Definition
pH indicates the acidity or alkalinity of the sample. Depending on the sample, the systematic symbol may be pH(a) for arterial blood or pH () for mixed venous blood. The analyzer symbol may be pH. pH is the negative logarithm of the hydrogen ion activity, pH = - log(aH⁺).

What does pH tell you
pH is the measure of the overall acid-base status of the blood. Most metabolic processes depend on pH being kept within a relatively narrow range; normally, blood pH is kept within a narrow range by dynamic buffering from the bicarbonate buffer system. In the blood, the physically dissolved CO₂ is partly hydrated to form carbonic acid (cHCO^-₃), which dissociates into protons and bicarbonate ions as per the following equation:

The Henderson-Hasselbalch equilibrium is maintained mainly through interactive renal and pulmonary control of carbonic acid and bicarbonate concentrations in the blood (i.e., by varying alveolar ventilation, and thus carbonic acid concentration, and varying renal bicarbonate excretion, respectively).

Reference ranges
pH(a) reference range (adult): 7.35 - 7.45
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Clinical interpretation
At any time, blood pH is determined by the concentration of carbonic acid (and thus by pCO₂) relative to the concentration of bicarbonate (as per the Henderson-Hasselbalch equation).

Thus, pH may be seen as composed of a “respiratory” component (i.e., determined by pCO₂, “respiratory acid”) and a “metabolic” component (i.e., determined by the bicarbonate concentration; note that the actual bicarbonate concentration is determined both by the physiological regulation of renal acid or base excretion – i.e., as H⁺ and cHCO^-₃ respectively – and by the titration of excess protons (“metabolic acid”) generated by the metabolism).

Any primary disturbance of the acid-base equilibrium is met by a secondary physiological attempt at “compensation” to normalize pH; in this respect, variations in alveolar ventilation and variations in renal acid-base excretion act as mutually opposing regulators.

Thus, e.g., alveolar hypoventilation (with resultant “respiratory” acidosis (1A on figure)) is sought compensated by increased bicarbonate retention in the kidneys (in principle, a “metabolic” alkalosis (1B on figure)); or a primary “metabolic” acid excess (e.g., lactic acid generation in anaerobic exercise, resulting in “metabolic” acidosis (2A on figure)) will be sought compensated by increasing alveolar ventilation (with resultant hypocapnia, in principle a “respiratory” alkalosis (2B on figure)), with the overall effect of normalizing pH (see figure):

Be aware of the risk of preanalytical errors on pH values.

For more information, go to Preanalytical considerations.

By simultaneous review of pH, pCO₂, and bicarbonate concentration (or the “base excess”, see this), any acid-base disturbance may be classified as follows:

(Plotting the values of pH, pCO₂ and bicarbonate measurements in the diagram below can usually provide information about the type of acid-base disturbance).

The Siggaard-Andersen Acid-Base Chart showing the expected response to primary and compensated acid-base anormalities:

click for enlargement

Acute respiratory acidosis is characterized by low pH, high pCO₂, and normal SBE. If the condition persists, bicarbonate excretion in the kidneys will decrease and acidosis will be partly or totally compensated for by increased bicarbonate concentration in the blood. Compensated respiratory acidosis is characterized by only slightly low (possibly normal) pH, high pCO₂, and high bicarbonate concentration.

Acute metabolic acidosis is characterized by low pH, low bicarbonate concentration, and normal pCO₂. Depending on the patient’s ventilatory capacity, this condition may be partly compensated for by hyperventilation, which results in low pCO₂.

Acute respiratory alkalosis is characterized by high pH and low pCO₂. If persistent (e.g., high-altitude dwelling), compensation occurs by an increased renal bicarbonate excretion, resulting in low bicarbonate concentration 

Acute metabolic alkalosis is characterized by high pH and high bicarbonate concentration. Spontaneously breathing patients may decrease their alveolar ventilation to compensate the alkalosis with an increased pCO₂.

Common causes of low pH (acidosis)

A. Respiratory acidosis:

• Alveolar hypoventilation 

B. Metabolic acidosis:

• Circulatory impairment
• Severe liver failure
• Renal failure
• Diabetic ketoacidosis
• Gastrointestinal loss of bicarbonate (diarrhea)
• Tissue necrosis
• Hyperkalemia

Common causes of high pH (alkalosis)

A. Respiratory alkalosis:

• Alveolar hyperventilation

B. Metabolic alkalosis:

• Diuretics
• Gastrointestinal loss of acid (vomiting)
• Hypokalemia (low cK⁺)
• Hepatic insufficiency

Considerations
Before treating acidemia that occurs with concomitant oxygenation problems, it should be considered whether an acidemia might be beneficial for tissue oxygenation, due to the right shift of the ODC.

Because of the compensatory mechanisms, a near-normal pH value does not exclude the presence of an acid-base imbalance. To evaluate the acid-base balance, even when pH is normal, pCO₂ together with cHCO^-₃, BE, or SBE must be evaluated.

While it may sometimes be difficult to differentiate between primary cause and secondary compensation in mixed acid-base disturbances (e.g., “metabolic” compensation of primary alveolar hypoventilation vs. respiratory compensation of primary metabolic alkalosis – in both cases, both pCO₂ and bicarbonate concentrations are high), the component that “pulls most” may be assumed to be primary (in the above example, hypoventilation may be considered primary if pH is low within the reference range, whereas metabolic alkalosis may be considered primary if pH is high in the reference range). Naturally, the primary deviation should be the therapeutic target.

Be aware of the risk of preanalytical errors on pH values.

For more information, go to Preanalytical considerations.