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Istituto di Anestesia e Rianimazione, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale Maggiore, Universita' di Milano, 20122 Milan, Italy
ABSTRACT
INTRODUCTION
METHODS
RESULTS AND DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Pelosi, P., M. Croci, I. Ravagnan, M. Cerisara, P. Vicardi,
A. Lissoni, and L. Gattinoni. Respiratory system mechanics in
sedated, paralyzed, morbidly obese patients J. Appl.
Physiol. 82(3): 811-818, 1997.
The effects of
inspiratory flow and inflation volume on the mechanical properties of
the respiratory system in eight sedated and paralyzed postoperative
morbidly obese patients (aged 37.6 ± 11.8 yr who had never smoked
and had normal preoperative seated spirometry) were investigated by
using the technique of rapid airway occlusion during constant-flow
inflation. With the patients in the supine position, we measured the
interrupter resistance (Rint,rs), which in humans probably reflects
airway resistance, the "additional" resistance (
Rrs) due to
viscoelastic pressure dissipation and time-constant inequalities, and
static respiratory elastance (Est,rs). Intra-abdominal
pressure (IAP) was measured by using a bladder catheter, and functional
residual capacity was measured by the helium-dilution technique. The
results were compared with a previous study on 16 normal anesthetized
paralyzed humans. Compared with normal persons, we found that in obese
subjects: 1) functional residual
capacity was markedly lower (0.645 ± 0.208 liter) and IAP was
higher (24 ± 2.2 cmH2O);
2) alveolar-arterial oxygenation
gradient was increased (178 ± 59 mmHg);
3) the volume-pressure curve of the
respiratory system was curvilinear with an "inflection" point;
4) Est,rs, Rint,rs, and Rrs were
higher than normal (29.3 ± 5.04 cmH2O/l, 5.9 ± 2.4 cmH2O · l
1 · s,
and 6.4 ± 1.6 cmH2O · l1 · s,
respectively); 5) Rint,rs increased
with increasing inspiratory flow, Est,rs did not change, and Rrs
decreased progressively; and 6) with
increasing inflation volume, Rint,rs and Est,rs decreased, whereas
Rrs rose progressively. Overall, our data suggest that obese
subjects during sedation and paralysis are characterized by hypoxemia
and marked alterations of the mechanical properties of the respiratory
system, largely explained by a reduction in lung volume due to the
excessive unopposed IAP.
morbid obesity; anesthesia and paralysis; functional residual
capacity; intra-abdominal pressure
INTRODUCTION AWAKE MORBIDLY OBESE PATIENTS present severe
alterations of respiratory mechanics, particularly an increase in
respiratory elastance (30) and resistance (41).
General anesthesia and paralysis, even in normal subjects, are
associated with alterations in respiratory function, such as increased
respiratory elastance, presence of atelectasis, and hypoxemia (8, 20).
It has been suggested that these alterations may be more pronounced in
morbidly obese people (36, 37, 38), who do, in fact, have a
substantially increased risk of perioperative respiratory complications
(19, 27).
Nevertheless, there are relatively few reports dealing with the changes
in mechanical properties of the respiratory system in these patients
during general anesthesia and muscle paralysis (22).
In this study we used the technique of rapid airway occlusion
during constant-flow ( METHODS The investigation was approved by the institutional ethics committee,
and informed consent was obtained preoperatively from each person.
There were eight patients (4 men and 4 women) scheduled for general
anesthesia for ileojejunal bypass or gastric binding. None had any
history of smoking or clinical evidence of cardiopulmonary disease.
Their preoperative pulmonary functional tests, done with the patients
in the seated position, gave the following values: average vital
capacity (VC) was 4.3 ± 1.2 liters (96.9 ± 7% of predicted), forced expiratory volume in 1 s
(FEV1) was 3.3 ± 0.9 liters
(91.7 ± 8.7% of predicted), and
FEV1/VC was 80 ± 5.8% (98.8 ± 8.1% of predicted). Mean age and body mass index were 37.6 ± 11.8 yr (range 20-55 yr) and 48.7 ± 7.8 kg/m2 (range 40.7-64.8
kg/m2), respectively.
