Clinical Acid-Base Disturbances
Approach to the Abnormal Blood Gas
Acid-base disorders can be approached with three questions:
What is wrong?
What caused it?
What’s being done about
it?
The answer to the first question, “What is
wrong?” is obtained by simple inspection of the values on the pH, PaCO2, and HCO3-.
If all three values are normal, the answer to “What is
wrong?” is “Nothing,” and the other two questions can be ignored.
If either pH, PaCO2, or HCO3- are abnormal, check the pH.
If it’s below 7.4, the answer to “What is wrong?” is “Acidosis.”
If above 7.4, “Alkalosis.”
If the pH is within the normal range, but the PaCO2 or
HCO3- (or both) are abnormal, an acid-base derangement exists, but the body has fully
compensated for it. For example, with a pH of 7.35 (normal) and a decreased bicarbonate of
18, an acidosis exists.
Check pH, PaCO2, HCO3-.
Anything abnormal? If no,
quit.
pH greater than 7.4 =
alkalosis
pH less than 7.4 = acidosis
The second question is “What caused it?” The
answer is “Metabolic” if bicarbonate has caused the observed change in pH from
7.4. If carbon dioxide caused it, the answer is “Respiratory.” If both are
guilty, the answer is “Mixed metabolic and respiratory.”
First look at the bicarbonate. Is it guilty?
Increased bicarbonate raises the pH. Low bicarbonate lowers
the pH. If you see a pH above 7.4 and the bicarbonate is elevated above normal, it means
bicarbonate is guilty of raising the pH. So a metabolic alkalosis exists.
If the bicarbonate is above 7.4 and the bicarbonate is
decreased or normal, bicarbonate is not guilty.
Similarly, if the pH is below 7.4 and the bicarbonate is
below normal, it means lack of bicarbonate is responsible for lowering the pH. Therefore a
metabolic acidosis exists.
Look at the CO2. Is it guilty?
Carbon dioxide is acidic. A high CO2 will lower the pH,
while a low CO2 will raise it. If the pH is above 7.4 and the PaCO2 is lower than normal,
lack of CO2 is responsible. A respiratory alkalosis exists.
If, however, the CO2 is normal or elevated while the pH is
above 7.4, then CO2 can’t be contributing to the disturbance.
If both PaCO2 and HCO3- are shifted in a direction that
would contribute to the pH abnormality, both are guilty. A mixed metabolic and respiratory
abnormality exists.
Check pH, PaCO2, HCO3-.
Anything abnormal? If no,
quit
pH greater than 7.4 =
alkalosis
pH less than 7.4 = acidosis
Who’s responsible?
HCO3- shifted in direction of
pH = guilty
CO2 shifted opposite of pH =
guilty
The final question is “What’s the body doing
about it?” We’re checking for compensatory changes — changes the body has
made to compensate for the abnormality. This is an inherantly inaccurate question, as
I’ll discuss later. Consider your answer a “best guess.”
Assume the body has only two mechanisms to affect pH:
respiratory and metabolic. Respiratory is CO2 and metabolic is HCO3-.
After you’ve identified the guilty party (CO2 or
HCO3-), look at the other value. If that other value is abnormal, but in a direction that
would move the pH back towards normal, then compensation is present.
If you’ve found that both HCO3- and CO2 are guilty,
then obviously compensation isn’t present. As an example, assume blood gases that
show pH=7.33, HCO3=16.5, and PaCO2=32. The problem is acidosis (any abnormality plus pH
>> 7.4). The guilty party is metabolic (HCO3- is low, shifted in a direction that
causes acidosis). Respiratory compensation is present (CO2 is abnormal in a direction that
would raise the pH back towards normal.
Compensation by respiratory means is very fast, occuring
within seconds or minutes. This compensation occurs via the body’s control of
respiratory rate through the brain respiratory center. Thus respiratory compensation for
metabolic abnormalities is seen almost immediately.
Metabolic compensation, on the other hand, is slow. It
occurs through elimination of acid or alkali by the kidney. Hours go by before significant
compensation is seen. Metabolic compensation will occur for chronic respiratory
disturbance, but also, metabolic correction through the kidney will be seen for metabolic
disturbances.
Check pH, PaCO2, HCO3-.
Anything abnormal? If no,
quit
pH greater than 7.4 =
alkalosis
pH less than 7.4 = acidosis
Who’s responsible?
