British Journal of Anaesthesia 1996; 76: 530–535
Carbon dioxide output in laparoscopic cholecystectomy
T. KAZAMA, K. IKEDA, T. KATO AND M. KIKURA
Summary
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Key words
Surgery, laparoscopy. Anaesthetics, volatile, sevoflurane. Ventilation, carbon dioxide response. Ventilation, deadspace. Oxygen, uptake.
Laparoscopic gynaecological procedures involve a
short duration of intraperitoneal carbon dioxide
insufflation and are performed usually in young or
otherwise healthy female patients. Changes in haemodynamic state and arterial blood-gas tensions with
insufflation of carbon dioxide have been studied
extensively and found to be relatively insignificant
[1–6]. However, peritoneal insufflation for laparoscopic cholecystectomy may be longer than that for
gynaecological procedures.
Insufflation of the abdominal cavity with carbon
dioxide may be associated with pulmonary atelectasis, decreased functional residual capacity and
high peak airway pressures. Absorption of carbon
dioxide via the peritoneum causes hypercapnia but
not impaired ventilation in healthy patients [7, 8].
Significant carbon dioxide retention has been demonstrated in patients with cardiopulmonary impairment
during carbon dioxide pneumoperitoneum for extended procedures such as laparoscopic cholecystectomy [7, 9], with possibly consequent cardiac
arrhythmias [10]. In pneumoperitoneum, carbon
dioxide eliminated in expired gas (carbon dioxide
output) contains both carbon dioxide of metabolic
production and also absorbed carbon dioxide from
the peritoneal cavity. Although there has long been
interest in the rate of carbon dioxide output during
long-lasting laparoscopic procedures, the reported
data [5, 10–12] are not consistent, possibly because
storage of carbon dioxide may be variable.
This study was conducted to assess excess carbon
dioxide output evoked by pneumoperitoneum with
stable carbon dioxide storage maintained by keeping
arterial P a CO constant at preinduction levels and to
investigate continued carbon dioxide load after
pneumoperitoneum using a pharmacokinetic
model.
2
Patients and methods
We studied 12 consenting, ASA I or II patients,
undergoing elective laparoscopic cholecystectomy.
TOMIEI KAZAMA, MD, KAZUYUKI IKEDA, MD, TAKASUMI KATO, MD,
MUTSUHITO KIKURA, MD, Department of Anaesthesiology and
Intensive Care, Hamamatsu University School of Medicine, 3600
Handa-cho, Hamamatsu, Japan 431-31. Accepted for publication:
October 27, 1995.
Correspondence to T.K.
CO2 output in laparoscopic cholecystectomy
531
Approval was obtained from the Human Studies
Committee at Hamamatsu University Hospital.
Patients were in good general health, with no signs or
laboratory findings of renal, pulmonary or hormonal
disease, or obesity (defined as a body mass index
9 29). All patients fasted overnight and were premedicated with hydroxygine 50 mg and atropine
0.5 mg 1 h before induction of anaesthesia. An i.v.
cannula was inserted during local anaesthesia. I.v.
infusion of sodium lactate solution was started, and
the rate of infusion was adjusted to 8–10 ml kg91 h91
during the study. Heart rate and ECG were
monitored continuously. An arterial cannula was
inserted into the radial or dorsalis pedis artery during
local anaesthesia for arterial pressure monitoring. An arterial blood sample was obtained from
the indwelling arterial cannula anaerobically and
analysed immediately (ABL 300 blood-gas analyzer, Radiometer, Copenhagen, Denmark). Rectal
temperature was displayed continuously on a
temperature module (Hewlett-Packard) using a
thermistor probe inserted 10 cm into the rectum.
Body temperature was maintained at 36–37 ⬚C by
external heating. The temperature of the operating
room was maintained at 24–26⬚C.
