmax,rs and Rmin,rs
was termed DR,rs. Because there was no appreciable
decrease in Pes i.e., I’1 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 con-
sidered negligible. As a consequence, maximal chest
wall resistance Rmax,w) is caused entirely by the vis-
coelastic 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 Pco,. Pulmonary oxygenation was assessedby
the arterial to alveolar oxygen tension ratio PaoJ
PAo,) and the alveolar to arterial difference [D A-
a)O,]. The Pao,/PAo, ratio was calculated as:
Pao,/ Pio, - PacoJ0.8)
whereas the D A-a)O, value was calculated as:
Pie,-PacoJ0.8) - Pao,
where Pio, is the partial pressure of inspired 0, and
0.8 is the respiratory quotient. PIO, was calculated by
the formula: Pio, = FIO, @‘b-47), where FIO, is the
fraction of inspired oxygen.
Measurement of the work of ventilation during pas-
sive inflation was obtained using a previously de-
scribed and validated method 14), as briefly summa-
rized 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 Pao, corrected for the resistive components of the
endotracheal tube) during inspiration over the infla-
tion volume. The mechanical work performed by the
ventilator to inflate the chest wall Wtot,w) was com-
puted, integrating the area subtended by Pes and vol-
ume. 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 fit-
tings, we used GraphPad PrismTM 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.
Results
The general characteristics of the patients are pre-
sented 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 -t- 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 5 0.090 L/s
for normal patients, moderately obese patients, and
morbidly obese patients, respectively.
The FRC decreased with BMI Figure 1). There was
a major decrease in FRC with a moderate increase in
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ANESTH ANALG
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* .
0
0
10 20 30 40 50 60 70
BMI (kg .m-‘ )
Figure 1. Relationsh ip between functional residual capacity (FRC)
and body mass index (BMI).
body mass (FRC = 11.97 X exp[-0.096 X BMI] + 0.46;
Y = 0.86; P < 0.01).
As shown in Figure 2, respiratory compliance de-
creased with BMI, and decreases were evident with
small increases in body mass (Cst,rs = 233.3 X
exp[-0.086 X BMI] + 40; Y = 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; Y= 0.45; P < 0.05).
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 < O.Ol), 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]; Y = 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).
As shown in Figure 4, oxygenation (Pao,/PAo,)
exponent ially decreased with increasing BMI (Pao,/
PAo, = 1.23 X exp[-0.037 X BMI] + 0.196; r = 0.81;
P < 0.01). Consequently, D(A-a)O, was linearly cor-
related with BMI (D[A-a]O, = -7.15 + 3.37 X BMI;
r = 0.84; P < 0.01). Pace, was not significantly related
to BMI (r = 0.06).
As shown in Figure 5, the work of breathing per-
formed by the ventilator on the respiratory system
linearly increased with increasing BMI (Wtot,rs = 0.10
+ 0.02 X BMI; r = 0.88; P < O.Ol), and it was related
both to the lung component (Wtot,L = 0.23 X
expI0.026 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).
Discussion
During general anesthesia with patients in the supine
position, 1) body mass is an important determinant of
PELOSI ET AL.
BODY MASS AND RESPIRATORY FUNCTION
657
O/
0 10 20 30
40 50 60 70
BMI (kg. m-*)
;. .
r= 0.81
/
p < 0.01
04
0 IO 20 30 40 50
60 70
BMI (kg m-*)
400
q 300
z
0
3 200
L
r= 0.45
I
< 0.05
l
s
5 100
l
0-l I
0 10 20 30 40 50 60 70
BMI (kg-m-*)
Figure 2. Relationsh ips between comp liance of the total respiratory
system (Cst,rs), lung (Cst,L), and chest wall (Cst,w) and body m ass
index (BMI).
lung volumes, oxygenat ion and respiratory mechan-
ics, mainly affecting the lung component; 2) alter-
ations in respiratory mechanics are present not only in
patients with severe obesity, but also in patients with
moderate obesity; 3) the work of breath ing 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
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658 PELOSI ET AL.
