Review
Acid-base balance
A review of current approaches
William H. Austin, M.D.*
Portland, Me.
Approaches to acid-base balance
Until 1948, when Singer and Hastings’
published their nomograph describing the
concept of buffer base, acid-base problems
were interpreted within the framework
of the Henderson-Hasselbalch equation
which describes the relation between
pH, pCOz (or H2C03), and bicarbon-
ate. Buffer base added a new parameter
designed to separate the respiratory and
nonrespiratory (metabolic) changes and
was originally defined as “the base equiv-
alent to the sum of buffer anion concen-
tration (including HCO,) in milliequiv-
alents per liter.” The physiologic basis
for this concept is the fact that changes in
carbonic acid are buffered by protein
anion. In respiratory defects, any increase
or decrease in the bicarbonate is initially
accompanied by an equal and opposite
change in the protein anion existing in the
basic form, leaving the buffer base un-
changed. When changes in the buffer base
occur, a metabolic component is judged
to be present. If in respiratory acidosis
an increase in the bicarbonate concentra-
tion occurs which is greater than can be
accounted for by a decrease in protein
anion, buffer base is increased beyond the
normal range, and a metabolic alkalosis,
primary or secondary, is diagnosed. Like-
wise in respiratory alkalosis when the bi-
carbonate decrease is greater than can be
accounted for by an increase in protein
anion, a coexisting primary or secondary
metabolic acidosis is present. This ap-
Received for publication Jan. 29, 1965.
*Director, Section of Renal Physiology, Cardiorenal
691
and techniques
preach attempts to make a clear-cut dis-
tinction between those changes in bicar-
bonate which are due to and balanced by
a change in the protein anion concentra-
tion and those changes which are secondary
to “metabolic” factors of primary or
secondary origin. The biochemical data
give no information about the nature of
the metabolic component, whether it is
the anticipated secondary change or a
coexisting, superimposed primary defect.
In the primary metabolic disorders the
diagnosis of pure or mixed disturbance is
based on the presence or absence of a
normal pCO2. In the case of metabolic
acidosis when the anticipated hyperven-
tilation and decrease in pCOz occurs,
“metabolic acidosis with secondary re-
spiratory alkalosis” is present according to
the Singer-Hastings system. So called “pure
metabolic acidosis” is said to exist with a
decrease in bicarbonate and buffer base
but with a normal pCOz. As will be pointed
out later, such a situation probably repre-
sents metabolic acidosis with superimposed
respiratory insufficiency of a relative de-
gree. The reverse situation is generally
true for metabolic alkalosis. However,
we agree that a normal pC0, is often seen
with an elevated bicarbonate, and from
the physiologic viewpoint such a situation
does probably represent “pure metabolic
alkalosis.”
In recent years, there has been a revival
of interest in the buffer base concept in
Department, Maine Medical Center, Portland, Me., 04102.
 the fornl of the “L4strup approach” ;~nd in organic acid level, and renal factors.‘“-‘”
the Siggaard-.~~ndersell non10gr;tm.2-Y In Both t!-pes of changes ma>- be cornpensa-
addition to buffer base, two new param- 1or-L. in nature. The>. are in a sense mcta-
eters, standard bicarbonate* and base bol& since the)- involve a change in bi-
excess,1 have been introduced. These two carbonate, \,et, at the same time, are
entities are also used as an index of non- secondar)- to changes in alveolar ventila-
respirator!, or metabolic changes. In the tion. The systems described above afford
Siggard-Andersen curve nomogram, buffer no distinction between superimposed pri-
base, standard bicarbonate, and base mar\- and secondary metabolic defects,
excess are superimposed on a pH.‘pCO? and a certain amount of confusion is pro-
plot. The construction and use of this duced by calling a primary- respirator).
graph is described elsewtlere.8 disturbance with its expected metabolic
The validity of both these approaches compensation a “mixed defect.” \T!e have
has been challenged by Schwartz and reserved the use of this term for two pri-
Relman” on conceptual and physiologic marl’ coexisting defects and consider a
grounds. They suggest that parameters defect pure when the primar!, disturbance
such as base excess ma>. add confusion is associated with the usual or expected
rather than clarity to the therapeutic con- degree of compensation.