The sampling cannula for measuring end-tidal
anaesthetic gas, oxygen, nitrogen and carbon dioxide
concentrations was inserted between a micro-pore
filter (Gambro Enström AB, Sweden) and the
tracheal tube. Mean inspired and expired gas samples
were obtained from bypass mini-mixing chambers
mounted in each inspiratory and expiratory limb of
the breathing circuit. These chambers have been
described previously [13]. Gas samples from each
chamber, and sampling cannula for end-tidal gas
measurement were introduced individually into a
mass spectrometer (MGA 1100, Perkin Elmer) calibrated against certified gas mixtures. The concentrations of oxygen, nitrous oxide, sevoflurane and
nitrogen were measured at 1-min intervals. Expired
minute volume was measured with an electric Wright
respirometer placed in the expiratory limb, and
calibrated previously against a dry gas of known
composition at physiological flow. The accuracy was
the same as that of the Fleisch pneumotachograph
(Gould). Expired minute volume normalized for
body surface area (BSA) was expressed at BTPS, and
carbon dioxide output and oxygen uptake were
expressed at STPD. Inspired minute volume was
calculated by an inert tracer gas dilution technique
[14–17]. Nitrogen was used as the “inert” gas and
was included in the inspired gas during anaesthesia
[16]. Pulmonary gas exchange was computed
as follows: V CO 2 :V E( F E CO − F I CO × F E N /F I N ) ;
VO2 :VE ( FI O2 × FE N2 − FI N2 − FE O2 ); RER : VCO2/
VO2 where VCO2 : carbon dioxide output, VO2 :
oxygen uptake, FI and FE : fractional mean
concentrations of mixed inspired and expired gas,
respectively; VE : expired minute volume and RER
: respiratory exchange ratio. F I CO , sampled from
the mixing chambers, was measured by mass spectrometer in order to exclude the effect of ageing on
carbon dioxide absorber. The equations for calculation are valid even in the presence of anaesthetic
gas [15, 18]. The ratio of deadspace to tidal volume
2
2
2
2
2
(VD/VT) was calculated using Bohr’s equation [19];
V D/V T:( P a CO − P E CO )/P a CO , where P E CO =
carbon dioxide partial pressure of mixed expired
gas.
Before induction of anaesthesia, all subjects were
permitted to breathe room air through the anaesthesia mask for 20 min and mean expired and
inspired concentrations of oxygen, carbon dioxide,
nitrogen and expiratory minute volume were
measured to obtain baseline carbon dioxide output
and oxygen uptake. Anaesthesia was induced with
thiopentone 5 mg kg91 i.v. and non-depolarizing
neuromuscular blocker (vecuronium 0.1 mg kg91).
Tracheal intubation was performed orally using a
cuffed tracheal tube. Inspired concentrations of
oxygen, nitrogen and nitrous oxide were adjusted to
30 %, 20 % and 50 %, respectively, during anaesthesia. The inspired sevoflurane mixture was
adjusted to give an end-tidal sevoflurane concentration of 1.37 % (0.8 MAC). The fresh gas flow rate
was 6–7 litre min91. The lungs of all patients were
ventilated mechanically with the same ventilator
equipped with an anaesthesia machine (Narcomed3,
North American Drager, USA). Tidal volume was
set at 10 ml kg91. Ventilatory frequency ( f ) was
adjusted mainly each minute to maintain P a CO at
preinduction levels with continuous monitoring of
end-tidal carbon dioxide pressure ( P E ′CO2) and intermittent measurement of arterial to end-tidal
carbon
dioxide
partial
pressure
difference
( P a CO − P E ′CO ) Arterial blood samples were
obtained every 15 min after stabilization of the
ventilator settings and analysed for pH, P a CO , P a O
and base excess. Before skin incision, baseline carbon
dioxide output and oxygen uptake were obtained
after they reached steady state. Neuromuscular block
was maintained with additional increments of vecuronium 0.025 mg kg91 when the train-of four ratio
exceeded 75 %. Carbon dioxide was introduced into
the peritoneal cavity by a carbon dioxide Pneu
(Wisap, Germany) pressure limiting automatic
insufflation apparatus and abdominal pressure was
maintained at 8 mm Hg in all patients. After
insufflation, multiple incremental changes in minute
volume were made to maintain P a CO at preinduction
levels. The table was tilted about 5⬚ of the reverse.
