ACID BASE DISORDER:

pH HCO3- Pco2 Primary Expected Compensated? Mixed Final

disorder compensation disorder diagnosis
<7.35 12 26 Metabolic Pco2= 1.5*HCO3 + 8 YES No Compensated
acidosis +/- 2 Expected value: 24-28 metabolic
acidosis
<7.35 15 50 Metabolic Same as above for NO, more than Respiratory Metabolic
acidosis metabolic acidosis expected acidosis acidosis +
Expected value:28.5- respiratory
32.5 acidosis
7.35- 15 24 Metabolic Same as above NO, LESS than Respiratory Metabolic
7.45 acidosis expected alkalosis acidosis +
Expected value:28.5- respiratory
32.5 alkalosis
>7.45 30 44 Metabolic PaCO2= 0.75*(change Yes No Compensated
alkalosis in HCO3 from 24) + 40 Expected value: 44.5 metabolic
alkalosis
>7.45 33 38 Metabolic Same as above No, less than expected Respiratory Metabolic
alkalosis For metabolic Expected value: 46.75 alkalosis alkalosis +
alkalosis respiratory
alkalosis
7.35- 42 67 Metabolic Same as above No, more than Respiratory Metabolic
7.45 alkalosis expected. acidosis alkalosis +
Expected value: 53.5 respiratory
acidosis
<7.35 25 55 Respiratory Acute: Yes, CLOSE to acute no Compensated
acidosis HCO3= 0.1* (change compensated value acute
in PaCO2 from 40) + Expected value: 25.5 respiratory
24 acidosis
<7.35 30 55 Respiratory Chronic: HCO3= Yes, close to chronic no Compensated
acidosis 0.4*(Change in PaCO2 compensated value chronic
from 40) + 24 Expected value: 30 respiratory
acidosis
>7.45 23 30 Respiratory Acute: HCO3= 24 - Yes, close to acute No Compensated
alkalosis 0.2* (Change in compensated value acute
PaCO2 from 40) Expected value:22 respiratory
alkalosis
>7.45 20 30 Respiratory Chronic: HCO3= 24 – Yes, close to chronic No Compensated
alkalosis 0.4*(Change in PaCO2 compensated value chronic
from 40) Expected value: 20 respiratory
alkalosis
<7.35 15 50 Respiratory Calculate as above for No, HCO3 value is less Metabolic Respiratory
acidosis acute and chronic for than expected, here acidosis acidosis +
respiratory acidosis the range is metabolic
and make a range 25-28 acidosis
7.35- 32 50 Respiratory Calculate as above for No, HCO3 value is Metabolic Respiratory
7.45 acidosis acute and chronic for more than expected, alkalosis acidosis +
respiratory acidosis here range is 25-28 metabolic
and make a range alkalosis
7.35- 18 30 Respiratory Calculate as above for No, HCO3 value is less Metabolic Respiratory
7.45 alkalosis acute and chronic than expected, here acidosis alkalosis +
respiratory alkalosis range is 20-22 metabolic
and make a range acidosis
>7.45 33 30 Respiratory Calculate as above for No, HCO3 value is Metabolic Respiratory
alkalosis acute and chronic more than expected alkalosis alkalosis+
respiratory alkalosis Here range is 20-22 metabolic
and make a range alkalosis

• MUST TO KNOW:
1. pH within normal limit doesn’t indicate compensation, rather it indicates mixed disorder.
2. Compensation take Ph to near normal, but never normal except chronic prolonged respiratory alkalosis, where it can be normal

Reference ranges:
• PaCO2: 35–45 mm Hg
• SaO2: >>= 95%
• pH: 7.35–7.45
• HCO3-: 21 to 27 mEq/L
• Resting PaO2 > 80 mm Hg is considered normal.

3. There are 4 steps:

We suggest the following four-step approach:
● Step 1: Establish the primary diagnosis:

•Metabolic acidosis is characterized by a low serum HCO3 and a low arterial pH; the serum anion gap
may be increased or normal.

