British Journal of Anaesthesia 82 (6): 843–6 (1999)
Oxygenator exhaust capnography as an index of arterial carbon
dioxide tension during cardiopulmonary bypass using a
membrane oxygenator
M. J. O’Leary*, S. P. MacDonnell and C. N. Ferguson
Department of Anaesthesia, St Bartholomew’s Hospital, West Smithfield, London EC1A 7BE, UK
*Corresponding author: Intensive Care Unit, The St George Hospital, Gray Street, Kogarah, NSW 2207, Australia
We have studied the relationship between the partial pressure of carbon dioxide in oxygenator
exhaust gas (PECO2) and arterial carbon dioxide tension (PaCO2) during hypothermic cardiopulmonary bypass with non-pulsatile flow and a membrane oxygenator. A total of 172 paired
measurements were made in 32 patients, 5 min after starting cardiopulmonary bypass and then
at 15-min intervals. Additional measurements were made at 34°C during rewarming. The
degree of agreement between paired measurements (PaCO2 and PECO2) at each time was
calculated. Mean difference (d) was 0.9 kPa (SD 0.99 kPa). Results were analysed further during
stable hypothermia (n530, d51.88, SD50.69), rewarming at 34°C (n522, d50, SD50.84),
rewarming at normothermia (n548, d50.15, SD50.69) and with (n578, d50.62, SD50.99) or
without (n591, d51.07, SD50.9) carbon dioxide being added to the oxygenator gas. The
difference between the two measurements varied in relation to nasopharyngeal temperature
if PaCO2 was not corrected for temperature (r250.343, P5,0.001). However, if PaCO2 was
corrected for temperature, the difference between PaCO2 and PECO2 was not related to
temperature, and there was no relationship with either pump blood flow or oxygenator gas
flow. We found that measurement of carbon dioxide partial pressure in exhaust gases from
a membrane oxygenator during cardiopulmonary bypass was not a useful method for
estimating PaCO2.
Br J Anaesth 1999; 82: 843–6
Keywords: partial pressure, carbon dioxide; partial pressure, arterial; monitoring, carbon
dioxide; heart, cardiopulmonary bypass; equipment, membrane oxygenator
Accepted for publication: January 26, 1999
Regular measurement of arterial carbon dioxide partial
pressure (PaCO2) during cardiopulmonary bypass (CPB) is
routine, usually by intermittent blood-gas analysis using a
bench blood-gas analyser. Capnography is used routinely
during anaesthesia before and after CPB to monitor endtidal carbon dioxide partial pressure, and its use in monitoring carbon dioxide partial pressure in exhaust gases
from the oxygenator (PECO2) during CPB has been reported
previously both in vitro and in vivo.1–3 These studies
suggested a reasonably close relationship between PECO2
and PaCO2 during the cooling and stable hypothermic
phases of CPB, but a far more variable relationship during
rewarming. Thus oxygenator exhaust capnography is not
used in clinical practice as a measurement technique. These
studies involved CPB, using bubble oxygenators rather
than modern membrane oxygenators. We investigated the
relationship between PECO2 and PaCO2 during CPB using a
membrane oxygenator.
Close control of PaCO2 is important as poor control has
been linked with poor psychomotor outcome after CPB.4
Although in-line blood-gas monitors which allow continuous monitoring of PaCO2 are available, they are expensive
and may be difficult to use. If oxygenator exhaust capnography were an accurate monitor of PaCO2, it would be a
simple, inexpensive and useful addition to patient management during CPB.
Patients and methods
We studied 32 adult patients undergoing elective cardiac
surgery using CPB. All gave informed consent to participate
in the study, which was approved by the East London
and City Health Authority Research Ethics Committee. A
standard anaesthetic technique was used. After premedication with papaveretum and hyoscine, anaesthesia was
induced with thiopental and fentanyl, and neuromuscular
block was produced with pancuronium. Ventilation was
adjusted to give an end-tidal carbon dioxide partial pressure of 3.6–4.4 kPa. Anaesthesia was maintained with
© British Journal of Anaesthesia
O’Leary et al.
