ADVANCES IN FLUID AND ELECTROLYTE

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PRACTICAL APPROACH TO
ACID-BASE DISORDERS
James E. Bailey, DVM, MS, and Luisito S. Pablo, DVM, MS

Acid-base balance is a general term for the way in which the body
maintains a relatively constant pH despite continuous production of
metabolic end products and is fundamental to physiologic homeostasis.
Disease states of animals lead to irregularities of body fluid, electrolyte,
and acid-base balance. With the advent of less expensive, accurate, as
well as portable blood gas and electrolyte analyzers, acid-base assess-
ment has become a standard of care in veterinary medicine. It is im-
portant that the veterinary practitioner understand acid-base pathophys-
iology to assure successful treatment of these disease states. The
literature is replete with excellent reviews of acid-base pathophysiology,
and production of another review would be redundant. 1- 22 The purpose
of this article is to provide a simple and concise description of traditional
and modern acid-base data interpretation and assist the practitioner
with application of these methods.

DEFINITIONS

Before proceeding, a discussion of acid-base terminology is manda-

tory. Please refer to the glossary at the end of this chapter for terms and
explanations of terms. Italicized words found in the text are explained in
the glossary. This glossary should prove useful in understanding further
reading on the pathophysiolgy of acid-base disorders.

From the Department of Large Animal Clinical Sciences, University of Florida, College of
Veterinary Medicine, Gainesville, Florida

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME 28 • NUMBER 3 • MAY 1998 645

646 BAILEY & PABLO

BLOOD SAMPLE COLLECTION AND HANDLING

Improper sample collection and handling will lead to measurement

error and flawed clinical judgment. Several factors must be considered
when taking blood for blood gas or serum chemistry measurements.
Plastic syringes are more gas permeable than glass syringes, but no
significant difference in acid-base values have been detected when using
plastic syringes. 2 Typically, a 25-gauge needle is securely attached to 3-
mL plastic syringe and a small amount of sodium heparin (100 units/
ml) is drawn into the syringe. The heparin is used to coat the walls of
the syringe to prevent coagulation, and all excess anticoagulant should
be expressed. Excess heparin may dilute the sample, produce false low
measurements of pH and partial pressure of carbon dioxide (PC02), and
cause hemolysis. Electrolyte measurements will also be in error. Sodium
heparin will cause a false high sodium (Na +) measurement and a false
low ionized calcium (iCa2+) measurement by introducing Na+ into the
sample and binding Ca2+, respectively. Any hemolysis will falsely ele-
vate the potassium (K+) and lower the iCa2+ concentration. Use of
balanced heparin, low concentration heparin (<10 IU/ml), commercially
available balanced heparin syringes, or purging of the syringe multiple
times after heparinization to minimize heparin content, may limit these
effects. Some of the portable, point-of-care blood gas and electrolyte
analyzers do not require anticoagulant, but timely collection and transfer
(< 3 minutes) is necessary to prevent coagulation and measurement
error. Also, underfilling of serum chemistry blood collection tubes will
result in a falsely low serum total carbon dioxide (TC02) and can contrib-
ute to improper clinical assessmenf.21
Arterial blood is preferred for pH and blood gas analysis because
the degree of hemoglobin oxygen saturation and oxygen delivery affect
metabolism and acid-base balance. Hypoxia may well be the cause of an
acid-base derangement. Arterial blood samples provide the most reliable
information, except during cardiopulmonary resuscitation when mixed
venous blood most accurately reflects the acid-base state of the animal
(especially the rapid increase in PC02). 23 Arterial blood samples are
easily acquired from the femoral, brachial, carotid, digital, and dorsal
pedal arteries after some practice. Venous blood can accumulate acid
metabolites, but bicarbonate and base deficit values are usually very
similar to arterial. When arterial blood collection is problematic, venous
blood can be obtained from the jugular, cephalic, or saphenous veins
and still provide useful acid-base information. Serum chemistry analysis
is commonly performed on venous blood for determination of electro-
lytes and TC02.
Many modern blood gas machines require less than 0.25 ml of blood
for analysis. However, to avoid dilutional effects of anticoagulant and
to assure adequate volume for older machines or additional tests (e.g.,
electrolytes, PCV, total protein), 1 to 1.5 milliliters of arterial blood are
withdrawn where possible. The sample should be extracted slowly and
anaerobically. Any air bubbles should be expressed immediately, and a
 PRACTICAL APPROACH TO ACID-BASE DISORDERS 647

