C o m p e n s a t i o n fo r

A c i d - B a s e D i s o rd e r s
a, b
Chiara De Caro Carella, DVM, MS *, Helio Autran de Morais, DVM, PhD

KEYWORDS
 Compensation  Acid-base  Ventilatory  Metabolic  Physiologic

KEY POINTS
 Hydrogen concentration is a critical determinant of many physiologic functions and is
tightly regulated.
 Any alteration in acid-base equilibrium sets into motion a compensatory response by
either the lungs or the kidneys.
 The compensatory response attempts to return the ratio between PCO2 and [HCO3 ] to
normal and thereby minimize the pH change.
 A primary increase or decrease in one component is associated with a predictable
compensatory change in the same direction in the other component, and the expected
compensation can be estimated clinically in dogs and cats.

THE CONCEPT OF COMPENSATION

Historically, simple acid-base disturbances, such as metabolic acidosis, respiratory

acidosis, metabolic alkalosis, and respiratory alkalosis, are used to classify patients’
acid-base status according to their primary origin. Primary respiratory disturbances
are usually produced by airway, pulmonary, and pleural cavity diseases, as well as
by neurologic, musculoskeletal, and restrictive extrapulmonary disorders, pain, and
anxiety. Iatrogenic respiratory acid-base disturbances may result from overzealous
or ineffective mechanical ventilation or administration of drugs, such as narcotics,
barbiturates, inhalational anesthetics, and neuromuscular blockers. All the aforemen-
tioned processes result in altered blood pH due to a primary increase or decrease in
partial pressure of carbon dioxide (PCO2), which is accompanied by an alteration in the
concentration of bicarbonate ([HCO3 ]). During compensation, [HCO3 ] moves in the
same direction of the alteration in PCO2. Primary metabolic disturbances are generally
the consequence of disease processes leading to alterations of the total concentration

The authors have nothing to disclose.

a
Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State
University, Baton Rouge, LA 70803, USA; b College of Veterinary Medicine, Oregon State
University, 700 Southwest 30th Street, Corvallis, OR 97331, USA
* Corresponding author.
E-mail address: cdecarocarella@lsu.edu

Vet Clin Small Anim - (2016) -–-

http://dx.doi.org/10.1016/j.cvsm.2016.11.003 vetsmall.theclinics.com
0195-5616/16/ª 2016 Elsevier Inc. All rights reserved.
2 De Caro Carella & de Morais

of weak acids ([Atot]) or strong ion difference (SID). This leads to alterations in pH and
[HCO3 ]. The secondary or adaptive response opposing the primary metabolic or res-
piratory disturbances, is referred to as compensation. Compensation is strictly regu-
lated by several physiologic mechanisms, with the essential goal of minimizing the pH
change caused by the primary disturbance. It is importance for [H1] (pH) to remain in
or near its physiologic range to preserve effective binding of hormones (eg, adrenaline,
insulin) to their specific receptors,1 maintain adequate myocardial contractility, and
preserve the ability of the brain to regulate its volume.2 Acid-base homeostasis is pre-
served under physiologic conditions by the harmonic collaboration of several “stake-
holders,” such as lungs (regulation of PCO2), kidneys (reabsorption and excretion of
H1), liver (synthesis of proteins that act as buffers), gastrointestinal system (absorption
and excretion of electrolytes, acids, and bases), and bone (storage of calcium carbon-
ate and phosphate).
The terms acidosis and acidemia, or alkalosis and alkalemia, are not synonyms.
Consider the case of a dog with chronic respiratory alkalosis whose arterial pH is
normal: alkalosis is the respiratory pathophysiologic process that induces net loss
of volatile acids in the body, whereas alkalemia is the actual blood pH, which is normal
due to the effective compensatory response in chronic respiratory alkalosis. The
magnitude of the compensation for primary acid-base disorders can be estimated
in dogs and cats. If the compensatory response exceeds or falls short of that ex-
pected, the presence of a mixed acid-base disorder should be investigated.2 A mixed
acid-base disturbance is characterized by the coexistence of 2 or more primary dis-
orders affecting the patient’s acid-base status.

