EPA-RI-72-002
July 1972 Environmental Health Effects Research
Physiological Adaptations
to Carbon Monoxide Levels
and Exercise in Normal Men
Office of Research and Monitoring
U.S. Environmental Protection Agency
Washington, D.C. 20460
-------
EPA-RI-72-002
Physiological Adaptations
to Carbon Monoxide Levels
and Exercise in Normal Men
by
C. R. Collier, J. M. Workman
J. G. Mohler, J. Aaronson, and 0. Cabula
University of Southern California
Department of Medicine
2025 Zonal Avenue
Los Angeles, California 90033
Contract No. 68-02-0334
Program Element No. 1A1007
Project Officer: Dr. John H. Knelson
Division of Health Effects Research
National Environmental Research Center
Research Triangle Park, North Carolina 27711
Prepared for
OFFICE OF RESEARCH AND MONITORING
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D. C. 20460
!
July 1972
-------
EPA REVIEW NOTICE
This report has been reviewed by the Environmental Protection Agency
and approved for publication. Approval does not signify that the
contents necessarily reflect the views and policies of the Agency,
nor d.oes mention of trade names or commercial products constitute
endorsement or recommendation for use.
11
\
\
-------
SUMMARY
Normal, young, non-smoking men were studied at rest and during
submaximal exercise with carboxyhemoglobin (COHb) levels of about
1% and after breathing CO to raise the COHb level to 8 to 9%.
Arterial and mixed venous blood was sampled. CO caused an increase
in minute volume and breathing frequency during exercise but not at
rest. CO caused no changes in cardiac output, heart rate, lactate,
lactate/pyruvate ratio, tidal volume, C0~ output or 2,3 DPG during
rest or exercise. CO caused a decrease in $2 consumption, in
arterial-venous Q content difference and in venous 0,, content and
venous Po™ during exercise and in the latter two also at rest.
Changes in On affinity are still being calculated.
-1-
-------
INTRODUCTION
Carbon monoxide is believed to exert its toxic effect almost entirely
through its binding on the active sites of hemoglobin. This reduces the
oxygen carrying capacity of hemoglobin and produces a hypoxemia similar
to that of anemia. However, the displacement of oxygen from active
sites has the equivalent effect of displacing the oxygen dissociation
curve of the remaining sites to the left and hence effectively increasing
the affinity of the remaining sites for oxygen. This effect has long
been known since Haldane . This phenomenon has little effect on
arterial oxygenation but has been believed to have a profound effect on
oxygenation of tissue and on oxygenation of venous blood. Because of .
normal arterial Po_ in CO poisoning, it is generally believed that the
body has limited physiological defense against CO compared with the
hypoxemia of altitude.
Of the many studies on the effects of carbon monoxide, only
234
Ayres, et al ' ' have directly sampled the blood from the pulmonary
arteries. In his studies, observations were made only at rest. In the
studies of Vogel, et al ' /observations were made at submaximal and
maximal exercise. The cardiac output was measured by dye dilution, but a
mixed venous sample was not obtained.
This study reports observations made on healthy, young, normal, male
subjects under conditions of rest and submaximal work before and after
giving a load of carbon monoxide to produce approximately 10% carboxy-
hemoglobin concentration. Pulmonary artery blood was sampled.
Observations were also done on levels of 2,3 diphosphoglycerate and
estimations were made of the oxygen affinity of the hemoglobin, both in
vitro and in vivo.
-2-
-------
METHODS
Nine, young, male, non-smoking subjects were chosen for study. The
physical characteristics of the last seven subjects are shown in Table I.
The first two subjects served mainly as pilot studies. A number of
pieces of information are missing about both of these. Essentially all
of the data desired is available on the last seven subjects, except that
one sample of blood from the pulmonary artery was actually a wedge sample
and was omitted from the data.
The subjects ate a light breakfast before 6 a.m. and reported to the
laboratory about 7 a.m. Blood carboxyhemoglobin was estimated by a method
modified slightly from Jones, et al . The subject warmed up for 10
minutes on the stationary constant load bicycle ergometer at a work load
of 50% of his estimated maximal 0 consumption (Vo~ max). The predicted
0
V02 max. as calculated according to the formula of Armstrong, et al
based on age and body weight and the corresponding bicycle load was
calculated from the empirical formula:
L = 570 Vo - 200
where L = bicycle load in KPM
•
Vo_ = desired 0 consumption in L/min.