1% isoflurane and 70% nitrous oxide in oxygen, with
incremental doses of fentanyl. After heparinization, CPB
was commenced using a roller pump (Sarns 7000MDX,
Sarns 3M Healthcare Group, Ann Arbor, MI, USA) and a
membrane oxygenator (CML Duo, Cobe Cardiovascular
Inc., Arvanda, CO, USA). Non-pulsatile pump flow at a
rate of 2.4 litre min–1 m2 was used throughout bypass.
Moderate hypothermia (32°C) and cold crystalloid cardioplegia were used for cardioprotection. Anaesthesia was
maintained during CPB using 1% isoflurane delivered from
a vaporizer in-line with the gas inlet to the oxygenator, and
with incremental doses of fentanyl.
Exhaust gas from the oxygenator was channelled from
the two scavenge ports to a 100-cm length of elephant
tubing incorporating a Heidbrink valve, to prevent membrane damage in the event of accidental occlusion of the
gas outlet, and a sidestream capnograph connection. Care
was taken to eliminate any leaks of exhaust gas before the
sampling point and to prevent entrainment of air. The
same capnograph was used throughout the study (Datex
Normocap CO2 Monitor, Datex Instrumentarium Oy,
Helsinki, Finland). The machine was calibrated according
to the manufacturer’s instructions using British Oxygen
Company (BOC) alpha standard gas cylinders, and was
allowed to warm up for 1 h before use.
Five minutes after institution of CPB and at 15-min
intervals thereafter, an arterial blood sample was obtained
and PaCO2 measured immediately using a bench blood-gas
analyser in the corridor next to the operating theatre (IL1312
Blood Gas Manager, Instrumentation Laboratories SpA,
Milan, Italy). The blood-gas analyser was calibrated to one
point every 20 min and two points every 3 h, and checked
against the manufacturer’s quality controls each day of use.
Both uncorrected and temperature corrected results were
recorded; temperature correction was performed automatically by the analyser using the following formula5:
PCO2 (corrected)5PCO2 (measured)3100.019(T–37)
where T5patient’s measured body temperature. At the same
times, the capnograph reading, pump flow, gas flows and
nasopharyngeal temperature were recorded. An additional
sample was obtained and recordings made at 34°C during
rewarming as a standard point between patients. A total of
172 paired measurements were made.
The degree of agreement between paired measurements
at each time was calculated using the method of Bland
and Altman.6
Results
When all measurements were considered together, the
mean difference between the two measurements was large,
whether uncorrected (0.9 (SD 0.99) kPa) or corrected for
temperature (0.22 (0.89) kPa) (Figs 1, 2). When results
obtained during the different phases of CPB (stable hypothermia, rewarming at 34°C and rewarming at normother-
Fig 1 Difference in the partial pressure of carbon dioxide in oxygenator
exhaust gas (PECO2) and arterial carbon dioxide tension (PaCO2) measured
by a capnograph and bench blood-gas analyser at all times, plotted
against the mean of the two measurements (PaCO2 was not corrected for
nasopharyngeal temperature).
Fig 2 Difference in the partial pressure of carbon dioxide in oxygenator
exhaust gas (PECO2) and arterial carbon dioxide tension (PaCO2) measured
by a capnograph and bench blood-gas analyser at all times, plotted against
the mean of the two measurements (PaCO2 was corrected for nasopharyngeal
temperature).