HCO3- shifted in direction of
pH = guilty
CO2 shifted opposite of pH =
guilty
If only one guilty, check
“innocent” value.
Shifted = compensation
present.
Is this accurate? No. Identifying the source of acidosis
and presence of compensation assumes that the same process has been going on all along. If
body’s state changes from one source of abnormality to another, or if two completely
separate pathological processes are present, your “guess” will be wrong.
For example, Phil Smith has a heart attack and goes into
V-fib. He develops both respiratory and metabolic acidosis. Then he gets defibrillated and
wakes up. As he realizes that he has to give up his favorite cholesterol-rich foods, he
hyperventilates. Now blood gases are drawn.
pH = 7.44
PaCO2 = 28 HCO3 = 18.6
Looking at these gases, you diagnose “fully
compensated (chronic) respiratory alkalosis.” Not true. Phil has an acute respiratory
alkosis superimposed upon a “slightly less acute” metabolic acidosis. Remember
that bicarbonate abnormalities cannot change quickly.
Computer interpretation (such as that used in Mad Scientist
Software's Blood Gases program) look for "zones" of blood gas values where
clinical disturbances tend to fall. This gives a 95% level of certainty about mixed
disorders and compensation. At the bedside however, you're on your own.
Whenever you diagnose a respiratory cause for an acid-base
abnormality, with metabolic compensation, consider whether the abnormal bicarbonate could
be a “leftover” or separate metabolic abnormality of the opposite type.
For example, in aspirin poisoning, both metabolic acidosis
and respiratory alkalosis occur as a result of the aspirin. Depending on whether the pH
happens to be above or below 7.4 at the moment, you might incorrectly call it a
“compensated respiratory alkalosis” or a “compensated metabolic
acidosis.” Always consider the clinical history. Then you can correctly decide
whether a “compensation” is really compensation, or a separate abnormality.
Like most everything else in medicine, blood gas
interpretation requires a consideration of the patient history and your examination
findings. Let's review our completed "bedside" algorithm.
Acid-base Disturbance
Diagnosis Algorithm
Check pH, PaCO2, HCO3-.
Anything abnormal? If no,
quit
pH greater than 7.4 =
alkalosis
pH less than 7.4 = acidosis
Who’s responsible?
HCO3- shifted in direction of
pH = guilty
CO2 shifted opposite of pH =
guilty
If only one guilty, check
“innocent” value.
Shifted = compensation
present.
History compatable with mixed
disorder?
Not true compensation.
Go to Index.
Metabolic Acidosis
Clinical causes of metabolic acidosis
Tissue metabolism normally results in about 12,500
milliequivalents of acid production per day. This acid is in the form of CO2, and after
circulation to the lungs, is removed from the body in expired air. If aerobic metabolism
ceases (due to lack of oxygen or inability to use available oxygen due to metabolic
poisoning), tissues are unable to completely oxidize sugar to CO2. Instead, sugar is only
partly oxidized to lactic acid. As this acid cannot be expired through the lungs as CO2
is, it remains in circulation, causing metabolic acidosis.
In untreated diabetes, normal sugar metabolism is deranged
due to lack of insulin. In this case, acid buildup is due to acetoacetic and
betahydroxybutyric acids.
A certain amount of acid is formed when dietary proteins
are metabolized. These proteins contain sulfate and phosphate groups that, after
metabolism, form sulfuric and phosphoric acid. These acids amount to only about 150 mEq
per day, however they must be excreted from the body through the slow process of kidney
filtration. If the kidneys fail, acidosis results after several days. Ingestion of
acidifying salts, and loss of bicarbonate through chronic diarrhea, are less common causes
of metabolic acidosis.
Example:
pH = 7.21 PaCO2 = 40 HCO3 =
15.6
Compensation for metabolic acidosis
As the blood becomes more acidic, the brain’s
respiratory centers are stimulated to increase the rate and depth of breathing. This
lowers the CO2 in the blood, decreasing its acidity.
The kidney then begins to remove the excess acid. As the
plasma is filtered, acid anions enter the urine. In the kidney tubules, hydrogen ion is
secreted. For each hydrogen ion that enters the urine, a sodium ion and a bicarbonate ion
are put back into the plasma. In this way, acid is eliminated from the body.
Example of compensated
metabolic acidosis:
pH = 7.34 PaCO2 = 28 HCO3 =
14.7
Go to Index.
