Brit. J. Anaesth. (1964), 36, 327
FACTORS INFLUENCING THE ARTERIAL OXYGEN TENSION DURING
HALOTHANE ANAESTHESIA WITH SPONTANEOUS RESPIRATION
BY
J. F. NUNN
With the technical co-operation of Miss D. C. CASSELLE
Medical Research Council External Staff, Hammersmith Hospital, London
SUMMARY
Factors influencing oxygenation of the arterial blood were studied, during routine
anaesthesia, in thirty-six patients anaesthetized with halothane and allowed to breathe
spontaneously, with a mean minute volume of 5 l./min. There was evidence of an
unsteady respiratory state during the first hour of anaesthesia. Oxygen consumption
was 87 per cent of basal. Physiological deadspace amounted to 33 per cent of the
expired tidal volume (all patients intubated). At high levels of inspired oxygen concentration, the mean alveolar-arterial Po, gradient was 184 mm Hg, corresponding to
a shunt of 14 per cent of pulmonary bloodflow. At lower levels of alveolar Po2, the
alveolar-arterial Po, gradient diminished but was above the value which would be
caused by a shunt of 14 per cent. This was probably due to uneven ventilation perfusion ratios (maldistribution) corresponding to a calculated venous admixture rising
as high as 30 per cent. It is concluded that, to ensure the maintenance of a normal
arterial Poa in the majority of patients, the alveolar Po, is required to be as high as
200 mm Hg and this needs an inspired oxygen concentration of 35 per cent under the
conditions investigated in this study.
Dr. Beddoes, quoted by Sir Humphry Davy
The present study was designed to make a
(1800), was probably the first to point out that simultaneous assessment of the principal factors
the inhalation of nitrous oxide might result in influencing arterial oxygenation during anaesdesaturation of the blood. Since that day a great thesia with spontaneous respiration. Analysis of
many publications have described desaturation arterial blood together with inspired and expired
during the course of anaesthesia. Unfortunately, air (sampled simultaneously) has given informathese studies have seldom given sufficient infor- tion on the interplay of oxygen consumption, inmation to indicate the precise cause of the hy- spired oxygen tension, alveolar ventilation, shuntpoxia, since a considerable number of factors can ing and maldistribution on the arterial oxygen
influence oxygenation. The position is somewhat tension. From the results it has proved possible
clearer when artificial ventilation is employed, and to formulate some recommendations as to the
studies by Campbell, Nunn and Peckett (1958), inspired oxygen concentration required under the
Frumin et al. (1959) and by Stark and Smith conditions of the study.
(1960) have denned some of the more important
DEFINITION OF TERMS
factors influencing arterial oxygenaaon under
these circumstances. When the patient is allowed T h e t e r m s "alveolar" and "deadspace" are now
to breathe spontaneously, however, very little is confused by alternative definitions. Throughout
known of the derangement of physiological fac- t h i s P 3 !** ^
* * d e f i n c d M follows:
tors influencing arterial oxygenation, although it Alveolar gas refers, not to end expiratory, but to
is established that appreciable shunting may occur
"ideal" alveolar gas as defined by Riley et al.
(Stark and Smith, 1960) and that saturation may
(1946). Arterial and ideal alveolar Pco3 are asbe as low as 70 per cent (Faulconer and Latterell,
sumed to be equal and the ideal alveolar Po, is
1949; Ikezono, Harmel and King, 1959).
derived by solution of the alveolar air equation.
327
BRITISH JOURNAL OF ANAESTHESIA
328
Deadspace refers to the physiological deadspace,
defined as that part of the tidal volume which
does not equilibrate with pulmonary blood, as
measured by solution of the Bohr equation
using the Pco3 of arterial blood (Enghoff, 1938).
Symbols are in accord with the recommendations
of the Committee for Standardisation of Definitions and Symbols in Respiratory Physiology
(Pappenheimer et al., 1950).
Primary symbols
V gas volume
V gas flow rate of exchange
F fractional concentration
P tension
R respiratory exchange ratio
f respiratory frequency
Secondary symbols
A alveolar
i inspired
E expired
D deadspace
T tidal
a arterial
STPD standard temperature and pressure dry.
BTPS body temperature and pressure saturated.
METHODS
Patients and anaesthesia.
A total of 40 studies were carried out in 36
patients (11 male) (table I). With the exceptions
noted, they showed neither clinical nor radiological evidence of cardiac or respiratory disease.
The nature of the study was explained to each
patient, and they remained under the care of
anaesthetists who were not directly concerned with
the study: premedication varied according to
their custom (table I).
Anaesthesia was induced with thiopentone
(200-500 mg). Patients were then intubated with
a cuffed endotracheal tube, during paralysis
obtained with suxamethonium (50-100 mg).
Anaesthesia was maintained solely by inhalational
agents, the patients being divided into three
groups according to the approximate composition
of the inspired gas as follows:
Nitrous
Oxygen
oxide
Halothane
Group I:
21%
78%
1%
Group II:
28%
71%
1%
Group HI: 98.5%
nil
1.5%
A non-rebreathing gas circuit was used prior to
the period of measurement, which varied between
14 and 73 minutes after induction of anaesthesia.
The same inspired gas mixture was used throughout this period, and ventilation was only assisted
before and after intubation during the brief period
of neuromuscular blockade.
Gas collection.
Measurement periods lasted for 3 minutes and
during this time gas was inhaled from the box,
and exhaled into the bag of a box-bag system (fig.
1), described in detail by Nunn and Pouliot (1962).
PATIENT
FRESH GAS Ah©
SAMPLING MANIFOLD
FRESH
GAS
SPIROMETER
\ /
HUMIDIFIERS
FIG 1
Gas circuit used for the measurement of gaseous exchange (Nunn and Pouliot, 1962).
TABLE ]
Details of patients studied.
Patient
Group T:
H.W.
E.S.
R.L.
T.R.
A.E.
A.M.
W.B.
W.M.
CM.
CB.
K.U.
J.O.
M.B.
E.P.
Height
(cm)
Weight
(kg)
Age
Sex
54
46
51
29
54
52
59
57
42
59
48
53
41
28
M
F
F
F
F
F
M
M
F
F
F
M
F
M
174
162
157
152
171
165
162
178
167
164
162
175
162
175
80
51
60
62
58
80
49
68
71
41
60
76
70
76
C
C
G
F
H
B
B
I
I
C
G
D
G
C
Group II:
R.H.
K.D.
D.P.
CH.
B.M.