rubber stopper should be placed over the needle tip. Air bubbles often
contain more oxygen and less C02 than the blood sample, exchange
with the sample, and cause increased P02, decreased PC0 2, increased
pH24 and decreased iCa 2 +. Air bubbles may also physically interfere
with contact between the analyzer electrode and blood sample. Blood
samples should be analyzed immediately. The blood in the nozzle of the
syringe should be purged, and the sample should be introduced slowly
and anaerobically. At room temperature, the blood sample will continue
metabolism, consume oxygen, produce C02 and lactic acid, and cause
measurement error. However, a delay in analyzing a sample stored at
room temperature for 10 minutes or stored in an ice-water bath for 2
hours will not affect accuracy significantly if the sample is properly
mixed before analysis. Potassium values will increase in iced samples.
Mixing can be performed by inverting the syringe multiple times (5 to
10) followed by rolling the syringe between the palms (vortexing) for 5
to 10 seconds.
Increased body temperature causes increased partial pressure of
gases (PC02 and P02 ) and decreased pH. Decreased body temperature
causes decreased partial pressure of gases (PC02 and P02 ) and increased
pH (pH changes 0.15 units per 0 C). This has led to two schools of
thought regarding temperature correction of blood gas data and acid-
base management of hypothermic patients: pH-Stat Management and
Alpha-Stat Management. Currently there is insufficient evidence to de-
mand temperature correction of blood gas data. However, the prac-
titioner must understand that the pH, as read in the blood gas analyzer
at 37°C, is actually higher in the hypothermic patient and lower in the
hyperthermic patient. Most blood gas machines are programmed with
nomograms that will correct the blood gas for temperature if the patient
temperature is entered.

BLOOD GAS

What can blood gas results reveal regarding acid-base homeostasis?

Blood gas analysis should be performed on all animals suspected
of having an acid-base disorder. The typical blood gas analysis provides
three measured parameters (pH, PC02, P02 ) and a variable number of
calculated values (e.g., actual bicarbonate, base excess). After consider-
ing the history and pathophysiology of the animal's disease, the first
parameter that should be examined is the pH. The pH is the most
valuable parameter for determining the animal's acid-base status and
will usually establish whether or not an acid-base disturbance exists. All
subsequent values are related back to pH. Normal small animal pH and
blood gas values are listed in Table 1. The sample pH may indicate
acidemia, alkalemia, or be normal (Fig. 1, Chart 1). Second, the arterial
partial pressure of carbon dioxide (PaC02) is examined. The sample may
show eucapnia, hypercapnia, or hypocapnia (see Fig. 1). The arterial partial
pressure of oxygen (Pa02 ) should also be evaluated to assure there
~
00

Date I I Patient Information

p •

Weight (kg)
History _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __

BLC>C>I> G-.A..S .A..N".A..LYSIS

Sample 1 Sample 2 Sample 3 Sample 4
pH
P.co 2 _ _ __

P.02
HC03-
BE
.A.. N" I C> N" G- .A..P
Sample 1 Sample 2 Sample 3 Sample 4 Normal Range
Na+
K+
Cl"
TC0 2
Anion Gap = (N a+ - - LmEq + K+ mEq) - (CI- - - LmEq + reo mEq) =
--L 2--L ~eNotes
 !CHART 11 Blood Gas

Normal Values

!canine I I Feline J IEquine I ]Bovine I

mEq/L 145-153 151-158 136-142 136-144
mEq/L 4.2-5.6 4.0-5.3 2.4-5.2 4.0-5.3
mEq/L 110-118 116-125 97-104 94-104
HCQ3·meq/L 17-24 17-24 24-27 23-25
TCO, mEq/L 20-27 15-25 26-35 24-34
Diarrhea Carbonic Anhydrase Inhibitors AG mEq!L 11-26 13-24 7-16 12-22
Hypoalbo.Jminemia Renal Tubular Acidosis Posthypocapnic Acidosis pH units 7.31-7.42 7.24-7.40 7.38-7.44 7.41-7.43
Dilutional Acidosis Cationic Amino Acids From the Department ol Clinical Pathology, University of Florida, Gai11esville, FL
HemodMion

Figure 1. Acid-base status report. Evaluation of blood gas and anion gap.

C'\
II'>
'J;)
650 BAILEY & PABLO

Table 1. NORMAL BLOOD GAS VALUES

Method Parameter Normal* Range•

Measured pH 7.4 7.35-7.45

PaC02 (mmHg) 40 35-45
Pa02 (mmHg) 100 (at FI02 0.21) 9Q-100
(mmHg) 500 (at Fl0 2 1.0) 90-650
Calculated HCO,- (mEq/L) 24 18-26
BE (mEq/L) 0 -4-+4

*Species dependent. Should be established by laboratory performing analysis. F/02 0.21 = room
air; 1.0 = 100% oxygen. STP.

