Acid-Base Principles and Practical Interpretation in Small Animals

W S A V A W C P , 2005
Luis Núñez Ochoa
Facultad de Medicina Veterinaria y Zootecnia
Unam, Mexico

The body maintains a balance of acids and bases in order to constantly maintain
blood pH within a narrow range, despite the continuous generation of metabolic
products. In turn, this allows the body to maintain cell enzyme systems in good
operation conditions, together with the proper concentration of ionized (active)
forms of various electrolytes such as Ca++ and Mg++. This influences the speed of
metabolic reactions and trans-membrane transportation systems
(pharmacokinetics and pharmacodynamics).
In veterinary medicine, acid-base disorders are common, since they appear in
frequently found conditions such as diarrhea, vomiting, renal insufficiency,
dehydration, anesthesia, pneumonia, or diseases with restricted pulmonary
expansion (effusion, traumatisms, hernia, tumors, etc.). Disease typically results in
altered local/systemic pH, due to electrolyte/water/CO2 movements. In order to
establish the appropriate therapy, electrolyte variations should be interpreted
considering self physiologic basics in association with clinical findings.
Several mechanisms exist that maintain this equilibrium between acids and bases,
resulting in a pH level within the reference range:
1.  Extracellular mechanism. This includes several buffers that either accept or
release protons (H+). Therefore, they minimize pH alterations such as
plasma protein, bicarbonate (HCO3-), phosphates, etc. Its operation is
immediate.
2.  Intracellular mechanism. Represented by proteins, hemoglobin,
organic/inorganic phosphates. It is immediate.
3.  Transcellular mechanism. It is mainly produced by K+/H+ ion exchange. It is
immediate.
4.  Respiratory mechanism. Enhancing the retention or elimination of PCO2 (as
a representative of carbonic acid, in other words, "volatile acids". Its
activation is relatively immediate.
H++ HCO3-↔ H2CO3 ↔ H2O+ CO2 (elimination)
5.  Renal mechanism (through the excretion or retention of H+ and HCO3-. In
other words, non-volatile acids. This is the longest-lasting mechanism,
since it starts in approximately 12-24 hours, and reaches its maximum
compensatory efficiency peaks in 2-5 days).
NaHCO3 + HCl (a non-volatile acid) ↔ NaCl + H2CO3 ↔ H2O+ CO2
DEFINITIONS