PHYSIOLOGY OF COMPENSATION

Carbon dioxide and buffers are the 2 main players responsible for preventing great os-
cillations in pH. The PCO2 is efficiently titrated by alveolar ventilation, which is controlled
by neural pathways regulating respiratory muscle activity, and therefore alveolar venti-
lation. These pathways originate in the respiratory centers of the medulla and are net-
worked with the pons, the cerebellum, and the forebrain to act in concert to regulate
respiratory patterns. These structures are interconnected with medullary modulatory
projections, as well as with chemo and mechanoreceptors located in the aortic and ca-
rotid bodies, and within the central nervous system (CNS).2 Altogether, they form a
complex sensory system that provides efferent information regarding changes in
PCO2 and PO2, allowing adaptation of the respiratory system to maintain homeostasis.
Chemoreceptors appear to possess variable sensitivity to oxygen and CO2. The ca-
rotid bodies, located at the bifurcation of the internal and external carotid arteries
are mainly responsive to variation in arterial partial pressure of oxygen (PaO2) and
are responsible for the hypoxic respiratory drive that accompanies hypoxemia
(PaO2 <60 mm Hg). These receptors are responsible for 90% of the increase in minute
ventilation3 that occurs during hypoxemia and can also sense pH and PCO2. The aortic
bodies are found within the aortic arch, and are most sensitive to variation in PO2 and
have limited importance in maintaining homeostasis during normal ventilation.4 The
CO2 and pH-sensitive chemoreceptors are mainly located within several structures
of the CNS, such as the retrotrapezoid nucleus, the raphe nuclei, the locus coeruleus,
the nucleus of the solitary tract, the pre-Bötzinger complex, and the cerebellar fastigial
nucleus.3 These receptors are so sensitive to changes in PCO2 that an increase of 1 mm
Hg in PCO2 increases minute ventilation by 20% to 30%.5
Buffers can be classified as bicarbonate (HCO3 ) and nonbicarbonate (eg, proteins,
phosphates, calcium carbonate), as well as extracellular (eg, HCO3 , hemoglobin,
 Compensation for Acid-Base Disorders 3

plasma proteins, and phosphates) and intracellular (eg, proteins such as histidine res-
idues). The efficacy of a given buffer in the body is dictated by 3 factors: (1) its abun-
dance in a given environment (intracellular and extracellular), (2) its dissociation
constant (pKa), and (3) the prevailing hydrogen ion concentration ([H1]).
Time is an important variable in compensation. The secondary respiratory response
carried by the lungs to a primary metabolic disorder occurs in minutes due to the volatile
nature of CO2, and it reaches its greatest efficacy within hours. On the other hand,
the secondary metabolic response carried by the kidneys to a primary respiratory distur-
bance does not reach its maximum before 2 to 5 days. Compensation rules are applicable
only after enough time has ensued to allow for full compensation to have occurred. Thus,
it is important to take into account the time of first occurrence of the pathologic process
before concluding that a mixed acid-base disorder is present.2
In general, it is safe to assume that if PCO2 and [HCO3 ] change toward the same
direction in all simple disorders, a mixed acid-base disorder is present whenever
PCO2 and [HCO3 ] are changing in opposite directions (one increases and the other
decreases). In the latter case, the resulting effect on pH is more intense6 because of
the potential additive synergism on pH from the coexisting disorders. A summary of
the guidelines for adequate use of compensatory rules is provided in Table 1. Some
guidelines for use of rules presented in Table 1 are presented in Box 1.