is not hypoxemia that could lead to anaerobic metabolism and lactic

acidemia.
Subsequent analysis will depend on calculated values. The actual
bicarbonate (HC03 -)may be calculated, but levels will vary with changes
in PaC02 by compensation through action described by the carbonic acid
equation (Table 2), and more rapid analysis is made by evaluating the
calculated Base Excess (BE). Base Excess calculation accounts for the
effects of C02 on carbonic acid equilibrium and identifies nonrespiratory
causes of acid-base disorder. It will also assist in separation of simple
(primary) acid-base disorders and mixed acid-base disorders (see Fig. 1, Chart
1). Large decreases or increases in BE indicate nonrespiratory causes of
acidosis and alkalosis, respectively. The actual base excess can also be
calculated and takes into account the effect of actual or calculated
oxygen saturation on the buffering effectiveness of hemoglobin.
Blood gas analysis is required to ascertain the acid-base status of
animals, however, calculation of base excess is inherently flawed. The
standard Siggaard-Anderson alignment nomogram is based on hemoglobin

Table 2. RULES OF THUMB DESCRIBING ANTICIPATED COMPENSATION TO

SIMPLE (PRIMARY) DISORDERS

Primary
Simple (Primary) Disorder Change Anticipated Compensation

Respiratory acidosis (acute) 11PaC02 11PaC02 10 mmHg => UpH 0.05

11HCO,- 1-2 mEq/L
max. 4 mEq/L acutely
Respiratory acidosis (chronic) 11PaC02 11PaC0 2 10 mmHg => 11HCO,- 3-4 mEq/L
Respiratory alkalosis (acute) UPaC02 UPaC02 10 mmHg => 1lpH 0.1
UHC0 3 - 2-3 mEq/L
max. 6 mEq/L acutely
Respiratory alkalosis (chronic) UPaC02 UPaC02 10 mmHg => .U.HCO,- 5-6 mEq/L
Metabolic acidosis UHC0,- UHCO,- 1 mEq/L => UPaC02 1 mm Hg
Metabolic alkalosis 11HCO,- 11HC03 - 1 mEq/L => 11PaC02 1 mm Hg

Normal PaC0 2 = 40 mmHg. Normal HCO,- = 24 mEq/L. TC02 may be used as a rough estimate
of HCO,-. Compensation is described by the carbonic acid equation. The kidneys contribute significantly
to the process of compensation in chronic respiratory disorders (maximal effect in 5--6 days).
 PRACTICAL APPROACH TO ACID-BASE DISORDERS 651

at a constant oxygen saturation. Any increase in the oxygen concentra-

tion due to air bubbles or poor sample handling will cause calculated
base excess to decrease 0.3 mEq · L - 1 • g Hbsat · dl- 1 • Also, nomograms
for determination of base excess are based on human blood and exclude
the effects of plasma proteins and electrolytes on acid-base equilibrium.
Further analysis, such as anion gap calculation, is necessary for assess-
ment of complex acid-base disorders.

ANION GAP
What Can Blood Electrolyte Results Reveal Regarding
Acid-Base Homeostasis?
Determining the anion gap will assist in evaluating mixed acid-base
disorders. It can also be used to recognize an acid-base problem from
the serum chemistry panel, indicating the need for blood gas analysis.
The anion gap is the difference between the quantity of unmeasured
cations and unmeasured anions in the blood. Major unmeasured cations
include calcium and magnesium. Major unmeasured anions include
phosphates, sulfates, and organic acids (e.g., lactate, citrate, ketones).
Changes in the concentration of unmeasured cations necessary to cause
changes anion gap are incompatible with life. Therefore, anion gap is
used to identify changes in the concentration of unmeasured anions.
Also, increases in anion gap are more common than decreases, thus
anion gap is primarily used to identify metabolic acidosis. Because the
difference between the unmeasured cations and anions must equal the
sum of the measured cations and anions, the calculation is made from
the difference between the quantity of measured values. The major
measured cations are sodium (Na+) and potassium (K+). The major
measured anions are chloride (Cl-) and bicarbonate (HC03 -). Auto-
mated chemistry analyzers can provide Na +, K +, CI- and TC02 rapidly,
but some blood gas machines have electrodes for measuring the major
electrolytes as well. The value for TC02 is a reasonable estimate of
HC03 - and is frequently substituted for [HC03 -] in the equation: Anion
Gap= ([Na+] + [K+]) - ([Cl-] + [HC03 -]). When using TC02 be sure
to compare it to calculated HC03 - to catch any laboratory error. Normal
anion gap is 11 to 26 mEq/L for dogs and 13 to 24 mEq/L in cats. A
significant increase in anion gap most often indicates metabolic acidosis
(Fig. 1, Chart 2).
An increased anion gap is not an absolute indication of metabolic
acidosis. Check the pH to confirm the diagnosis. Next consider whether
or not the results are compatible with disease history of the animal.
Metabolic acidosis is associated with conditions such as diabetic ketoaci-
dosis, renal disease, acute diarrhea, and various intoxicants. Metabolic
alkalosis is associated with conditions such as vomiting and use of loop
or thiazide diuretics. Respiratory acidosis is associated with conditions
such as aspiration/ obstruction, pneumothorax, and use of narcotic anal-
gesics. Respiratory alkalosis is associated with conditions such as hypox-
emia, pulmonary disease, or septicemia. Consider a mixed acid-base
652 BAILEY & PABLO