S.M.
B.B.
A.B.
A.V.
E.M.
A.L.*
52
49
41
65
47
40
47
55
23
58
30
F
F
F
M
F
M
M
F
M
F
F
170
160
68
68
175
175
167
175
178
167
167
162
160
54
78
84
95
75
80
64
52
51
A
C
C
D
E
C
E
G
C
C
G
V.C.
40
F
162
64
D
Group III
M.P.
43
A.G.
81
62
W.F.t
D.D.
66
LE.
50
B.B.
67
K.F.
36
R-B.J
46
A.H.
59
J.S.
36
F
F
F
F
F
F
M
F
F
M
167
162
151
165
157
160
183
—
—
175
64
55
50
64
54
51
89
59
B
E
A
C
C
73
Premedication
c
c
cG
Interval
between
induction
and
study (min)
26
73
21
38
20
65
37
31
14
20
21
54
24
25
19
15
25
25
60
43
45
33
42
22
25
30
25
—
15
35
20
20
A
—
Operation
Position:
supine or
lithotomy
Herniorrhaphy
Mastectomy
Dilatation and curettage
Skin graft
Radium to cervix
Varicose veins
Amputation of leg
Herniorrhaphy
Dilatation and curettage
Radium to cervix
Radium to cervix
Herniorrhaphy
Dilatation and curettage
Circumcision
S
S
L
S
L
S
Radium to cervix
Varicose veins
Radium to cervix
Herniorrhaphy
Mastectomy
Herniorrhaphy
Herniorrhaphy
Mastectomy
Herniorrhaphy
Mastectomy
Radium to cervix
L
S
L
S
Varicose veins
Herniorrhaphy
Radium to cervix
Radium to cervix
Radium to cervix
Radium to cervix
Radium to cervix
Radium to tongue
Radium to cervix
Radium to cervix
Herniorrhaphy
Rectal (°C)
temperature
Medical state
36.5
35.7
36.4
36.4
36.5
36.4
37.8
36.9
36.1
36.1
36.0
36.2§
36.0
36.5
Hypertension
Fit
Fit
Hyperkeratosis
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
S
37.0
36.1
37.5
37.0
36.2
36.2
35.2
35.8
36.0
35.0
36.2
36.2
36.2
S
L
L
L
L
L
S
L
L
S
35.9
36.3
35.0
36.1
34.0
35.0
36.6
36.1
36.0
36.0
Fit
Fit
Fit
Fit
Fit
Fit
s
sL
L
L
S
L
S
s
s
s
s
s
sL
Fit
Fit
Fit
Fit
Fit
Fit
Fit
Fit
•This patient was studied a second time after an interval of one week (same operation).
JTwo studies were carried out during the same operation.
tThree studies were carried out during the same operation.
§ Nasopharyngeal
A — Pethidine 75 mg, atropine 0.6 mg
D — Pethidine 100 mg, atropine 0.6 mg, promethazine 25 mg
G — Morphine 10 mg, atropine 0.6 mg
B — Atropine 0.6
rag
E — Pethidine 50 mg, atropine 0.6 mg
H — Papaveretum 20 mg, atropine 0.6 mg
C — Pethidine 100 mg, atropine 0.6 mg
F — Pentobarbitone 200 mg, atropine 0.6 mg
I — Papaveretum 20 mg, hyoscine 0.4 mg
330
The system permits the separate measurement of
inspired and expired minute volumes and the
sampling of each (Donald and Christie, 1949).
The direction of gas flow was controlled by a unidirectional valve box giving a total apparatus
deadspace of 55 ml in the earlier studies, and 30
ml after modification. Gases were sampled immediately after collection, and errors due to diffusion through the walls of the bag were found to
be negligible. Fresh gases were humidified and
it was, therefore, possible to correct gas volumes
to BTPS or STPD as required. Any temperature
changes in the system were noted and the appropriate corrections made. No gas samples were
studied for the patients in Group in, since alveolar Poa may be calculated without measurement
of gas exchange when the inspired oxygen concentration approaches 100 per cent.
Gas analysis.
Oxygen concentration was determined with a
polarograph and carbon dioxide concentration
with a carbon dioxide sensitive electrode, the
same methods being used for the blood samples
(see below). The use of the polarograph for analysis of a gas mixture carries only a moderate level
of accuracy (coefficient of variation of random
error—1.2 per cent). Nevertheless, the method is
not affected by the presence of nitrous oxide,
which excludes practically all other methods, with
the exception of a paramagnetic analyzer, which
was not available at that time. Analysis of carbon
dioxide concentrations by the use of a carbon
dioxide sensitive electrode is satisfactory, being
uninfluenced by the presence of nitrous oxide and
having an accuracy comparable to that of the Haldane apparatus. The limitations due to the accuracy of these techniques are discussed at length
by Nunn and Pouliot (1962).
Blood analysis.
Blood samples of 12 ml were collected from the
radial artery into an all-glass syringe the deadspace of which was filled with heparin (50 mg
per ml). Analysis was carried out within 15 minutes. The samples were not cooled, but a correction was applied for changes in Po. and PcOj due
to metabolic activity of the blood (Capel and
Nunn, unpublished).
was determined with a carbon dioxide
BRITISH JOURNAL OF ANAESTHESIA
sensitive electrode (Severinghaus and Bradley,
1958), maintained close to body temperature and
held constant to within ±0.1°C. The output was
measured potentiometrically using a Vibron Electrometer as a null indicator. The sensitivity of the
electrode was determined daily with 100 per cent
carbon dioxide and a 5 per cent carbon dioxide
in oxygen mixture, and each blood sample was
bracketed between known gas mixtures, analyzed
with the Lloyd-Haldane apparatus (Lloyd, 1958);
1.5-ml samples were analyzed in duplicate.
Po3 was determined with a Clark cell covered
with a 60[j. polyethylene membrane. The electrode
was mounted in a Bishop cuvette (Bishop and
Pincock, 1958) and stirred at 500 r.p.m. The electrode was polarized with a voltage of 600 mV and
the current passed was bucked using the circuit
described by Severinghaus and Bradley (1958),
null balance being determined with a Vibron
Electrometer. Zero was obtained with carbon
dioxide gas (Cater et al., 1963) and calibration was
with air-equilibrated water, allowing a ratio of
0.95 for the difference in reading between blood
and water of the same Po2; 4.5-ml samples were
analyzed in duplicate. The measured blood-gas
tensions were corrected for any difference between
the patient's rectal temperature and the running
temperature of the electrodes (Bradley, Stupfel
and Severinghaus, 1956; Nunn, Bergman, Bunatyan and Coleman, unpublished).
