-
Can you interpret pH, PCO2
and bicarbonate (HCO3) on venous as
well as arterial samples?
The short answer is “yes.” Arterial samples are ideal because
oxygenation of blood can be evaluated (important for patients with
pulmonary and cardiovascular disease), and the sample is not
affected by stasis of blood and local tissue metabolism. Much
valuable information, however, can be obtained from careful review
and interpretation of venous blood gases using the principles we
discussed during the Webinar. Due to peripheral tissue metabolism,
venous blood will have a higher
PCO
2 and lower pH than arterial blood.
Consider, for example, the following data derived from normal
un-anaesthetised dogs that appeared in the
Journal of Veterinary
Internal Medicine (2001;5[5]:294–298).
|
Parameter
|
Arterial blood
|
Jugular venous blood
|
|
pH
|
7.395 ± 0.028
|
7.352 ± 0.023
|
|
PCO
2 (mm Hg)
|
36.8 ± 2.7
|
42.1 ± 4.4
|
|
Bicarbonate (mEq/L)
|
21.4 ± 1.6
|
22.1 ± 2.0
|
back to the top
-
Are pH, PCO2
and bicarbonate adequate for diagnosis?
Again, the short answer is “yes.” The literature contains many
concepts for assessing acid-base balance. Some, such as standard
bicarbonate and base excess, are predicated on the notion (which is
an oversimplification) that the buffering capacity of whole blood
reflects the whole animal’s buffering capacity. Others, such as the
strong ion difference, are conceptually sound but mathematically
sophisticated and too cumbersome for general everyday use. I
believe that if you have a good understanding of the principles of
acid-base chemistry and physiology, “yes,” pH,
PCO
2 and bicarbonate are sufficient as
discussed in the Webinar.
back to the top
-
How helpful is total CO2 alone for assessing acid-base balance?
Total CO
2 is determined by adding a strong
acid to plasma or serum and measuring
the amount of CO
2 released from the reaction: H
+
+ HCO
3
-
→ H
2CO
3 → CO
2 + H
2O.
The term total CO
2 refers to the fact that this method
includes both the dissolved CO
2 and bicarbonate present in the
sample. As a result, total CO
2 determined on an anaerobically
handled sample is approximately 1 or 2 mEq/L higher than the
bicarbonate concentration because dissolved CO
2 (in mEq/L) =
PCO
2 (in mm Hg) × 0.03 (the solubility
coefficient for CO
2). However, when the sample is
handled aerobically (as typically is the case for blood samples
sent to a laboratory), the dissolved CO
2 is released to the atmosphere, and
the value obtained essentially is equal to the bicarbonate
concentration of the sample. That’s a long way of saying that total
CO
2 on a routinely handled biochemical
profile is the same thing as the bicarbonate concentration. The
value of that information will depend on the clinician’s
understanding of acid-base balance. For example, what does a low
bicarbonate concentration mean? Most often, it will signify the
presence of metabolic acidosis, but (although much less likely) it
also could reflect a decrease in the bicarbonate concentration as
compensation for a primary respiratory alkalosis. Blood-gas
analysis would be necessary to answer this question definitively if
the answer is not already clear from the patient’s clinical
presentation. As another example, what does a high bicarbonate
concentration mean? Most often, it will signify the presence of
metabolic alkalosis, but it also could reflect an increase in the
bicarbonate concentration as compensation for a primary respiratory
acidosis. Again, blood-gas analysis would be necessary to answer
this question definitively if the answer is not already clear from
the patient’s clinical presentation. Thus, a good understanding of
acid-base principles will help you interpret the meaning of the
total CO
2 on a biochemical profile.
back to the top
-
How often should one monitor
acid-base parameters in response to therapy?
This depends on whether or not the patient is stable. The more
unstable the patient, the more frequently acid-base parameters
should be monitored. In critical patients, monitoring could be
necessary every few hours. In critically ill patients judged to be
in need of sodium bicarbonate therapy (based on presence of a
severely low pH such as 7.0–7.1), one common practice is to
administer a low dose of bicarbonate (e.g., 1–2 mEq/kg)
slowly by the intravenous route and then re-evaluate blood gases in
a few hours.
back to the top
-
When supplementing
bicarbonate, should constant rate infusion (CRI) be used?