Anesthesia was induced with intravenous thiopental sodium (5-7
mg/kg). Muscle relaxation to facilitate endotracheal intubation was
provided with succinylcholine (1 mg/kg), and paralysis was maintained
with pancuronium bromide. Patients were intubated with a
Portex cuffed endotracheal tube (6.5-7.5 mm ID) and mechanically ventilated (tidal volume 8-10 ml/kg of ideal body weight,
respiratory rate 11-14 breaths/min). Anesthesia was maintained
with 0.5-1% isofluorane in
O2-N2O
(50:50%). The average time of the surgical procedure was 128 ± 45 min. After surgery, the N2O was
withdrawn and patients were transferred to our intensive care unit
(ICU) still sedated and paralyzed. The time elapsed from the end of the
surgical procedure and the beginning of the protocol ranged between 1 and 2 h. The entire study was performed in the ICU. During the study,
all subjects were sedated with intravenous diazepam (0.1-0.2
mg/kg) and paralyzed with pancuronium bromide (0.1-0.2 mg/kg).
Mechanical ventilation was provided with a Siemens Servo Ventilator 900 C ventilator. The baseline ventilator setting during the study was as
follows: tidal volume of 0.72 ± 0.04 liter and inspiratory flow of
0.66 ± 0.04 l/s with a mean inspired
O2 fraction of 44 ± 9% and
balance N2 (air supplemented with
O2). The inspired O2 fraction was set to maintain
arterial O2 saturation higher than
90% and respiratory frequency to maintain normocapnia (12.4 ± 1.8 breaths/min). The duration of expiration averaged 3.81 ± 0.72 s
(range 2.88 to 5.04 s). Arterial PO2
and PCO2 averaged 98 ± 15 and
36.3 ± 4 Torr, respectively.
) inflation (5, 11, 13,
15) to investigate the following in sedated,
paralyzed, morbidly obese patients:
1) the effects of
, volume (V), and time on the mechanical properties of the respiratory system, i.e., elastance and resistance, and 2) the adaptability of the
spring and dashpot model proposed by Bates et al. (3) for interpreting
respiratory mechanics. We also measured functional residual capacity
(FRC) and intra-abdominal pressure to provide a further picture of the
changes in respiratory system mechanics induced by sedation and
paralysis in these patients. We compared our data with those reported
by D'Angelo et al. (11) in normal anesthetized paralyzed subjects
using the same technique.
Vi, where Vi is the initial gas volume in the anesthesia bag
and [He]i and
[He]f are the initial
and final helium concentrations in the bag, respectively.
Respiratory mechanics.
was measured with a heated pneumotachograph
(Fleish no. 2) inserted between the endotracheal tube and the Y piece
of the ventilator. It was connected to the breathing circuit by a cone and to a differential pressure transducer (Validyne MP 45 ± 2 cmH2O, Northridge, CA). The
equipment dead space (not including the endotracheal tube) was 80 ml.
Volume was obtained by digital integration of the flow signal. The
response of the pneumotachograph, calibrated with the same gas mixture
used during measurements, was linear over the experimental range of
flows. Airway pressure (Pao) was measured proximal to the orotracheal
tube by a pressure transducer (Bentley Trantec, Bentley Laboratories,
Irvine, CA). The pressure-flow relationships of the orotracheal tubes
were determined after each experiment by using the experimental gas mixture as described by Behrakis et al. (7) to compute the resistive
pressure of the endotracheal tubes for any given flow tested. All
variables were recorded on a four-channel pen recorder (Gould Brush
2400S, Gould, Cleveland, OH) and processed by an analog-to-digital
converter to an IBM-compatible personal computer for storage and
computations.
Respiratory mechanics were assessed by the
constant- end-inspiratory occlusion method (5, 11,
13, 15). After the occlusion, there was an immediate drop in Pao from a
maximal value (P
max) to a lower value
(P1), followed by a gradual
decrease, until an apparent plateau
(P2) was achieved. These plateau
pressures were reached in 3-4 s, so Pao at 4 s was taken as the
static end-inspiratory elastic recoil pressure of the total respiratory
system (Pst,rs). During this period the reduction in pressure due to
volume loss from continuing gas exchange should be negligible (11).