In a study of this nature, considerable importance attaches to the absolute accuracy of the
measurement of blood gas tensions. Analysis of
116 samples of tonometer-equilibrated blood before, during and after the study revealed no significant systematic error for either electrode, but
a random error with coefficient of variation 4 per
cent for carbon dioxide and 5 per cent for oxygen.
This would include errors in tonometer-equilibration and sampling. Using these methods we
obtained the following values for arterial tensions
in normal conscious supine subjects, whose ages
ranged from 24 to 46 (Nunn and Bergman, 1964).
Breathing air:
Pco, 39 (SE 1.3) mm Hg
Po2 91(SE0.8)mmHg
Breathing oxygen:
Pco3 37 (SE 2.1) mm Hg
Po 3 650(SE 26)mmHg
Breathing 11 % oxygen: Pco, 37 (SE 1.4) mm Hg
Po3 35(SE3.8)mmHg
FACTORS INFLUENCING THE ARTERIAL OXYGEN TENSION
Calculation of results.
The ideal alveolar Pa, was derived from a
special form of the alveolar air equation which is
applicable when the inert gas (nitrous oxide in
this instance) is not in equilibrium (Nunn, 1963):
(i)
(For patients in Group III the alveolar Po,
was taken to equal the dry barometric pressure less the arterial Pco,.)
The alveolar-arterial Po, difference ((A-a)Po2) was
derived by subtraction and the calculated shunt
estimated from a mixing equation on the following assumptions:
(1) End pulmonary capillary Po, equal to alveolar Poa.
(2) Arteriovenous oxygen content difference of
3.5 vols per cent, which is the value suggested from published data of cardiac output and oxygen consumption during anaesthesia.
(3) The form of the haemoglobin dissociation
curve described by Severinghaus (1958).
(4) The solubility of oxygen in whole blood
(O.OO3O3 vols per cent/mm Hg) derived by
Sendroy, Dillon and Van Slyke (1934) for
ox blood being valid for human blood.
The importance of these assumptions is quite
critical at some of the levels of oxygenation found
in these studies. The values for the calculated
shunt must therefore be interpreted with caution.
The physiological deadspace was derived from
the following form of Bohr's equation:
—5
— I ~ apparatus deadspace (ii)
The apparatus deadspace was determined by
water displacement.
Values of oxygen uptake, carbon dioxide output and nitrous oxide uptake were derived by the
method of Nunn and Pouliot (1962). Oxygen consumption is also expressed as a percentage of
basal according to calorific data of Aub and
Dubois (1917) and Boothby and Sandiford (1924).
The value for the respiratory exchange ratio
(R) relates to the expired gas and would not be
expected to equal the metabolic respiratory
quotient of the patients, since they were clearly
not in steady respiratory states.
331
RESULTS
Minute volume (inspiratory) of Groups I and II
had a mean value of 5 l./min BTPS (table II).
The mean expiratory minute volume was 240 ml/
min less, the major part of the difference being
due to nitrous oxide uptake which is shown
plotted against duration of anaesthesia (fig. 2).
Mean respiratory frequency was 27 b.pjn.
2O
4O
6O
TIME FROM INDUCTION — MINUTES
80
Flo. 2
Nitrous oxide uptake (ml/min STTPD) plotted against
time from induction. The lines indicate the range of
observations in six subjects studied by Severingnaus,
1954.
Arterial Pcot was above the normal limit in
almost all cases. In the first two groups the mean
values were almost identical, with an overall mean
of 50.3 mm Hg. The level was lower (42.3 mm
Hg) in the patients breathing a high oxygen concentration. The mean of this group was considerably influenced by one result which was probably
in error.
Physiological deadspace is plotted against expired tidal volume in figure 3. The mean ratio
was 33 per cent and the majority of results lie
within the range 20-40 per cent.
Oxygen uptake is plotted against rectal temperature in figure 4. The mean was 87 per cent of
basal (Groups I and II) at 36.3°C. The correlation between oxygen consumption and temperature is not significant.
Carbon dioxide output and respiratory exchange ratio were below the possible metabolic
limits for the oxygen uptake and indicated unsteady respiratory states. Figure 5 shows the res-
TABLE II
Measured and derived data.
Flo,
Patient
%
(A-a)
Po
difference
Vl
VE
fl./m (ml
Pao,
Pa**
PAo,
f
BTPS) B T P S ) (BPM) (mmHg)(mm Hg) (mm Hg)(mmHg)
Vo,
V D (phys)
Calculatcd
shunt
%
ml
BTPS
VD/VT
ratio
VNjO
(ml/min
Voo,
ml/m
%
STPD
% of (ml/m
STPD)
basal
R
STPD)
Group I
H.W.
E.S.
R.L.
I.R.
A.E.
A.M.
W.B.
W.M.
CM.
C.B.
K.U.
J.O.
M.B.
E.P.
Mean
20.07
21.80
2229
22.76
20.97
20.40
22.64
21.80
20.55
21.07
21.79
21.72
20.29
20.01
5.71
3.64
2.64
7.21
4.36
6.87
7.48
7.48
2.31
4.31
4.77
5.17
4.43
4.21
220
97
95
138
134
210
250
246
129
102
181
199
141
145
24.6
33.0
24.0
52.0
30.0
31.4
29.0
27.0
13.0
39.0
23.0
24.0
29.0
26.0
48.6
51.5
49.6
53.4
54.6
39.4
41.7
44.5
66.1
65.8
41.3
47.1
47.0
59.7
91
103
107
83
89
111
128
116
90
58
94
109
97
77
• 66
84
79
71
65
84
80
83
51
40
81
71
74
55
25
19
28
12
24
27
48
33
39
18
13
38
23
22
23
11
12
11
22
12
18
14
46
41
8
24
15
32
63
16
16
85
62
83
91
81
39
45
82
68
44
51
29
16
17
61
47
40
36
33
30
44
45
34
32
35
223
129
129
156
191
186
210
330
163
231
212
188
265
217
89
69
66
78
95
83
110
139
73
136
105
76
123
83
141
47
54
46
80
138
179
187
59
80
77
132
106
108
0.63
0.37
0.42
0.29
0.41
0.74
0.85
0.57
0.36
0.35
0.37
0.70
0.40
0.51
101
278
226
65
167
228
240
600
446
443
321
253
91
391
21.34
5.04
163
28.9
50.7
97
70
26
21
59
36
202
95
102
0.50
275
13.6
10.2
11.7
34
31
100
67
67
59
53
103
19
26
32
40
27
29
31
40
178
177
155
214
188
198
190
177
83
84
76
91
79
70
73
78
113
63
126
110
126
140
118
108
0.50
0.36
0.81
0.52
0.67
0.71
0.62
0.61
149
149
208
155
158
140
163
103
SD
3.7
SB of mean
2.8
3.2
Group II
R.R
K.D.
