1- Gato de 18 aos de edad, golpeado por un auto que le caus colapso traqueal

Anlisis sanguneo de gases

pH
PO2 PCO2 Bicarb Tot CO2 Exceso de base O2 SAT
Units

mmHg mmHg

(7.36-7.42)

7.30

90

mM/L

(36-42) (17-24)
54

mM/L

mM/L

(18-25)

(-2.5-2.5)

27.5

25.9

1. Qu tipo de sangre fue muestreada?

2. El paciente tiene una

Acidemia

3. Por qu aument la pCO2?

Arterial

Venosa

Alcalemia

___________________________________________

4. Por qu est aumentado el bicarbonato? __________________________________

5. Cul componente es el principal responsable del trastorno cido-base del paciente?
Respiratorio

Metablico

6. Cul proceso es el responsable del trastorno cido-base del paciente?

a) Ganancia de cido o prdida de base
b) Prdida de cido o ganancia de base
c) Ganancia de CO2
d) Prdida de CO2
7. El paciente tiene

acidosis respiratoria alcalosis metablica

2. Cachorro de 8 meses de edad con vmitos las ltimas doce horas

Anlisis sanguneo de gases
pH
PO2 PCO2 BICARB TOT CO2 BASE EXCESS O2 SAT
Units

mmHg mmHg

mM/L

mM/L

mM/L

(7.36-7.42)

(36-42)

(17-24)

(18-25)

(-2.5-2.5)

7.46

40

40

27.6

28.8

4.5

63

1. Qu tipo de sangre fue muestreada?

2. El paciente tiene una

Acidemia

Arterial

Venosa

Alcalemia

3. Por qu est aumentado el bicarbonato? __________________________________

4. El aumento en el bicarbonato provoc el aumento en la pCO2 Falso Verdadero
5. Cul componente es el principal responsable del trastorno cido-base del paciente?
Respiratorio

Metablico

6. Cul proceso es el responsable del trastorno cido-base del paciente?

a) Ganancia de cido o prdida de base
b) Prdida de cido o ganancia de base
c) Ganancia de CO2
d) Prdida de CO2
7. El paciente tiene
a) acidosis respiratoria
b) alcalosis respiratoria
c) acidosis metablica
d) alcalosis metablica
8. Sin tomar en cuenta la historia clnica, con base slo en los datos cmo sabe que ha
habido prdida de cido?

3. Perro de seis aos de edad, con pulmona

Anlisis sanguneo de gases
pH
PO2 PCO2 BICARB TOT CO2 BASE EXCESS O2 SAT
Units

mmHg mmHg

mM/L

mM/L

mM/L

(7.36-7.42)

(36-42)

(17-24)

(18-25)

(-2.5-2.5)

7.33

65

33.3

35.3

7.1

1. El paciente tiene una

Acidemia

2. Por qu aument la pCO2?

Alcalemia

___________________________________________

3. Por qu est aumentado el exceso de base? ___________________________________

4. En general cules dos procesos pueden originar aumento en el bicarbonato?
__________________________________

________________________________

5. Cul de esos dos procesos es el principal responsable del aumento en el bicarbonato en

este caso?
____________________________________________________________
6. Cul componente es el principal responsable del trastorno cido-base del paciente?
Respiratorio

Metablico

7. Cul proceso es el responsable del trastorno cido-base del paciente?

a) Ganancia de cido o prdida de base
b) Prdida de cido o ganancia de base
c) Ganancia de CO2
d) Prdida de CO2
8. El paciente tiene
a) acidosis respiratoria
b) alcalosis respiratoria
c) acidosis metablica
d) alcalosis metablica

4. Paciente que ha recibido Furosemida (diurtico) por largo tiempo

Anlisis sanguneo de gases
pH
PO2 PCO2 BICARB TOT CO2 BASE EXCESS O2 SAT
Units

mmHg mmHg

mM/L

mM/L

mM/L

(7.36-7.42)

(36-42)

(17-24)

(18-25)

(-2.5-2.5)

7.55

55

45.7

47.4

23.0

1. El paciente tiene una

Acidemia

2. Por qu aument la pCO2?

Alcalemia

___________________________________________

3. En general cules dos procesos pueden originar aumento en el bicarbonato?

__________________________________

________________________________

4. Cul de esos dos procesos es el principal responsable del aumento en el bicarbonato en

este caso?
____________________________________________________________
5. Por qu est aumentado el exceso de base? ___________________________________
6. Cul componente es el principal responsable del trastorno cido-base del paciente?
Respiratorio