Table 1 Relationship between PCO2 measured by a capnograph and bench
blood-gas analyser during different phases of CPB (PCO2 not corrected and
corrected for nasopharyngeal temperature). n5Number of observations, Mean5
mean difference between the two measurements, SD5SD of mean difference,
95% LA595% limits of agreement
CPB phase
Temp. uncorrected
All measurements
Stable hypothermia
Rewarming, 34°C
Rewarming, 36–38°C
Temp. corrected
All measurements
Stable hypothermia
Rewarming, 34°C
Rewarming, 36–38°C
n
Mean
SD
95% LA
172
30
32
48
0.9
1.88
0
0.15
0.99
0.69
0.84
0.69
–1.09 to 2.88
0.5 to 3.26
–1.28 to 1.28
–1.23 to 1.53
172
30
32
48
0.19
0.43
-0.49
0.22
0.77
0.72
0.65
0.71
–1.35 to 1.73
–1.07 to 1.87
–1.79 to 0.81
–1.2 to 1.64
mia) were analysed separately, there was still a large
difference between the measurements whether uncorrected
or corrected for temperature (Table 1). Results were analysed
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Oxygenator exhaust capnography
Table 2 Relationship between PCO2 measured by a capnograph and bench
blood-gas analyser during CPB with and without carbon dioxide (CO2) added
to the oxygenator. n5Number of observations, Mean5mean difference between
the two measurements, SD5SD of mean difference, 95% AL595% limits
of agreement
No CO2 added
CO2 added
n
Mean
SD
95% AL
78
91
0.62
1.07
0.99
0.9
–1.36 to 2.6
–0.91 to 2.88
Fig 3 Relationship between the difference between the two measurements
(partial pressure of carbon dioxide in oxygenator exhaust gas (PECO2) and
arterial carbon dioxide tension (PaCO2)) and nasopharyngeal temperature
(°C) (PaCO2 was not corrected for nasopharyngeal temperature).
further for patients with and without carbon dioxide added
to the oxygenator (Table 2); there was no improvement in
agreement between the measurements. There appeared to
be no pattern for the relationship between the two measurements, which may suggest a systematic error, and unlike in
a previous study,3 there was no trend towards an improved
relationship during any phase of CPB. At some times, PECO2
was higher than PaCO2 (in patients without carbon dioxide
added to the oxygenator).
In an attempt to define which factors may influence the
difference between PECO2 and PaCO2 during CPB, and
consequently explain our results, we examined the relationship between the difference and nasopharyngeal temperature, pump blood flow and oxygenator gas flow using
simple regression analysis. The magnitude of the difference
between the two measurements was found to correlate
closely with nasopharyngeal temperature (r250.343,
P,0.001), increasing as temperature decreased (Fig. 3), but
there was no relationship if temperature correction was
made (r250.002, P50.6). Changes in the difference between
the measurements was not related to any of the other
variables: for PaCO2 uncorrected for temperature vs pump
blood flow and pump gas flow, r250.1, P50.19 and
r252.301E–4, P50.84, respectively, whereas for PaCO2
corrected for temperature, the relationships were r25
2.664E–4, P50.84 (blood flow) and r250.015, P50.12
(gas flow).
Discussion
Our results showed a poor relationship between carbon
dioxide tension in exhaust gas from a membrane oxygenator
during CPB and PaCO2. Indeed, the relationship between
the two measurements was extremely variable even during
stable phases of CPB. This finding is in contrast with that
from a previous study using a bubble oxygenator.3
Although the physical processes which occur during gas
exchange are the same in an oxygenator as in the lung,
namely convection, diffusion and chemical reaction, the
diffusional distances in an oxygenator are much greater
than those in the lung (100–500 µm compared with 10 µm)
and the surface area for gas exchange considerably less
(,10 m2 compared with approximately 70 m2). Gas
exchange is thus much less efficient in the oxygenator, and
the ventilating gases do not usually reach equilibrium with
the bloodstream.7 None the less, one might expect a
consistent relationship between gas tensions in the exhaust
and arterial blood, and a previous study suggested that this
may be the case, at least during some phases of CPB.3
There are important differences between bubble and
membrane oxygenators with respect to transfer of carbon
dioxide. In bubble oxygenators, oxygen uptake and carbon
dioxide elimination are intrinsically linked and dependent
on bubble size. The smaller the bubbles the more efficient
oxygen uptake and the more inefficient carbon dioxide
removal become. Most bubble oxygenators are designed to
compromise between these factors, designing for bubble
size to produce a ratio of carbon dioxide elimination to
oxygen uptake of 0.8.8 Therefore, there is an obligatory
link between oxygenation and carbon dioxide removal with
bubble oxygenators such that it is not possible to vary
oxygenation and ventilation independently. In contrast,
membrane oxygenators allow variation of ventilation (that
is PaCO2) by varying gas flow rate, and variation of
oxygenation by varying the fraction of oxygen in gas
supplied to the oxygenator. It is probable that the relationship
between exhaust gas PCO2 and arterial PCO2 is more stable
with bubble oxygenators.