siderations. The finding of a positive base AA third and relatively unheralded ap-
excess or increased standard bicarbonate proach is that one advocated b>. I’oppell
does not necessarily- indicate the need for and associateszu and Roberts and associ-
measures to reverse these values to normal, ates.” These investigators, employing the
since the!. may reflect the usual compensa- classic parameters of pH, ~(‘02, and (‘02
tory changes. The>* further question the content, attempted to define the magnitude
validity of standard bicarbonate in vivo of changes encountered in various acid-
and in vitro. The lack of correlation was base disorders. For this they emplo\- a
subsequently documentedlfl,ll in dogs and pCOz/COz content plot which the>- found
human beings bl- determining the bicar- to be most convenient to represent the
bonate concentration of a sample of blood changes. The)- studied the magnitude of
exposed to a given pCOr and the concen- ventilatory change in metabolic disorders
tration actually present when the subject in patients with normal and abnormal pul-
was exposed to the same partial pressure monary function. The>. likewise made ob-
of carbon dioxide. ActualI,-, similar studies servations of the bicarbonate alterations
were made bl- Siggaard-L4ndersen,” but the in primary pulmonary disorders without
difference between in vivo and in vitro re- associated metabolic disease. From this
sults was not thought to be of clinical information they were able to determine
significance. the expected or llsual degree of compensa-
From Schwartz’s studies it appears that torq’ change in various primary. defects.
part of the bicarbonate generated from This also allowed the detection of super-
whole blood buffers in respiratory acidosis imposed problems which, with the use of
diffuses into the interstitial space. This the broader definitions, would go unnoticed
ina). in part account for the “metabolic (e.g., metabolic acidosis and pulmonar>
acidosis” which is said to exist in acute insufficiency). We combined their obser-
respiratory acidosis as diagnosed using the vations with over 400 of our own and in-
Singer-Hastings approach.‘* It seems some- cluded some important additions by Rob-
what arbitrary to make a distinction be- in.“’ The findings are expressed graphicall).
tween changes in bicarbonate which re- in Fig. 1, which delineates the various pat -
sult from whole blood buffers and those terns referred to earlier. Here, pCOs and
occurring secondary to ion transfer, changes BHCOx,* two components of the Hender-

*The standard bicarb~~ilte is e~~ual t<, the CO:! wntent oi *I’oppell originally used pCOp and (‘0: content in his graph. I
plasma separated from whole blood equilibrated with a believe that bicarbonate tends to be less confusing, al-
pCOz of 40 mm. Hg. at 38’C. though its use changes the iorm of the plot very little.
tThe base excess is defined as a titratable base on titration L<> Slightly different pI;‘s and wlubility coefficients wwc
normal pH at normal pCOz and normal temperature. calcu- used. but again n small deviation of Pnppell’s origlnnl plot
lated as a deviation of standard bicarbonate times 1.2.2 RSllltR.
 Volume 69
Number 5 Acid-base balance 693

son-Hasselbalch equation, are put into BHC03* plot. The pH, although useful
apposition. The use of pCOz and bicar- and necessary, is not specifically made
bonate makes a linear plot, and it is con- part of the diagram presented here, mainly
venient to think of these two parameters for reasons of simplicity.
as representing respiratory and metabolic The following features are worthy of
factors, respectively. Fig. 1, the pCOt/bi- note. Although implied, some of these
carbonate plot modified from PoppellZo and facts are not readily apparent from inspec-
associates, is based on the blood measure- tion of the graph.
ments described later. The expected range 1. Metabolic acidosis rarely exists as a
of values for metabolic acidosis, respiratory compensated defect when the BHCOs is
alkalosis, metabolic alkalosis, and respira- below 16 to 18 mM. per liter and is
tory acidosis is appropriately labeled. increasingly uncompensated below this
Mixed defect 1 results when chronic or value. Even in the absence of pulmonary
acute ventilatory insufficiency (relative disease, with bicarbonate levels above 16
or absolute respiratory acidosis) is super- to 18 mM. per liter, the acidosis is fre-
imposed on a defect producing a low bi- quently compensated (pH above 7.36).