The immediate and slow changes in Pao were obtained by computed fitting
curves, as previously described (4). The initial drop in Pao corrected
for the resistive pressure drop as the result of the endotracheal tube
(Pmax P1), where Pmax is
the peak airway pressure corrected for the endotracheal tube
resistance, divided by the immediately preceding steady
provides the interrupter resistance
(Rint,rs). In the calculation of the Rint,rs, correction was made for the errors due to the closing time of the ventilator valve, as previously described (4). The slow decay of
pressure (P1 P2) divided by the
preceding the occlusion yields the effective
"additional" resistance (Rrs) as previously reported (5, 11,
13, 15). The sum of Rint,rs and Rrs presents the total
resistance of the respiratory system (Rrs).
P2 (Pst,rs) divided by V
provides the static elastance of the total respiratory system (Est,rs),
and P1 divided by V gives the
dynamic elastance (Edyn,rs).
Two sets of experiments were carried out in each patient.
1) In the iso-V experiment, V
was kept constant at its baseline value and test breaths were performed
by randomly changing the inspiratory for one
breath from the basal setting to values of 0.2, 0.4, 0.6, 0.8, and 1 l/s. This was done by regulating the inspiratory time
(TI) with the appropriate
button on the ventilator. 2) In the
iso- experiment, the basal was
kept constant, and V was changed for single breaths from the basal
setting to values of 0.2, 0.4, 0.6, 0.8, and 1 liter in random order by
changing the respiratory frequency on the ventilator. This part of the experiment served to compute the volume-pressure curve of the respiratory system. At each test breath, end-inspiratory occlusion lasting 4-5 s was performed by pressing the end-inspiratory hold button of the ventilator. After each test breath, baseline ventilation was resumed until volume, flow, and pressure records returned to
baseline values.
Model fitting.
Our data were analyzed in terms of the model of the respiratory system
of Bates et al. (3). In its simplest form this consists of two
compartments in parallel: a dashpot representing Rint,rs and a Kelvin
body (Fig. 1). The latter consists of a
spring representing the Est,rs in parallel with a Maxwell body, i.e, a
spring (E2) and a dashpot
(R2) arranged serially.
E2 and
R2 represent the viscoelastic
properties of the tissues of the lung and chest wall, and Est,rs and
Rint,rs are standard elastic and resistive components, respectively.
This four-element model predicts that during constant-
inflation, Rrs should increase with
TI according to the following exponential function (11, 13, 15)
|
(1) |
2 is the time constant of the
Maxwell body (=
R2/E2).
Equation 1 is based on the assumption that Rrs reflects only the viscoelastic behavior. Measurements of
Rrs, however, may comprise contributions due to time-constant inequalities within the lung (pendelluft) and /or chest
wall (28, 31). Such contributions may be taken into account by adding a
constant (A) to Eq. 1 (15)
|
(2) |
2 were assessed by fitting
Eq. 2 to the experimental data of
Rrs vs. TI. The time constant
of the exponential was allowed to vary independently.
Because during constant- inflation
TI = V/,
Eq. 2 can be rewritten
|
(3) |
V Rrs will decrease with increasing
, whereas at a constant Rrs
will increase exponentially with V.
Statistical analysis.
Analysis of regression was done by using the least squares method.
Morbidly obese patients and 16 normal anesthetized paralyzed subjects
(11) were compared by using Student's unpaired
t-test (2).
P < 0.05 was accepted as
statistically significant. Values are means ± SD.
RESULTS AND DISCUSSION
|
(4) |
is the pressure at V of 1 liter and b is a dimensionless
number. The average coefficients
a and
b in obese patients were,
respectively, 24.9 ± 4.6 and 0.65 ± 0.09 cmH2O/l, significantly different
(P < 0.01) from those reported in
normal subjects (a = 14 ± 2 and b = 0.95 ± 0.01 cmH2O/l).
V)-pressure (Pst) curve of total respiratory
system in 8 morbidly obese patients and 16 normal anesthetized paralyzed persons (11). Data are expressed as means ± SD. Average curve was obtained by using individual regressions.