Metabolic Acidosis
Metabolic acidosis was the most common acid-base disorder in dogs and cats in a
few studies.7,8 Several disease processes can lead to this disturbance; the most com-
mon are diarrhea, hypoadrenocorticism, diabetic ketoacidosis, and lactic and uremic
acidosis. Metabolic acidosis can occur due to (1) loss of HCO3 -rich fluid of the body
(diarrhea), (2) addition to a fixed acid, or (3) lack of excretion of fixed acid by kidneys.2
Metabolic acidosis is characterized by a primary decrease in plasma [HCO3 ], in-
crease in plasma [H1], decrease in blood pH, and a compensatory decrease in
PCO2. The compensatory response to metabolic acidosis is predominantly an increase
in ventilation, leading to a decrease in PCO2, and minimizing pH changes. Increase in
renal ammoniagenesis also helps by increasing [HCO3 ]. The secondary adaptive
mechanisms in metabolic acidosis consists of 3 parts: body buffer, respiratory, and
renal responses. During the body buffer response, between 40% and 50% of the
acute acid load is buffered by intracellular buffers (proteins and phosphates),9–11
40% by extracellular HCO3 , and 10% by red cell buffers (hemoglobin) in nephrec-
tomized dogs.11 Intracellular buffer seems to contribute approximately 50% of the
buffer response in non-nephrectomized dogs.12 The combination of H1 with HCO3
ions generates CO2, which activates peripheral and central chemoreceptors, inducing
an increase in alveolar ventilation. The body buffer response is complete in approxi-
mately 30 minutes, with interstitial fluid receiving the acid load, and intracellular space
receiving H1 in exchange for Na1 and K1 ions. The respiratory response starts with
the increase in H1 and PCO2 by increasing alveolar ventilation, which induces a hypo-
capnic state (decreased PCO2). Hypocapnia minimizes changes in pH. In dogs, for
each 1 mEq/L decrease in [HCO3 ], a decrease in 0.7 mm Hg in PCO2 is expected.9
The respiratory pattern associated with metabolic acidosis in human beings, Kuss-
maul ventilation with deep and rhythmic chest excursions, is not commonly observed
in small animals. During chronic metabolic acidosis, secondary hypocapnia has
been shown to further reduce plasma [HCO3 ] by decreasing renal reabsorption of
HCO3 and [HCO3 ] to close to 40%.13 The renal response to an acute acid load is
aimed to excrete fixed acids from the body by increasing ammoniagenesis. Renal
ammoniagenesis uses glutamine as the primary metabolic substrate, generating
4 De Caro Carella & de Morais

Table 1
Compensatory response in simple acid-base disorders in dogs and cats

Expected Expected
pH Primary Compensatory Compensatory
Disorder Origin Timing Change Response in Canine Response in Felinea
Acidosis Metabolic Y [HCO3 ] 1.0 mm Hg PCO2 does not
decrement in PCO2 change
for each 1 mEq/L
decrement in
[HCO3 ]
Respiratory Acute [ PCO2 0.15 mEq/L 0.15 mEq/L
increment in increment in
[HCO3 ] for each [HCO3 ] for each
1 mm Hg 1 mm Hg
increment in PCO2 increment in PCO2
Chronic [ PCO2 0.35 mEq/L Unknown
increment in
[HCO3 ] for each
1 mm Hg
increment in PCO2
Long-standing [ PCO2 0.55 mEq/L Unknown
(>30 d) increment in
[HCO3 ] for each
1 mm Hg
increment in PCO2
Alkalosis Metabolic [ [HCO3 ] 0.7 mm Hg 0.7 mm Hg
increment in PCO2 increment in PCO2
for each 1 mEq/L for each 1 mEq/L
increment in increment in
[HCO3 ] [HCO3 ]
Respiratory Acute Y PCO2 0.25 mEq/L 0.25 mEq/L
decrement in decrement in
[HCO3 ] for each [HCO3 ] for each
1 mm Hg 1 mm Hg
decrement in PCO2 decrement in PCO2
Chronic Y PCO2 0.55 mEq/L 0.55 mEq/L
decrement in decrement in
[HCO3 ] for each [HCO3 ] for each
1 mm Hg 1 mm Hg
decrement in PCO2 decrement in
PCO2b
a
Data from limited number of cats.
b
Similar to dogs. Exact degree has not been determined, but cats with chronic respiratory alkalosis
tend to maintain normal arterial pH.
From de Morais HSA, Leisewitz A. Mixed acid-base disorders. In: DiBartola SP, editor. Fluid, elec-
trolyte, and acid-base disorders. 4th edition. Elsevier: Philadelphia; 2011. p. 304; with permission.

