Brit. J. Anaesth. (1967), 39, 450
THE INFLUENCE OF CARDIAC OUTPUT ON ARTERIAL OXYGENATION:
A THEORETICAL STUDY
BY
G. R. KELMAN, J. F. NUNN, C. PRYS-ROBERTS AND R. GREENBAUM
Department of Anaesthesia, University of Leeds, and The General Infirmary at Leeds,
England
SUMMARY
Recent measurements of cardiac output have shown that, during anaesthesia, departures
from normality are of common occurrence. In the presence of pulmonary venous
admixture, such changes of cardiac output may affect the arterial Poa to a considerable
extent. This paper explores the nature of the theoretical relationship between cardiac
output, percentage pulmonary venous admixture, and (A-a) Poa difference, and from
the results draws certain conclusions: (1) Appreciable reductions in arterial Po3
during and after anaesthesia may be caused largely by reductions of cardiac output.
(2) When allowance is made for the probable changes of cardiac output, it appears
that the percentage pulmonary venous admixture during anaesthesia may not be
greatly increased above the normal range. (3) Since with certain anaesthetic techniques
there is a linear relationship between Pacoa and cardiac output, an increase of alveolar
ventilation may under such circumstances cause a paradoxical decrease of the
arterial Po,.
In the absence of inert gas exchange, three major
factors determine the alveolar oxygen tension:
(1) The oxygen uptake of the patient.
(2) The oxygen tension of the inspired gas
mixture.
(3) The alveolar ventilation.
(1) Pulmonary arteriovenous anastomoses.
(2) Drainage of venous blood into the left heart
and pulmonary veins.
(3) Blood flow through atelectatic areas of lung.
(4) Blood flow through relatively underventilated areas of lung.
Within reasonable limits the cardiac output is
not a factor, although clearly, if the circulation
were arrested while ventilation continued, the
oxygen uptake would fall to zero and the alveolar
Po3 would become equal to the inspired oxygen
tension.
Many recent studies have demonstrated that the
(A-a) Po, difference is increased during
anaesthesia, and this is associated with a reduction
in the arterial Po, to a considerable extent. If we
ignore the possible role of limitations of oxygen
diffusing capacity, the principal factor which
causes this difference is the "venous admixture
effect" or "physiological shunting" which comprises a number of components including the
following:
The relationship between this venous admixture
and the resultant (A-a) Po3 difference is, however,
complex and depends inter alia upon the cardiac
output. This latter factor has received little attention hitherto, partly because accurate measurements have seldom been available, and also
because early studies suggested that gross
deviations from the normal were unusual during
anaesthesia.
More recent work indicates that we should
pay more attention to the cardiac output since
the magnitude of the venous admixture during
anaesthesia is such that moderate changes of
cardiac output will have a substantial effect on
the (A-a) Po, difference. Furthermore, recent
measurements of cardiac output have demon-
INFLUENCE OF CARDIAC OUTPUT ON ARTERIAL OXYGENATION
strated quite severe deviations outside the normal
range with certain commonplace anaesthetic
techniques. Observed reductions in cardiac
output are, in fact, sufficient to account for
marked falls in arterial Po, and this has been
clearly demonstrated in the sudden fall of
arterial Po, which results from the acute
reduction of cardiac output following the
administration of intravenous tbiopentone (PrysRoberts, Kelman and Greenbaum, 1967).
The purpose of this paper is to explore more
fully the quantitative relationship between cardiac
output and arterial Po,, and to re-evaluate the
magnitude of the calculated venous admixture
previously reported by one of us (J.F.N.) using
values of cardiac output and arteriovenous oxygen
differences mere in keeping with current findings
than those assumed in the original study.
Qualitatively, the effect of cardiac output on
arterial Po, is as follows:
If the cardiac output falls while the oxygen
consumption remains constant, the oxygen
extraction must increase and the mixed venous
blood oxygen content must fall. Therefore, the
blood passing to the left heart through the
"physiological shunt" will also have a lower
oxygen content. Provided that the pulmonary
end-capillary Po, and the percentage of venous
admixture remain constant, the admixture of
blood with a lower oxygen content must
inevitably lower the oxygen content of the
mixed arterial blood.