pH. Is the negative logarithm of H+ (ratio is inverse, i.e., the higher the H+ ion
concentration the lower the pH. The lower the H+ ion concentration the higher the
pH). pH is determined by the PCO2 : HCO3- ratio.
pH = 6.1+ log (HCO3-/ 0.03PCO2)
Where: 6.1 is the dissociation constant of carbonic acid in body fluids, 0.03 is the
CO2 solubility constant (as a conventional evaluation of H2CO3).
Acidemia. Decreased blood pH as compared to reference values.
Acidosis. A process that involves a gain of acids, a loss of bicarbonate, or
both.This results in decreased pH.
Metabolic acidosis. This is the most frequent process. It is characterized by a
non-volatile acid gain (mainly lactic acid) or a bicarbonate loss, or both, with an
incomplete physiological respiratory compensation (PCO2 or hypocapnia). This
results in decreased pH.
Respiratory acidosis. This process is characterized by alveolar hypoventilation
that results in increased PCO2 (hypercapnia) caused by obstruction of the airways,
depression of the breathing center (trauma, or drugs) breathing restrictive
processes (thoracic effusion, pneumothorax, diaphragmatic hernia, abdominal
distension and fractures or lesions of the thoracic walls), pulmonary disease, or a
mixture of two or more causes.
Alkalemia. Increased blood pH as compared to reference values.
Alkalosis. A process characterized by a chlorine loss or decreased PCO2. This
results in increased pH.
Metabolic alkalosis. A process that involves a chlorine loss or increased HCO3-
(due to excess therapy), with an incomplete physiologic respiratory compensation
(chemoreceptors of the breathing center detect the alkalosis and respond with
hypoventilation that results in increased PCO2 [0.7 mm Hg for each mmol/L] that
increases HCO3-). This results in increased pH. The most frequent causes are
vomit or sequestration of chlorine in the stomach in cases of torsion. Other
causes include the use of furosemide or mineralocorticoids.
Respiratory alkalosis. This is the least frequent pH disorder. It is characterized
by alveolar hyperventilation that results in decreased PCO2 levels (hypocapnia)
caused by hypoxemia, direct stimulation of the breathing center, stimulation of the
nociceptive (pain sensitive) receptors, as in pulmonary edema, pneumonia,
embolism, etc. It is accompanied by an incomplete physiological metabolic
compensation (HCO3- ).
Metabolic. A problem that results from a primary alteration in H+ or HCO3-.
Respiratory. A problem that results from a primary PCO2 change due to an
alteration in CO2 elimination.
Buffers. Substances that accept or release protons (H+). They minimize pH
changes such as plasma proteins, bicarbonate, phosphates, hemoglobin, etc.
PCO2 represents H2CO3 as a respiratory component of the acid-base balance.
TCO2 is the total amount ofCO2 that can be extracted from plasma. It includes
dissolved CO2 and HCO3-, where H2CO3 and CO2 represent 5% of the total, while
HCO3- is the remaining 95%. Therefore, TCO2 is considered as an acceptable mean
of HCO3- minus 1-2 mmol/L in normal individuals.
Base excess or deficit (BE+ or BE-). This represents only the metabolic
component of changes in non-volatile acids or bicarbonate, since it is estimated
under ideal conditions. In other words, with a PCO2 of 40 mm Hg, a temperature of
38°C, and the buffering capacity of hemoglobin is not considered.
Reference values are typically maintained at 0 ± 3.
Values >3 = metabolic alkalosis; <- 3 = metabolic acidosis
If this value is positive, the animal does not require a bicarbonate therapy, since an
excess exists. In animals with negative values, the need to correct the acid-base
imbalance can be calculated using the following equation:
HCO3- dose (mmol/L)= 0.3 (treatable space) X weight in kg X BE (mmol/L)
Treatable space = extracellular fluid. Some authors consider it to be 20%.
Example: a 20 kg dog with a BE of-27 (hence a base deficit), therefore:
HCO3- dose (mmol/L) = 0.3 X 20 kg X 27
HCO3- need (mmol/L) = 162 mmol
Expected physiologic compensation. It is important to determine if the
compensation is adequate or not. The following values are valid for dogs. (Cat
values need to be further verified.)
 In metabolic acidosis, for each mmol/L that the HCO3- decreases, a PCO2
decrease of 0.7 mmHg is expected.
 In metabolic alkalosis, for each mmol/L that HCO3- increases a PCO2
increase of 0.7 mmHg is expected.
 In chronic respiratory acidosis, for each mmHg that the PCO2 increases, there
will be a HCO3- increase of 0.35.
 In chronic respiratory alkalosis, for each mmHg that the PCO2 decreases, a
HCO3- decrease of 0.55 will occur.
Evaluation of blood pH/gases

The theory presented in the paragraphs above, will be explained using some
examples:
SIMPLE ACID-BASE DISORDERS

Results Interpretation Reference

pH 7.2 Acidemia 7.35-7.46

PCO2 62 Respiratory acidosis (hypercapnia) 26-42

HCO3- 30 Physiological metabolic compensation 18-24

BE +12 Chronic process, because this (-) 3-(+) 3

compensation takes more than 12-24
hours

Metabolic compensation: 62-42= 20 (PCO2); 20 X 0.35= 7; 24+7= 31

Example: pneumonia.

Results Interpretation Reference

pH 7.2 Acidemia 7.35-7.46

PCO2 23 Physiological respiratory 26-42

compensation

HCO3- 15 Metabolic acidosis 18-24

BE -10 Base deficit due to loss or to its (-) 3-(+) 3
buffering function

Example: diarrhea.

Results Interpretation Reference

pH 7.5 Alkalemia 7.35-7.46

PCO2 52 Physiological respiratory 26-42

compensation (hypercapnia)

HCO3- 37 Metabolic alkalosis 18-24

BE +12 Base excess as a result of chlorine (-) 3-(+) 3

loss

Example: vomiting.

Results Interpretation Reference

pH 7.5 Alkalemia 7.35-7.46

PCO2 20 Respiratory alkalosis (hypocapnia) 26-42

HCO3- 15 Physiological metabolic compensation 18-24

BE +12 Base excess (-) 3-(+) 3

Example: fear, pain, toxins, etc.