D.P.
C.H.
B.M:
S.M.
E.B.
A.B.
28.19
29.30
30.20
30.00
27.75
29.15
26JK)
26.77
5.58
3.37
5.66
5.49
6.28
7.50
5.74
5.00
176
120
314
167
248
202
170
261
30.2
26.1
17.2
31.0
24.3
36.0
32.2
17.9
37.1
61.7
40.9
67.4
36.1
38.7
51.3
50.7
161
112
192
131
160
170
137
142
141
58
104
95
121
81
99
82
20
54
88
36
39
89
38
60
4
38
12
11
6
25
9
19
V D
Patient
Flo,
%
Po,
CalcuVi
VE
differlated
(l./m
(ml
f
Pa«>,
PAo,
Pao, ence
shunt
ml
BTPS) BTPS) (BPM) (mm Hg)(mm Hg) (mm Hg) (mm Hg)
%
BTPS
Group If (continued)
A.V.
28.20
4.41
E.M.
27.40
2.92
A.L.
28.85
4.72
26.80
4.55
V.C.
30.10
3.09
Mean
28.43
SD
SE of mean
Group Til
M.P.
A.G.
W.F.
D.D.
J.E.
B.B.
K.F.
R.B.
A.H.
J.S.
97.50
99.00
98.00
99.00
99.00
98.00
99.00
98.50
99.00
98.50
98.50
98.50
98.00
Mean
98.50
SD
SE of mean
4.95
210
119
177
149
160
20.1
23.0
25.0
28.5
18.0
45.5
69.9
49.8
46.7
53.5
158
131
154
146
140
165
107
115
104
116
-7
24
39
42
24
190
25.4
49.9
149
107
27
7.5
54.0
50.5
44.0
43.3
40.2
47.9
16.3*
39.5
40.0
40.7
43.6
35.9
53.5
637
653
653
661
664
642
692
664
668
671
667
667
640
532
438
521
494
478
476
510
517
514
424
456
569
259
105
215
132
167
186
166
182
147
154
247
211
98
381
8
16
10
13
14
13
14
11
12
17
15
8
25
42.3
660
476
76
21
184
73
20
14
4.4
1.2
42
26.4
7.3
VD/VT
ratio
%
ml/m
STPD
% of
basal
Voo,
(ml/m
STPD)
VN.O
R
(ml/min
STPD)
0
6
6
7
4
45
26
42
51
46
21
22
24
34
29
158
107
220
155
143
68
57
116
81
68
116
72
112
65
65
0.73
0.67
0.51
0.42
0.46
129
64
236
163
156
11
10.4
2.9
56
29
174
79
103
0.58
152
* This value would seem to be in error, but is
included as there was no valid reason for its
exclusion. The effect on the calculated shunt is
about 1 per cent
BRITISH JOURNAL OF ANAESTHESIA
334
, I4O
o
NUNN t HILL
•
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28O
32O
VOLUME — ML
Fio. 3
Physiological deadspacc (ml, BTPS) plotted against expired tidal volume.
piratory exchange ratio plotted against time. The
correlation coefficient closely approaches the customary level of significance (0.05<P<0.1).
The arterial Po2 varied markedly between the
different groups. In Group I the mean value was
70 mm Hg (table n). In Group n , the mean value
was 107 mm Hg, and in Group m , 476 mm Hg.
For each pair of groups the difference was highly
significant (P<0.001). The relationship between
the inspired oxygen concentration and the arterial
Po3 is shown in figure 6.
The alveolar-arterial Poi difference is listed in
table II and shown plotted against alveolar Po2
in figure 7. The mean value in Group I was 26
mm Hg and in Group n , 42 mm Hg, the difference being significant (P=0.05). In Group HI the
values for (A-a) Poa were larger, mean value being
184 mm Hg. The difference between Group II
and Group ELI is highly significant (P<0.001).
Below an alveolar Po3 of 200 mm Hg, the alveolararterial Poa difference only once exceeds half the
the alveolar Po a .
The calculated shunt is listed in table H and
shown plotted against alveolar Po, in figure 7.
Below an alveolar Poa of 200 mm Hg, there is a
significant negative correlation between alveolar
Po2 and calculated shunt ( R = -0.50; 0.01<P<
0.025). Shunts were calculated to be over 30 per
cent of cardiac output at the lowest levels of
arterial Po2. There is no significant difference between the calculated shunts in Groups II and DI
(11 per cent and 14 per cent respectively).
DISCUSSION
Two factors tend to raise the arterial Po3 of the
anaesthetized patient. The first is the sub-basal
level of oxygen uptake which, in this study, confirms the value of 86 per cent at a mean rectal
temperature of 36.4°C found by Nunn and
Matthews (1959) (fig. 4). The magnitude of the
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NUNN 4 MATTHEWS 1959
PRESENT'STUOY
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35
36
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BODY TEMPERATURE - °C
FlO. 4
Oxygen consumption (expressed as percentage of basal;
Aub and Dubois, 1917) plotted against rectal
temperature.
FACTORS INFLUENCING THE ARTERIAL OXYGEN TENSION
benefit obtained from this effect may be calculated from the following form of the alveolar air
equation:
^^Fio,-^)
(iii)
The increase in alveolar POj due to a 13 per cent
reduction of oxygen uptake normally amounts to
less than 10 mm Hg, but will be greater under
conditions of underventilation. Our results are
only slightly below 100 per cent of the metabolism
standards suggested by Robertson and Reid
(1952). These standards also apply to drug-induced sleep (Fraser and Nordin, 1955).
The second favourable factor is the concentration effect of nitrous oxide uptake on alveolar
Po2 (Fink, 1955).
Against these favourable factors, there appear
to be no less than four factors tending to lower
the arterial Po3 during anaesthesia with spontaneous respiration:
(1) Underventilation.
(2) Increased deadspace.
(3) Increased shunting.
(4) Inequality of ventilation perfusion ratios.
Underventilation.