Simple though this qualitative statement is, the
quantitative effects of changes of cardiac output
are complex since some of the relationships
involved are highly non-linear.
QUANTITATIVE RELATIONSHIPS
It is a common practice in electrical engineering
to describe complex circuit elements such as
transistors and thermionic tubes in terms of simple
"equivalent circuits" (Hill, 1963). The advantage
of this technique is that analysis of the equivalent
circuit is relatively easy. A similar technique can
profitably be applied to respiratory physiology
where the inadequacies of blood gas exchange
in the lungs may be similarly described. Figure 1
shows an equivalent circuit suitable for consideration of the venous admixture effect in the lungs.
451
In this simple model the blood entering the
lungs along the pulmonary artery immediately
splits into two streams. Part (Qs) of the total
cardiac output «Jt) bypasses the functioning
lung tissue completely, the remainder (Qt—Qs)
comes into complete equilibrium with the ideal
alveolar gas. The two separate blood streams
then unite and leave the lungs via the left heart.
The percentage of the cardiac output thus
bypassing the lungs (Qs/Qt X100) is known as
the "physiological shunt" or "calculated
pulmonary venous admixture". This percentage
is calculated as if all the (A-a) Po3 difference
were due to a direct admixture of mixed venous
blood with the pulmonary end-capillary blood as
it leaves the alveoli. This is, of course, not what
actually happens but the simplifying assumption
is necessary for quantification of the phenomenon.
Thus the net effect of true anatomical shunt,
ventdlation/perfusion abnormalities (and diffusion
limitations if any), may be described in terms of
the single parameter Qs/Qt.
T1
FIG. 1
"Equivalent circuit" of lungs
and pulmonary circulation.
J
L
—1
Q
This simple model is only strictly applicable
when the alveolar oxygen tension is constant,
since, for a given degree of ventilation/perfusion
abnormality, a change of the alveolar oxygen
tension will alter the calculated pulmonary venous
admixture. However, if the PA<>, is constant, then
the simple model will respond to changes of
cardiac output in the same way as do the actual
lungs. It is instructive to examine with the aid
of this model the changes of arterial and mixed
venous oxygenation which will arise from changes
of cardiac output when the ideal alveolar oxygen
tension remains constant This will provide valuable information about the probable behaviour
of the actual lungs under similar circumstances.
The amount of oxygen taken up from the
alveoli in unit time is
where Cc' o , is the oxygen content of the blood
452
BRITISH JOURNAL OF ANAESTHESIA
at the end of the pulmonary capillaries leaving
the alveoli, and therefore assumed to be in complete equilibrium with the ideal alveolar gas,
and Cv 0 , is the oxygen content of the mixed
venous blood.
During a steady state* this rate of oxygen
uptake from the alveoli must equal the body's
oxygen consumption. Now, if the alveolar ventilation and the body's oxygen consumption remain
constant, the ideal alveolar oxygen tension, and
therefore the pulmonary end-capillary oxygen
content will also be unchanged. This must be
so since the ideal alveolar tension may be
calculated from the alveolar air equation given
by Nunn (1962), viz.
P A O , = P B dry [ F I O J - ( ^ O 3 / ^ A ) F ] ,
where F equals 1 - Fio, (1 - R). In the situation
under consideration all the terms on the r.h.s.
are constant so PAo, must also be constant.
If we now take the usual form of the Fick
equation, Le. Qt=>/o,/(Cao, -Cv 0 3 ), solve this
for Cvoj, and substitute in the equation Vo,=
(Qt - <Js) x (Cc'o, - Cvo3), we obtain fa>, = (Qt <£s) ( C c ' c - C a o j + V o ^ Q t ) which may be rearranged into the form:
The scaling factor 1/10 is necessary to allow
for the normal inconsistency of the units
(Cc'oa and Ca 0 , - ml/100 ml, Vo, - ml/min, and
Qt—litres/min).