disorder when the pH change is in the opposite direction of what would

be expected. Question the results if they do not fit the disease. Consider
sample error if there was any problem in blood collection.
Blood gas analysis and anion gap are useful tools for assessing an
animal's acid-base status, but may not identify all disorders. This is
particularly true when multiple counterbalance disorders exist. Such
mixed disturbances often occur in critically ill patients with failing
homeostatic mechanisms. A classic example of an animal with multiple
counterbalancing acid-base disorders is a dog with gastric dilatation-
volvulus. There may be lactic acidosis from stagnant hypoxia (and possi-
bly histotoxic hypoxia) simultaneous to metabolic alkalemia from acute
vomiting and sequestration of acid. Prompt identification of mixed acid-
base disorders is vital to proper therapeutic intervention. Blood gas and
anion gap are usually satisfactory tools for acid-base analysis. However,
they may fall short when additional problems such as hypoalbuminemia
exist, because they do not take into account the effect of plasma proteins
on buffering capacity. Alternative analysis may be useful for assessment
of highly complex acid-base disorders.

STEWART'S ANALYSIS
What Is Stewart's Acid-Base Analysis and How Is It
Performed?
Stewart's quantitative acid-base analysis is an alternative way of
viewing acid-base equilibrium. In the traditional approach to acid-base
disorders described earlier, the hydrogen ion and bicarbonate ion con-
centration are considered independent variables affected directly by disease
processes and mechanisms of homeostasis. Stewart's quantitative ap-
proach, on the other hand, involves applying fundamental physical
and chemical principles to acid-base equilibrium. 6 It is based on the
assumption that the hydrogen ion (and bicarbonate ion) concentration
are dependent variables reliant on the effects of four independent variables:
(1) strong ions, (2) weak nonvolatile acids (A,a1), (3) free water, and (4)
PC0 2 • Further, it is the interaction of these independent mechanisms,
not one single mechanism, that determines the acid-base state.
The effect of strong ions is calculated as the strong ion difference
(SID). Strong ion difference can be estimated as the difference between
mean normal [Na+] and the corrected [Cl-] (Fig. 2). The corrected [Cl-]
is determined by dividing the mean normal [Na+] by the [Na+] of the
animal and multiplying by the [Cl-] of the animal. Normally the SID is
positive. Increased SID produces nonrespiratory alkalosis and decreased
SID manifests as nonrespiratory acidosis (Fig. 2, Chart 3).
Free water affects [Na +] (the major strong cation) of the extracellular
fluid which in turn affects the SID.' It is calculated as the difference
between the [Na+] of the animal and the mean normal [Na+]. This value
is then multiplied by the normal SID divided by the normal mean [Na+]
(Fig. 2). In basic terms, it indicates the amount of water necessary to
return the sodium concentration to normal. Negative values (increased
 PRACTICAL APPROACH TO ACID-BASE DISORDERS 653

free water) suggest dilutional acidosis and positive values (decreased

free water) indicate concentration or contraction alkalosis (Fig. 2, Chart
3).
Chloride ion is the most important strong anion to consider. Changes
in [HC03 -] are dependent on changes in [o-]. Changes in chloride
concentration are calculated as the difference between mean normal
[Cl-] and the corrected [Cl-] (Fig. 2). Positive values suggest hypochlore-
mic alkalosis and negative values suggest hyperchloremic acidosis (Fig.
2, Chart 3). Other unmeasured anions (organic and inorganic acids) will
also affect the SID. Unmeasured anions (UA) make up the balance of
the BE and can be calculated as in Figure 2. Negative values (increased
unmeasured anions) suggests organic acidosis (Fig. 2, Chart 3).
Proteins are the largest constituent of the weak nonvolatile acids
(A1a 1), and albumin is the primary contributing protein. Abnormalities in
albumin can be calculated by subtracting the patient albumin from the
normal albumin and multiplying by a correlation factor of 3.7 (a decrease
plasma albumin 1 g/ dl will increase BE 3.7 mEq/L). Negative values
suggest hyperproteinemic acidosis and positive values denote hypopro-
teinemic alkalosis. Phosphorus is also a weak acid and supplemental
calculations (Fig. 2) may identify negative values signifying hyperphos-
phatemic acidosis (molecular weight of phosphorus is 30.974 g/mole; 1
mmole phosphate = 1.8 mEq phosphate).
The effect of PC0 2 on acid-base equilibrium was discussed in the
section on blood gases. Changes in PC02 indicate respiratory causes of
acid-base imbalance. Examining the BE will also assist in separation
of respiratory and nonrespiratory causes of acid-base disorder (Fig. 1,
Chart 1).
The complex polynomial equations of Stewart's quantitative acid-
base analysis have been modified and simplified for practical application
in Figure 2. Inexpensive computer programs are available that will
perform the simultaneous equations with greater precision and accuracy
and are an excellent teaching tool.* Even so, there are numerous assump-
tions that must be made in applying quantitative analysis. Several
"constants" are applied in these equations. The appropriateness of these
constants has been questioned, particularly when extrapolating across
species.