carbonate value (i.e., metabolic acidosis 2. Metabolic acidosis usually exists as
or respiratory alkalosis). Mixed defect 2 an uncompensated defect in the presence
is present when ventilatory insufficiency of chronic pulmonary disease at all values
is superimposed on metabolic alkalosis, for BHC03 (mixed defect 1).
and an identical picture may be present 3. Respiratory alkalosis usually exists
in respiratory acidosis when there is a de- with a variable pH ranging from normal
crease in pCO2 without a simultaneous fall to high. Below 16 mM. per liter the pH
in the bicarbonate. This sustained eleva- tends to be more nearly normal. The range
tion of bicarbonate may be secondary to of expected pCOz values is much wider
depletion of chloride,22 and replacement of than in uncomplicated metabolic acidosis.
chloride will restore the picture to one of Respiratory alkalosis rarely exists alone
respiratory acidosis. Loss of chloride with a BHCO, below 12 mM. per liter.
through vomiting in a patient with respira- 4. Primary respiratory alkalosis and
tory acidosis will also produce this mixed metabolic acidosis coexisting as primary
defect. Some investigatorsz3 found that the defects cannot be diagnosed accurately
administration of bicarbonate produced but can be suspected when a moderately
metabolic alkalosis with an elevated pC0, low BHCOS exists with a near normal pH.
(mixed defect 2), but this is not a common 5. Metabolic alkalosis unassociated with
finding in our experience. A is an indetermi- primary pulmonary disease is character-
nate area. Points following this region ized by a high bicarbonate and a normal or
could represent one of several possibilities; only slightly elevated PCO~.~OJ~ (One in-
however, precise characterization is not vestigator reported elevated pC0, in pa-
always possible on biochemical grounds. tients receiving bicarbonate,2G but recalcu-
The line separating respiratory acidosis lated pCOrs from his pH and bicarbonate
and mixed defect 2 is not an exact boundary
*Some may object to the use of [BHCOJ instead of [HCO;];
between the two regions, and interpreta- however, it should be remembered that [BHCOa] times the
tion in this area, as always, should be activity coefficient (y), which in practice is incorporatedinto
the workingionization constant. equals [HCO;]: [BHCOa] x
tempered by the clinical situation. In
HzCOz %CO3
general, acute changes fall in the left half y= [HCOQ: [H+] =p Ka, or [H’] = __- Ka.
of the respiratory acidosis area, and the WCOil [==WY
more chronic changes, in the right. Plots HtCQ
Since Ka/r = K’, then [Hi] = -- K’ (Ka and Ii’ are
of pH/log pCO2 and pH/bicarbonate F’HCQI
could be used to express the same informa- the true apparent ionization constants, respectively).2~
The negative log of this apparent constant (I;‘) becomes
tion; however, we believe that the clinician an apparent PK', for the above-mentioned and other rea-
gains greater insight into the dynamics of sons. (IHCO51 in this discussion is used to indicate bi-
the acid-base situation and is able to carbonate activity, although others have employed the
notation for bicarbonate concentration. This inconsistent
transpose the laboratory findings to the usage of [HCOi] is another reason for the use of [BHC03]
clinical situation more easily with a pCO,/ for bicarbonate concentration.)
694 A ustin
60
t
PC02
mm’&
I-
DEFECT
0 5 10
Fig. 1. pCO,/BHCO, plot for venous blood. Mixed
with ventilatory insufficiency.
tory insufficiency or improving
BHCO,. A is an indeterminate
values failed to reveal any elevation of
pCO? [above 45 mm.] during the time the
subjects were breathing room air.)
6. Metabolic alkalosis associated with
severe depletion of potassium, some de-
gree of primary pulmonary disease, or im-
proving pulmonary disease without ade-
quate replacement of chloride”” may give
the picture of an elevated bicarbonate and
moderately elevated pCOz with alkaline
to normal pH (mixed defect 2).
7. Chronic respiratory acidosis is as-
sociated with an elevated pCOz and BHCOS
and a normal to markedly lowered pH.