•Metabolic alkalosis is characterized by an elevated serum HCO3 and an elevated arterial pH.

•Respiratory acidosis is characterized by an elevated arterial PCO2 and a low arterial pH.

•Respiratory alkalosis is characterized by low arterial PCO2 and an elevated arterial pH.

•With the exception of chronic respiratory alkalosis and mild to moderate respiratory acidosis (see
'Mixed acid-base disorders' below), compensatory responses do not usually return the arterial pH to
normal.

Thus, a normal arterial pH in the presence of substantial changes in both serum HCO3 and arterial
PCO2 is usually indicative of a mixed acid-base disorder (which could include an iatrogenic acute
respiratory alkalosis if discomfort from the arterial puncture causes the patient to hyperventilate).

●Step 2: Assess the degree of compensation as defined above for the individual disorders. If the
compensatory response is inadequate or excessive for the patient's clinical circumstances, then a
mixed acid-base disorder exists. (See 'Compensatory respiratory and renal responses' above.)

Determination of the expected compensatory response requires historical information. This is

particularly true for the respiratory acid-base disorders, in which compensation evolves from acute
(minutes to a few days) to chronic (three to five days or more). The normal compensatory response to
acute respiratory acidosis is an increase in the serum HCO3 concentration by approximately 1 mEq/L
for every 10 mmHg (1.3 kPa) elevation in the PCO2. When the respiratory acidosis persists for more
than three to five days, the HCO3 increases by approximately 3.5 to 5 mEq/L for every 10 mmHg (1.3
kPa) elevation in the PCO2. (See 'Response to respiratory acidosis' above.)

●Step 3: Determine whether or not the anion gap is elevated. This is especially important for patients
with metabolic disorders. If metabolic acidosis exists and the anion gap is increased, compare the
increase in anion gap to the decrease in the HCO3 concentration. This delta anion gap/delta HCO3
ratio should be approximately 1 when a simple anion gap metabolic acidosis exists.
The serum AG is calculated from the following formula, which represents the difference between the
primary measured cation (sodium [Na]) and the primary measured anions (chlorine [Cl] and
bicarbonate [HCO3]):
Serum AG = Na - (Cl + HCO3)
Some clinicians also include the serum potassium (K) in the formula; when this is done, the normal
range increases by approximately 4 mEq/L:
Serum AG = (Na + K) - (Cl + HCO3)

●Step 4: The fourth and final step is to establish the clinical diagnosis. Once the acid-base disorder, or
disorders, is identified, the underlying cause or causes of each disorder should be determined and
addressed.

WHY HISTORY IS IMPORTANT:

Case 1 — A patient with an unknown past history presents with respiratory distress. Arterial blood
shows a pH of 7.32, PCO2 of 70 mmHg (9.3 kPa), and HCO3 of 35 mEq/L. The patient is acidemic and
has a high PCO2. This is consistent with respiratory acidosis. The PCO2 is approximately 30 mmHg
above its normal range. If this is chronic then the HCO3 should increase by approximately 12 mEq/L
(and it was increased by 11 mEq/L from a normal value of 24 mEq/L). Thus, these values are
compatible with a diagnosis of a simple (fully compensated) chronic respiratory acidosis.
However, the results are also compatible with a mixed acid-base disorder. This patient could have
developed metabolic alkalosis due to gastroenteritis and vomiting. This may have increased his HCO3
from 24 to 32 mEq/L. Perhaps the patient then developed acute respiratory acidosis (from ingestion
of a drug that depressed the respiratory center) causing an acute increase in PCO2 from 40 (5.3 kPa)
to 70 mmHg (9.3 kPa). This acute respiratory acidosis would further increase the HCO3 by
approximately 3 to 36 mEq/L. These two acid-base diagnostic possibilities (chronic respiratory acidosis
versus acute respiratory acidosis and metabolic alkalosis) have identical laboratory findings. The only
way to differentiate them is an accurate history.