MIXED ACID-BASE DISORDERS

Results Interpretation Reference

pH 7.4 Normal 7.35-7.46

PCO2 62 Respiratory acidosis (hypercapnia) 26-42

HCO3- 37 Metabolic alkalosis 18-24

BE +12 Base excess as a result of chlorine (-) 3-(+) 3

loss.

Expected metabolic compensation: 62-42= 20 (PCO2); 20 X 0.35= 7; 24+7= 31

Example: vomiting and pneumonia.

Results Interpretation Reference

pH 7.4 Normal 7.35-7.46

PCO2 20 Respiratory alkalosis (hypocapnia) 26-42

HCO3- 12 Metabolic acidosis 18-24

BE -12 Base deficit as a result of bicarbonate (-) 3-(+) 3

loss.

Example: diarrhea and pain or cranial traumatism.

This interpretation is based on the following law: Compensation is never able to
return pH back to reference values

Results Interpretation Reference

pH 7.27 Acidemia 7.35-7.46

PCO2 39 Respiratory acidosis, since the 26-42

expected compensation is not
observed (a restrictive problem due to
abdominal distension or pain)

HCO3- 17 Metabolic acidosis 18-24

BE -12 Base deficit due to its buffering (-) 3-(+) 3

function because of acid gain

Expected respiratory compensation: 18-17= 1 (HCO3); 1 X 0.7= 0.7; 26-1= 25

Example: Advanced gastric torsion, advanced pancreatitis.
A rule exists where PCO2 and HCO3- always follow the same direction, in the event
of a simple problem. When direction is opposite, then it is a mixed problem, since
a 20:1 ratio should exist between HCO3- and PCO2.
Electroneutrality law. A balance between cations (negative charge) and anions
(positive charge) exists in the body, This electrical neutrality is always maintained.
In other words, if an anion is gained, a cation is also gained. If a cation is lost,
another cation is gained or an anion is lost. This maintains an always perfect
balance.
 

ME: Cations represented by Calcium, Magnesium, Zinc, immunoglobulins, and other

microelements.
NVA: non-volatile acids (both organic and inorganic acids, or anion gap), represented by lactic acid,
sulfates, phosphates, ketone bodies, salts of uremic acids, and exogenous acids such as
salicylates and oxalates.

Sodium and potassium represent approximately 98% of cations. Chlorine and

bicarbonate represent 88% of anions. This difference represents the content of
non-volatile acids (both organic and inorganic acids, or an anion gap).
The calculation of non-volatile acids (NVA) is then performed by the sum of the
principal cations Na+ and K+, minus the sum of the principal anions HCO3- and Cl-.
Example: an animal with the following results:

Na+ : 151
mmol/L

K+ : 5 mmol/L

HCO3 20 mmol/L
-

Cl- 118
mmol/L

Then, developing the equation:

Fixed or non-volatile acids = [(Na+) 151+ (K+) 5]-[(HCO3-) 20 + (Cl-)118]
(151+ 5)-(20+118)
156-138 = 18 mmol/L
Taking the electroneutrality law into account:
1.  If a chlorine loss occur due to vomiting, gastroduodenal foreign body,
torsion volvulus or ileus, this results in sequestration, and it will always
exist a bicarbonate increase as renal compensation mechanism (after 12
hours). Therefore: hypochloremic metabolic alkalosis.
2.  Should a bicarbonate loss occur due to diarrhea or nephropathy, increased
chlorine levels will always exist. Therefore: hyperchloremic metabolic
acidosis.
3.  Shouldan organic acid gain occur, decreased bicarbonate levels will always
result because it is used to buffer such organic acids.
Usefulness of calculating non-volatile or "fixed" acids (Anion Gap or
Organic/Inorganic Acids)
1.  Detecting the gain of "fixed" acids. In other words, metabolic acidosis
conditions.
2.  Establishing a prognosis for sick animals.
3.  Using the different analytes (Na+ , K+ , HCO3-, and Cl- ) to estimate the
concentration of non-volatile acids, metabolic acidosis or alkalosis
processes can be determined, the problem can be located (high or low
intestinal obstructions, loss of bases only, or with the generation/gain of
acids, as it occurs in diarrhea with dehydration), and finally, to establish the
appropriate fluid therapy.
Metabolic acidosis categories
 1.  Metabolic acidosis with no acid gain (non-volatile acids within the normal
range). In other words, due to bicarbonate loss (diarrheas).
2.  Metabolic acidosis with acid gain (high non-volatile acid levels). Examples:
endogenous acidosis due to lactic acid gain (tissue hypoxia due to
hypovolemia caused by profuse hemorrhage, dehydration, shock, etc.),
ketone bodies, phosphates, sulfates, or in exogenous acidosis caused by
the ingestion of salicylates (aspirin), oxalic acid (ethylene glycol) or
methanol, among the most important ones.
Electrolyte evaluation