The diagnosis of a superimposed metabolic
acidosis without an absolute decrease in
bicarbonate (below 24 mM. per liter) is
difficult to make with the current infor-
mation but may be suspected when values
fall in the left half of the respiratory aci-
dosis area.‘O**r
This device is only a guide, and too much
reliance should not be placed on it. The
bar for metabolic acidosis represents two
standard deviations, in our hands, but
other areas are not so well defined at the
present time. Various situations may pro-
duce misleading plots; for instance, the
combination of vomiting and diarrhea
15 20 25 30 35 40 45 50
BHC03 mM/L
defect 1: Metabolic acidosis
Mixed defect 2: Metabolic alkalosis with ventila-
respiratory acidosis with sustained elevation of
area. See text.
may result in a normal picture in the face
of marked depletion of chloride and bi-
carbonate. Such a device, however, is
helpful as a summary of the “natural
patterns” of acid-base disorders, and thus
is an aid to diagnosis and treatment. The
absolute validity of the figures presented
here may be questioned by some, but the
approach represents a clinical corollary
rather than a biochemical preoccupation.
Acid-base problems are troublesome enough
for those who deal with them regularly
and are more of a problem for the
clinician who sees them only occasionally.
For this reason, a few familiar parameters,
provided that they adequately define the
situation, seem to be preferable to a multi-
tude of less “tangible” ones, particularly
if they only add needlessconfusion.
The blood sample
The choice of which type of blood sample
to use for routine determinations has been
hotlv debated.26-32Arterial blood is most
desirable but more difficult to obtain when
frequent measurements are desired. This
is not a serious drawback, but if either
venous or capillary blood gives the same
 Volume 69
Number 5 Acid-base balance 695

information, sampling would be simplified. content will occur for about 1 hour.33
Wide variations between arterial and ven- Unpublished work indicates that at room
ous pH and pCOz have been reported28 temperature the pH changes by .0004 pH
and are said to be related to oxygen satu- units per minute, and at 37 or 38°C. the
ration, cardiac output, and high pH values. changes are of the order of .OOl per minute.
Gambino2gf36 found less variation between Severinghaus34 and Siggaard-Andersen35
plasma values and a wide scatter with found that plasma pH is higher than
whole blood. He apparently used fluoride whole blood pH by approximately .Ol
in some samples, which may have unpre- units, and some workers have routinely
dictably affected the pH values.33 Brooks added this value to whole blood pH. Gam-
and Wynn2’ report that venous blood bino could not find any consistent differ-
taken from the dorsum of the unheated ence between whole blood and plasma.36
hand gives results similar to those with His work is difficult to evaluate, not only
arterial blood. It is not always feasible to because fluoride was used, but because of
sample in this manner, particularly without instrumentation. The inherent error of
stasis. Capillary blood, when it can be ob- his pH meter alone exceeds the difference
tained with relative ease, gives values very in whole blood and plasma pH reported
close to arterial samples.26~28~30Large errors by some observers .34,36Salenius’ findings
occasionally may be made unwittingly, of a .048 difference is subject to some ques-
especially when the operator is not tion.37 If the temperature separation does
thoroughly experienced with microtech- have an effect on the pH in the manner
niques necessary for capillary samples. described by Rosenthal,38 then Salenius’
We find, as did Poppell and associates,20 results could be due to separation of plasma
less variation in pH and pCO2 when the at temperatures below 37 or 38°C. We
venous blood is drawn without stasis or re-evaluated this problem in the manner
pumping of the hand. Normal values for described by Severinghaus34 but used a
pCOz calculated from pH and pCO2 con- shorter centrifugation time (less than 5
tent range from 40 to 47 mm. Hg. We minutes). Our differences were slightly
hasten to add that this finding is at vari- greater than .Ol pH units between plasma
ance with that of others who note a greater and whole blood. The slightly higher
range and difference in the pCO2. It should values are undoubtedly due to the use of
be noted that venous pC02 determined a liquid-junction which was not thermo-