equivalent amounts of NH41 and HCO3 . The produced HCO3 is preferentially trans-
ported across the basolateral plasma membrane, absorbed into peritubular capil-
laries, and returned to the systemic circulation. The net result is an increase in
NH41 and Cl excretion, accompanied by an increase HCO3 regeneration moving
extracellular [HCO3 ] toward normal. In cats, renal proximal tubules do not increase
production of ammonia or glucose from glutamine during acidosis and renal excretion
of ammonia does not change much during acidosis.14
Secondary ventilatory compensation seems to be absent in the domestic cats with
spontaneous or experimentally induced metabolic acidosis.14–19 Therefore, formulas
 Compensation for Acid-Base Disorders 5

Box 1
Guidelines for adequate use of compensatory rules from Table 1

Time
Sufficient time must elapse for compensation to reach steady-state:
 Acute respiratory disorders: 15 minutes
 Chronic respiratory disorders: 7 days
 Long-standing respiratory acidosis: 30 days
 Metabolic disorders: 24 hours
pH
Compensation does not return the pH to normala
Overcompensation does not occur
Values in the Expected Compensatory Range
Do not prove that there is only one disturbance
Provide support for a simple acid-base disturbance, if consistent with the remaining clinical
data
a
Exceptions: chronic respiratory alkalosis (>14 days), and potentially long-standing respira-
tory acidosis (>30 days).
From de Morais HSA, Leisewitz A. Mixed acid-base disorders. In: DiBartola SP, editor. Fluid,
electrolyte, and acid-base disorders. 3rd edition. Elsevier: Philadelphia; 2006. p. 296; with
permission.

to calculate compensation in humans and dogs should not be extrapolated to cats,

and finding a normal PCO2 in the presence of metabolic acidosis should prompt the
diagnosis of a mixed disorder in cats. It is also important to allow enough time for
compensation to occur before using formulas in Table 1. The respiratory response
to metabolic acidosis takes at least 17 to 24 hours to fully develop.9 Therefore, appli-
cation of the formula to calculate compensation during the first 24 hours from onset of
the acidosis can lead to underestimation of the secondary response, and to the incor-
rect conclusion that a mixed disorder is present.

Metabolic Alkalosis
Metabolic alkalosis is less common than metabolic acidosis in dogs and cats,7,20 and
usually results from loss of gastric fluid or therapy with diuretics. It also may occur in
hyperadrenocorticism, hyperaldosteronism, or from excessive administration of
NaHCO3. Mechanistically, metabolic alkalosis can result from (1) loss of chloride-
rich fluids (via gastrointestinal tract or kidneys), and (2) chronic administration of al-
kalis.2 The latter does not lead to metabolic alkalosis if renal function is normal due
to very good ability of the kidneys to eliminate these compounds. Metabolic alkalosis
is characterized by a primary increase in plasma [HCO3 ], decrease in plasma [H1],
increase in blood pH, and a compensatory increase in PCO2.
The compensatory response to metabolic alkalosis is predominantly a decrease in
ventilation, leading to an increase in PCO2, and minimizing pH changes. The initial
response is the acute buffer response, with approximately 32% of the alkali load buff-
ered by intracellular buffers, whereas 68% moved to the extracellular fluid (ECF) in
nephrectomized dogs.21 The decrease in plasma [H1] also stimulates peripheral
and central chemoreceptors leading to a decrease in alveolar ventilation. For each
1 mEq/L increase in [HCO3 ], an increase of 0.7 mm Hg in PCO2 is expected in dogs
and cats.2,10,22–26 Mild hypoxemia has been observed in experimentally induced
metabolic alkalosis in dogs22 (arterial PO2 5 60–70 mm Hg). Severe hypoxemia can
6 De Caro Carella & de Morais