These data indicate an overall higher elastance in obese subjects and the presence of an "inflection point," or "zone," at pressures between 5 and 15 cmH2O, after which the volume increases linearly with pressure. In normal subjects no inflection zone was identified. In accordance with the pattern of the volume-pressure curves, the Est,rs measured at fixed flow during baseline ventilation is higher (P < 0.01) in obese patients than in normal subjects (29.3 ± 5.04 vs. 14.5 ± 2.1 cmH2O/l; Table 1). More importantly, whereas Est,rs in normal subjects did not change with increasing volume (straight volume-pressure curve), in obese patients it dropped sharply along the inflection zone (from 0 to 0.6 liter), subsequently remaining roughly constant (Fig. 3A). As expected (11), Est,rs was not influenced by
(Fig.
3B).
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
) and dynamic (
) elastance with V
(A) and flow (;
B) in 8 morbidly obese patients and
16 normal anesthetized paralyzed persons (11). Data are expressed as
means ± SD. Average curve was obtained by using individual
regressions.
Increased stiffness of the respiratory system, i.e., a higher Est,rs, has already been described in conscious obese persons (30). Possible causes include increased stiffness of the chest wall and/or lung parenchyma or a decrease in overall lung volume. Naimark and Cherniak (30) found abnormal chest wall elastance in conscious obese subjects and attributed the increase to the greater adiposity around the ribs, diaphragm, and abdomen or to limited movement of the ribs caused by thoracic kyphosis and lumbar hyperlordosis from excessive abdominal fat content (30, 36, 37). However, Suratt et al. (35) found no alterations to chest wall elastance. Whatever the real behavior of the chest wall elastance, the lung volume reduction we observed might explain the higher elastance of the respiratory system. It is well established, in fact, that Est,rs depends on lung volume (the lower the volume, the higher the elastance) (1). Moreover, the possible negative effects of anesthesia duration on Est,rs can be reasonably ruled out because several authors found no deterioration in respiratory mechanics during the course of anesthesia after induction (6). The changes in Est,rs with increasing pressure and volume in obese subjects may be interpreted as a recruitment of atelectatic lung regions. Increasing pressure recruits the atelectasis due to the displacement of the diaphragm, i.e., counteracting the previously unopposed intra-abdominal pressure (16, 24, 29). This recruitment of atelectatic regions may sharply change elastance along the inflection zone, after which the increase in inflation volume does not really decrease Est,rs, as the recruitment is very likely complete. Rint,rs. In obese subjects, Rint,rs was three times that in normal subjects (5.9 ± 2.4 and 2.3± 0.5 cmH2O · l
1 · s,
respectively, at comparable and V; Table 1), as
previously reported in awake, seated, obese patients using body
plethysmography (5 ± 0.05 cmH2O · l1 · s)
(41), and sharply decreased with increasing volume
(P < 0.01, Fig.
4A).
Consequently, the conductance (Gint,rs), i.e., 1/Rint,rs, increased
with volume, according to the following equation
|
(5) |
. The average values of
a and
b in obese patients were 0.005 ± 0.11 l · cmH2O1 · s1
and 0.35 ± 0.34 cmH2O1 · s1,
respectively, which are significantly
(P < 0.0.1) different from normal
values (0.39 ± 0.09 l · cmH2O1 · s1
and 0.15 ± 0.09 cmH2O1 · s1).
V
(A) obtained at constant
of 0.66 l/s and between Rint,rs and
(B) obtained at
constant V of 0.7 liter, in 8 morbidly obese patients and 16 normal
anesthetized paralyzed persons (11). Data are expressed as means ± SD. Average curve was obtained by using individual regressions.
While Rint,rs decreased with increasing volume, at the same tidal volume (iso-
V) it rose dramatically with flow, compared with normal
(Fig. 4B). Expressing the
Rint,rs-flow relationship with Roher's equation
|
(6) |
1 · s,
which is similar to normal
(K1 = 1.94 ± 0.51 cmH2O · l1 · s),
whereas
K2,
the "turbulent" component, was significantly (P < 0.01) increased (8.1 ± 6.3 and 0.52 ± 0.08 cmH2O · l2 · s2,
respectively).