by the Astrup equilibration technique will stated. The observed pH difference be-
yield a low pCO2 when the pH of the un- tween whole blood and plasma is apparently
saturated venous sample is put into the due to a change in the liquid-junction
pH/pCOs plot .32 This could be predicted potentials created by the use of concen-
from the work of Peters and Van Slyke24 trated KCl, since the difference is obliter-
and is related to the fact that oxygenated ated with isotonic saline bridges.3g The
blood has a lower pH than reduced blood temperature of the liquid-junction as
at the same pCO2. The absolute difference previously referred to has a very definite
between arterial and venous blood is of effect on the pH, decreasing the value by
little importance, provided that the find- .OOl units for every degree centigrade
ings in various defects fall into consistent below 38°.35 Despite some evidence to the
patterns. Like that of Poppell and Roberts, contrary, we think that whole blood should
our experience with venous blood has shown be used for pH measurements and .Ol
this to be the case. Fig. 1 is based on venous added to the observed value. Separating
samples drawn in the manner described, plasma at 37 or 38°C. for pH measurement
but a similar system for arterial blood is is inconvenient and does not really improve
perfectly feasible and perhaps even more the accuracy. Glycolysis which takes place
desirable. The patterns found with arterial during separation over a 20-minute period
blood have not been worked out in detail, results in a decrease in plasma pH equal
but they are apparently fairly similar to to or exceeding the difference between
those found with venous blood.20 whole blood and plasma.
Once the sample is obtained, if it is Fortunately, the CO2 content is not sig-
stored in ice, little change in pH or CO2 nificantly altered by the temperature of
 696 A l/Sfiff
separation.:{:j,:j.‘,3”
(‘entrifuging sail~ples for
(‘0, content under mineral oil does not
result in significant loss of (‘O,, as is often
stated.i” In 20 paired samples, one set
spun in a syringe, the other under oil in
the routine fashion, the average difference
in CO, content was 0.2 mM. per liter, with
the greatest being 0.9 mM. per liter.
Buffers and pH measuring
Two buffers in the physiologic range
(6.840 and 7.387) are by far the most useful
for calibrating a pH measuring system for
physiologic work. The buffer salts* (phos-
phate) are prepared by the National Bureau
of Standards. The value cited above for
the 7 buffer is slightly higher than that
given by the National Bureau of Stand-
ards, because of the presence of liquid-
junction potentials encountered with clini-
cal electrodes.41 These buffers are not
difficult to make, are more reliable than
most of those commercially available, and
are less expensive. They ma) be used to
calibrate buffers which are made with less
precision. The higher buffer is slightly less
stable than the 6.8 buffer, and its deteriora-
tion may be detected by a decrease in the
pH difference between the two.
At present there are on the market a
number of excellent pH meters that have a
high degree of accuracy. The ENIF-pH
ratio of the pH meter may be checked with
the potentiometer (61.64 mv. per pH at
37.X.) to be sure that the response of the
instrument is appropriate. However, this
is usually unnecessary with the better in-
struments. The over-all response of the
electrometer and the electrode taken as a
unit is actually the more important factor.
The electromotive efficiency of the elec-
trode may deviate from the theoretical
value, but any significant variation in
electrode output may be detected by the
use of the two buffers described. If the
output of the electrode is low, the slope
control or the temperature control (which
controls the millivolts required to give a
certain pH value) may be adjusted until
the two buffers agree. Deviations in electro-
motive efficiency should not be confused
with buffer inaccuracy. This can be checked
by making new batches of buffer. Once a
*Salts may be obtained from the National
Washington, D. C.. 20234. along
preparation of the two buffers referred
s\‘stenl’s response has been appi-opriatel\.
set, the 7.387 buffer alone illa!- be used lo
standardize the equipment, provided that
periodic checks are made against the lower
buffer. Highly alkaline buffers have little
place in physiologic s\,stems because of
the alkaline error of nlost glass electrodes.