Trendelenburg position and then slightly to the left
lateral position. Laparoscopic cholecystectomy was
performed by a standard procedure. Intraperitoneal
gas was evacuated after cholecystectomy and regression of carbon dioxide output in the postinsufflation state was measured 30 min under stable
P E ′ CO2 every 1 min by manual control of ventilatory
frequency. After carbon dioxide output returned to
control level, neuromuscular block was antagonized
with neostigmine 2.0–2.5 mg i.v. and atropine 1.0 mg
i.v. The trachea was then extubated.
Anaesthesia was divided into five periods: (1)
preinduction phase, (2) anaesthesia phase (control
period of anaesthesia before skin incision), (3)
pneumoperitoneum phase (during laparoscopy at
intra-abdominal pressure of 8 mm Hg), (4) postpneumoperitoneum phase (0–30 min after evacuation of carbon dioxide from the peritoneal cavity),
and (5) recovery phase (40 min after extubation).
2
2
2
2
2
2
2
2
2
2
532
British Journal of Anaesthesia
To fit the regression curve for carbon dioxide
output during the post-pneumoperitoneum phase to
multicompartment models, the least squares method
was used and the number of compartments was
determined by minimum AIC (an information
criterion) based on the maximum likelihood estimation method [20].
Statistical analysis was carried out using analysis
of variance (ANOVA), Fisher’s test and Student’s t
test, where appropriate. P : 0.05 was considered
statistically significant. All values are expressed as
mean (SEM).
Results
We studied 12 premedicated patients, who were
essentially normal in the pre-anaesthesia state (table
1). Steady states for VCO2/BSA and VO2/BSA were
obtained during the following phases: preinduction,
anaesthesia, pneumoperitoneum and recovery.
Although it was difficult to maintain P a CO constant
during the 10 min after tracheal intubation and the
start of P E′CO surgery, concentrations were maintained at 5.0–5.4 kPa.
Compared with the preinduction phase, minute
ventilation (VE) decreased from 5.26 (0.33) to 3.33
(0.27) litre min91 (P : 0.05) in the anaesthetic phase
and increased to 5.14 (0.30) litre min91 in the
pneumoperitoneum phase (P : 0.05). Respiratory
minute volume during pneumoperitoneum thus had
to be made 1.54 times that in the anaesthesia phase to
maintain P a CO2 constant (table 2). Carbon dioxide
output and oxygen uptake decreased, respectively,
from 83.5 (5.2), 101.6 (5.1) to 68.5 (4.2), 81.1
Figure 1 Changes in carbon dioxide output ( ) and oxygen
uptake ( ) in the pre-induction (Pre.) anaesthesia (Anaes.) and
pneumoperitoneum (Pneumo.) phases while maintaining P E ′CO2
constant at the normal value for the preinduction phase (mean,
SEM; n : 12). I : Intubation, SI : skin incision.
2
2
(4.6) ml min91 m92 (ATPS, P : 0.05) with sevoflurane
anaesthesia and RER did not change. During
pneumoperitoneum,
carbon
dioxide
output
increased 49 % (102.4 (5.0) ml min91 min92, P :
0.05) while oxygen uptake remained stable and RER
increased from 0.84 (0.02) to 1.16 (0.03) (P: 0.05,
table 2, figs 1, 2). These variables returned to
preinduction levels during recovery. P a CO2 , pH, base
excess and Sa O2 in the preinduction phase were
normal (table 2) and were maintained throughout the
experiment.
Table 1 Characteristics of patients, pneumoperitoneum (pneumo.) and anaesthesia (mean (SEM or range))
Age (yr)
Sex (M : F)
Weight
(kg)
Height
(cm)
Duration of
anaesthesia
(min)
52.5 (37–69)
5:7
57.1 (16.7)
154.1 (11.0)
196.2 (5.4)
Duration of
pneumo.