9
The subject then lay on a bed while a Swan-Ganz^ catheter was inserted in an
antecubital vein in one arm and advanced to the pulmonary artery. A
plastic arterial cannula was placed percutaneously in a brachial artery
of the other arm. The subject then moved to the bicycle where he
remained for the rest of the experiment. After moving, the position of
the catheter tip was rechecked. Observations of inspired minute volume
and of heart rate were made during a rest period of five minutes, the
last three minutes of which samples of expired air, arterial blood and
mixed venous blood were obtained. Exercise was then performed at a load
—3—
-------
of 75% of the estimated Vo« max. for a period of 5 minutes. Heart rate,
EGG, respiratory rate and inspired minute volume was observed for the
entire period. Mixed venous and arterial blood samples were obtained
during the last two minutes of exercise and expired air was collected
for the last minute of exercise.
The subjects were then loaded with carbon monoxide, first to about
7% carboxyhemoglobin, and then to 10% carboxyhemoglobin by breathing a
measured volume of 1% carbon monoxide in air. The dose was calculated
according to the formula of Pitts and Pace^. After a period of from
20 to 45 minutes, the studies at rest and exercise were repeated as
described for control state. During the exercise period, the subject
breathed air containing 60-70 ppm CO. Following the second exercise
study the catheter was withdrawn and the subject breathed 100% oxygen
for approximately 30 minutes. A few of the subjects experienced a mild
phlebitis and thrombosis in the vein the cardiac catheter had been
placed in. All the subjects were able to complete the protocol except
one, K.S., who passed out and would have fallen from the bicycle after
4 minutes and 40 seconds of exercise. The subjects knew the protocol.
Several of them stated that the second exercise period was easier than
the first.
Blood samples were measured for pH, Po2 and Pco2 using radiometer
electrodes and Model PHM72 readout system. Expired air volume was
measured in a large spirometer and a sample taken for analysis by the
micro-Scholander method. Blood was analyzed for 0 , C02 and CO content
by the method of Van Slyke. Hemoglobin concentration was measured as
cyanmethemoglobin photometrically. Lactate and pyruvate were 2,3
diphosphoglycerate was determined by specific enzymatic methods using
commercial kits.*
_4_ .
* Lactate and pyruvate were determined by use of kits from Boehringer
Mannheim and 2,3 DPG by using a kit from Calbiochem.
-------
Blood was equilibrated in a swirl tonometer with approximately 3%
and 4% oxygen" and; 5% CG-- in- nitrogen /'respectively;^ 'aM'? oxygen1' c'onteh't , t °
and pH were determined1 as"1 described 'above. Th'e cardiac output
was calculated from the Pick' equation and in' vitro andt 'in? vivo ••pnn \ will
be computed from the data of the mixed < venous'* sample by methods to be
developed. The difference between means of -. control and after CO was '
tested for statistical significance by student's "t" test- for paired
data..
The base excess of the extracellular fluid was computed according
to Collier, Hackney and Mohler V".
RESULTS
Table II contains a summary of the most- pertinent data; obtained;. The
mean and standard deviation, is shown for all' data obtained1. ; The! mean r
carboxyhemoglobin concentration was 8.9% -after, loading: iahd duringcn: •.
exercise this lowered slightly to 7.8% even though: 60. to 70.ppin of
carbon monoxide was breathed during the exercise period.: .There-.wasn a;.r:i ;
significant increase in minute volume during- exercise after*' CO. IcThds.was
due entirely to an increase in respiratory frequency: as ;the; tidalh .volume
did not change significantly. The increase in minute volume during
exercise caused a islight lowering pf: -the arterial. P.co A, -,. but -the-. Change
was not statistically significant. There were no significant changes in
arterial Pco^ caused by carbon monoxide'. However ,.•> the mixed; venous POA
was significantly lowered at both rest and' during exercise ,-ibeingr lowered
to 22.2 torr during exercise after CO. ; .The lowest mixed;; yenous. Pdo i l<
observed was 20 torr on two occasions. The] alveolar rarte'rtlal - oxygen
tension dif f erence :was Increased; during) bothvresti and- exercise.cli.The
t
difference was not significant during exercise but was during rest. This
f>
may have been due to observation during an unsteady state from the previous
exercise.
-5-
-------
The arterial oxygen content was, of course, lowered as this was
essentially a manipulated variable. The mixed venous oxygen content,
however, was also significantly reduced, being approximately 1 volume %
lower than the control. However, the arterial-venous oxygen content
difference was also lowered by CO during both rest and exercise. The
change caused by CO was not statistically significant at rest but was
statistically significant during exercise. This was made possible not
by a change in blood flow which did not change significantly due to CO
during either rest or exercise but was caused by a reduction in oxygen
consumption during exercise. There were no statistically significant
changes in C02 output but there was slight drop after CO during
exercise so the respiratory exchange ratio was essentially unchanged.