lead to hypoxic-driven ventilation, a defense mechanism that impedes the total aboli-
tion of the ventilatory stimulus. The respiratory pattern of humans with metabolic alka-
losis can be slow and shallow, although this respiratory pattern is less predictable than
the one seen in metabolic acidosis.27 The renal response to an acute alkali load (or
Cl loss) is aimed to excrete HCO3 from the body. Because kidneys are extremely
efficient in excreting HCO3 , metabolic alkalosis persists only if the glomerular filtra-
tion rate is impaired in patients with low Cl concentration, if alkalis are administered
continuously, or if Na1 is retained by the kidney in the face of hypochloremia.2
Maximum respiratory compensation may take up to 24 hours to develop. Caution
must be exercised when using formulas for calculating expected compensation before
time has elapsed for full compensation to be present.

Respiratory Acidosis
Respiratory acidosis (or primary hypercapnia) is characterized by increase in PCO2,
increase in [H1], and a decrease in pH, with a compensatory increase in [HCO3 ].
The acute phase of the compensatory response to respiratory acidosis occurs within
15 minutes and consists of titration of nonbicarbonate buffers. The second phase is
the renal compensation that starts concomitantly with the first phase and is not fully
completed before 2 to 5 days. The kidneys increase the net excretion of acids,
increasing HCO3 reabsorption while decreasing Cl reabsorption. From a compen-
satory perspective, respiratory acidoses can be divided into acute and chronic. In
acute respiratory acidosis, CO2 concentration raises intracellularly, increasing
[HCO3 ] because of the increased dissociation of the newly formed carbonic acid
(H2CO3) into HCO3 and H1. Bicarbonate ions are then released from the erythrocytes
in exchange for Cl . Intracellular buffers are capable of managing up to 97% of the H1
acute load in canines,28,29 with the remaining 3% being buffered by extracellular
buffers. The compensatory response of [HCO3 ] in acute respiratory acidosis in
dogs has been estimated as a 0.15-mEq/L increase for each 1 mm Hg of PCO2.9
Although there is paucity in experimental data, compensation in cats with acute
respiratory acidosis is similar to the one in dogs. In anesthetized and mechanically
ventilated cats made hypercarbic, a compensatory increase in [HCO3 ] of 0.07 to
0.1 mEq/L was observed for each 1–mm Hg increase in PCO2.30 Conscious cats
exposed to a FiCO2 of 4% showed an increase in [HCO3 ] of 0.16 mEq/L per each
1 mm Hg of increase in PCO2, which resembles the canine response to hypercarbia.31
During chronic respiratory acidosis, renal adaptation increases [HCO3 ], reaching a
steady-state within 5 days.32 Hydrogen ions accumulating in the renal tubular cells
are exchanged for Na1 and excreted as NH41Cl .33 Chloride ions are excreted,
whereas HCO3 is reabsorbed, leading to hypochloremia, increase in SID, moving
plasma pH toward the reference range,2 although this fails to return to completely
normal.34 An increase in [HCO3 ] of 0.35 mEq/L is expected per each 1 mm Hg in
PCO29 in dogs. In situations in which the respiratory acidosis lasts for more than 30
consecutive days, pH may return to normal in humans.35 This has been called long-
standing respiratory acidosis and also has been observed in dogs, with changes in
[HCO3 ] up to 0.55 mEq/L per 1 mm Hg of increase in PCO2.2,36 It is not currently
known if cats with long-standing respiratory acidosis may have normal blood pH.