Metablico

7. Cul proceso es el responsable del trastorno cido-base del paciente?

a) Ganancia de cido o prdida de base
b) Prdida de base o ganancia de cido
c) Ganancia de CO2
d) Prdida de CO2
8. El paciente tiene
a) acidosis respiratoria
b) alcalosis respiratoria
c) acidosis metablica
d) alcalosis metablica

5. Potro de tres semanas de edad con diarrea profusa los ltimos cuatro das. Est
aptico, su piel flcida, los ojos hundidos, su temperatura es de 36.7 C, su respiracin
es profunda y con una frecuencia de 30 por minuto.
Anlisis sanguneo de gases
pH
PO2 PCO2 BICARB TOT CO2 BASE EXCESS O2 SAT
Units

mmHg mmHg

mM/L

mM/L

mM/L

(7.36-7.42)

(36-42)

(17-24)

(18-25)

(-2.5-2.5)

7.20

ND

16

6.1

-20.5

1. El paciente tiene una

Acidemia

2. Por qu disminuy la pCO2?

Alcalemia

___________________________________________

3. Por qu hay un exceso de base negativo? ___________________________________

4. El paciente tiene
a) acidosis respiratoria
b) alcalosis respiratoria
c) acidosis metablica
d) alcalosis metablica
5. El paciente ha empezado a compensar el trastorno cido-base

Falso Verdadero

6. Gatito al que se dio una sobredosis de aspirina

Anlisis sanguneo de gases
pH
PO2 PCO2 BICARB TOT CO2 BASE EXCESS O2 SAT
Units

mmHg mmHg

mM/L

mM/L

mM/L

(7.21-7.41)

(28-50)

(16-23)

(17-24)

(-8.5-1.5)

7.16

28

14.1

14.9

-13

1. El paciente tiene una

Acidemia

Alcalemia

2. Cul sistema buffer est disminuido?

______________________________
3. A qu se debe tal disminucin?
_________________________________________________________________________
4. Cul componente es el principal responsable del trastorno cido-base del paciente?
Respiratorio

Metablico

5. Cul proceso es el responsable del trastorno cido-base del paciente?

a) Ganancia de cido o prdida de base
b) Prdida de base o ganancia de cido
c) Ganancia de CO2
d) Prdida de CO2
6. El paciente tiene
a) acidosis respiratoria
b) alcalosis respiratoria
c) acidosis metablica
d) alcalosis metablica
7. Por qu la pCO2 est dentro del rango normal?
_________________________________________________________________________
8. En qu sentido esperas que cambie la pCO2?
_________________________________________________________________________

7. Perro de seis aos de edad con debilidad severa generalizada, atrofia muscular,
respiracin superficial y cianosis.
Anlisis sanguneo de gases
pH
Units

PO2 PCO2 BICARB TOT CO2 BASE EXCESS O2 SAT

mmHg mmHg

mM/L

mM/L

mM/L

%
-

(7.31-7.42)

(29-42)

(17-24)

(18-25)

(-2.5-2.5)

7.345

45.4

53.2

28.4

30.1

2.8

1. El pH de la sangre est en el rango normal significa esto que no hay alteracin del
balance cido-base? por qu?
_________________________________________________________________________
2. Por qu aument la pCO2?
_________________________________________________________________________
3. Por qu est aumentado el exceso de base? ___________________________________
4. El paciente tiene
a) acidosis respiratoria
b) alcalosis respiratoria
c) acidosis metablica
d) alcalosis metablica
e) ninguna de las anteriores

8. Oveja de dos aos de edad, deprimida, permanece recostada, deshidratada,

frecuencia respiratoria de 80 y estaba en engorda a base de granos
Anlisis sanguneo de gases
pH
PO2 PCO2 BICARB TOT CO2 BASE EXCESS O2 SAT
Units

mmHg mmHg

mM/L

mM/L

mM/L

%
-

(7.32-7.54)

(37-46)

(20-25)

(21-28)

(-)

7.00

60

25

-22.9

1. El paciente tiene una

Acidemia

Alcalemia

2. Cul componente es el principal responsable del trastorno cido-base del paciente?

Respiratorio

Metablico

3. Por qu disminuy la pCO2?

_________________________________________________________________________
4. Por qu hay un exceso de base negativo? ___________________________________
_________________________________________________________________________
5. El paciente tiene
a) acidosis respiratoria
b) alcalosis respiratoria
c) acidosis metablica
d) alcalosis metablica
6. Por qu est aumentada la frecuencia respiratoria?
_________________________________________________________________________