There were no significant changes in lactate, pyruvate, or lactate/
pyruvate ratios caused by CO during exercise. The changes observed
after CO at rest were probably related to the first exercise period.
There were no significant changes in DPG caused by either CO or exercise.
Table III shows the results of some of the most pertinent acid-base
data for arterial and venous blood. The lactate values are again shown
in this table but in meq./L, for comparison with the acid-base data.
Fig. 1 shows the arterial and venous acid-base measurements at rest and
during exercise.
DISCUSSION
The reduction in oxygen consumption which was observed after CO
during exercise was also observed during maximal 3 minute exercise in an
12
earlier study in our laboratory but not observed during submaximal 3
minute exercise. It may be that some of our subjects were close to Vo« max.
-6-
-------
One of our subjects, K.S., exercised at Vo2 max. because he was unable to
complete the work. Our empiric formula for computing the bicycle load
may have given too high a work load. In comparison with the formula of
Cotes , our subjects were working at about 84% of Vo2 max. and if
compared with Astrand and Rodahl were working at 87% of Vo^ max., rather
than at the expected 75%. This reduction in oxygen consumption which is
observed after CO during exercise seems tenable only if we assume that
there is an increase in oxygen debt because it does not seem logical
that carbon monoxide would cause an increase in mechanical efficiency.
However, this could not be absolutely ruled out without further study.
A reduction in oxygen consumption after CO was also reported by
Chevalier, et al . The total amount of oxygen consumed before CO for
5 minutes of exercise was 5.99 L. (an average of 10 subjects) and after
CO the same workload required only an extra 5.79 L. This difference
was not significant but neither was the oxygen debt which was 1.65 L.
control and 1.84 L. after CO. However, the percentage of the oxygen debt
of the total, or the sum of these two was significant at the 5% level.
The sum of 02 consumed during work plus the 02 debt is identical before
and after CO.
Three other studies do not report a change in oxygen consumption
during exercise. Asmussen and Chiodi , reporting on 3 subjects, and
Klausen, et al^ , reporting on 8 subjects, both showed no difference in
oxygen consumption. Vogel, et al reported that there was no difference
in oxygen consumption at the same work load and shows a graph on which
oxygen consumption is plotted against work load for a number of
individuals. In view of our data, it might be well to look at the
individual cases in his study.
-7-
-------
The cardiac output which we found unchanged was also reported
unchanged by Asmussen and Chiodi and by Klausen, et al . However,
in their studies the cardiac output was measured by an indirect
"bloodless" method. The acetylene method was used by the first group
and a CCL rebreathing method by the second. Vogel, et al ,using the
dye-dilution method, report that there is an increase in cardiac output
for suhnaximal exercise. However, in Vogel's presentation, he
plotted the cardiac output as a function of oxygen consumption rather
than as workload. If there were small reductions in oxygen consumption
at the same workload, this might change the data somewhat. Vogel's
subjects were at a higher COHb (about 20%) and the difference in response
of cardiac output probably represents a true difference in response at
18
the higher CO load. Chiodi, et al found an increase in cardiac output
at high CO levels but no increase at lower CO levels.
The dye-dilution method which Vogel used gives approximately the
same value for cardiac output as the direct Pick method in patients at
19
rest or during .mild exercise but has not been adequately compared at
20
high workloads in normals. The normal data of Tabakin, et al using
dye dilution and treadmill exercise gives higher cardiac outputs at a
21
given work load than the data of Reeves, et al using the direct Fick.
Our subjects show only slightly higher cardiac outputs than those of
Reeves. Even though the direct Fick method may be preferable to the dye-
dilution method at heavy exercise, the difference in methods probably
does not account for the difference in response of cardiac output to CO
in our two studies.
The heart rate which we found unchanged was found to be increased by
most other observers ' ' ' ' However, Chevalier, et al report a
-8-
-------
reduction in heart rate during exercise following CO inhalation. Another
study in our laboratory also showed no change in heart rate after CO.
In our first study, the subjects were sham loaded in a single blind
procedure; but in the present study, the subjects knew that the CO load
followed the control study. The ECG showed no changes after CO at rest
22
or exercise. This was also found in the young subjects of Fortuin, et al
The alveolar-arterial Po difference was quite high in all of our
subjects, perhaps because they tended to hyperventilate. CO caused an
increase in this difference which was statistically significant at rest.