This depends upon the clinical condition and the clinician’s
preference. In most instances, the decision to administer
bicarbonate is made in a critically ill patient (e.g., blood pH =
7.1), and often a low dose of bicarbonate (1–2 mEq/kg) is
administered slowly by the intravenous route. Alkalinising
crystalloid fluids (e.g., lactated Ringer’s solution) are often
administered also. When blood gases are checked several hours
later, it is not unusual to observe that the acidosis is well on
its way to resolution and nothing more needs to be done in terms of
bicarbonate administration. In the unusual situation where severe
metabolic acidosis and extremely low bicarbonate concentration are
refractory to initial treatment, the clinician may elect to start a
constant rate infusion of bicarbonate, but important questions
remain. For example, what volume of distribution (V
d) should be used in the calculation of the amount of
bicarbonate to give? The general formula is mEq bicarbonate = V
d × body weight (kg) × bicarbonate deficit (mEq/L). You
will see values of 0.2 (extracellular space) to 0.6 (total body
water) used for V
d in this equation, and (experimentally at least) the V
d for bicarbonate in dogs with severe chronic metabolic
acidosis can even exceed 0.6! If you are going to use this kind of
equation, you should probably pick a low value such as 0.2 for V
d until you see how the patient responds. Another
question is how to calculate the “bicarbonate deficit.” Do you
simply subtract the patient’s bicarbonate concentration from the
normal value of 21 mEq/L and plug that result into the equation
above as the “bicarbonate deficit?” You probably shouldn’t, because
your goal is not to return the patient’s bicarbonate concentration
to completely normal but just enough to increase the pH out of the
danger zone (i.e., to above 7.2). The amount of bicarbonate needed
to do so likely will be less than the amount calculated from the
equation. From these considerations, you can see that it is not
simply a matter of plugging numbers into an equation. Consequently,
often it is preferable to give repeated small doses of sodium
bicarbonate until the patient’s blood pH stabilises above 7.2. This
approach requires serial re-evaluation of the patient’s blood gases
and adjustments to treatment based on the results obtained.
back to the top
-
How does one use base
excess to evaluate acid-base status?
Opinions differ about the value of base excess in the evaluation of
acid-base status. Base excess is defined as the amount of strong
acid or base required to titrate 1 litre of blood to pH 7.40 at
37°C while
PCO
2 is held constant at 40 mm Hg. Base
excess is changed only by non-volatile (or fixed) acid and thus is
considered to reflect the magnitude of metabolic acid-base
disturbances. A negative value indicates metabolic acidosis and a
positive value metabolic alkalosis (normal base excess is
approximately -3 to +3 mEq/L). People often use changes in base
excess to determine the presence of a metabolic acid-base disorder.
However, the observed change in the patient’s bicarbonate may
reflect a normal adaptive renal response to the presence of a
primary respiratory acid-base disorder. If the clinician
understands the implications of the Henderson-Hasselbalch equation
and follows the guidelines for interpreting blood-gas data that we
discussed during the Webinar, there is no real need to bring base
excess into the discussion.
back to the top
-
What is the anion gap and
how is it used to evaluate acid-base status?
The “anion gap” simply is the
difference between the
“commonly measured” cations (sodium and potassium) and the
“commonly measured” anions (chloride and bicarbonate). In reality,
the law of electroneutrality must be satisfied and there is no
actual anion gap. It’s just that there are more
un-measured anions (i.e.,
negative charges on proteins, phosphate, sulfate and lactate as
well as other organic anions) than
un-measured cations (i.e.,
only calcium and magnesium). In some types of metabolic acidosis,
fixed acids decrease serum bicarbonate concentration, and the
anions of these acids accumulate as un-measured anions. Examples
include diabetic ketoacidosis (where organic ketoanions
accumulate), ethylene glycol poisoning (where organic anion
metabolites of ethylene glycol accumulate), renal failure (where
phosphate accumulates) and, pictured in the diagram above on the
left, lactic acidosis (where the organic anion lactate
accumulates). This type of acidosis is called a “high anion gap” or
“normochloraemic” acidosis because the un-measured anion increases
in proportion to the decrease in bicarbonate and serum chloride
concentration is unchanged. This is the most common type of
metabolic acidosis encountered in veterinary medicine. The other
type of acidosis, pictured in the diagram above on the right, is
called a “normal anion gap” or “hyperchloraemic” acidosis, because
there is no accumulated un-measured anion and serum chloride
concentration increases in proportion to the decrease in serum
bicarbonate. This type of acidosis is somewhat less common in
veterinary medicine and is exemplified by small-intestinal
diarrhoea. In this situation, bicarbonate-rich fluid is lost in the
diarrhoea, the animal becomes dehydrated and the kidneys increase
their absorption of sodium and water. Because of the lower serum
bicarbonate concentration, the filtered load of bicarbonate is
decreased and the kidneys must reabsorb more of the sodium with
chloride, leading to hyperchloraemia. Other causes of
hyperchloraemic acidosis, such as renal tubular acidosis, are rare.
back to the top
-
Our normal values for pH
are 7.35–7.45. How can this information be used to assess
acid-base balance?
You’ve hit upon a very important issue—namely that we
determine the patient’s expected compensatory response by doing
calculations based on “average” normal values, whereas in reality,
we must deal with normal reference ranges from laboratories and we
don’t really know what the actual “normal” value is for any
individual patient. In the case of pH, we typically use 7.38 as an
average “normal” value for arterial samples. As a consequence of
this uncertainty, we conclude that an acid-base disturbance is a
simple disorder as long as
the observed
compensatory
PCO
2 (in the case of metabolic
disorders) or compensatory bicarbonate concentration (in the case
of respiratory disorders) is within 2–3 mm Hg (for
PCO
2) or 2–3 mEq/L (for bicarbonate) of
the calculated value. Only when the observed values are more than
2–3 mm Hg or 2–3 mEq/L away from the calculated values do we
consider the possibility of a
mixed disorder, and it is
always important to ask yourself if your conclusions are warranted
by the patient’s clinical presentation.
back to the top
|