(min)
CO2
volume for
insufflation
(litre)
89.3 (4.4)
77.2 (5.1)
Table 2 Metabolic and respiratory variables during the four phases of the procedures (mean (SEM)). P E′CO2 :
end-tidal carbon dioxide pressure; VE : expired minute volume; VCO2/BSA : carbon dioxide output/body
surface area; VO2/BSA : oxygen uptake/body surface area; RER : respiratory exchange ratio; VD/VT :
deadspace to tidal volume ratio; ( P a CO2 − PE′CO2 ) :arterial to end-tidal carbon dioxide tension. * Significant
difference from pre-induction, ** significant difference from anaesthesia
PE′
CO2 (kPa)
Sa O2 (%)
Tidal volume (litre)
VE(litre min91)
VCO2/BSA (ml min91 m92)
VO2/BSA (ml min91 m92)
RER
End-tidal sevoflurane (%)
VD/VT
( P a CO2 − PE′CO2 ) (kPa)
pH
Pa O2 (kPa)
Pa CO2 (kPa)
Base excess
Preinduction
Anaesthesia
Pneumoperitoneum
5.4 (0.11)
98 (1.3)
0.39 (0.033)
5.26 (0.33)
83.5 (5.2)
101.6 (5.0)
0.82 (0.013)
0
0.43 (0.017)
0.16 (0.11)
7.430 (0.005)
11.7 (0.44)
5.6 (0.09)
2.8 (0.5)
5.4 (0.12)
99 (1.2)
0.43 (0.028)
3.33 (0.27)*
68.5 (4.2)*
81.1 (4.6)*
0.84 (0.015)
0.70 (0.09)*
0.31 (0.02)*
0.12 (0.09)
7.426 (0.009)
18 (0.9)
5.5 (0.08)
2.4 (0.5)
5.4 (0.06)
99 (0.9)
0.5 (0.033)
5.14 (0.3)**
102.4 (5.04)**
88.8 (4.8)
1.16 (0.025)**
1.69 (0.10)**
0.32 (0.017)
0.28 (0.16)
7.409 (0.009)
19.8 (0.92)
5.6 (0.08)
1.6 (0.9)
Recovery
(40 min after
extubation)
5.3 (0.13)
98 (1.1)
0.32 (0.031)
5.6 (0.32)
86.5 (6.1)
103.6 (5.2)
0.83 (0.03)
0.05 (0.01)
0.42 (0.023)
0.48 (0.29)***
7.385 (0.014)
10.8 (0.55)
5.7 (0.09)
2.1 (1.0)
CO2 output in laparoscopic cholecystectomy
533
Figure 2 Changes in PE′CO2 ( ) and respiratory exchange ratio
(RER) ( ) in the preinduction (Pre.), anaesthesia (Anaes.) and
pneumoperitoneum (Pneumo.) phases (mean, SEM ; n : 12).
I : Intubation, SI : skin incision.
during induction, pneumoperitoneum or after
pneumoperitoneum.
The regression equation for excess VCO2/BSA
after removal of carbon dioxide from the abdominal
cavity is shown in figure 3. VO2 and P E′ CO2 were
stable. A two-compartment model was judged to
give the best fit by AIC. Excess carbon dioxide
output pharmacokinetic variables and AIC values in
each model are shown in table 4. Time constants of
the first (rapid) and second (slow) compartments
were 8.2 and 990 min, respectively. At the end of
pneumoperitoneum, the rapid compartment was
thought to be equilibrated, as T was short (5.7 min)
and carbon dioxide output was constant. The excess
rate of carbon dioxide output/BSA was still
5.5 ml min91 m92, 30 min after removal of carbon
dioxide from the peritoneal cavity.
There was no clinical evidence of hypoxaemia, no
change in standard bicarbonate before and after
peritoneal insufflation, and no postoperative complications.
Discussion
Figure 3 Changes in excess carbon dioxide output ( ) after
removal of carbon dioxide from the abdominal cavity. Oxygen
uptake ( , top) and PE′CO2 ( ) were stable (mean, SEM;
n : 12). (Y : 39.4 e9t/8.18 ; 6.07e9t/990.13).