A further complication is the assumption that by using
PECO2 as a measurement technique for PaCO2, a similar gas
is being measured as when measuring end-tidal carbon
dioxide tension during anaesthesia. However, there are
fundamental differences between the relationship between
carbon dioxide tension in the exhaust gas from a membrane
oxygenator and PaCO2 and the relationship between endtidal carbon dioxide tension and PaCO2. In the latter, the
end-tidal gas is assumed to be representative of alveolar
gas. Differences between arterial and alveolar gas tensions
are generally caused by ventilation–perfusion mismatching,
whereas in the oxygenator, there are significant differences
between gas and blood partial pressures. There is a significant barrier to diffusion between the gas and blood phase in
an oxygenator compared with the lung. The partial pressure
of carbon dioxide in the gas phase in both bubble and
845
O’Leary et al.
membrane oxygenators varies significantly under normal
operating conditions.6 The tension of carbon dioxide in the
exhaust is influenced significantly by gas flow along and
blood flow across the membrane. In contrast, in a bubble
oxygenator the principal determinant of carbon dioxide
elimination is bubble size.8
We attempted to control for the relationship between
PECO2 and gas and blood flow through the oxygenator by
analysing the results according to different flows, but this
failed to improve the agreement between the measurements.
We were also unable to demonstrate any consistent relationship between pump gas or blood flow and the difference
between PECO2 and PaCO2. Not surprisingly, the difference
between the measurements was increased during hypothermia if PaCO2 was not corrected for temperature; this finding
reflects the increased solubility of carbon dioxide at low
temperatures, the effect disappearing when temperature
correction of blood gases was performed.
Because of the large variability between measurements
and lack of a systematic error, we considered a technical
problem as an explanation for our results. Possible technical
errors are incorrect calibration of the capnograph or bloodgas analyser or entrainment of air or other gases in the
sampling tube. Calibration of the capnograph and blood-gas
analyser were performed according to the manufacturer’s
instructions. Fletcher pointed out that when results from a
capnograph and blood-gas analyser are being compared,
they should be cross-calibrated with the same gas.9 We did
not perform a cross-calibration, but a discrepancy would
have caused a systematic error and would not explain the
wide variability of our results. Although dilution of sampled
gases cannot be excluded completely as an explanation for
our observations, we consider this unlikely as we ensured
that all exhaust ports of the oxygenator were either sealed
tightly or connected to our sampling chamber. The sampling
tube was connected to the proximal end of 100 cm of
elephant tubing which should be more than adequate to
prevent air entrainment.
In several patients without carbon dioxide added to the
oxygenator, PECO2 was greater than PaCO2. This finding was
surprising; if blood flow and gas flow are in opposite
directions (the counter-current principle) it is theoretically
possible that the maximum PECO2 may be equivalent to
venous PCO2, but the Cobe oxygenator relies on a crosscurrent system with blood flow perpendicular to gas flow.
Interestingly, this is somewhat similar to the bird lung, where
air flows from the rear to the front through parabronchi
and the gas exchanger is arranged along the parabronchi,
perfused with blood according to a cross-current system.
This system allows mixed blood leaving the lung to have
a higher PO2 than expired air,10 but in our case it was the
mixed exhaust gas which had a higher PCO2 than the mixed
blood leaving the oxygenator.
In summary, we have demonstrated that measurement of
carbon dioxide partial pressure in the exhaust gas from the
oxygenator during CPB was not a useful method for
estimating PaCO2.
Acknowledgements
We thank Mr S. J. Edmondson for allowing us to study patients under his
care, and Mr Stephen Clark, Senior Anaesthetic Technician, and the
perfusion team for practical assistance. Dr M. J. O’Leary was supported
by the Joint Research Board of St Bartholomew’s Hospital and BMI
Columbia Healthcare Ltd. This study was presented as a poster at the
Autumn Meeting of the Anaesthetic Research Society, 1996.
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