23
Brody and Coburn first reported this phenomenon which is due to the
decrease in mixed venous Po~ and 0» content after CO.
The acid-base data given in Table III shows that the acid-base
changes are mostly due to lactate production during exercise. Neither
lactate production nor acid-base changes are affected by the CO load.
The lactate concentration at rest after CO was elevated but this is
probably because the resting sample after CO was taken from 38 to 73 min.
(average 59 min.) after the first exercise and the lactate had not yet
been metabolized to control values. Asmussen and Chiodi reported an
increase in lactate production during exercise caused by CO but their
COHb levels were 20-30%.
n i
Visser, et al have investigated the relation between lactate and
arterial blood acid-base changes following acute exercise and found
that the change in blood lactate was almost identical with the change
in plasma bicarbonate concentration corrected for changes in Pco?.
(This change is essentially the change in base excess of the arterial
plasma (BEp).) The addition of lactic acid to in vitro blood gives a
lesser change in BEp, making it necessary to postulate some unknown
acids in the body. -There are two errors in this analysis which have been
-9-
-------
clarified by more recent work. First, the correction for changes in Pco-
was based on an in vitro CCL dissociation slope for blood. Because of
dilution effective of the buffer value of blood with interstitial fluid,
the ECF has a buffer value which is about 1/3 of that of blood. Thus
if there was a change in Pco~ during exercise in his patient population,
Visser would have calculated a false change in base. We have obviated
this by calculating the base excess of the ECF . Second, inspection of
figure 1 shows that the exchange of CO from venous to arterial blood is
along an in vitro blood slope and not along the ECF or in vivo slope.
This is due to the fact that the pulmonary capillary exchange is only
with the blood and does not include an appreciable interstitial fluid
? c
pool. This relationship was first stated by Roos and Thomas . 'This
fact makes it necessary to use the mixed venous blood for such comparison.
Arterial blood can be used only if the A-V LHCO'j difference is constant
in the two situations. This is certainly not true when comparing rest
and exercise. Figure 1 and Table IV show the much greater change in
base excess of arterial blood than of mixed venous blood. The close
equimolecular correlation of lactate and base deficit is only fortuitous
and has no scientific basis. There seems to be no need in searching for
other sources of acid.
-10-
-------
REFERENCES
1. Haldane, J.B.S.: "The Dissociation of Oxyhemoglobin in Human Blood
During Partial CO Poisoning". J. Physiol. 45: XXII-XXIV, 1912-1913.
2. Ayres, S. M., Gianelli, S., Jr. and Armstrong, R. G.:
"Carboxyhemoglobin: Hemodynamic and Respiratory Responses to Small
Concentrations". Science 149: 193-194, 1965.
3. Ayres, S. M., Mueller, H. S., Gregory, J. J. , Gianelli, S., Jr. and
Penny, J. L.: "Systemic and Myocardial Hemodynamic Responses to
Relatively Small Concentrations of Carboxyhemoglobin (COHb)".
Arch. Environ. Health 18: 699-709, 1969.
4. Ayres, S. M., Gianelli, S., Jr. and Mueller, H.: "Myocardial and
Systemic Responses to Carboxyhemoglobin". Ann. N.Y. Acad. Sci.
174: 268-293, 1970.
5. Vogel, J. A., Gleser, M. A., Wheeler, R. C. and Whitten, B. K.:
"Carbon Monoxide and Physical Work Capacity". Arch. Environ.
Health 24: 198-203, 1972.
6. Vogel, J. A., Gleser, M. A. and Mello, R. P.: "Oxygen Transport
during Exercise with Carbon Monoxide Exposure". Fed. Proc. 30:
371, 1971.
7. Jones, R. H., Ellicott, M. F., Cadigan, J. B. and Gaensler, E. A.:
"The Relationship between Alveolar and Blood Carbon Monoxide
Concentrations during Breathholding". J. Lab. Clin. Med. 51:
553-564, 1958.
8. Armstrong, B. W., Workman, J. N., Hunt, H. H., Jr. and Roemich, W. R.:
"Clinico-Physiologic Evaluation of Physical Working Capacity in
Persons with Pulmonary Disease". Amer. Rev. Resp. Dis. 93: 90-99,
1966.