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1998;87:65&60
25
l
10 20 30 40 50 60 70
BMI (kg. m-*)
0 10 20
30 40 50
60 70
BMI (kg. m-*)
l
l l l
l
0 10 20 30 40
50 60 70
BMI (kg m-2)
l
l
va
l l
l
.
l
l
l
l
l
l
l
l
Figure 3. Relations hips between the resistance of the total respira-
Figure 4. Relationsh ips between the oxygenation index (PaoJ
tory system (Rmax,rs), lung (Rmax,L), and chest wall (Rmax,w) and
PAo,), the alveolar-a rterial oxygen differen ce (D[A-a]O,), and
body mas s index (BMI).
Pace, and body mass index (BMI).
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 ventila-
tion. The loss of the diaphragmatic tone induced by
anesthetics makes the movement of the diaphragm
passively dependent on the relative pressures present
1.00
0.75
0”
a4
lN 0.50
0
a”
0.25
0.00
0
l
B
I
E 150-
5
0”
zgoo -
3
a
50 -
10 20 30 40 50 60 70
BMI (kg - m-P)
0-l
0 10 20 30 40 50 60 70
BMI (kg. m-*)
l
l
l
cl 10 20 30
40 50 60 70
BMI (kg m-*)
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 distri-
bution 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 gravita-
tional intraabdominal pressure gradient is likely in-
creased, with an increased load particularly on the
most dependent lung regions and a consequent, and
more important, cephalad displacement and reduction
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659
BODY MASS AND RESPIRATORY FUNCTION
1 r=0.88 1
0.0-l
0 IO 20 30 40
50 60 70
BMI (kg m-“)
0.0-l
0 lo 20 30 40
50 60 70
BMI (kg m-2)
r = 0.47
I
< 0.01
0.00-l
0
10 20 30 40 50 60 70
BMI (kg. m-2)
Figure 5. Relations hips between the work of breathing of the total
respiratory system (Wtot,rs) lung (Wtot,L), and chest wall (Wtot,w)
and body mas s index (BMI).
in the passive movements of the dependent part of the
diaphragm. This preferential alteration of the dia-
phragm likely favors the development of more atelec-
tasis in the dependent lung regions 17,18). However,
studies performed in normal subjects using a three-
dimensional fast computed tomography scan ques-
tioned the role of the diaphragm alone in determining
atelectasis formation and reducing FRC 4,5). It is
likely that the interaction of several potentially signif-
icant 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 compli-
ance 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 val-
ues of chest wall compliance in anesthetized and par-
alyzed obese subjects. The most likely cause of the
reduction in lung compliance with BMI is simply the
reduction in FRC, with the intrinsic mechanical char-
acteristics of the lung being approximately normal.
From our data, it is quite clear that chest wall com-
pliance is only weakly influenced by the increase in
BMI. Several factors may, however, explain the slight
influence of BMI on chest wall compliance: the pres-
ence 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 progres-
sively 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 com-
pliance in obese subjects 20).
We found that respiratory system resistance in-
creased with increasing BMI, mainly because of an
increase in lung resistance, whereas chest wall resis-
tance seemed unaffected. The increase in lung resis-
tance 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 obe-
sity. Moreover, they also observed that airway resis-
tance was approximately twice as high in patients
with severe obesity compared with those with mini-
mal 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. In-
deed, 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 differ-
ence 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 Pao,/
PAo, 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 re-
ported in supine obese subjects during both spon-
taneous breathing and anesthesia and paralysis
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(8,17,13). Moreover ventilation-perfusion mismatch
has been reported even in awake, seated, obese sub-
jects (23). The lung bases are well perfused, but they
are underventila ted because of airway closure and
alveolar collapse. This effect is likely more pro-
nounced and enhanced in obese subjects in the supine
position during anesthesia and paralysis.
In contrast, Pco, was not correlated to BMI, as pre-
viously reported in awake and anesthetized obese
subjects without obesity hypovent ilation 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 venti-
lator 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 breath-
ing 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 breath ing may have
been overestimated.
In conclusion, we found that the BMI is an impor-
tant determinant of lung volumes, respiratory me-
chanics, and oxygenation in anesthetized patients in
the supine position.
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