From this equation it will be seen that, when
Qs/Qt and \fo3 are constant, the alveolar-arterial
oxygen content difference is reciprocally related
to the cardiac output. This relationship is plotted
in figure 2 as a series of rectangular hyperbolae
with different percentages of physiological shunt
as parameter, ^ o , is equal to 200 ml/ml.
In figure 3 variations of the oxygen content
of (a) pulmonary end-capillary blood, (Jo)
arterial blood, and (c) mixed venous blood are
plotted against cardiac output for various percentages of calculated pulmonary venous
admixture. As before VA and Vo, are assumed
constant. Since the ideal alveolar tension is con• In the case of oxygen (in contrast to carbon dioxide)
a steady state is attainable within a few minutes.
.46
Q litres/minute
FIG. 2
Relationship between pulmonary end-capillary to
arterial oxygen content difference and cardiac output
for several values of Qs/Qt
stant, the pulmonary end-capfllary oxygen content is also constant, whereas the arterial oxygen
content falls with decreasing cardiac output in
the manner predicted by figure 2. In plotting this
diagram the ideal alveolar oxygen tension was
assumed to be equal to 180 mm Hg, which is a
reasonable value during artificial ventilation when
the Flo, is in the region of 30 per cent as it
commonly is during nitrous oxide anaesthesia.
Using the dissociation curve recently proposed
by Severinghaus (1966), an oxygen solubility in
blood at 37°C of 0.003 ml/100 ml per mm Hg
(Sendroy, Dillon and Van Slyke, 1934), and an
oxygen capacity of 20.85 ml/100 ml (Le.
capillary
• arterial
= mixed venous
5
7
6 litres/minute
FIG. 3
Relationship between Cc'o« Caoi, and CVo, and cardiac
output for several values of 0 s / Q t PAo, = 180 mm Hg.
INFLUENCE OF CARDIAC OUTPUT ON ARTERIAL OXYGENATION
haemoglobin concentration 15 g per cent) this
gives an end-capillary oxygen content of 2123
ml/100 ml.
The mixed venous content falls for two
reasons. The major factor is that a decrease of
cardiac output increases the mixed venous to
arterial oxygen content difference. This follows
from the Fick equation since, if the oxygen consumption of the body is constant, the extraction
of oxygen from die blood must be increased at
lower cardiac outputs. It is for this reason that
the arterial oxygen content falls with decreasing
cardiac output since, as die mixed venous blood
becomes progressively stripped of oxygen, the
effect of any given degree of physiological shunting becomes magnified. This fall of arterial oxygen
content will cause an additional slight decrease of
the mixed venous oxygen content
die Leeds University English-Electric-LeoMarconi KDF 9 digital computer. Figure 4 was
based on an oxygen capacity of 20.85 g per cent,
a temperature of 37° C, a pH of 7.40, and a Pco,
of 40 mm Hg. The dissociation curve used was
that employed in die computer sub-routine
described by Kelman (1966), which in turn was
based on die dissociation curve recendy propounded by Severinghaus (1966).
Figure 4 confirms die dependence of (A-a) Po3
difference on die cardiac output shown in figure
2 and 3. The simple hyperbolic relationship is
now distorted because of die non-linearity of
tie dissociation curve below full saturation. The
rate of change of Pao3 with Qt is particularly
marked at low values of venous admixture.
5
Q
40
.5
7
Q litres/minute
FIG. 4
Relationship between arterial Po, and cardiac output
for several values of O S / Q L Haemoglobin concentration 15 g per cent
It is difficult mentally to convert oxygen contents into tensions so that in figure 4 die arterial
oxygen contents shown in figure 3 have been
converted into oxygen tensions. The conversion
of content into tension by inverse interpolation
is normally tedious and time-consuming, but diis
has been gready simplified by die use of a set of
tables relating tension to content at various
hydrogen ion concentrations, carbon dioxide
tensions, and temperatures, and for different
haemoglobin concentrations. These tables were
produced automatically on die line printer of
453
7
ttm/minute
FIG. 5
Relationship between arterial Po, and cardiac output
for several values of Qs/Qt. Haemoglobin concentration 10 g per cent.