The results for haemodynamic state and temperature are summarized in table 3. After induction
of anaesthesia there were decreases in heart rate,
systolic arterial pressure, mean arterial pressure and
diastolic arterial pressure. Significant increases in
arterial pressure in the pneumoperitoneum phase
were noted, but no cardiac arrhythmia was detected
During laparoscopy, the large volume of carbon
dioxide for pneumoperitoneum is passively absorbed
from the peritoneal cavity into the blood and most of
it is removed from the circulation by hyperventilation. The respiratory effects of carbon dioxide
absorbed from the peritoneal cavity into the blood
have been studied previously [7, 21–27]. The quantity of carbon dioxide and bicarbonate ion in the
body is large. When ventilation is not in accord with
carbon dioxide output, hypercapnia continues. Sustained elevation in PaCO2, typical of that associated
with pneumoperitoneum, probably recruits wholebody storage depots, such as skeletal muscle and
bone [28], in addition to intraperitoneal organs.
Thus to study carbon dioxide output during
laparoscopic cholecystectomy, the body storage of
carbon dioxide must not be allowed to change.
Although it is not certain that a constant P a CO2
necessarily implies constant storage, it is a reasonable
assumption.
In the present study, VE was adjusted to maintain
P a CO2 constant at the preinduction level with constant
monitoring of P E′ CO2 and intermittent measurement
of (PaCO2−PE′ CO2). This method for estimating PaCO2 is
invalid if the alveolar deadspace increases with
(PaCO2−PE′ CO2), a situation that may occur during
the period of carbon dioxide insufflation. Bramton
Table 3 Haemodynamic variables and temperatures during the four phases of the procedures (mean (SEM)). SAP
: systolic arterial pressure; MAP : mean arterial pressure; DAP : diastolic arterial pressure; HR : heart rate. *
Significant difference from preinduction; ** significant difference from anaesthesia
SAP (mm Hg)
MAP (mm Hg)
DAP (mm Hg)
HR (beat min91)
Rectal temp. (°C)
Room temp. (°C)
Preinduction
Anaesthesia
Pneumoperitoneum
138.9 (4.0)
102 (3.7)
79.8 (3.5)
75.5 (3.7)
36.48 (0.08)
26.2 (0.6)
106 (1.7)*
76.7 (1.4)*
58.8 (1.3)*
67.6 (1.9)
36.49 (0.09)
25.9 (0.7)
130.9 (5.1)**
101.9 (3.9)**
73.9 (3.2)**
76.0 (2.8)
36.46 (0.09)
25.5 (0.4)
Recovery
(40 min after
extubation)
132.8 (3.7)**
96.0 (3.5)**
76.1 (3.2)**
70.1 (2.7)
36.45 (0.08)
25.4 (0.6)
534
British Journal of Anaesthesia
Table 4 Excess carbon dioxide output pharmacokinetic variables and AIC values in each model. AIC : An
information criterion [20]. V1, V2, V3 : volumes of each compartment, Vss : total volume of distribution
One-compartment model
A1
A2
A3
Time constant 1 (min)
Time constant 2 (min)
Time constant 3 (min)
AIC
V1 (ml m−2)
V2 (ml m−2)
V3 (ml m−2)
Vss (ml m−2)
Two-compartment model
41.1
39.4
6.1
13.2
8.2
990
161.1
543
151.6
323
1849
543
2172
and Watson reported that monitoring of PE′CO2
during laparoscopy could be used to reflect P a CO2 ,
except at the start of pneumoperitoneum [29].
Fitzlerald and colleagues demonstrated that there
were no changes in ( P aCO2 − P E ′ CO2) during He
pneumoperitoneum in mechanical ventilation [7]. In
the present study, VD/VT was almost constant except
during preinduction when an anaesthesia mask was
used for ventilation. P a CO2 during pneumoperitoneum was thought to be nearly constant, since
PE′CO2 and ( P aCO2− P E ′ CO2) were nearly constant (table
2, fig. 2).
During anaesthesia, the metabolic rate is reduced
by about 15–30 % below that of the awake state [16,
30]. In this study, oxygen uptake and carbon dioxide
output decreased 20.2 % and 18.0 % respectively.