TREATMENT
Treatment of acid-base disorders should focus first and foremost on
any underlying disease process. The aim of any therapy is to return pH
to normal. Correction of the disease process may well be all that is
necessary to restore acid-base equilibrium. For example, metabolic acido-
sis from diabetic ketoacidosis would be treated with insulin and fluids.
Also, remedy of respiratory acidosis is accomplished by gradually elimi-
*ACIDBASICS, The Stewart Model of Acid-Base Relationships, Insight Services, Inc.
Copyright, Philip D. Watson, Ph.D., 1996.
a-
~

.A..:N'.A..LYSIS

mEq
SID -_ (N a+mean normal---mEq *
L _ CJ- corrected--- L = --L
mEq)
Na+ mEq
[ Cl- correctel---m{q = ( CJ- mEq X mean normal T )_ mEq]
patient--- L Na+ mEq - - - - L
patient T
Factors Contributing to Change in SID

11 H20 Free
SIDnormal ¥-q {N + mEq N + mEq ) mEq
- Na+ mEq a patient---T - a meannormai---T = ---T
mean normal T

11Cl- -_ (Cl- mean normal---mEq *

L _ CJ- corrected---mEq)
L -_ ---mEq
L
• 11 Unmeasured Anions = BE- ( 11 Free H20 + 11 Cl- + 11 Albumin+ 11PhosphoruseffectivJ = __m
1Eq
Factors Contributing to Change in Weak Acids (A101 )

11 Albumin = 3.7(AlbuminmeannormaJ--~f - Albuminpatient--~f) = --mLEq

!J. Phosphoruseffective = 1.8(/J.Phosphorusadjusted--m~ol) = __mLEq
[
11 Phosphorusadjusted = (Phosphorusmeannormal--~f - Phosphoruspatient--~f) = --~f J
= 0.3229(Phosphorusadjusted--~f) = _ _m~oi
Notes
 [CRART-31 Blood Gas

pH, P,C02 , BE

Respiratory Respiratory
Acidosis Alkalosis

Mean Normal Values

/Canine! /Feline I /Equine! /Bovine!

Na• mEq/L 149 155 139 140
Cl· mEq/L 114 121 101 99
Phos mg/dl 4.3 5.3 3.2 6.8
Alb mg/dl 3.1 2.2 3.5 3.5
SID mEq/L 35 34 38 41
pH units 7.37 7.32 7.41 7.42
From lhe Deparlment of Clinical Pathology. Unive~i~ of Aorida, Gainesvile, FL

Figure 2. Quantitative acid-base analysis.