Figure 5 shows die change of arterial Po, with
cardiac output when die haemoglobin concentration is 10 g per cent. This value was arbitrarily
chosen to represent tie lower limit likely to be
encountered during routine elective surgery. It
corresponds to an oxygen capacity of 13.09
ml/100 ml. The tensions are generally lower
dian in die 15 g case and die rate of change of
arterial tension widi cardiac output is even more
marked at low percentages of pulmonary venous
admixture.
Figure 6 shows tie changes of mixed venous
oxygen tension for two values of percentage
venous admixture based on an oxygen capacity of
20.85 ml/100 ml and a normal oxyhaemoglobin
BRITISH JOURNAL OF ANAESTHESIA
454
terms of the product of cardiac output and
arterial oxygen content (Richards, 1943-44; Nunn
and Freeman, 1964). A decrease of cardiac output
at a constant percentage pulmonary venous
admixture will decrease both of the factors
determining the oxygen availability. For this
reason it might be thought that the relationship
between this factor and the cardiac output would
be markedly curvilinear. In fact, however, the
cardiac output is the dominant factor and, in a
plot of oxygen availability against cardiac output,
it is difficult to detect the slight departure from
5
7
linearity induced by the fall of arterial oxygen
6 litres/minute
content with cardiac output Despite this, however, an increase in the percentage pulmonary
FIG. 6
Relationship between mixed venous Po, and cardiac venous admixture will cause a greater percentage
output for two values of Qs/Qt Haemoglobin concen- fall of the total oxygen available when the cardiac
tration 15 g per cent.
output is low (table I).
It is difficult to translate these concepts into
dissociation curve. Only two values of physio- practical terms, since there is as yet no general
logical shunt are plotted since the cardiac output agreement about the level of arterial oxygenation
is a much more important determinant of the or tissue oxygen flow at which hypoxic tissue
mixed venous oxygen tension than is the per- damage is likely to occur (Payne and Hill, 1966).
centage venous admixture. The rate of fall of It is, however, dear that quite moderate decreases
venous Po, with decreasing cardiac output of cardiac output may, when coupled with
increases as the output falls below 3 l./min.
increased pulmonary venous admixture (from
whatever cause), result in a surprisingly large
(A-a) Po3 difference. The effect of a reduction
IMPLICATIONS
of cardiac output on the oxygen content of the
The influence of cardiac output on arterial Po, mixed venous blood is even more striking,
has several implications in relation to clinical although in this case the oxygen content is not
practice and as regards the interpretation of greatly influenced by changes of the percentage
previous research data.
pulmonary venous admixture. Both of these
effects are especially marked when there is a
Oxygen availability and tissue oxygenation.
concomitant reduction in the oxygen capacity of
It is convenient to discuss the total amount of the blood, and it should be remembered that
oxygen available to the body per unit time in reductions of haemoglobin concentration to 10 g
TABLE I
Percentage fall of total oxygen availability due to an increase of percentage pulmonary venous
admixture from 5 to 30 per cent.
1
4
Cardiac output (L/m)
2
6
8
10
Qs/Qt 5 per cent
Coo, (ml/100 ml)
Oxygen availability (ml/min)
20.18
201.8
20.70
414.2
20.97
838.7
21.06
1263
21.10
1688
21.13
2113
Qs/Qt 30 per cent
Cao, (ml/100 ml)
Oxygen availability (ml/min)
12.66
126.6
16.95
339.0
19.09
763.5
19.80
1188
20.16
1613
20.37
2037
37.26
18.16
8.97
5.95
4.46
3.56
Percentage fall oxygen availability
(Qs/Qt 5 —y 30 per cent)
455
INFLUENCE OF CARDIAC OUTPUT ON ARTERIAL OXYGENATION
per cent are of common occurrence in patients
undergoing routine surgery.
It is axiomatic that the oxygen tension in the
blood leaving a tissue cannot be reduced to zero
if the tissue is not to suffer damage. Krogh (1919)
suggested that this critical tension was of the
order of 5-20 mm Hg but more recent work
suggests that it may in fact be somewhat higher.