Thus RER remained constant, even during anaesthesia. Surgical stimulation may alter carbon
dioxide output and oxygen uptake by increasing
metabolic rate. End-tidal total MAC multiples of
sevoflurane and nitrous oxide during pneumoperitoneum were maintained at 1.39, which was
sufficient to prevent the effect of surgical stimulation
on metabolism, as oxygen uptake did not change
during surgery. The increased intra-abdominal
pressure may have interfered with the elimination of
carbon dioxide from abdominal organs and lower
extremities by causing the veins to collapse. Carbon
dioxide output and oxygen uptake increase after
completion of pneumoperitoneum in this situation.
However, an intra-abdominal pressure of 8 mm Hg,
which was maintained automatically, did not hinder
elimination of carbon dioxide, as oxygen uptake
during and after pneumoperitoneum remained
stable.
Marked increases in P a CO2 and excess carbon
dioxide output, 66.9 mm Hg and 41 ml min91, respectively, 12 min after pneumoperitoneum were
reported by Lewis and co-workers in young gynaecological patients anaesthetized with halothane during spontaneous ventilation [10]. Mullet and
colleagues reported excess carbon dioxide output to
be 32 ml min91 with a 25 % increase in Pa CO2 [12].
Wurst, Schulte-Steinbberg and Finsterer noted a
30–40 % increase in carbon dioxide output during
pneumoperitoneum [11]. These values are less than
the
carbon
dioxide
output
of
102.4
(5.0) ml min91 m92 and excess carbon dioxide output
of 34.1 (3.9) ml min91 m92 (54.0 (4.6) ml min91)
observed in the present study, possibly because of
Three-compartment model
39
1.8
4.6
8.2
111
1006
155.6
320
1178
1067
2565
the following three factors: a decrease in tissue
storage of carbon dioxide as a result of hyperventilation before insufflation of carbon dioxide,
hypoventilation after insufflation and unstable conditions for measuring carbon dioxide output. Viale
and colleagues demonstrated that the transient
increase in RER at the start of anaesthesia was
caused by increased carbon dioxide output during
mechanical ventilation, as the standard controlled
ventilation used (tidal volume : 10 ml kg91, ventilatory rate : 12 b.p.m.) may have caused alveolar
hyperventilation. They found that 60 min was
necessary to attain steady state after starting mechanical ventilation [15].
The regression equation for excess VCO2/BSA
showed the best fit with the two-compartment model
(rapid and slow compartments) after removing
carbon dioxide from the abdominal cavity. The halftimes of the rapid and slow compartments were 5.7
and 686 min, respectively. A very small pressure
difference causes carbon dioxide diffusion because
carbon dioxide diffuses rapidly into the tissues. PCO2
of arterial blood entering the tissues is 5.3 kPa; tissue
capillary blood reaches almost complete equilibrium
with interstitial PCO2 when venous blood leaves the
tissues [31]. The carbon dioxide insufflated to
establish pneumoperitoneum diffuses into the abdominal organs and abdominal wall through the
peritoneum, partly accumlates in tissue, and is then
carried by the blood to the lungs. Therefore, the
rapid compartment represents abdominal circulatory
blood, liver, kidneys and other well-perfused tissues.
The slow compartment represents tissues with low
blood flow. Although the carbon dioxide load in the
present study was clinically safe in patients without
cardiac or pulmonary disease with controlled ventilation during and after pneumoperitoneum, excess
VCO2/BSA was still 5.5 ml min91 m92, 30 min after
pneumoperitoneum. Therefore, patients receiving
sedative drugs, patients with significant cardiac or
pulmonary disease, or those with impaired ventilation in the pneumoperitoneum phase may be
adversely affected by hypercapnia associated with
carbon dioxide insufflation, even in the postoperative
phase [9, 7].
Acknowledgments
We thank Koji Morita, PhD, and Yoshimitsu Sanjo, PhD for help
and advice.
CO2 output in laparoscopic cholecystectomy
535
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