An Acid/Base Primer
Base Excess
While pH, PCO2, and bicarbonate may be familiar terms to you, the concept of
base excess may not be. Base excess (BE) is defined as the amount of acid
which must be added to blood to return the pH to normal. While that definition
may be easy to memorize and may be helpful in some circumstances, the
practical application of this definition is pretty obscure. [NOTE: Sometimes
base excess is reported as base deficit. That's because base excess can be
negative...and that's a base deficit. Base excess seems to be the term most
commonly used and the one that we'll use here, but either term is valid.]
So, what do we really mean by the term base "excess"? Let's give an example.
If you have an animal with a base excess of zero, that would mean that the
animal's blood has a normal amount of buffer base in it. So, what's a normal
amount of buffer base?
(1) Buffer Base = [HCO3-] + [Buf-]
The meaning of HCO3- is probably obvious. Buf- represents all the conjugate
bases of all the non-bicarbonate buffers. The non-bicarbonate buffers include
hemoglobin, oxyhemoglobin, organic and inorganic phosphates, and proteins.
Of these, hemoglobin is the most abundant non-bicarbonate buffer. The
bicarbonate system represents about 55% of the buffering capacity of the
blood and the non-bicarbonate buffers about 45%.
You can see from equation (1) that buffer base is the sum of Buf- and
HCO3-...or the total amount of buffers in the blood. The exact value for buffer
base varies from individual to individual (stemming largely from differences in
hemoglobin content) and, because of this variation, is not a particularly useful
measurement. The value for base excess, on the other hand, represents the
deviation from the normal buffer base for a particular individual.
Understanding how BE works requires a little chemistry. OK...for some of you,
it's a lot. Here's just two equations that are important for understanding BE:
(2) CO2(dissolved) + H2O <==> H+ + HCO3(3) HBuf <==> H+ + Buf where: Buf represents all of the non-bicarbonate buffers (e.g. hemoglobin)
Now, you should recognize that these equations describe two different
buffering systems in the blood but that both buffers act simultaneously, not
independently. This means that whatever affects one equation will also have
an effect on the other. Let's apply this. See the H+ in the two equations? That's
the same H+. If H+ is put into the blood, it will react according to both
equations, not one or the other. This is the so-called isohydric principle...blood

only has ONE (iso) pH (hydric) and that pH affects both equations
simultaneously.
The other thing you should note is that these equations represent chemical
reactions that are in equilibrium. This is to say that the equations will move in
either direction according to the law of mass action.

If we add H+ to the blood, which way will equation (2) go?

+

(2) CO2(dissolved) + H2O <==> H + HCO

If we add H+ to the blood, which way will equation (3) go?

(3) HBuf <==> H+ + Buf -

If we add H+ to the blood, what will happen to base excess? (Hint)

If we remove H+ from the blood, which way will equation (2) go?
+

(2) CO2(dissolved) + H2O <==> H + HCO

If we remove H+ from the blood, which way will equation (3) go?
(3) HBuf <==> H+ + Buf -

If we remove H+ from the blood, what will happen to base excess?

If we add CO2 to the blood, which way will equation (2) go?
(2) CO2(dissolved) + H2O <==> H+ + HCO3-

If we add CO2 to the blood, which way will H+ go?

If we add CO2 to the blood, which way will equation (3) go? (Hint)
+

(3) HBuf <==> H + Buf

Compensation

Izquier
Derech

Izquier
Derech

Aumen
Disminu
Igual

Izquier
Derech

Izquier
Derech

Aumen
Disminu
Igual

Izquier
Derech

Aumen
Disminu
Igual

Izquier
Derech

(No...this isn't referring to how much you are being paid for doing this!)

We know that when there is an acid/base disturbance, the body will attempt to
correct the disturbance because H+ concentrations that are too high or too low
are very dangerous. Buffer systems are a very effective first line of defense
against exaggerated changes in H+ concentrations in the ECF.
The respiratory system and the kidney are an integral part of the body's buffer
systems and they are designed to specifically address changes in H+
concentration. As you know, if H+ concentration and PCO2 rise due to a
change in ventilation, the peripheral and central chemoreceptors are
stimulated. The output from these receptors activates the respiratory center in
the medulla resulting in an increase in ventilation. Consequently, PCO2 and
H+ concentration will be returned to normal levels. This respiratory response to
a primary respiratory abnormality is termed a correction. The initial problem
has been corrected. The same line of thinking can be applied to the metabolic
component.
Now, what happens if there is some problem with the respiratory system which
prevents it from responding appropriately to signals stemming from high H+
and high PCO2? In this case the respiratory system is incapable of correcting
for the acid/base disturbance. The kidneys must then take over responsibility
for returning the pH to normal (or near normal) levels. We speak of the kidneys
in this capacity as compensating for the failure of the respiratory system to do
its job.