This problem has been reviewed recently by
Bendixen and Laver (1965), who suggest that
there is probably an average critical level of
venous Po, which lies in the region of 20-30
mm Hg. At normal pH and temperature this
corresponds to an oxygen saturation of 35—55 per
cent, which is equivalent to an oxygen content of
7-11 ml/100 ml when the oxygen capacity is
20 ml/100 ml. Under these conditions and with
a normal oxygen consumption of 200 ml/min,
this critical level is likely to be reached when
the cardiac output falls to the region of 2 l./min
(fig. 6), and recent work has shown that, during
artificial ventilation with a lowered arterial Pco,,
the cardiac output may routinely fall to the
region of 2\ l./min (Prys-Roberts and Kelman,
1966).
The coefficient of oxygen utilization varies
greatly from tissue to tissue so that some tissues
have a bigger oxygen reserve than others. Oxygen
reserve may conveniently be defined as the normal
venous oxygen content minus the critical venous
oxygen content (Bendixen and Laver, 1965).
Tissues with a large coefficient of oxygen utilization (e.g., the myocardium) have a venous oxygen
content which is normally near to the critical
level, and therefore have little or no oxygen
reserve. Other tissues (e.g., the kidney) have an
extremely small oxygen extraction and therefore
a large oxygen reserve. The effect of arterial
hypoxaemia, therefore, falls much more heavily
on some tissues than on others, and tissues with
a low oxygen reserve may suffer hypoxia even
when the artificial oxygen flux is considerably
above the body's total oxygen requirements.
Effects of artificial ventilation on
During artificial ventilation and nitrous oxide/
oxygen anaesthesia, a lowering of the arterial Pco,
will result in a decrease in the cardiac output
(Prys-Roberts et al., 1967). In the presence of
an intrapulmonary physiological shunt this will
in turn result in an increase of the (A-a) Po,
difference. There are thus two factors which tend
to change the Pao. in opposite directions—
alveolar hyperventilation raises the PAOS towards
the inspired oxygen tension, and thus tends to
raise the arterial Po2; whilst the simultaneous
increase of the (A-a) Po, difference occasioned
by the fall of cardiac output tends to lower the
arterial Po s . It therefore appears possible for an
increase of alveolar ventilation to result, in certain
circumstances, in a paradoxical fall of the arterial
oxygen tension.
220 r
200
180
160
140
£120
| 100
Cf 80
60
40
20
0 1
2 3 4 5 6 7
VA Litres/minute
8
9
FIG. 7
Relationship between arterial Po, and alveolar ventilation for several values of Os/Qt. Fio,=0.3.
This is demonstrated in figure 7 which represents the effects of variations of alveolar ventilation on the Paoj of a hypothetical but typical
patient with the following variables maintained
constant: temperature 37°C, Flo, 30 per cent
(Pio2 214 mm Hg), Vo, 200 ml/min, Vco,
160 ml/min, R 0.8, weight 70 kg. The hypothetical change of cardiac output with ventilation
was estimated using the following regression
equation (Prys-Roberts et al., 1967):
Q (l./min per 70 kg)=0.039 Pace, + 2.23.
It is seen that, in the presence of a physiological
shunt greater than 5 per cent of the total cardiac
BRITISH JOURNAL OF ANAESTHESIA
456
output, alveolar hyperventilation will often result
in a decrease rather than an increase of the
arterial oxygen tension. The effect of hyperventilation on arterial saturation is less marked
because the oxyhaemoglobin dissociation curve
is shifted to the left by the respiratory alkalosis,
so that the saturation falls less rapidly with
increasing alveolar ventilation than it would otherwise do without this compensatory mechanism.
Coleman (1965), and then to recalculate their
degrees of venous admixture. This had been
done in figures 8(a) and (b) which show that the
recalculated values are about half those originally
reported. The mean recalculated (a-v) oxygen
content difference is 7.00 ml/100 ml (SD 0.93
ml/100 ml).
Calculation of percentage venous admixture.
Almost all calculations of physiological shunt
during anaesthesia have been based on measurements of the (A-a) Po3 difference without simultaneous measurements of the arterial-mixed
venous oxygen content difference. This latter
parameter is, however, required for the solution
of the shunt equation (slightly rearranged for
convenience):
(a)
Q s C c ' p , — Ca 0 .