9. Swan, H. J. C., Ganz, W., Forrester, J., Marcus, H., Diamond, G. and
Chonette, D.: "Catheterization of the Heart in Man with Use of a
Flow-Directed Balloon-Tipped Catheter". N. Engl. J. Med. 283:
447-451, 1970.
10. Pitts, G. C. and Pace, N.: "The Effect of Blood Carboxyhemoglobin
Concentration on Hypoxia Tolerance". Am. J. Physiol. 148: 139-151,
1947.
11. Collier, C. R., Hackney, J. D. and Mohler, J. G.: "Use of Extra-
cellular Base Excess in Diagnosis of Acid-Base Disorders: A
Conceptual Approach". Chest 6: Supplement 6S-12S, 1972.
12. Workman, J. M. and Collier, C. R.: "Effects of Carbon Monoxide on
Human Physical Performance". Report on Contract CPA 70-99 performed
for Environmental Protection Agency, Durham, N.C.
-11-
-------
13. Cotes, J. E.: "Lung Function". 2nd edition, pp. 312-315, F. A. Davis,
Philadelphia, 1968.
14. Astrand, P. 0. and Rodahl, K.: "Textbook of Work Physiology", p. 615,
McGraw-Hill, New York, 1970.
15. Chevalier, R. B., Krumholz, R. A. and Ross, J. C.: "Reaction of
Nonsmokers to Carbon Monoxide Inhalation". J.A.M.A. 198: 1061-
1064, 1966.
16. Asmussen, E. and Chiodi, H.: "The Effect of Hypoxemia on Ventilation
and Circulation in Man". Am. J. Physiol. 132: 426-436, 1941.
17. Klausen, K., Rosmussen, B., Gjellerod, H., Madsen, H. and Petersen, E.:
"Circulation, Metabolism and Ventilation during Prolonged Exposure
to Carbon Monoxide and to High Altitude". Scand. J. Clin. Lab. Invest.
Suppl. 103: 26-38, 1968.
18. Chiodi, H., Dill, D. B., Consolazio, F. and Horvath, S. M.:
"Respiratory and Circulatory Responses to Acute Carbon Monoxide
Poisoning". Am. J. Physiol. 134: 683-693, 1941.
19. Eliasch, H., Lager.lbf, H., Bucht, H., Ek, J., Eriksson, K. , Bergstrb'm, J
and Werko, L.: "Comparison of the Dye Dilution and the Direct Pick
Methods for the Measurement of Cardiac Output in Man". Scand. J.
Clin. Lab. Invest. Suppl. 20: 73-78, 1955.
20. Tabakin, B. S., Hanson, J. S., Merriam, T. W., jr., and Caldwell, E. J.:
"Hemodynamic Response of Normal Men to Graded Treadmill Exercise".
J. Appl. Physiol. 19: 457-464, 1964.
21. Reeves, J. T., Grover, R. F., Blount, S. G., Jr. and Filley, G. F.:
"Cardiac Output Response to Standing and Treadmill Walking".
J. Appl. Physiol. 16: 283-288, 1961.
22. Fortuin, N. J., Anderson, E. W., Strauch, J. M. and Knelson, J. H.:
"Cardiovascular Effects of Exposure to Low Levels of Carbon Monoxide
in Man". Unpublished paper.
23. Brody, J. S. and Coburn, R. F.: "Carbon Monoxide-Induced Arterial
Hypoxemia". Science 164: 1297-1298, 1969.
24. Visser, B. F., Kreukniet, J. and Maas, A. H.: "Increase of Whole
Blood Lactic Acid Concentration during Exercise as Predicted from pH
and Pco2 Determinations". Pfliig. Arch, ges. Physiol. 281: 300-304,
1964.
25. Roos, A. and Thomas, L. J., Jr.: "The In-vitro and In-vivo Carbon
Dioxide Dissociation Curves of True Plasma". Anesthesiology 28:
1048-1063, 1967.
-12-
-------
Table I VITAL DATA ON SUBJECTS STUDIED
Subject
AR
SG
RA .
KS
JB
JS
VS
Age
yr.
34
22
27
23
30
19
21
Weight
kg.
81.6
75.7
70.3
72.6
68.0
66.7
96.8
Height
on.
