Normal serum pH ranges from 7.34-7.45. This is a tightly regulated range, and any disturbances lead to acid-base imbalances. The imbalances include
The situation is more complex as patients can have mixed disturbances involving both respiratory and metabolic disorders. The body will attempt to move towards a normal pH; however, in a mixed disorder, this is not possible.
ABGs are useful in monitor acid-base changes as well as compensatory changes.
Arterial Blood Gas Test
The ABG will report
A PCO2 of 40 is used for equations to determine predicted pH. The size of the discrepancy between predicted and measure pH can help determine the type of alkalosis or acidosis present.
To evaluate ABGs to determine acid-base imbalances:
Metabolic acidosis occurs if the measured pH is greater than the calculated pH.
Metabolic alkalosis occurs if the measured pH is lower than the calculated pH.
Note that in compensated abnormalities, the body can respond using increased or decreased ventilation to push the pH back to normal. For example, in a primary metabolic acidosis, respiratory compensation will lead to hyperventilation (or respiratory alkalosis) to try and blow off excess CO2. Another example is respiratory acidosis, in which the kidneys would metabolically compensate by retaining the bicarbonate to increase pH back to normal. Be aware that respiratory compensation is usually immediate, while metabolic compensations may take 8-48 hours to take effect. The compensation will stop if the pH is normalized.
This acid-base imbalance can occur due to chronic obstructive pulmonary diseases (COPD) in which the patient retains CO2. With increasing PCO2, there is respiratory acidosis. The kidneys will gradually compensate for this by reabsorbing HCO3 to oppose the acidosis. This is a metabolic alkalosis compensation.
Notice that the physiologic mechanisms to compensate are unlikely to go too far and overcompensate, rather they approach normal pH. So if a patient in respiratory failure (primary respiratory acidosis) has a pH that is alkalotic, it is unlikely that it is due to compensatory metabolic alkalosis. Rather there is likely an associated primary metabolic alkalosis driving the pH higher than normal. Such a cause may be hypokalemic or hyperchloremic metabolic alkalosis due to furosemide treatment in a patient who did not get adequate supplementation with potassium chloride. This knowledge helps determine primary versus compensatory conditions.
This calculated number can determine the etiology of acid-base imbalance. The positive cations (potassium and sodium) should be about equal to the negative anions (bicarbonate and chloride). However, a gap remains due to unmeasured anions such as lactic acid and ketones. The anion gap indicates the difference between major cations and anions:
The normal range is 7+/- 4 mEq/L. Normal gap acid-base imbalances indicate that the imbalances are due to bicarbonate and chloride. For example, in diarrhea, metabolic acidosis is secondary to lost bicarbonate and compensated by retained chloride. This is a normal gap acidosis. However, if the anion gap is high (over 11 mEq/L), unmeasured anions are contributing to acidosis (i.e., ketones and lactic acid) or not enough compensation with chloride. Diabetic ketoacidosis is a well-known case of a high-gap acidosis.