In the absence of direct measurements most
workers have assumed a value for the (a-v) Coj
difference which they have realized may have
been incorrect. Campbell, Nunn and Peckett
(1958) calculated Qs/Qt for two values of (a-v)
Co3 difference and showed the large effect of
the different values. Sykes, Young, and Robinson
(1965), also showed by calculation the effect of
variations in the assumed (a—v) Co, difference.
Nunn (1964) and Nunn, Bergman and Coleman (1965), used a single assumed value for the
probable difference obtaining during anaesthesia
which was based on measurements of oxygen
consumption and cardiac output taken from the
literature. Although the value of VOj (200 ml/min)
which they assumed was probably a reasonable
estimate, the value of cardiac output (5.7 l./min)
appears in the light of recent work to have been
too high. The value of cardiac output assumed
by Nunn and associates was representative of the
values which had been reported in the literature
up to that time; but the studies from which it
was derived were made under somewhat different
clinical conditions.
Using the regression equation found by PrysRoberts, Kelman and Greenbaum (1967), it is
possible to predict the probable cardiac outputs
of the patients studied by Nunn, Bergman and
RECALCULATED
(b)
6
8
10
12
14
16
18 20 22
24
26
FIG. 8
Histogram of calculated pulmonary venous admixture
determined by Nunn, Bergmann and Coleman (1965):
(a) original values;
(b) recalculated values.
Nunn (1964) also measured the (A-a) Poa
difference during halothane anaesthesia, and again
assumed an (a-v) Co, difference of 3.5 ml/100
ml. Preliminary studies in this department (PrysRoberts and Kelman, unpublished) suggest that
INFLUENCE OF CARDIAC OUTPUT ON ARTERIAL OXYGENATION
457
the cardiac output is reduced during halothane Hill, D. W. (1963). Some fundamentals of medical
electronics. I l l : Thermionic valve amplifiers.
anaesthesia, and that the output depends both on
Brit. J. Anaesth., 35, 194.
the blood halothane level and on the Paco2- The Kelman, G. R. (1966). Digital computer subroutine for
values which have been obtained so far suggest
the conversion of oxygen tension into saturation.
J. appl. PhysioL, 21, 1374.
that the cardiac output under the conditions of
Nunn's study may have been reduced to between Krogh, A. (1919). The number and distribution of
capillaries in muscles with calculations of the oxy2 and 3 l./min with an oxygen consumption in
gen pressure head necessary for supplying the
tissues. J. Physiol. (Lond.), 52, 409.
in the region of 200 ml/min. This corresponds to
an (a-v) Co2 difference of the order of 8 ml/100 Nunn, J. F. (1962). Predictors for oxygen and carbon
dioxide levels during anaesthesia. Anaesthesia, 17,
ml. If these figures are confirmed then the
182.
calculated venous admixtures found by Nunn
(1964). Factors influencing the arterial oxygen
will have to be reduced by approximately 50 per
tension during halothane anaesthesia with spontaneous respiration. Brit. J. Anaesth., 36, 327.
cent, and will then lie scarcely outside the normal
Bergman, N. B., and Coleman, A. J. (1965). Facrange.
tors influencing the arterial oxygen tension during
It appears that the enlarged (A-a) Po,
anaesthesia with artificial ventilation. Brit. J.
Anaesth., 37, 898.
difference which occurs during anaesthesia is not
Freeman, J. (1964). Problems of orygenatkm and
necessarily due to "atelectasis" or even to excesoxygen transport during haemorrhage. Anaessive scatter of ventilation/perfusion ratios. It may,
thesia, 19, 206.
to a large extent, be caused by a decrease of Payne, J. P., and Hill, D. W. (1966). Oxygen Measurements in Blood and Tissues, p. 261. London:
cardiac output with a relatively normal oxygen
Churchill.
consumption in the presence of a degree of
Prys-Roberts,
C , and Kelman, G. R. (1966). Haemovenous admixture which is essentially within the
dynamic influences of graded hypercapnia in
normal range. Previous failures to demonstrate
anaesthetized man. Brit. J. Anaesth., 38, 661.