Metabolic Alkalosis
Causes of metabolic alkalosis
Fruits are the normal source of alkali in the diet. They
contain the potassium salts of weak organic acids. When the anions are metabolized to CO2
and removed from the body, alkaline potassium bicarbonate and sodium bicarbonate remain.
Metabolic alkalosis may be found in vegetarians and fad dieters who are ingesting a
low-protein, high fruit diet.
A more efficient way to get alkali into the body is to
consume sodium bicarbonate. This common heartburn remedy is probably the most common cause
of symptomatic metabolic alkalosis.
If acid is eliminated from the body, it has the same effect
as adding alkali. Persons with protracted vomiting of acidic stomach juices will often
develop metabolic alkalosis, as acid is secreted into the stomach then vomited out of the
body.
Example:
pH = 7.51 PaCO2 = 39 HCO3 =
30.4
Compensation for metabolic alkalosis
Short term, a decrease in respiratory rate leads to an
increase in serum carbon dioxide levels. (The carbon dioxide is transported as hydrogen
ion — buffered by hemoglobin — and bicarbonate.) This lowers the pH towards
normal, partially compensating for the additional alkali present in the blood.
The slow process of eliminating bicarbonate through the
kidney then begins. Hydrogen ions are transported from the filtered urine back into
plasma, with sodium ions and bicarbonate left behind. Alkaline sodium bicarbonate is thus
eliminated.
Example:
pH = 7.45 PaCO2 = 46 HCO3 =
31.2
Go to Index.
Respiratory Acidosis
Causes of respiratory acidosis
Buildup of carbon dioxide occurs when ventilations are
inadequate. This is usually due to absense of adequate respiratory effort — such as
when central control of respiration is depressed due to narcotics or barbiturates. When
respiration ceases due to cardiac arrest, of course, respiratory acidosis is an immediate
result.
Respiratory acidosis can also result when obstruction of
air motion leads to carbon dioxide buildup. Severe asthma and foreign body obstruction are
examples.
Example:
pH = 7.21 PaCO2 = 55 HCO3 =
22
Compensation of respiratory acidosis
Whereas respiratory changes can occur within seconds or
minutes, metabolic changes take hours to days. Compensation for respiratory acidosis must
occur through elimination of acid through the kidney, as discussed above under metabolic
acidosis. Only in chronic respiratory problems, such as severe obstructive airway disease,
will compensation be seen.
Example:
pH = 7.34 PaCO2 = 56 HCO3 =
29.5
Go to Index.
Respiratory Alkalosis
Causes of respiratory alkalosis
Respiratory alkalosis occurs due to hyperventilation. The
hyperventilation may be due to psychological causes — in fact, this is the most
common cause.
In other causes, the hyperventilation may be due to
abnormal stimulation of ventilation due to disease. Changes in the lung due to pulmonary
embolism, asthma, or pulmonary edema often trigger increased respiratory rate, resulting
in respiratory alkalosis.
Central stimulation of respiration occurs in aspirin
poisoning. This respiratory alkalosis is a separate effect from the metabolic acidosis
produced by aspirin.
Example of respiratory
alkalosis:
pH = 7.57 PaCO2 = 24 HCO3 =
21.5
Compensation of Respiratory Alkalosis
Respiratory alkalosis must exist for hours before metabolic
compensation can be seen. Alkaline sodium hydroxide is eliminated by the kidney, returning
the pH back towards normal, as discussed above under metabolic alkalosis.
Example:
pH = 7.46 PaCO2 = 22 HCO3 =
15.3
Go to Index.
Therapy of Respiratory Acidosis
The treatment of respiratory acidosis isn’t difficult
— in theory. All you have to do is increase the ventilation of the lungs. This
removes carbon dioxide from the blood stream, raising the pH. The increase in ventilation
may be easy in the intubated cardiac arrest or drug OD patient. Just turn up the
ventilator, or tell the “bagger” to bag a little faster and deeper.
In the conscious patient with severe asthma or pulmonary
edema, a decision must be made whether to await results from conservative therapy, or to
take control the airway through intubation and assisted ventilation. (This decision, in
practice, is based more on “gestault” of the clinical picture rather than on the
level of carbon dioxide.) You either improve air motion with drugs, or force better air
motion with an artificial airway.