A routine that must be imposed in the evaluation of electrolytes is the clinical

strong-ion difference (SIDc) Na+ and Cl-.
The reference values of sodium minus chlorine difference is 30 to 40 mmol/L
Example: Na+ 151 mmol/L and Cl- 118 mmol/L, then 151-118 = 33
If the difference exceeds 40, then it is a hypochloremic metabolic alkalosis (i.e.,
vomiting).
If the difference is lower than 30, then it is a hyperchloremic metabolic acidosis
(i.e., diarrhea).
In hypochloremic metabolic alkalosis conditions, the trend is to increase blood pH
(alkalemia). Therefore, the transcellular mechanism is activated in an attempt to
keep pH as lease elevated as possible, through an intracellular hydrogen ion
exchange with extracellular potassium ions. Therefore, in these cases we observe
the trend to decreasing serum potassium levels (hypokalemia).
 

In metabolic acidosis conditions due to bicarbonate loss (diarrhea, low intestinal

obstruction, or iliocaecal obstruction), the tendency is to decrease the pH
(acidemia). Here, the transcellular mechanism is activated in an attempt to keep
pH as least low as possible through an extracellular hydrogen ion exchange with
intracellular potassium ions. If is a simple acid-base disorder, these cases will
show increased serum potassium levels (hyperkalemia).
 
Summary of the most common pH/electrolyte changes associated with various clinical
situations
 
Vomiting Diarrhea Shock Dehydration

K+

Na+ Normal Normal Normal Normal or

Cl- Normal Normal

HCO3-

Base excess or
deficit (BE)

pH

PCO2
(compensatory)

SIDC Normal Normal

Non volatile acids Normal Normal

References
1.  Adams, LG; Polzin, DJ. Mixed acid-base disorders. Vet. Clin of North Am Small An. Fluid and
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2.  Autran de Morais, HS. Mixed acid-base disorders. In Fluid therapy in small animal practice. DiBartola
ed. W. B. Saunders, Phil. 1992: 276-296.

3.  Bailey, JE; Pablo, LS. Practical aproach to acid-base disorders. Vet. Clin of North Am Small An.
Advances in fluids and electrolyte disorders. 1998, 28: 3, 645-662.

4.  Carlson, GP. Fluid, Electrolyte and acid-base balance. In Clinical Biochemistry of Domestic Animals.
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5.  DiBartola, SP. Introduction to acid-base disorders. In Fluid therapy in small animal practice. DiBartola
ed. W. B. Saunders, Phil. 1992: 193-215.

6.  DiBartola, SP. Metabolic acidosis. In Fluid therapy in small animal practice. DiBartola ed. W. B.
Saunders, Phil. 1992: 216-243.

7.  DiBartola, SP. Metabolic alcalosis. In Fluid therapy in small animal practice. DiBartola ed. W. B.
Saunders, Phil. 1992: 244-257.

8.  DiBartola, SP; Autran de Morais, HS. Respiratory acid-base disorders. In Fluid therapy in small
animal practice. DiBartola ed. W. B. Saunders, Phil. 1992: 258-275.

9.  Orsini, JA. Pathophysiology, diagnosis, and treatment of clinical acid-base disorders. Comp Cont
Educ. Small An. 1989, 11: 5, 593-604.

10. Polzin, DJ; et al. Clinical application of the anion gap in evaluation of acid-base disorders. Comp
Cont Educ. Small An. 1982, 4: 12, 1021-1032.

11. Robertson, SA. Simple acid-base disorders. Vet. Clin of North Am Small An. Fluid and electrolytes
disorders. 1989, 19: 2, 289-306.

S I
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Luis Núñez Ochoa (/apputil/content/defaultadv1.aspx?

pId=11196&authorId=6976)
Facultad de Medicina Veterinaria y Zootecnia
Unam, Mexico
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