such "atelectasis" by radiological or other means
Greenbaum, R. (1967). The influence of
circulatory factors on arterial oxygenation during
may be explained in part by the fact that the
anaesthesia in man. Anaesthesia, 22, 257.
calculated venous admixture is considerably
Robinson, R. (1967). Circulatory insmaller than has been thought previously. This
fluences of artificial ventilation during nitrous
oxide anaesthesia in man. Results: the relative
may also be the explanation for reported failures
influence of mean intrathoracic pressure and
to raise the arterial Po, by hyperinflation of the
arterial carbon dioxide tension. Brit. J. Anaesth.
lungs (Panday and Nunn, in preparation).
(in press).
Studies are currently being undertaken to Richards, D. W. (1943-44). The circulation in traumatic shock in man. Harvey Lecture Series, 39,
determine the relative role of decreases of cardiac
217.
output and of increases of oxygen consumption
Sendroy, J. jr., Dillon, R. T., and Van Slyke, D. D.
in the causation of postoperative hypoxaemia. It
(1934). Studies of gas and electrolyte equilibria in
appears probable that these factors may prove
blood J. biol. Chem., 105, 597.
sufficient to explain the increased (A-a) Po, Severinghaus, J .W. (1966). Blood gas calculator. J.
appl. Physiol, 21, 1108.
differences without invoking the presence of large
Sykes,
M. K., Young, N. A., and Robinson, B. (1965).
increases of venous admixture.
Factors influencing the arterial oxygen tension
during anaesthesia with artificial ventilation. Brit.
J. Anaesth., 37, 314.
ACKNOWLEDGEMENTS
This work was aided by a grant from the Medical
Research Council. One of us (R.G.) is in receipt of a
L'INFLUENCE DU DEBIT CARDIAQUE SUR
Leverhulme Research Fellowship.
L'OXYGENATION ARTERIELLE: UNE ETUDE
THEORIQUE
REFERENCES
Bendixen, H. H., and Laver, M. B. (1965). Hypoxia
in anesthesia: a review. Clin. Pharmacol. Ther.,
6, 510.
Campbell, E. J. M., Nunn, J. P., and Peckett, B. M.
(1958). A comparison of artificial ventilation and
spontaneous respiration with particular reference
to ventilation-blood flow relationships. Brit. J.
Anaetth., 30, 166.
SOMMATRE
Des mesures rtantes du dibit cardiaque ont montre*
que durant l'anesthesie, des deviations de la normale
sont fre'quentes. En presence d'une mixtion pulmonaire
veineuse, des alterations pareilles du dibit cardiaque
peuvent influencer considirablement le POj artirieL Ce
travail explore la nature de la relation thtorique
existant entre le dibit cardiaque, le pourcentage de
458
BRITISH JOURNAL OF ANAESTHESIA
mixtion pulmonaire veineuse, et la difference Po, (A-a),
et tire certaines conclusions des resultats: (1) Une
reduction appreciable du Po, arteriel durant et apres
l'anesthesie peut en grande partie £tre causee par la
reduction du dibit cardiaque. (2) Les alterations
probables du dibit cardiaque etant donnees, il semble
que le pourcentage de mixtion pulmonaire veineuse
durant l'anesthesie ne dipasse que peu les valeurs
normales. (3) Puisqu'il existe durant certaines techniques d'anesthisie une relation lineaire entre le Paw,
et le dibit cardiaque, une augmentation de la ventilation alvtolaire peut causer dans ces circonstances une
diminution paradoxale du Po, artiriel.