Minute volumes of respiration found in this
study were slightly higher than those found in a
comparable study of patients anaesthetized without the use of halothane (Nunn and Hill, 1960).
Arterial Pco3 was marginally lower in the present
study. However, it is important to realize that
these comparatively innocuous levels of Pco3 do
not guarantee adequate ventilation. This deduction may only be made in a steady state, and the
values for the respiratory exchange ratio found in
this study suggest that a steady state for carbon
dioxide was not attained for a considerable time
after the start of the anaesthetic. Reduction in
ventilation causes a rapid fall of alveolar Po,
(half-time about 30 seconds; Farhi and Rahn,
1955a), but the rate of carbon dioxide build-up
is limited by the rate of production and retention
of carbon dioxide and the large storage capacity
of the body for this gas. The time course of carbon dioxide retention during underventilation has
not yet been established, but clearly the rate must
be very much slower than the rate of depletion
during hyperventilation (half-time about 4 min-
335
utes; Fahri and Rahn 1955a; Nunn and Matthews,
1959). The practical point is that a patient may
be suffering from hypoxia due to underventilation
at a time when the Pco, is still within reasonable
limits. The customary definition of ventilation by
the arterial Pcoa thus requires qualification in the
unsteady state.
Increased deadspace.
The physiological deadspace amounted to
about a third of the tidal volume, with half of the
anatomical deadspace excluded by endotracheal
intubation (Nunn, Campbell and Peckett, 1959).
Nunn and Hill (1960) found an identical deadspace/tidal volume ratio in patients anaesthetized
without halothane (fig. 3). They also demonstrated that the physiological deadspace was about
double the anatomical deadspace, indicating deadspace at the alveolar level, probably arising from
maldistribution of inspired gas relative to pulmonary bloodflow. It should be remembered that
the deadspace may be further increased in elderly
and emphysematous patients (Donald et al.,
1952) and after haemorrhage (Freeman and Nunn,
1963). Deadspace is further increased during
anaesthesia by the inevitable addition of apparatus
deadspace.
Increased shunting.
True shunt is most conveniently measured at
high levels of alveolar Po3. The mean calculated
value of 14 per cent of pulmonary bloodflow
obtained in this study may be compared with a
calculated shunt of less than 1 per cent found in
normal conscious supine subjects using the same
techniques (Nunn and Bergman} 1964). The latter
finding is almost identical with the results
obtained under comparable circumstances by Cole
and Bishop (1963), who concluded the major part
of the shunt must consist of Thebesian veins
draining into the left heart. It seems unlikely that
the large shunt observed during anaesthesia
should be caused by an increase in the flow
through the Thebesian veins and the explanation
is probably perfusion of totally unventilated parts
of the lung.
Whatever may be the interpretation of our findings, it is clear that, during the inhalation of high
concentrations of oxygen, the arterial Po2 of the
anaesthetized patient will be about 200 mm Hg
BRITISH JOURNAL OF ANAESTHESIA
336
less than the alveolar Po3 (compared with a difference of about 15 mm Hg in the conscious subject). It is fortunate that this is seldom of significance in the heakhy patient, since the alveolar
Po3 is usually so far above the normal level that
the arterial blood remains fully saturated in spite
of the increased alveolar-arterial Po, difference.
We considered the possibility that large shunts
might be due to demonstrable atelectasis. Patient
J.S. was X-rayed immediately after surgery, but
no localized lung lesion was seen. This does not
exclude the possibility of major atelectasis. Bendixen, Hedley-Whyte and Laver (1963) have recently reported that grossly visible atelectasis in
the dog could not be seen on X-ray examination
of the isolated lung.
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TIME FROM INDUCTION —MIN
1.
80
Fia. 5
Respiratory exchange ratio, measured on expired gas,
plotted against duration of anaesthesia.
Similar increases in true shunt have been reported during anaesthesia by Stark and Smith
(1960), and in the postoperative period (Gordh,
Linderholm and Norlandex, 1958). Interpretation
of the findings of the latter group is complicated
by the very high values for shunt which they
obtained in their control pre-operative measurements.
Inequality of ventilation/perfusion ratios (maldistribution).
At the lower levels of alveolar Po, in this study,
the observed alveolar-arterial Poa difference cor-
responds to a significantly larger calculated venous
admixture than at high levels of alveolar Po,. It
is necessary to consider three possible components
of the alveolar-arterial Po2 difference within this
range:
component due to shunt;
component due to failure of attainment of
diffusion equilibrium;
component due to inequality of ventilation/
perfusion ratios.
The first component has been discussed above
and it is generally assumed that the magnitude
of the shunt remains unchanged at lower levels
of alveolar Po,. However, due to the shape of the
haemoglobin dissociation curve, the resulting
alveolar-arterial Po, gradient is diminished as the
alveolar Po, is reduced. Thus a shunt of 10 per
cent causes a gradient of about 130 mm Hg at
high levels of alveolar Po3, but only about 15 mm
Hg at an alveolar Po, of 97 mm Hg. Therefore,
the shunt demonstrated at high Po, can account
for little more than half of the alveolar-arterial
Po, difference found at the lower levels of Po, in
this study.
Hitherto it has been thought that the limitation
imposed by the diffusing capacity of oxygen accounts for an appreciable part of the total alveolararterial Po, difference at lower levels of alveolar
Po2, although not at higher levels (Lilienthal et
aL, 1946). On this traditional view, our results
might be explained by a combination of increased
shunt and impairment of diffusing capacity. However, recent studies, reviewed by Staub (1963),
suggest that the diffusion component of the total
alveolar-arterial Po, gradient is much less than
had formerly been supposed. It now seems unlikely that any conceivable impairment of diffusing capacity could make a substantial contribution to the total alveolar-arterial Po, gradients
observed in this study.
We are left with inequality of ventnation/perfusion ratios (maldistribution) as the most likely
cause of that part of the total alveolar-arterial Po,
gradient which cannot be explained by shunt.
Regions of high ventilation/perfusion ratio interfere with carbon dioxide elimination, but do not
appreciably influence oxygenation of the arterial
blood. Regions of low ventilation/perfusion ratio,
on the other hand, have little effect on carbon
FACTORS INFLUENCING THE ARTERIAL OXYGEN TENSION
337
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% OXYGEN INSPIRED GAS
FIG. 6
Arterial Po, plotted against percentage of oxygen in inspired gas.