Can the kidney correct for a metabolic disturbance?

S
No

Can the kidney compensate for a metabolic acidosis?

S
No

Can the kidney correct for a disturbance caused by the respiratory system?

S
No

Can there be compensation if there is a mixed disturbance?

S
No

Classifying acid/base disturbances: Part I

Respiratory/Metabolic - Acidosis/Alkalosis

Clinically, acid/base disturbances are classified on the basis of the component

(respiratory or metabolic) that is primarily involved and the process (acidosis or
alkalosis) causing the disturbance. For example, a respiratory alkalosis
signifies that the respiratory component is primarily involved and that there is
an alkalosis. Mixed disturbances can also occur, in which more than one type
of disorder is present simultaneously. Thus, an animal could have a respiratory
acidosis and a metabolic alkalosis at the same time.
To classify an acid/base disturbance, you begin by identifying the component
that is affected (metabolic or respiratory) and then by determining the type of
disturbance (acidosis or alkalosis.)

The goal of compensation for an acid/base disturbance is to return the pH of

the blood to a value within the normal range. Of course, the adjustment of an
acid/base derangement requires a finite amount of time; it does not occur
instantaneously. Specific terms are used to describe the extent of the response
to an acid/base disturbance.
At the outset, before any compensation has occurred, we would refer to the
system as being uncompensated. So, for instance, in a case of partial
tracheal obstruction, we would have an acute respiratory acidosis (acute
addition of CO2 to the blood). The addition of CO2 will drive the bicarbonate
buffer equation [CO2 + H2O <==> H+ + HCO3-] to the right, generating H+.
Assuming that the obstruction is not relieved within a couple of days, the
kidney will begin to respond by excreting H+ and the pH will move back toward
normal. As it does, what variable in the blood gas panel will begin to change?
In the example case we're talking about here, why wouldn't this variable be
changed before the kidney began to excrete H+. [Need a review of this?] The
system at this point will have an increased base excess along with a (still)
abnormal pH. This circumstance is termed partial compensation. After the
kidney has been working long enough, the pH will (hopefully) be returned to
the normal range. The base excess will be even higher, but the pH will be
normal. The system is then fully compensated. Thus, acid/base disturbances
are classified as uncompensated, partially compensated, or fully
compensated.

Another way of looking at acid/base responses is to describe the degree of the

response based upon the physiological potential to respond to the primary
abnormality. In many acid/base disorders, compensation may progress as far
as possible but the pH is still not within the normal range. Full restoration of
normal pH will have to await repair of the primary abnormality.

The maximal physiological response of an otherwise normal individual to a

given acid/base disturbance is termed maximal compensation. Maximal
compensation is characterized by a sustained plateau of blood pH and this pH
is often NOT within the normal range. Establishing the standards for maximal
compensation requires the study of large numbers of individuals with
uncomplicated acid/base disturbances. Once such data is obtained, a
judgement can be made as to whether or not an observed response is as
much as one might expect under a given set of circumstances.
Why does blood pH usually fail to return to normal when the system is
maximally compensated? In other words, why aren't maximal and full
compensation the same thing?

The respiratory system:

an open bicarbonate buffer system
We will evaluate the following statement: Since HCO3- has increased, the
bicarbonate buffer equation is driven to the left, increasing the PCO2.
CO2(dissolved) + H2O <==> H+ + HCO3The fundamental issue here requires an appreciation for the fact that, in
animals, bicarbonate is part of an open buffer system as opposed to a closed
system. In a closed buffer system [a flask with an air-tight cork in the mouth], if
HCO3- is added to the fluid, CO2 will, indeed, increase as you would expect.
However, with a functional respiratory system, when HCO3- is added, the CO2
that is formed is immediately removed from the system by the lung. So...in an
open system, CO2 does not accumulate as HCO3- is added. Of course, if the
respiratory system is NOT functional, that is, it is dysfunctioning, then PCO2
WILL increase. When the respiratory system dsyfunctions, an acid/base
disorder ensues.
In the case involving a vomiting puppy, there is no indication that there is any
abnormality in the respiratory system. Hence, as HCO3- increases, yes, CO2
will be formed. BUT, the additional CO2 will be breathed off as rapidly as it is
formed. [You can imagine that in an open system like this in which one of the
major components does not accumulate, the effectiveness of the buffer is
enhanced markedly.]
So why is the CO2 increased in this vomiting puppy?
In vomiting, H+ is being lost from the body. The buffer equation moves to the
right simply due to what law? Because of this, CO2 will initially be removed
from the ECF but, because we are dealing with an open system, ventilation will
decrease, restoring PCO2. Remember, however, that H+ is one of the drives
for ventilation. As H+ declines (it's being lost in the vomitus), there will be a
diminished drive for respiration, ventilation will decrease further, and CO2 will
begin to rise above normal, driving the buffer equation toward the right, raising
the concentration of H+. This process will also cause a further increase in
HCO3- but the body is much more interested in keeping H+ concentrations
normal than worrying about HCO3-!