170
169
179
183
175
170
189
Body Surfai
M2
1.93
1.86
1.88
1.94
1.83
1.77
2.24
-13-
-------
Table II MEASURED AND COMPUTED DATA
COHb
*E
f
VT
Paco2
Pao2
A-a Do2
Pv-o2
L Ca°2
^^
Cvo-
Cao2-Cvb2
yo2
Q
fH
Vco2
R
Lactate
Pyruvate
Lact./pyr. ratio
2,3 DPG
Units
L/min
/min
L
torr
torr
torr
torr
vol %
vol %
vol %
L/min
L/min
/min
L/min
mg %
mg %
trg/gm,
R
Control
Mean
1.1
12.9
13.5
0.97
34.0
86.3
23.4
35.9
18.9
12.9
5.9
0.35
6.0
81
0.32
0.90
18.9
0.92
30.0
, Hb 11.7
S.D.
0.6
4.7
3.9
0.29
5.7
8.0
5.4
1.7
1.2
1.3
1.0
0.06
0.9
13
0.09
0.15
5.7
0.95
13.5
3.1
E S T
E X E R C I S
After CO
Mean
8.9
15.2
17.0
0.98
32.0
85.3
26.0
31.4
17.4
11.9
5.5
0.38
7.2
104
0.34
0.90
30.4
1.60
32.5
12.7
S.D.
1.7
4.9
5.8
0.46
6.5
8.3
6.2
2.2
0.9
1.6
1.2
0.07
1.9
15
0.09
0.17
12.6
1.33
31.5
3.8
P
N.S.
N.S.
N.S.
N.S.
N.S.
<0.05
<0.01
-
<0.1
N.S.
N.S.
N S.
-------
Table III ACID-BASE AND LACTATL DATA
REST
EXERCISE
Units
Arterial
Pco_ torr
PH
(.HCOo J meq./L
BE£CF meq./L
Mixed Venous
Pco- torr
pH
1 HCO« J meq./L
BE meq . / L
ECF
Lactate meq./L
Control
Mean
34.0
7.43
22.3
-1.5
40.6
7.40
24.6
0.4
2.1
S.D.
5.7
0.04
1.9
1.7
5.1
0.03
1.7
1.6
0.6
After
Mean
32.0
7.43
20.6
-3.2
38.4
7.39
22.6
-1.5
3.4
CO
S.D.
6.5
0.07
1.3
1.0
5.2
0.05
1.3
1.3
1.4
Control
P
N.S.
N.S.
<0.02
<0.02
N.S.
N.S.
<0.02
<0.02
<0.02
Mean
31
7
15
-9
57
7
21
-5
10
.0
.31
.3
.8
.9
.19
.3
.2
.3
S.D.
2.5
0.04
2.1
2.3
4.6
0.05
1.3
1.8
1.8
After CO
Mean
29.4
7.31
14.7
-10.4
55.0
7.18
20.0
-6.7
10.3
S.D.
3.5
0.02
1.1
1.2
4.7
0.03
1.4
1.3
1.9
P
N.S.
, N.S.
N.S.
N.S.
N.S.
N.S.
N.S.
<0.05
N.S.
-------
Table IV CHANGES IN ACID-BASE AND LACTATE PRODUCED BY EXERCISE
Control After CO
(Exercise - Rest) (Exercise - Rest)
meq./L, meq./L
A Laotate +8.2 +6.9
'. BE Venous -5.6 •*>•-•
ECF
Arterial -fi-3 ~7-?
-------
meq./L.
30
20
10
7.0
7.2
7.4
Pco2 s 4O
7.6
ECF
-------
LEGENDS
Table I Vital data on subjects studied
Table II Measured and computed data
COHb % saturation of Hb with CO
Vp Expired minute volume
fR Respiratory frequency
V Tidal volume
\
Paco_ Arterial Pco-
Pao2 Arterial Po-
Pvo9 Mixed venous Po«
A-a Do2 Alveolar-arterial Po_ difference
Qs/Qt Total effective R to L shunt as % of total blood
flow
Cao2 Arterial CL content
Cvoo Mixed venous Qj content
Vo7 0 consumption
Q Cardiac output
f Heart rate
H
Vco C02 output
R Respiratory exchange ratio
2,3 DPG 2,3 Diphosphoglycerate concentration
S.D. Standard deviation
P Probability that the difference between the means
before and after CO is due to chance
N.S. No statistically significant difference
Table III Acid-Base and Lactate Data
T HCO-T ; Calculated concentration of bicarbonate in the
3 - p
plasma
BE Base excess of extracellular fluid
ECF
-------
Table IV Changes in Acid-Base and Lactate Produced by
Exercise
(Differences between average data of Table III)
Figure 1 Average acid-base data for rest and exercise
before CO
v Mixed venous blood
a Arterial blood
ECF Average normal non-bicarbonate buffer line for
extracellular fluid in humans
------- |