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dioxide elimination, but cause a marked impairment of oxygenation of the arterial blood (Severinghaus and Stupfel, 1957). In this study we are,
therefore, more concerned with regions of relative over-perfusion. Using the multibreath nitrogen washout method, Bergman (1963) has demonstrated a normal pattern of distribution of
inspired gas during anaesthesia with spontaneous
respiration. There is thus some evidence that the
primary abnormality is uneven distribution of
pulmonary bloodflow rather than inspired gas.
It is not possible to ascribe a numerical value
to the degree of regional relative overperfusion,
unless the pattern of maldistribution is known.
Farhi and Rahn (1955b) have considered the possibility of a log-normal scatter of ventilation/perfusion ratios. West (1963), however, has demonstrated that horizontal layers of lung tissue have
ventilation/perfusion ratios governed primarily
by the effects of gravity on the distribution of the
pulmonary bloodflow. We may expect this effect
to be diminished in the supine position, but at
present one can only speculate about the probable
form of maldistribution in the anaesthetized
patient.
Although it is not possible to make a quantitative presentation of the degree of maldistribution,
the alveolar-arterial Po2 difference (fig. 7) defines
the resultant disturbance of function, without
speculating as to its cause. The calculated venous
admixture (also in fig. 7) shows the degree of
venous admixture which would be needed to
explain the observed alveolar-arterial Poa difference, but should not be taken to imply that the
disturbance is, in fact, due to simple venous
admixture.
The degree of regional relative overperfusion
found in this study appears roughly comparable
with the degree of regional relative over-ventilation demonstrated by the increased alveolar deadspace found by Nunn and Hill (1960). It is tempting to believe that the two studies have measured
different aspects of the same fundamental disturbance.
The degree of maldistribution found in this
study also appears compatible with the postoperative data of Nunn and Payne (1962). Their
findings could be explained by regional relative
overperfusion producing the effect of a 25 per
cent venous admixture at an alveolar Po, of 100
mm Hg, a figure closely corresponding to the
mean value in figure 7.
Clinical implications.
It must be stressed that, although cyanosis may
be present in severe hypoxia, its absence does not
guarantee normal or even near-normal levels of
oxygenation (Comroe and Botelho, 1947). In this
BRITISH JOURNAL OF ANAESTHESIA
338
4OO
ALVEOLAR—ARTERIAL POj DIFFERENCE -- mmHg
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20 h
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ALVEOLAR POj — mmHg
Fio. 7
Alveolar-arterial Po, difference and venous admixture plotted against ideal
alveolar Po,.
study, cyanosis was not apparent in the four
patients with arterial oxygen tensions below 60
mm Hg (86 per cent saturation). On the other
hand, faulty lighting or venous congestion gave
the appearance of cyanosis in other patients whose
saturation was in excess of 99 per cent. It is clear
that observation of the patient is not by itself
sufficient for the maintenance of normal Po3 during anaesthesia; practical application must also be
made of the theoretical factors influencing arterial
oxygenation.
Many anaesthetists take the view that adequate
oxygenation is of such importance that the patient
should receive more than 90 per cent oxygen in
the inspired gas. The present study suggests that
this will ensure higher than normal arterial Po3
in a routine case.
Unfortunately, the use of high concentrations
of oxygen excludes the effective use of nitrous
oxide, which requires a concentration in excess of
65 per cent to ensure loss of consciousness. Therefore, anaesthetists who wish to use nitrous oxide
must be prepared to administer oxygen in a concentration which is no higher than is needed for
normal arterial oxygenation.
The problem is to define the minimum concentration of oxygen required.
We may start from the premise that 100 mm
Hg is an adequate arterial Po,, this being not only
the normal level, but also sufficiently far above
the bend of the dissociation curve to give a valuable margin of safety. In figure 7, it will be seen
that the maximal alveolar-arterial Po2 gradient
approximates to half the alveolar Po3 (below an
FACTORS INFLUENCING THE ARTERIAL OXYGEN TENSION
alveolar Poa of 200 mm Hg). Therefore, the minimal arterial Po, will also be half the alveolar Po a .
Thus an alveolar Po3 of 200 mm Hg is required
to ensure an arterial Po, of 10 mm Hg in the
majority of patients (say 95 per cent) under the
conditions of this study. The problem now consists of adjusting the inspired oxygen concentration to the minute volume so that the alveolar Po,
will be above 200 tnm Hg, account being taken
of the probable sub-basal metabolism of the
patient This is a relatively simple problem and
equation (iii) may be rearranged to indicate the
inspired oxygen required for any given ventilation, or alternatively to indicate the minimum
acceptable ventilation for any given inspired
oxygen concentration. Assuming an oxygen consumption of 225 ml/m (BTPS) and VD/VT ratio
of 33 per cent, the equation simplifies to:
Required inspired oxygen
concentration (%)
= 28 +
33
minute volume (l./min BTPS)
Sample values are given in table ID, but intermediate values for a wide range of circumstances
can be read off the predictor described by Nunn
(1962). Figure 6 shows that in this study, with an
average minute volume of 5 l./min, an inspired
oxygen concentration of 26-31 per cent was sufficient to maintain normal arterial Po s in the average patient but not for the majority. Interpolation
suggests that 35-40 per cent would be required,
and this accords with the observed minute
volumes and the values quoted in table HI. Unfortunately, this concentration of oxygen does not
permit the use of a sufficiently high concentration
of nitrous oxide to ensure unconsciousness in all
cases (Rosen, 1959).
This study has dealt with problems of oxygenation. Concern for the maintenance of normal oxygen levels should not blind the anaesthetist to
the problems of carbon dioxide homeostasis. It
is for each anaesthetist to decide whether he is
prepared to accept the degree of respiratory acidosis, which appears inseparable from the type of
anaesthesia with which this study is concerned.
Caution should be exercised in extrapolating
these findings to situations which lie outside the
339
TABLE III
Inspired oxygen concentrations required for maintenance of normal arterial Po, in the majority of
intubated patients, anaesthetized with halothane and
breathing spontaneously at sea level.
Minute volume of
respiration l./min
(BTPS)
Inspired oxygen concentration (per cent)
oo
20
10
7
6
5
4
3
2
1
28
29.5
31.5
32.5
33.5
34.5
36.5
39
44.5
61
circumstances of our study. Information is available about the effect of other anaesthetic agents
on the minute volume, but nothing is known of
their effect on the alveolar-arterial POj gradient
below an alveolar Po2 of 200 mm Hg, during
spontaneous respiration. Rebreathing, failure to
intubate, fever, severe haemorrhage, right-to-left
shunts, and many respiratory diseases, will each
affect oxygenation adversely.