L\cid buffers, such as phthalate, are less
objectionable, but their distance from the
systems pH being measured map- introduce an
error not seen with the use of buffers
nearer the pH of blood. These acid buffers
are of value in calculating the system over
a greater span. Semple and associate#
have described a 7.416 phosphate buffer
with an ionic strength similar to that of
blood (.13). This buffer has no great ad-
vantage over the buffers of the National
Bureau of Standards. Bates has described
several reasons for using buffers with an
ionic strength below . I, and the reader is
referred to his excellent book on pH meas-
urements for further details.“’
For best results, thermostated reference
electrodes and liquid-junctions should be
employed, as well as temperature control
of the glasselectrode. As referred to earlier,
the use of a liquid-junction at room temper-
ature35 will yield plasma pH values ,015
higher than those with junctions controlled
at 37 or 38°C. We have been able to con-
firm the existence of this phenomenon in
whole blood and suggest that thermostated
junctions be adopted to better standardize
pH results.
The use of pC0, electrodes such as those
described by Severinghausd3 has gained
wide acceptance. They have the advantage
of giving rapid results without the need
for separating the blood. Those who prefer
pH/pCOz plots will find this technique
particularly suitable, since calculations
are eliminated and the bothersome prob-
lem of pK’ is obviated. Values of pCOz ob-
tained with the electrode agree well with
other direct measurements of pCO2.
The Astrup microtonometer technique
of determining pCO? by equilibrating
blood with two gasesof known pCOz is sim-
ple and rapid.Y As alluded to earlier, if the
original sample is unsaturated, falsely low
pCOzs will result. In most situations this
would not be a problem, provided that
either arterial or capillary blood was used.
Bureau of Standards.
with instructions for
This system has the same general ad-
to above. vantages of the pCOz electrode in the

rapidity with which the answers can be
obtained.
CalculatiGn of conversion
tables and pKs
Experimental pK’ for the carbonic acid
buffer system in plasma differs consider-
ably from the true pK for carbonic acid.
The apparent pK’ is a composite of the
first dissociation constant of carbonic acid,
the activity coefficient for bicarbonate,
and a factor which permits dissolved
carbon dioxide to be treated as carbonic
acid. In addition, the temperature, pH,
and solubility coefficient have a real or
apparent effect on the pK’. The solubility
coefficient of COz is itself a function of
temperature, electrolyte, protein, lipid,
and water content of plasma. There is
little wonder that there has been disagree-
ment in published values for pK’. One
author suggests that each individual de-
termine his own PK’.~~ Several objections
could be raised to this. One of these is that
several variables and sources of error are
inherent in the procedure itself. Variations
from laboratory to laboratory would most
likely represent technical errors in equili-
bration and sample handling rather than
true differences in the pK’, even though
determinations of pH and carbon-dioxide
content may be made with a high degree
of accuracy.33r34*41Therefore, it seems
reasonable to adopt pK’ at 37S”C. ad-
justed for pH using the appropriate solu-
bility coefficient for COZ. The value may
be arbitrarily chosen or based on current
experimental data. The latter is the logi-
cal approach. The choice of 37.5”C. has
physiologic significance, although if a
given investigator chooses to use 37 or
38”C., he can still employ pK’ for 37.5X.
without significantly altering the calcu-
lations.
The whole problem may be considerably
simplified by using a nomogram or set of
tables (incorporating appropriate pK’s) for
making calculations, in lieu of solving the
Henderson-Hasselbalch equation. A nomo-
gram employing a fixed pK’, such as that
of Singer and Hastings,’ is preferred by
some. The nomogram is somewhat cum-
bersome to use and is subject to small
inaccuracies.
The alternative to a nomogram has
been suggested by Milch, Bane and Rob-
Acid-base balance 697
erts.44 From the rearranged Henderson-
Hasselbalch equation a “pC0, factor”
may be determined for various pHs. This
factor is given by the term [l+ antilog
(pH-pK’) ] . S, where S* is the solubility
factor calculated as follows: S = at/.76 .
22.26. The pCOz factor may be divided into
the CO* content to yield pCO2. With the
advent of the pCOz electrode some investi-
gators and clinicians find it easier to de-
termine pH and pCOz. In order to arrive
at a figure for bicarbonate from a deter-
mined (or calculated) pCO2, we have
calculated a second set of factors given by
the expression [l+ antilog (pH - pK’)] .