a-
(11
(II
656 BAILEY & PABLO

nating the cause of hypoventilation. Treatment of respiratory causes of

acid-base disorder is directed at correcting the cause while supporting
ventilation. Acidosis with pH values less than 7.1 to 7.2 may lead to
significant cardiovascular depression. Sodium bicarbonate (NaHC03 )
can be administered to raise the pH above 7.2. The dose is roughly
calculated as NaHC0 3 mEq = body weight (kg) X 0.3 X base deficit
(mEq/1); where the extracellular fluid volume is estimated as 0.3 of the
body weight and 1 kilogram = 1 liter. The use of NaHC03 should be
avoided in respiratory acidosis because it will decrease respiratory drive
thus worsening any hypoxemia, may cause transient hypercapnia as
bicarbonate is converted to C02 and H 20, and alkalemia may develop
with resolution of hypoventilation. Complications associated with use
of NaHC0 3 include transient hypercapnia, paradoxical CSF acidosis,
leftward shift of the oxyhemoglobin dissociation curve leading to de-
creased downloading of oxygen, intracellular shift of potassium in ex-
change for hydrogen ions causing hypokalemia, transient hypernatremia
possibly inducing volume overload, tetany due to decreased ionized
calcium, late alkalosis as organic acids are metabolized producing addi-
tional bicarbonate, and overshoot alkalosis. Despite these potential com-
plications, use of bicarbonate may be necessary to stabilize the acid-base
status. Alternatively, tromethamine (THAM) can be used, providing
equal buffering capacity without transient hypernatremia or hypercap-
nia.2s
Treatment of metabolic alkalosis is also focused on the underlying
cause. For example, loss of acid through the gastrointestinal system can
be reduced by reducing secretion (e.g., cimetidine). Any alkalinizing
agents should be discontinued. Chloride may be provided in the form
of 0.45% to 0.9% NaCl solution (with added KCl) to treat chloride
responsive metabolic alkalosis. Treatment of respiratory alkalosis is di-
rected at eliminating the cause of hyperventilation and hypocapnia. For
example, hyperventilation induced by pain is treated with analgesic
agents.
When using the quantitative approach to acid-base disorders, treat-
ment is guided by SID and A 101• Treatment of acid-base disorders is still
focused on the underlying disease process first. The aim of further
therapy is to return SID and A101, and thus pH, to normal. For example,
in cases where volume expansion is desired, increased SID from hypo-
chloremic alkalosis is treated by infusion of 0.9% NaCl solution to lower
plasma SID (KCl is added if hypokalemic). If volume expansion is
not desired, nonsodium containing salts (e.g., KCl, CaCb), ammonium
chloride, or acetazolamide may be used to decrease SID. Hypoproteine-
mic (hypoalbuminemic) causes of alkalosis may be treated by instilling
plasma.
The pH should be considered prior to any therapeutic maneuver.
Multiple disease processes may be responsible for the observed pH. If
multiple disease processes are suspected, the effects of treatment should
be assessed simultaneously. Treating one disorder without considering
concurrent disorders may lead to dangerous shifts in acid-base status.
 PRACTICAL APPROACH TO ACID-BASE DISORDERS 657

Disorders that have additive effects such as respiratory acidosis with

metabolic acidosis may require more aggressive therapy than counterbal-
ancing disorders such as metabolic acidosis with respiratory alkalosis.

GLOSSARY

Acid: A substance that tends to dissociate in solution and release

hydrogen ions (protons); a proton (H+) donor. Volatile acid: an acid in
solution that depends on the concentration of one of its components in
the gas phase in contact with the solution. The only volatile acid of
clinical importance is carbonic acid (H2C03), and its concentration de-
pends on the amount of C02 in the alveoli and blood (see also carbonic
acid equation). Nonvolatile (Fixed) Acid: An acid that does not have
significant vapor pressure at body temperature. These acids, primarily
derived from protein metabolism, must be metabolized or excreted for
elimination. Lactic acid is an example.
Acidemia: An increase in the hydrogen ion concentration or a de-
crease in the pH of the blood; a blood pH below 7.35.
Acidosis: An increase in the hydrogen ion concentration or a de-
crease in the pH of the body as a whole. Acidosis does not necessarily
imply acidemia.
Actual Bicarbonate: The total C02 minus the C02 found as carbonic
acid and dissolved C02; the plasma bicarbonate content (mEq/L). De-
rived from the Henderson-Hasselbalch equation.
Alkalemia: A decrease in the hydrogen ion concentration or an
increase in the pH of the blood; a blood pH above 7.45.
Alkalosis: A decrease in the hydrogen ion concentration or an
increase in the pH of the body as a whole. Alkalosis does not necessarily
imply alkalemia.
Alpha-Stat Management: Treatment strategy during hypothermia
directed at maintaining PaC02 at 40 mmHg and pH at 7.4 as measured
in the blood gas analyzer at 37°C. The pH and PC02 are not corrected
for the actual patient temperature. This treatment strategy is directed at
maintaining the H+:OH- ratio, buffering and TC02 constant. (See also
pH-Stat Management).
Anion: A negatively charged ion. The major anions of the extracellu-
lar fluid are Cl-, HC03 -, plasma proteins, organic acid anions (lactate),
phosphate, and sulfate.
Anion Gap (Unmeasured Anions): The difference between the quan-
tity of unmeasured cations and unmeasured anions in the blood. An
increase in anion gap most often indicates metabolic acidosis. A misno-
mer in that there is no true gap as electroneutrality must be maintained.
Atot: The total amount of both dissociated and undissociated forms
of all weak acids. In plasma, the weak acids are proteins (primarily
albumin) and inorganic phosphate. Albumin constitutes most of Atot in
normal animals. Increases in Aot cause metabolic acidosis and decreases
in Atot cause metabolic alkalosis.
658 BAILEY & PABLO