It is still too early to define the precise nature
of the impairment of oxygenation occurring during artificial ventilation. Early studies by Campbell, Nunn and Peckett (1958) and Frurnin et al.
(1959) have indicated alveolar-arterial Po 3 gradients intermediate between normal values and
those found in this study. Studies of arterial
saturation during anaesthesia have shown lower
levels than would be expected in conscious subjects at comparable minute volumes (Ikezono et
al., 1959; Cole and Parkhouse, 1961; Dobkin and
Song, 1962; Wakai, 1963; Conway and Payne,
1964).
ACKNOWLEDGMENTS
The author is indebted to the anaesthetic and surgical
staff of the Postgraduate Medical School and Hammersmith Hospital for their willing co-operation in these
studies.
These studies were carried out while the author was
in receipt of a Leverhulme Research Fellowship and
a Medical Research Council Grant.
340
BRITISH JOURNAL OF ANAESTHESIA
REFERENCES
Aub, J. C , and Dubois, E. F. (1917). The basal metabolism of old men. Arch, intern. Med., 19, 823.
Bendixen, H. H., Hedley-Whyte, J., and Laver, M. B.
(1963). Impaired oxygenation in surgical patients
during general anesthesia with controlled ventilation. New Engl. J. Med., 269, 991.
Bergman, N. A. (1963). Distribution of inspired gas
during anesthesia and artificial respiration. /. appl.
Physioi, 18, 1085.
Bishop, J. M., and Pincock, A. C. (1958). A method
of measuring oxygen tension in blood and gas
using a covered platinum electrode. /. Physioi.
(Land.). 145, 20P.
Boothby, W. M., and Sandiford, I. (1924). Basal metabolism. Physioi. Rev., 4, 69.
Bradley, A. F., Stupfel, M., and Severinghaus, J. W.
(1956). Effect of temperature on Pco, and Po, of
blood in vitro. /. appl. Physioi., 9, 201.
Campbell, E. J. M., Nunn, J. F., and Peckett, B. W.
(1958). A comparison of artificial ventilation and
spontaneous respiration with particular reference
to ventilation-bloodflow relationships. Brit. J.
Anaesth., 30, 166.
Cater, D. B., Hill, D. W., Lindop, P. J., Nunn, J. F.,
and Silver, I. At (1963). Oxygen washout studies
in the anaesthetised dog. /. appl. Physioi, 18, 888.
Cole, P. V., and Parkhouse, J. (1961). Blood oxygen
saturation during anaesthesia with volatile agents
vaporized in room air. Brit J. Anaesth., 33, 265.
Cole, R. B., and Bishop, J. M. (1963). Effect of varying
inspired O, tension on alveolar-arterial O, difference in man. /. appl. Physioi., 18, 1043.
Comroe, J. H. jr., and Botelho, S. (1947). The unreliability of cyanosis in the recognition of arterial
anoxaemia. Amer. J. med. Sci., 214, 1.
Conway, C. M., and Payne, J. P. (1964). Hypoxaemia
associated with anaesthesia and controlled respiration. Lancet, 1, 12.
Davy, Sir Humphry (1800). Researches, Chemical and
Philosophical; chiefly concerning nitrous oxide, or
dephlogisticated nitrous air, and its respiration.
London: J. Johnson.
Dobkin, A. B., and Song, Y. (1962). The effect of
methoxyflurane-nitrous
oxide anesthesia on
arterial pH, oxygen saturation, Paco, and plasma
bicarbonate in man. Anesthesiology, 23, 601.
Donald, K. W., and Christie, R. V. (1949). The respiratory response to carbon dioxide and anoxia
in emphysema. Clin. Sci., 8, 33.
Renzetti, A., Riley. R. L., and Cournand, A.
(1952). Analysis of factors affecting the concentrations of oxygen and carbon dioxide in gas
and blood of lungs: results. /. appl. Physioi., 4,
497.
Enghoff, H. (1939). Volumen inefficax. Bermerkungen
zur Frage des shadlichen Raumes. Upsala LSk.Foren. Forh., 44, 191.
Farhi, L. E., and Rahn, H. (1955a). Gas stores of the
body and the unsteady state. /. appl. Physioi, 7,
472.
(1955b). A theoretical analysis of the
alveolar-arterial O, difference with special reference to the distribution effect /. appl. Physioi.,
7, 699.
Faulconer, A., and Latterell, K. E. (1949). Tensions
of oxygen and ether vapour during use of the
semi-open, air-ether method of anesthesia. Anesthesiology, 10, 247.
Fink, B. R. (1955). Diffusion anoxia. Anesthesiology,
16, 511.
Fraser, R., and Nordin, B. E. C. (1955). The basal
metabolic rate during sleep. Lancet, 1, 532.
Freeman, J., and Nunn, J. F. (1963). Ventilation-perfusion relationships after haemorrhage. Clin. Sci.,
24, 135.
Frumin, M. J., Bergman, N. A., Holaday, D. A.,
Rackow, H., and Salanitre, E. (1959). Alveolararterial O, differences during artificial respiration
in man. /. appl. Physioi., 14, 694.
Gordh, T., Linderholm, H., and Norlander, O. (1958).
Pulmonary function and oxygen tension of arterial
blood. Ada anaesth. scana., 2, 15.
Ikezono, E., Harmel, M. H., and King, B. D. (1959).
Pulmonary ventilation and arterial oxygen saturation during ether-air anesthesia. Anesthesiology,
20, 597.
Lilienthal, J. L., Riley, R. L., Premmel, D. D., and
Franke, R. E. (1946). An experimental analysis
in man of the oxygen pressure gradient from alveolar air to arterial blood during rest and exercise
at sea level and at altitude. Amer. J. Physioi., 47,
199.
Lloyd, B. B. (1958). A development of Haldane's gasanalysis apparatus. /. Physioi. (Lond.), 143, 5P.
Nunn, J. F. (1962). Predictors for oxygen and carbon
dioxide levels during anaesthesia. Anaesthesia,
17, 182.
(1963). Indirect determination of the ideal alveolar oxygen tension during and after nitrous oxide
anaesthesia. Brit. J. Anaesth., 35, 8.
Bergman, N. A. (1964). The effect of atropine on
pulmonary gas exchange. Brit. J. Anaesth., 36, 68.
Campbell, E. J. M., and Peckett, B. W. (1959).