In a patient with poor gas exchange due to intrapulmonary
causes — that is, disease within the lung itself — increasing ventilatory rate
and depth may be only marginally helpful. In this case, only improvement of the disease
process will help.
Some cases of carbon dioxide retention are better
untreated. For example, consider this patient with CHF and emphysema:
pH = 7.32 PaCO2 = 78 HCO3 =
39.3 PaO2 = 43
Review of past hospital records consistantly shows a CO2
around 70 at discharge. This patient has a chronic (compensated) respiratory acidosis.
Trying to “normalize” this patient’s blood gases would be dangerous. And
even if you succeeded, once the patient was breathing on his own he would retain CO2 again
acutely, resulting in a severe acute respiratory acidosis of pH =7.1! If the patient must
be intubated, sufficient “dead space” must be provided within the ventilator
tubing to keep the CO2 in the patient’s usual range. Go to Index.
Therapy of Metabolic Acidosis
Mild cases of metabolic acidosis are best left alone.
Usually no treatment is needed if the pH is above 7.1, and rarely is it needed if the pH
is above 7.2, although the patient’s level of discomfort and compensating
hyperventilation must be considered.
Metabolic acidosis is treated with sodium bicarbonate,
given intravenously. There is considerable question, however, how beneficial acidosis
treatment is for certain patients.
For the semi-comatose diabetic in ketoacidosis,
there’s no question that bicarbonate will raise the serum pH. But as the acid is
neutralized in the blood, CO2 is formed (you remember the chemical reaction). The increase
in pH decreases respiratory drive, which slows the elimination of this extra carbon
dioxide. The CO2 diffuses into the cerebrospinal fluid, causing a paradoxical lowing of pH
around the brain, with deepening of coma. The moral: give bicarb slowly and maintain the
hyperventilatory state, even if bag-valve assist or intubation is required.
For the patient in cardiac arrest, raising the pH
hasn’t been shown to improve the ultimate outcome. And alkalosis caused by too much
bicarbonate is positively deadly for the arrest victim. On the other hand, since the
American Heart Association changed its standards to eliminate the routine use of
bicarbonate, I’m seeing a lot of arrested patients from the field with pHs of 6.9
— which may lengthen the “code time” if there's pulseless electrical
activity because the patient can’t be declared dead until he's both “warm and
dead” and “acid-base normal and still dead.” For now, treat the cardiac
arrest patient with bicarbonate only based on proven need by blood gases.
Bicarbonate dosage recommendations vary widely — most
sources recommend from 0.1 to 0.3 times the weight of the patient in kilograms times the
(negative) base excess (BE) expressed in milliequivalents per liter. In my experience, 0.2
x weight x BE is about right for the typical patient. The calculated result of this
formula will have units of milliequivalents — the number you calculate is the dose in
milliequivalents.
However, the recommendation I’ll give to you (and the
formula given in both the Blood Gases disk and the ACLS training software) is based on the
more conservative recommendation of the American College of Emergency Physician’s
textbook. This formula is 0.1 x weight x BE. The minus sign on the base excess is ignored.
Bicarb Dose = 1/10 of weight
in kg times base excess
Bicarb = 0.1 x wt x BE
After giving bicarbonate, a repeat blood gas analysis
should be performed (after a couple of minutes to “blow off” the CO2 that is
formed). Often, an additional dose must be given. If you decide that use of bicarbonate is
needed in a situation where blood gases are NOT available, for example with a tricyclic
overdose or diabetic patient in coma far from a hospital, you need a reasonable way of
calculating an empiric dosage.
In this situation, give the patient one mEq for every
kilogram of body weight:
Emperic Bicarb = 1 mEq x
weight in kg
In the cardiac arrest victim, a continuing dosage may be
necessary IF BLOOD GASES ARE NOT AVAILABLE. This dose is 1/2 mEq per kilogram every 10
minutes. However, you’ll probably never use this 1) because you should be getting
blood gases, and 2) because if your CPR is so ineffective that acid continues to build up
at that rate you’ll never save the patient anyway. The final words on bicarbonate
therapy are: Have a good reason for using it, be aware of its problems and complications,
and monitor your therapy with repeat blood gas analysis. Go to Index.
Back to Main Manual Index.
Copyright 1996 Mad Scientist Software
Citation:
Argyle, B., Blood Gases Computer Program Manual.
Mad Scientist Software, Alpine UT, 1996.