Case 2 — A patient presents with diarrhea. Arterial blood shows a pH of 7.24, PCO2 of 24 mmHg (3.2
kPa), and HCO3 or 10 mEq/L. The low pH indicates acidemia, and the low serum HCO3 concentration
indicates metabolic acidosis. The serum HCO3 concentration of 10 mEq/L is approximately 14 mEq/L
below normal. This should stimulate respiratory compensation, and the Winters' equation suggests
that the PCO2 should be approximately 23 mmHg (3.1 kPa). The HCO3 + 15 rule suggests that the
PCO2 should be approximately 25 mmHg (3.3 kPa). Thus, the patient's PCO2 of 24 mmHg (3.2 kPa) is
in the appropriate range for compensation for this degree of metabolic acidosis. In addition, the PCO2
is the same as the decimal digits of the arterial pH. (See 'Response to metabolic acidosis' above.)
If the PCO2 had been significantly higher than 24 mmHg (3.2 kPa) these results would be consistent
with a mixed metabolic acidosis and respiratory acidosis. This might occur, for example, if the patient
were obtunded and had respiratory center depression. If, on the other hand, the PCO2 had been
significantly lower than 24 mmHg (3.2 kPa), then mixed metabolic acidosis and respiratory alkalosis
exists. Mixed metabolic acidosis and respiratory alkalosis often develops with salicylate intoxication or
septic shock

Case 3 — Determining the appropriate compensatory response may be more difficult with respiratory
acid-base disorders because compensatory responses differ in acute and chronic disturbances.
Consider a patient with the following arterial blood values: pH 7.27, PCO2 70 mmHg (9.3 kPa), and
HCO3 31 mEq/L. The low pH and hypercapnia indicate that the patient has respiratory acidosis. If this
patient has acute hypercapnia, then the 30 mmHg (4 kPa) rise in PCO2 should increase the serum
HCO3 concentration by approximately 3 mEq/L (to approximately 27 mEq/L). If this patient has
chronic hypercapnia, the serum HCO3 should increase by approximately 11 mEq/L (to approximately
35 mEq/L). The observed value of 31 mEq/L is between these expected levels and could have multiple
explanations, including:
● Chronic respiratory acidosis with a superimposed metabolic acidosis that has reduced the serum
HCO3 from 35 to 31 mEq/L. This might occur in a patient with chronic obstructive pulmonary disease
who developed diarrhea due to viral gastroenteritis or lactic acidosis from sepsis.

● Acute respiratory acidosis with a superimposed metabolic alkalosis that has increased the HCO3
from 27 to 31 mEq/L. This could occur in a patient with respiratory depression due to a sedating drug
who also developed vomiting or was taking diuretics.

● Acute respiratory acidosis superimposed on mild chronic respiratory acidosis. Suppose, for example,
that a patient has chronic respiratory acidosis with a PCO2 of 55 mmHg (7.3 kPa) and an appropriate
serum HCO3 of 30 mEq/L. The patient then develops pneumonia, which acutely causes a further
increase in the PCO2 to 70 mmHg (9.3 kPa). The serum HCO3 would rise further to approximately 31
mEq/L.

● Acute respiratory acidosis that is evolving into a chronic disorder (between one and three days).

Thus, the correct diagnosis in a primary respiratory acid-base disorder can be established only when
correlated with the patient's history and physical examination. This is true even when the arterial
blood values appear to represent a simple disorder. If the serum HCO3 concentration had been 35
mEq/L in this example, the findings would have been compatible with an uncomplicated chronic
respiratory acidosis. However, similar findings could have been induced by acute respiratory acidosis
plus metabolic alkalosis. The history usually helps to distinguish among the possibilities.

Compiled by:

Dr. Sagor Dey, MBBS (SMC), FCPS P-1(Rheumatology)

ADMIN (MEDICINE MANIAC)