Respiratory Alkalosis
Respiratory alkalosis (or primary hypocapnia) is characterized by decrease in PCO2,
decrease in [H1] and an increase in pH, with a compensatory decrease in [HCO3 ].
It occurs when alveolar ventilation is increased and an excessive amount of CO2 is
eliminated. The first phase of the compensatory response to acute respiratory
 Compensation for Acid-Base Disorders 7

alkalosis occurs within 15 minutes, when H1 is released from intracellular nonbicar-

bonate buffers. In the second phase, the kidneys increase net acid excretion, with
an increase in HCO3 reabsorption and a decrease in Cl reabsorption. The renal
adaptation may take 2 to 5 days to achieve the steady-state.37–39 In dogs with acute
respiratory alkalosis, a compensatory decrease of 0.25 mEq/L in [HCO3 ] accom-
panies each 1–mm Hg decrease in PCO2.9 In cats, this response has been studied
only under general anesthesia, where a decrease in HCO3 of 0.26 mEq/L for each
1–mm Hg decrease in PCO2 was observed.40 In dogs with chronic respiratory alkalosis,
a decrease in [HCO3 ] of 0.55 mEq/L is expected for each 1–mm Hg decrease in
PCO2.9,41 In this disturbance, pH usually returns to the reference range within 5 to
7 days for dogs9 and 14 days in humans.42 Although experimental data are not avail-
able for cats, compensation appears to be similar to the ones seen in dogs.2

Calculation of Expected Compensation

Calculation of the expected compensatory acid-base response using the formulas in
Table 1 allows characterization of acid-base disorders as simple or mixed. A mixed
acid-base disorder occurs whenever 2 or more primary acid-base disorders are pre-
sent in the same patient.2 A respiratory acid-base disorder is considered to be a sim-
ple disorder (respiratory acidosis or respiratory alkalosis) if the calculated expected
[HCO3 ] falls within 2 mEq/L of the patient’s [HCO3 ]. If the difference is greater
than 2 mEq/L, the patient likely has a primary metabolic acid-base disorder in addition
to the primary respiratory acid-base problem (mixed disorder). A metabolic acid-base
disorder is considered to be a simple disorder (metabolic acidosis or metabolic alka-
losis) if the calculated expected PCO2 falls within 2 mm Hg of the patient’s PCO2, other-
wise the patient has a mixed acid-base disorder with a primary respiratory and a
primary metabolic acid-base disorder. Compensatory rules should be used with
care in cats, because they were derived from a limited number of cats. A cat with
metabolic acidosis and with PCO2 within the reference range is considered to have a
simple acid-base disorder, whereas cats with PCO2 outside the reference range are
considered to have a mixed disorder with a primary metabolic acidosis and a primary
respiratory alkalosis if PCO2 is below the reference range or a primary respiratory
acidosis if PCO2 is above the reference range.
Estimation of the compensatory response is performed by using the midpoint in the
reference range for the analytes. For instance, if the reference range for [HCO3 ] varies
from 19 to 23 mEq/L, the corresponding midpoint would be 21 mEq/L, whereas the
midpoint would be 36 mm Hg for a PCO2 reference range between 31 and 41 mm
Hg. Midpoint should be established based on the reference values provided by the
laboratory being used. The following is a stepwise approach to estimate compensa-
tion in acid-base disorders:
1. Establish the primary acid-base disorders (the one changing in the direction pre-
dicted by the patient’s pH)
2. Estimate the expected compensation. If the primary disorder is respiratory, ex-
pected [HCO3 ] should be calculated, whereas in a primary metabolic disorder, ex-
pected PCO2 should be estimated.
a. Calculate the change in the patient’s primary parameter (D[HCO3 ] in patients
with a primary metabolic disorder; DPCO2 in patients with primary respiratory dis-
order): D[HCO3 ] 5 Patient’s [HCO3 ] midpoint [HCO3 ] or DPCO2 5 Patient’s
PCO2 midpoint PCO2.
b. Calculate the change in the secondary parameter. For metabolic acid-base dis-
orders, multiply the DPCO2 by 0.7 in dogs and cats with metabolic alkalosis and
8 De Caro Carella & de Morais