Balanced Heparin: Calcium is added to the heparin in sufficient

quantity to fill the calcium binding sites of heparin (with no excess),
thus preventing changes in ionized calcium levels of samples.
Base: A substance that tends to bind hydrogen ions (protons) in
solution; a proton (H+) acceptor.
Base Excess (BE): The base concentration of whole blood (mEq/L).
Measurement is made under standard conditions (PC0 2 of 40 mmHg
and temperature of 37°C) by titrating the blood to a pH 7.4 using a
strong acid or a strong base. It can also be derived from a nomogram
if pH, PC02 and hemoglobin concentration are known. Base excess
calculations are inherently in error because they refer to human [HC03 -]
and nomogram (see also nomogram). For this reason BE may range from
- 4 to + 4 mEq/L in small animal patients and be considered normal.
Positive values indicate a deficit of noncarbonic acids; negative values
indicate an excess of noncarbonic acids. Standard Base Excess is the
concentration of titrable base of extracellular fluid. It is an in vivo
expression referring to a model of extracellular fluid and is calculated
using a standard value for hemoglobin concentration of the total extra-
cellular fluid (3 mmol/L). Actual Base Excess is the concentration of
titrable base of blood determined at standard conditions and at the
actual oxygen saturation.
Base Deficit: A negative Base Excess (BE).
Buffer: A substance that tends to preserve the original hydrogen ion
concentration ([H +]) in solution, maintaining pH despite an addition of
acid or base. Physiologic buffers act to minimize acute changes in acid-
base, but respiratory and metabolic mechanisms act to maintain acid-
base balance. The major buffer systems of the body are bicarbonate,
phosphate, a-amino serum proteins, ammonium, and hemoglobin.
Carbonic Acid: H 2C03; an unstable acid solution made by dissolving
C02 in H 20 (See also carbonic anhydrase and carbonic acid equation).
Carbonic Acid Equation: An equation describing the carbonic acid/
bicarbonate buffer system. C02 + H 20 ~ H 2C03 ~ H+ + OH- (See
also carbonic anhydrase).
Carbonic Anhydrase: An enzyme found in red blood cells, gastroin-
testinal mucosa, kidney tubules, and glandular epithelial cells that cata-
lyzes the reversible reaction of C02 and H 20 to form carbonic acid
(H2C03 ) as described in the carbonic acid equation.
Cation: A positively charged ion. The major cations of the extracel-
lular fluid areNa+, K+, Mg2 +, Ca2 +.
Compensation: Occurs when an abnormal pH is returned to normal
by changing an acid-base component other than the principal component
affected. Full Compensation occurs when the pH is normal, but other
components of acid-base are moved out of normal range in response to
the principal component affected. Partial Compensation occurs when the
pH is not returned to normal after other components of acid-base are
altered from normal range in response to the principal component af-
fected. However, the body will not overcompensate. For example, respi-
 PRACTICAL APPROACH TO ACID-BASE DISORDERS 659

ratory compensation for a metabolic acidosis will not overcompensate

and cause alkalosis.
Dependent Variables: Variables whose value is determined by the
system, other variables and the equation governing the system; internal
to the system.
Eucapnia: A normal amount of C02 in the blood; PaCOz = 35 to
45 mmHg.
FI0 2: Inspired oxygen fraction. Room air contains 21% oxygen and
provides an inspired oxygen fraction of 0.21.
Free Water: Extracellular fluid water without electrolytes. Increased
free water leads to dilutional acidosis and decreased free water leads to
concentration or contractional alkalosis.
Henderson-Hasselbalch Equation: A formula for calculating the re-
lationship of a buffer system. Applied in acid-base physiology to calcu-
late the carbonic acid/bicarbonate buffer system relationship. pH = pK
+ log ([HC03 - ] -:- [H2C03 ]). The equation is used to calculate actual
bicarbonate given measured values for pH and PC02 • The pK for this
system is 6.1. The term [H2C03 ] can be replaced by the terms a(PCOz),
where a is the solubility coefficient of C02 and equals 0.0301. Often
simplified for teaching purposes as pH = HC03 - -:- PaC02 = Kidney
function -:- Lung function.
Hypercapnia (Hypercarbia): An excessive amount of C02 in the
blood; PaC02 > 45 mmHg.
Hypocapnia (Hypocarbia): A deficiency of C02 in the blood; PaCOz
< 35mmHg.
Hypoxemia: Insufficient oxygenation of the blood; Pa02 < 60
mmHg.
Hypoxia: Relative lack of oxygen transported to or utilized by the
tissues. Anemic Hypoxia: Due to reduced hemoglobin content or function,
leading to reduced oxygen carrying capacity. Anoxic (hypoxic) Hypoxia:
Due to inadequate oxygenation of hemoglobin. Histotoxic Hypoxia: Due
to impaired tissue oxygen utilization. Stagnant (Ischemic) Hypoxia: Due
to inadequate oxygen transport to the tissues because of inadequate
blood flow.
Independent Variables: Variables not affected by changes in the
system, other variables or the equation governing the system; outside of
the system.
Metabolic Acidosis: A condition in which there is an accumulation
of nonvolatile acids (not C02 ) or loss of base from the body. It is
characterized by acidemia and compensatory increases in ventilation to
decrease the PC02 •
Metabolic Alkalosis: A condition in which there is an accumulation
base or loss of acid (but not loss of C02 ) from the body. It is characterized
by alkalemia and compensatory decreases in ventilation to increase
the PC02 •
Mixed Acid-Base Disorder: A combination of two simple (primary)
acid-base disturbances resulting in either an additive effect or a compen-
satory, neutralizing effect.
660 BAILEY & PABLO