The Rint,rs in anesthetized humans usually reflects airway resistance,
although it may include an "ohmic" component of the chest wall,
~27% according to D'Angelo et al. (12). Rint,rs not only represents
the interrupter resistance of the lung and chest wall in series but
also parallel "gaps" in homogeneity within the lungs. With these
limitations in mind, our data suggest that the lung volume reduction
plays a major role in the increase in Rint,rs. Airway caliber is
closely related to lung volume (39), and a large reduction in caliber,
due to the smaller lung volume, could account for an increased
turbulent component, i.e., higher K2,
observed at a rate that only minimally affects airway resistance in
normal persons. Other possible factors, such as recruitment of
previously collapsed lung regions, during tidal volume may be involved
in the increase in Rint,rs, but, at the moment, this remains a matter
of speculation.
Rrs and Rrs.
Rrs at the baseline ventilator setting was significantly
(P < 0.01) higher than normal (6.4 ± 1.6 and 2.8 ± 0.6 cmH2O · l1 · s,
respectively; Table 1), and it was markedly dependent on and V, decreasing with and
increasing with V (Figs.
5A and
6A).
Consequently, Rrs was significantly
(P < 0.01) increased in obese
subjects (12.3 ± 3.1 compared with 5.1 ± 0.9 cmH2O · l1 · s
for normal patients; Table 1), but it was neither
nor V dependent (Figs. 5B and
6B).
Rrs;
A) and total respiratory system
resistance (Rrs; B) with
in 8 morbidly obese patients and 16 normal
anesthetized paralyzed persons (11) at constant V of 0.7 liter. Data
are expressed as mean ± SD. Average curve was obtained by using
individual regressions.
Rrs (A) and Rrs
(B) with V in 8 morbidly obese
patients and 16 normal anesthetized paralyzed persons (11) at a
constant of 0.66 l/s. Data are expressed as means ± SD. Average curve was obtained by using individual regressions.
The increase in
Rrs in our patients might reflect higher
time-constant inequalities within the respiratory system and/or altered stress-adaptation properties of the thoracic tissues (lung and
chest wall). The reduction in lung volume itself may increase Rrs
(11). Unfortunately, the end-inspiratory occlusion method does not
distinguish between stress-adaptation phenomena and time-constant differences. However, during mechanical ventilation, in obese patients
the distribution of ventilation is markedly uneven (22) and, although
the structures responsible for the viscoelastic behavior of the
respiratory system are not known, mechanical alterations of both lung
and chest wall may contribute to the increase in Rrs (13).
Spring and dashpot model of respiratory mechanics.
We found that the spring and dashpot model presented in Fig. 1 can be
applied not only to normal subjects (11, 13) but also to morbidly
obese, sedated, paralyzed patients. In all patients, the relationship
between Rrs and TI closely
fitted (P < 0.01) the theoretical
exponential function (Eq. 2, Fig.
7). The individual values for the constants
in Eq. 2 in obese subjects are listed in Table 2, which also provides the
E2
(R2/2)
values. Both R2 and
2 were significantly
(P < 0.01) higher than in normal
anesthetized paralyzed persons (18.3 ± 6.9 vs. 5.9 ± 1.8 cmH2O · l1 · s
and 4.4 ± 2.9 vs. 1.3 ± 0.3 s, respectively).
E2, however, was close to normal
(5.6 ± 3.0 vs. 4.5 ± 0.9 cmH2O/l. The
values of A were small and not
significantly different from zero. Moreover, according to the model in
Fig. 1, Rrs increased exponentially with V and decreased with
, as expected from Eq. 3. In obese patients, however, the standard time
constant of the respiratory system (= Rint,rs/Est,rs) was 0.21 ± 0.09 s (Table 1), which is slightly higher than normal (0.14 0.17 s) (11). Although the nature of the increase in
R2 and
2 in obese patients is not known and the anatomic correlates of
R2 and
E2 have yet to be determined, up
to the volume investigated Rrs was consistent with the linear
viscoelastic model shown in Fig. 1.
Rrs and inspiratory time
(TI) in a representative obese
patient from iso-V () and iso- ()
experiments.
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ACKNOWLEDGEMENTS
We are particularly indebted to Prof. E. D'Angelo for useful suggestions and criticism in preparing the revised version of this manuscript. We also thank the surgeons and nurses who helped in performing this study.
FOOTNOTES
Address for reprint requests: P. Pelosi, Istituto di Anestesia e Rianimazione, Ospedale Maggiore, via Francesco Sforza 35, 20122 Milano, Italy.
Received 29 March 1995; accepted in final form 23 September 1996.
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