in dogs with metabolic acidosis. For respiratory acid-base disorders, multiply

DHCO3 by the factor presented in Table 1 for the disturbance in question
(eg, 0.15 for dogs and cats with acute respiratory acidosis).
c. Calculate the expected compensation by adding the change in the secondary
parameter to the midpoint HCO3 (primary respiratory disorder) or PCO2 (primary
metabolic disorder): PCO2expected (mm Hg) 5 36 1 calculated change in the sec-
ondary parameter or [HCO3 expected] (mEq/L) 5 21 1 calculated change in the
secondary parameter.
If the patient’s PCO2 or [HCO3 ] differs from the PCO2expected or the [HCO3 expected]
by more than 2 mm Hg or 2 mEq/L, respectively, the patient likely has more than 1 pri-
mary acid-base disorder. The presence of a coexisting acid-base disorder must be
suspected.
Two case examples displaying calculation of expected compensation in acid-base
disorders are provided in Box 2. Midpoint reference values of 21 mEq/L for [HCO3 ]
and 36 mm Hg for PCO2 were used in the calculations.

Box 2
Case examples

Case 1: 7-year-old dog with chronic respiratory disorder

 pH 5 7.31
 PCO2 5 47 mm Hg
 [HCO3 ] 5 23 mEq/L
1. Primary disorder: respiratory acidosis (chronic based on history)
2. Compensation:
a. Calculate change in the primary parameter
i. DPCO2 5 47 36 5 11 mm Hg
b. Calculate change in the secondary parameter (DPCO2  0.35)
i. 11  0.7 5 3.85
c. Calculate the expected compensation
i. [HCO3 expected] 5 21 1 3.85 5 24.85
ii. [HCO3 expected] range: 22.85 to 26.85
3. Conclusion: Patient [HCO3 ] (23 mEq/L) falls inside the range for [HCO3 expected] 5 >
simple acid-base disorder
a. Diagnosis: Simple chronic respiratory acidosis
Case 2: 12-year-old dog with chronic heart disease
 pH 5 7.34
 PCO2 5 27 mm Hg
 [HCO3 ] 5 14 mEq/L
4. Primary disorder: metabolic acidosis
5. Compensation:
a. Calculate change in the primary parameter
i. D[HCO3 ] 5 14 21 5 7 mm Hg
b. Calculate change in the secondary parameter (D[HCO3 ]  0.7)
i. 7  0.7 5 4.9
c. Calculate the expected compensation
i. PCO2expected 5 36 4.9 5 31.1
ii. PCO2expected range: 29.1 to 33.1
6. Conclusion: Patient PCO2 (27 mm Hg) falls below the range for PCO2expected 5 > primary
respiratory alkalosis
a. Diagnosis: Mixed acid-base disorder: primary metabolic alkalosis and primary
respiratory alkalosis
 Compensation for Acid-Base Disorders 9

Hydrogen concentration is a critical determinant of many physiologic functions and is

tightly regulated. Any alteration in acid-base equilibrium sets into motion a compensa-
tory response by either the lungs or the kidneys. The compensatory response attempts
to return the ratio between PCO2 and [HCO3 ] to normal and thereby minimize the pH
change. Those responses tend to be consistent in different studies in dogs and cats.
Thus, a primary increase or decrease in one component is associated with a predictable
compensatory change in the same direction in the other component, and the expected
compensation can be estimated clinically in dogs and cats. Lack of appropriate
compensation is evidence of a mixed acid-base disorder. Compensation is said to be
inappropriate if a patient’s PCO2 differs from expected PCO2 by more than 2 mm Hg in
a primary metabolic process or if a patient’s [HCO3 ] differs from the expected
[HCO3 ] by more than 2 mEq/L in a respiratory acid-base disorder.

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