Anatomical subdivisions of the volume of respiratory dead space and effect of position of the
jaw. /. appl. Physioi., 14, 174.
Hill, D. W. (1960). Respiratory dead space and
arterial to end-tidal CO, tension difference in
anaesthetized man. /. appl. Physioi., 15, 383.
Matthews, R. L. (1959). Gaseous exchange during
halothane anaesthesia. Brit. J. Anaesth., 31, 330.
Payne, J. P. (1962). Hypoxaemia after general
anaesthesia. Lancet, 2, 631.
Pouliot, J. C. (1962). The measurement of
gaseous exchange during nitrous oxide anaesthesia. Brit. J. Anaesth., 43, 752.
Pappenheimer, J. R., Comroe, J. H., Cournand, A.,
Ferguson, J. K. W., Filley, G. F., Fowler, W. S.,
Gray, J. S., Helmoltz, H. F., Otis, A. B., Rahn,
H., and Riley, R. L. (1950). Report of the committee for the standardisation of definitions and
symbols in respiratory physiology. Fed. Proc., 9,
602.
Riley. R. L., Lilienthal, J. L., Prommel, D. D., and
Franke, R. E. (1946). On the determination of
the physiologically effective pressures of oxygen
and carbon dioxide in alveolar air. Amer. J.
Physioi., 147, 191.
Robertson, J. D., and Reid, D. D. (1952). Standards
for the basal metabolism of normal people in
Britain. Lancet, 1, 940.
Rosen, J. (1959). Hearing tests during anaesthesia with
nitrous oxide and relaxants. Ada anaesth. scand.,
3, 1.
Sendroy, J. jr., Dillon, R. T., and Van Slyke, D. D.
(1934). Studies of gas and electrolyte equilibria in
blood. /. biol. Chem., 105, 597.
FACTORS INFLUENCING THE ARTERIAL OXYGEN TENSION
Severinghaus, J. W. (1954). The rate of uptake of
nitrous oxide in man. /. din. Invest., 33, 1183.
(1958), in Handbook of Respiration (edited by
D. S. Dittmer and R. M. Grebe), p. 73. Philadelphia: Saunders.
Bradley, A. F. (1958). Electrodes for blood Po,
and Pco, determination. /. appl. Physiol., 13, 515.
Stupfel, M. (1957). Alveolar dead space as an
index of distribution of blood flow in pulmonary
capillaries. /. appl. Physiol., 10, 335.
Stark, D. C. C , and Smith, H. (1960). Pulmonary
vascular changes during anaesthesia. Brit. J.
Anaesth., 32, 460.
Staub, N. C. (1963). Alveolar-arterial oxygen tension
gradient due to diffusion. /. appl. Physiol., 18, 673.
Wakai, I. (1963). Human oxygenation by air during
anaesthesia. The relation of ventilatory volume
and arterial oxygen saturation. Brit. J. Anaesth.,
35, 414.
West, J. B. (1963). Distribution of gas and blood in
the normal lungs. Brit. med. Bull., 19, 53.
LES FACTEURS QUI INFLUENCENT LA
TENSION DE L'OXYGENE ARTERIEL AU
COURS DE L'ANESTHESIE AU HALOTHANE
AVEC RESPIRATION SPONTANEE
SOMMAIRE
Etude des facteurs qui influencent l'oxygenation du
sang arte'riel pendant l'anesthesie de routine chez 36
malades narcotises par l'halothane et respirant spontanement ayec un volume/minute moyen de 5 l./min.
On obseryait nettement pendant la premiere heure de
l'anesthesie un stade respiratoire instable. La consommation d'oxygene ^tait de 87%, calculee a partir de
la valeur basale. L'espace mort physiologique
atteignait
33% du volume circulant expire1 (tous les malades
dtaient intubes). Aux fortes concentrations de l'oxygene inspire le gradient alve'olaire arte'riel Po, £tait en
moyenne de 184 mm/Hg, ce qui correspond a un
shunt de 14% du flux sanguin pulmonaire. Aux faibles
taux du Po, alviolaire le gradient alve'olaire art^riel
Po, diminuait, mais restait au-dessus des valeurs qui
341
correspondraient a un shunt de 14%. Cela 6tait probablement du a un taux de ventilation inadequat (maldistribution) correspondent a un melange contenant
30% de sang veineux. On en conclut que pour assurer
chez la plupart des malades un Po, arteriel normal,
le Po, alveolaire doit fitre de 200 mm/Hg et cela exige
dans les conditions realises dans cette 6tude une concentration de 35% de l'oxygene inspird.
UBER DIE ARTERIELLE SAUERSTOFFSPANNUNG BEI HALOTHANE-NARKOSE MIT
SPONTANER ATNfUNG BEEINFLUSSENDEN
FAKTOREN
ZUSAMMENFASSUNG
Wahrend 36 routinemaOig durchgefuhrten HalothaneNarkosen mit einer Spontanatmung bei einem Minutenvolumen von durchschnittlich 5 l./min wurden die
Faktoren untersucht, die Sauerstoflsfittigung des
arteriellen Blutes beeinflussen. Es fand sich eine unbestSndige Atmungslage wfihrend der ersten Stunde
der Narkose. Der Sauerstoffverbrauch lag bei 87% der
Norm. Der physiologische Totraum belief sich auf 33%
der exspirierten Atemluft (AUe Patienten waren intubiert). Bei einem hdheren Niveau der eingeatmeten
Sauerstoffkonzentration betrug das durchschnittliche
alveolar-arterielle Po,-Gefalle 184 mm/Hg, entsprechend einer Verschiebung der Lungendurchblutung
urn 14%. Bei niedrigerem Stand des alvcolaren Po,
verringerte sich das alveolare-arterielle Po, Gefglle,
stieg aber tlber den Wert an, der durch eine Verschiebung urn 14% verursacht wiirde. Dies war wahrecheinlich den ungleichmafiigen Durchluftungs-DurchstrSmungsverhaltnissen (ungleichmafiige Verteilung) zuzuschreiben, tlbereinstimmend mit einer berechneten
venosen Beimischung, ansteigend bis zum Wert von
30%. Es lfifit sich schlufifolgern, dafi zur sicheren
Einstellung eines normalen Po,-Wertes in der flberwiegenden Mehrzahl der FSlle der alveolare Po,-Wert
an die 200 mm/Hg bctragen sollte. Das erfordert eine
Sauerstoffkonzentration der Einatmungsluft von 35%
unter den in dieser Arbeit beschriebenen Voraussetzungen.