S - S. These bicarbonate factors may be
multiplied by the pCOe to yield bicarbon-
ate. From such a set of factors, pCOz and
BHCO, may be calculated with ease. The
method of calculating pCO2 and bicarbon-
ate is presented in the footnotes to Table I.
As alluded to earlier, preparation of a set
of factors poses a major problem in respect
to the choice of pK’. The best modern ex-
perimental data, although limited, are
those determined by Siggaard-Andersen45
using highly accurate buffers and pH
measuring systems. He found the pK’ at
7.4 and 38” to be 6.104. Severinghaus*‘j
noted a change in the pK’ with temperature
of approximately -.006 pH units per de-
gree centigrade. Austin, Lacombe, Rand
and Chatterjee47 recently determined the
solubility factors for COz in human serum
with known water content (.935 grams per
milliliter at 23°C.) and found slightly
higher values than those used by Siggaard-
Andersen. If his work is corrected for
temperature and a slightly different solu-
bility coefficient, the pK’ becomes 6.11
at 37.5”C. and 7.40.
The apparent change in pK’ with pH
(possibly due to the presence of carbo-
nate45) is well known. Through the physi-
ologic range it may be considered to be
linear. The pK’-pH regression coefficient
is -.047,44 but a value of -.05 may be
used without introducing any significant
error. Actually, this means a variation of
only .04 in the pK’ throughout the range
of 6.9 to 7.7. From the foregoing informa-
tion, pK’s for various pHs have been de-
termined and have been used in the calcu-
*S= HzC03 (mM./L.)/pCOz (mm. Hg).
ta= Solubility coefficient in ml. COz/ml. plasma.
 Am. Heart 1.
698 Austin May, 1965

Table I. Conversion factors for calculation of PC02 and BHCOI at 37.5’C.”

pH 1 $2 ~ “;:i? 1 PH 1 i::: i ;z3 1 $JH 1 ;::; ~ ;:ki?

6.90 ,207 ,177 7.20 ,396 ,366 7.50 .785 ,755

,211 ,181 1 ,404 ,374 ,803 ,773
2 ,216 .186 2 .413 ,383 ,821 .791
,220 ,190 3 ,422 ,392 ,839 ,809
4 .224 ,194 4 .433 ,403 ,858 ,828
,229 ,199 5 ,443 ,413 5 ,877 ,847
6 ,235 ,205 6 ,455 .425 6 .907 ,877
7 ,241 .211 7 ,465 ,435 .927 .897
8 ,246 .216 8 ,475 .44s 8 .948 .918
9 ,250 ,220 ,485 ,455 9 ,969 ,939
7.00 ,256 ,226 7.3: ,496 .466 7.60 .992 ,962
,261 ,231 1 so7 ,477 1 1.01 ,984
,266 ,236 2 ,518 ,488 2 1.03 1.00
,272 ,242 3 ,529 .499 1.06 1.03
,277 ,247 4 ,541 ,511 4 1.08 1.05
5 ,284 ,254 5 ,553 ,523 5 1.11 1.08
6 ,292 ,262 6 ,571 .541 6 1.14 1.11
,298 ,268 7 ,583 ,553 1.17 1.14
8 ,304 ,274 8 ,596 .566 8 1.20 1.17
9 ,312 282 609 ,579 9 1.23 1.20
7.10 ,318 ,287 7.4; .623 .593 7.70 1.25 1.22
.324 ,294 I ,637 ,607 1.28 1.25
,331 ,301 2 ,651 ,621 2 1.31 1.28
.338 ,308 3 ,665 ,635 1.34 1.31
,345 ,315 4 .680 ,650 4 1.37 1.34
,352 ,322 5 ,696 ,666 1.40 1.37
.364 .334 6 ,714 .683 1.44 1.41
.371 ,341 7 .731 ,701 1.48 1.45
.379 ,349 8 .749 ,719 1.52 1.49
.387 ,357 9 .767 ,737 1.56 1.53

*pK’at 7.40=6.11; ApK’/pH= -.OS; a=.514; dubilityfactor= .0304; temperature=37,YC. (37-3PC.).

co2 content.
tPC02 =
pcoz factor

~BHCO.T= PC& x BHCOa factor.

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