In other words, CO2 is not increased in a case of vomiting as a result of added

bicarbonate driving the buffer equation to the left. It is increased because the
respiratory system is purposely allowing PCO2 to rise in order to restore the
normal H+ concentration.

The lung and the base excess

Here are the buffer equations again:
(1) CO2(dissolved) + H2O <==> H+ + HCO3(2) HBuf <==> H+ + BufThese are the two equations that describe buffering in the extracellular fluid.
"Buf" represents all the non-bicarbonate buffers in the ECF, particularly
hemoglobin.
Look what happens when PCO2 increases. H+ and HCO3- (the latter is part of
the buffer base) are both formed. But the H+ that is formed by equation (1) is
not different from the H+ in equation (2). As H+ increases, equation (2) will be
driven to the left (by what law?). An increase in H+ in equation (2) will cause a
decrease in Buf-, the other component of buffer base. In fact, for every HCO3that is generated by equation (1), one Buf- is consumed in equation (2). There
is, therefore, no net change in the buffer base. Since
Buffer Base = [HCO3-] + [Buf-], then you can see that if HCO3- increases and
Buf- decreases, buffer base won't change.
Examples:
1. In Problem Set #1, we had a cat with a collapsed trachea. The PCO2 and
bicarbonate were both increased, but the base excess was zero. There must
have been equivalent, but opposite, changes in HCO3- and Buf-.
2. The dog in Problem Set #3 also had a respiratory dysfunction. The blood
gas panel indicated an increased PCO2 and increased bicarbonate, but in that
case there was a base excess. We can't use the respiratory system to explain
the increase in base excess in this dog. Therefore, we must presume that the
base excess is increased by some action of the metabolic component. So what
was the body doing to add base to the ECF? There was no obvious pathologic
loss of H+ or gain of base. We had no evidence of vomiting or any other
organic disease apart from the respiratory system. We must conclude that the
kidney was retaining HCO3- on purpose in response to the increased H+ that
was resulting from the hypoventilation. This response of the kidney is called
metabolic compensation. The kidney compensated for the dysfunction of the
lung. The point is that if the base excess is changed in a respiratory acid/base
disturbance, it is changed either because of a metabolic disturbance or
because compensation is underway, NOT because the respiratory disturbance

has altered it. What are the two facts that you wrote on the back of your left
hand?

Bottom line: What was the difference between the dog and the cat, both of
which had primary respiratory disease. One had a base excess, the other
didn't. The difference was that the dog was compensating for the respiratory
dysfunction and the cat was not. The dog (via compensation) was generating a
base excess, the cat was not. The dog had a metabolic response to the
respiratory dysfunction, the cat did not.
So what's the cat's problem, anyway? Well, if her kidneys are normal, she
probably just needs a little time. It takes 1 or 2 days for the kidneys to mount
an effective response.

Maximal and Full Compensation

Take, for example, a case of metabolic acidosis with a BE of -10 mEq/L and a
pH of 7.24 BEFORE COMPENSATION. At maximal compensation, the PCO2
will be about 30 and the pH will be 7.33. In order to get the pH back into the
normal range, PCO2 would have to drop even further.
Be aware that what's driving respiration is the high H+ concentration. As
respiration is stimulated and the pH is gradually raised by blowing off CO2,
there will be less and less drive from low pH to keep ventilation increased. At
the same time, the consequence of lowering the PCO2 (the thing responsible
for raising the pH) is to also decrease that part of the ventilatory drive which is
due to PCO2.
The end result is that pH almost never makes it back to normal. Restoration of
blood pH completely back into the normal range will have to await either
medical intervention or repair of the primary abnormality.
Richard E. Rawson, D.V.M., Ph.D.
Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853