Mixed Venous Blood: Pulmonary arterial blood.

Nomogram: A graphic illustration of interrelated values. A computa-
tion table for solving complex problems. Used to determine an unknown
variable given other related known variables. Siggaard-Anderson Align-
ment Nomogram: For interrelating base excess, total C02 and HC03 -
when pH and PC02 are measured. Singer-Hastings Nomogram: Also for
interrelating base excess, total C02 and HC03 - when pH, PC02 are
measured, but uses fully oxygenated blood values and correction scales
for venous blood.
Partial Pressure: The pressure a gas contributes to the total pressure
of a mixture of gases. Partial Pressure of Carbon Dioxide (PC02); Partial
Pressure of Oxygen (P02). An arterial or venous source are designated
by subscript letters "a" or "v", respectively.
pH: Defined as the negative log of the hydrogen ion concentration
([H+]). pH = -log [H+]. The pH varies inversely with the [H+]. An
increase in [H+] decreases pH, and a decrease in [H+] increases pH.
pH-Stat Management: Treatment strategy during hypothermia di-
rected at maintaining PaC02 at 40 mmHg and pH at 7.4 at the actual
body temperature. The pH and PC02 are corrected for temperature
when measured by the blood gas analyzer at 37°C (See also alpha-Stat
Management).
pK: The pH at which 50% of an acid or base is ionized.
Respiratory Acidosis: A condition in which the primary problem is
an accumulation of C02 in the body (PC02 > 45 mmHg). It is character-
ized by acidemia, an increase in PC0 2, and possible compensatory in-
crease in plasma bicarbonate with time.
Respiratory Alkalosis: A condition in which the primary problem
is excess elimination of C02 from the body (PC02 < 35 mmHg). It is
characterized by alkalemia, a decrease in PC02, and possible compensa-
tory decrease in plasma bicarbonate with time.
Simple (Primary) Acid-Base Disorder: Any of the four primary
acid-base disorders (respiratory acidosis, respiratory alkalosis, metabolic
acidosis, and metabolic alkalosis) with anticipated compensation.
Standard Bicarbonate: The plasma bicarbonate concentration (mEq/
L) after the whole blood sample is brought to 38°C and is equilibrated
with C02 to a PC02 of 40 mmHg. Because of the constant PC02, nonres-
piratory causes of acid-base balance can be identified.
Stewart's Quantitative Acid-Base Analysis: Application of funda-
mental physical and chemical principles to acid-base equilibrium. It is
based on the assumption that the hydrogen ion (and bicarbonate ion)
concentration are dependent variables reliant on four independent vari-
ables: (1) free water, (2) strong ions, (3) weak acid buffers, and (4) PC02 •
STP: Standard temperature (37°C) and barometric pressure (760
mmHg).
Strong Ions: The ions of salts that dissociate completely in water.
Principle measured strong ions are Na +, K + and Cl-. Other important
strong ions include Ca 2 +, Mg2 +, lactate, betahydroxybutyrate, acetoace-
tate, and sulfates.
 PRACTICAL APPROACH TO ACID-BASE DISORDERS 661

Strong Ion Difference (SID): The difference between all positive and
negative strong ions. SID = [Na+] + [K+] - [Cl-]. Increases in SID
usually indicate metabolic alkalosis and decreases in SID indicate meta-
bolic acidosis.
Total Carbon Dioxide (TC0 2 ): The amount of C02 in the blood or
plasma liberated with acidification of the sample (mEq/L). TC0 2 is
composed of bicarbonate (HC03 -) carbonic acid (H2C03 ) and carbon
dioxide (C0 2). A more clinically useful measurement is actual bicarbon-
ate.

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Address reprint requests to

James E. Bailey, DVM, MS
University of Florida
College of Veterinary Medicine
Department of Large Animal Clinical Sciences
P.O. Box 100136
Gainesville, FL 32610-0136