DER EINFLUSS DES HERZMINUTENVOLUMENS AUF DIE ARTERIELLE
SAUERSTOFFSATTIGUNG: THEORETISCHE
UNTERSUCHUNG
ZUSAMMENFASSUNG
Neuerc Messungen des Herzminutenvolumens haben
gezeigt, dafi wahrend der Narkose Abweichungen von
der Norm haufig vorkommen. Bei Vorhandensein einer
pulmonalven6sen Beimischung konnen derartige Verand:rungen des Herzminutenvolumens einen betracbtlichen Einflufl auf den arteriellen Sauerstoffdruck
ausuben. Die vorliegende Arbeit untersucht die Art
der theoretischen Beziehung zwischen Herzminutenvolumen, Prozentsatz der pulmonalvenosen Beimischung und Sauerstoffdruck-Differenz (A-a) und kommt
aufgrund der Ergebnisse zu bestimmten SchluOfolgtrungen: (1) Eine merkliche Reduizierung des
arteriellen Sauerstoffdrucks wShrend und nach einer
Narkose kann weitgehend durch eine Reduzierung des
Herzminutenvolumens verursacht sein. (2) Wenn man
die vermutlichen Anderungen des Herzminutenvolumens berficksichtigt, so scheint es, daO der
Prozentsatz der pulmonalvenosen Beimischung wShrend
der Narkose nicht erheblich fiber den Normalbereich
gesteigert zu sein braucht. (3) Da bei bestimmten
Narkosetechniken eine lineare Beziehung zwischen
arteriellem CO,-Druck und Herzminutenvolumen
besteht, kann eine Steigerung der alveolaren Ventilation
unter derartigen Bedingungen eine paradoxe Abnahme
des arteriellen Sauerstoffdrucks hervorrufen.
BOOK REVIEW
Peridural Analgesia and Anesthesia. By P. C. Lund.
Published by Charles C. Thomas, Springfield,
Illinois. Pp. xiv+379. Price $13.50.
Readers of anaesthetic literature will immediately
recognize the name of Dr. Peere Lund from his many
contributions to our knowledge of regional anaesthesia.
It is fitting that such an experienced worker should
prepare a monograph on this topic and even more
fitting that the foreword should be written by Dr.
Harold R. Griffith. This former president of the World
Federation of Societies of Anaesthesiology and
Emeritus Professor of Anaesthesia at McGill University, Montreal, was once Dr. Lund's chief in the
Royal Canadian Air Force.
Peridural or epidural anaesthesia is more widely
practised in the United States than in Great Britain.
Indeed many British anaesthetists never use this
method of anaesthesia. However, in recent years there
has beeen a renewal of interest in this technique and
its applications. This book deals in a most comprehensive manner with all aspects of epidural anaesthesia. The chapters relating to the anatomical, physiological and pharmacological problems are excellent.
The new local analgesic prilocaine (propitocaine;
Citanest) is discussed in great detail and the findings
presented add weight to the view that it is the drug
of choice for this form of anaesthesia where only one
dose is required. Repetitive administrations, however,
carry a high risk of methaemoglobinaemia.
The various methods of identifying the epidural
space are critically examined and the author selects
the loss of resistance method using a syringe as the
one of choice. British anaesthetists may not agree that
the mere wearing of sterile gloves is sufficient protec-
tion against contamination, particularly if a catheter is
to be inserted into the epidural space. The use of a
stilette for facilitating introduction of the catheter increases the risk of tissue damage and breakage unless
the directions given are adhered to closely. The Lee
nylon catheter has replaced the vinyl plastic catheters
mentioned.
Peridural anaesthesia offers most advantages over
general anaesthesia to the patient with chronic respiratory disease and in obstetrics. The heavy preoperative sedation advocated would certainly counterbalance some of the benefits obtained. Two per cent
lifpiocaine will increase the motor nerve paresis and
with high blocks the severity of the respiratory
depression. The chapter on the use of peridural anaesthesia in obstetrics is very good and one feels that
more use should be made of this form of analgesia
here. However, from the figures presented, one cannot
agree with the author's conclusion that this form of
anaesthesia definitely reduces neonatal mortality, and
is therefore the method of choice where the foetus is
at risk. The teaching of peridural techniques to anaesthetists in training is very difficult and the method
presented has much to commend it.
There are usually several solutions to every anaesthetic problem. In some situations peridural anaesthesia
offers the greatest safety and comfort for the patient.
It is the duty of every anaesthetist to master this
technique. Dr. Lund's book will be of great value to
both the beginner and the established anaesthetist. It
is well written, illustrated in a clear manner, and contains an excellent bibliography.
James Moore
John W. Dundee