Interpretation of arterial blood gases

Arterial blood gases give information on oxygenation, ventilation and acid-base status.

Oxygenation

Oxygenation is assessed using the PaO2. This value must always be interpreted in light of the fractional inspired oxygen concentration (FiO2). This is most simply expressed in terms of the PaO2/FiO2 or P:F ratio. With the PaO2 measured in kPa, the normal P:F ratio is approximately 60. A P:F ratio <25 indicates severe respiratory failure. Do not remove oxygen supplementation in order to measure blood gases with the patient breathing room air.

Use the alveolar gas equation to distinguish hypoxia due to hypoventilation from hypoxia due to shunting or diffusion abnormalities. In the former there will be a normal gradient between alveolar and arterial oxygen tension, while in the latter this gradient will be increased. Assuming a normal barometric pressure at sea level, and a normal respiratory quotient, the alveolar gas equation simplifies to:

PAO2 = FiO2 x 94.5 - PaCO2 x 1.25 [in kPa]

PAO2 = FiO2 x 713 - PaCO2 x 1.25 [in mmHg]

Ventilation

Ventilation has to be assessed in combination with acid-base status as ventilation is an integral part of acid-base homeostasis. A rise in PaCO2 indicates hypoventilation while a fall indicates hyperventilation.

Acid-base disturbance

Metabolic acidosis results in compensatory hyperventilation. Ventilatory compensation for metabolic alkalosis is a fall in ventilation. Conversely, hypoventilation, which produces a respiratory acidosis results in compensatory increase in renal bicarbonate retention while respiratory alkalosis results in increased renal bicarbonate loss (table 1).If there is a mixed acid base disturbance the “compensatory” change may lie outside the range expected as a result of compensation (table 1a & 1b).

Table 1a. Expected compensatory changes resulting from acid base disorders, with partial pressure measured in kPa. § Alternatively use Winter’s formula (for metabolic acidosis only):
Expected PaCO2 = [ ( 1.5 × HCO3 ) + 8 ± 2 ] × 0.133

Table 1b. Expected compensatory changes resulting from acid base disorders, with partial pressures measured in mmHg. § Alternatively use Winter’s formula (for metabolic acidosis only):
Expected PaCO2 = [ ( 1.5 × HCO3 ) + 8 ± 2 ]

Metabolic acidosis

Causes can be divided into those that cause an increased anion gap acidosis and those that cause a normal anion gap acidosis.

Anion gap = Na - Cl - HCO3

Normal anion gap = 8-16

Table 2. Causes of metabolic acidosis

Lactic acidosis

Common in critically ill patients. Unless there is clear evidence to the contrary, lactic acidosis should be assumed to be due to inadequate tissue perfusion. In patients with sepsis there are several pathways of lactate production, one of which is inadequate tissue perfusion (shock).

Table 3. Causes of lactic acidosis. Type A is due to tissue hypoxia

Ketoacidosis
NB detection of ketonuria by stick testing and of ketonaemia by testing serum dilutions with nitroprusside (Acetest) reagent may occasionally be misleading as these tests only react to acetoacetate and not β hydroxybutyrate. The predominant ketone in alcoholic ketoacidosis is β hydroxybutyrate.

Respiratory compensation

Respiratory compensation for primary metabolic acidosis does not restore the pH to normal. The presence of a normal pH in a patient with a metabolic acidosis should raise suspicion of an associated alkalosis. Respiratory compensation for acute acidosis tends to be greater than for chronic metabolic acidosis. The minimum level of PaCO2 that can usually be attained is approx 1.3 kPa. Levels <2-2.7 kPa are rarely maintained in chronic metabolic acidosis.

Metabolic alkalosis

Usually initiated by increased loss of acid from stomach or kidney. Excretion of bicarbonate at high plasma concentrations is normally so rapid that alkalosis will not be sustained unless bicarbonate reabsorption is enhanced or alkali is continuously generated at a great rate.

Maintenance of alkalosis is most often due to stimulation of bicarbonate reabsorption by a volume (chloride) deficit. During volume depletion renal conservation of sodium takes preference over other homeostatic mechanisms. In alkalosis a large fraction of plasma sodium is paired with bicarbonate so complete reabsorption of filtered sodium requires reabsorption of bicarbonate as well. Alkalosis is, therefore, sustained until volume depletion is corrected by administration of sodium chloride. This diminishes the tubular avidity for sodium and provides chloride as an alternative anion for reabsorption with sodium. The excess bicarbonate can then be excreted.

The other major mechanism which can maintain metabolic alkalosis is hypermineralocorticoidism. Elevation of plasma bicarbonate is initiated by increased urinary loss of protons as ammonium and titratable acidity. Stimulation of tubular acid secretion also enhances bicarbonate reabsorption thus sustaining the alkalosis. These patients are not volume or chloride depleted.

Measuring urinary chloride may be helpful if the cause of alkalosis is not evident. It is low (<10 mmol/L) when the alkalosis associated with volume contraction but higher (>20 mmol/L) when alkalosis due to hyperadrenocorticoidism or severe potassium depletion.

Table 4. Causes of metabolic alkalosis.

Respiratory acidosis

Patients with acute hypercapnia are always acidaemic. Those with chronic hypercapnia are usually acidaemic, however some patients with minimal or moderate hypercapnia may have normal or even slightly raised pH. Significant elevation of pH in patients with chronic hypercapnia is almost always due to co-existent metabolic alkalosis (eg due to diuretics, low-sodium diets or post-hypercapnic alkalosis). The causes of hypoventilation (and hence respiratory acidosis) are discussed in the chapter on acute respiratory failure.

Respiratory alkalosis

An acute reduction in CO2 releases hydrogen ions from tissue buffers and minimizes the alkalaemia by reducing plasma bicarbonate. Acute alkalosis also enhances glycolysis, increases production of lactic and pyruvic acids, lowers serum bicarbonate and raises plasma concentrations of corresponding anions by 1-2 mmol. In chronic hypocapnia the plasma bicarbonate is further reduced because decreased PaCO2 inhibits tubular reabsorption and generation of bicarbonate.

Table 5. Causes of respiratory alkalosis

Clinical features

Respiratory alkalosis can cause tetany. This is probably mainly due to direct enhancement of neuromuscular excitability by alkalosis rather than modest decrease in ionized calcium induced by alkalosis. Severe respiratory alkalosis may also cause confusion or loss of consciousness, which may be due to cerebral vasospasm.

Mixed acid-base disorders

Metabolic acidosis and respiratory alkalosis

Common causes include:

Metabolic acidosis and respiratory acidosis

This is the typical acid-base disorder after cardiac arrest or severe pulmonary oedema. It is usually associated with very severe acidaemia. If the arterial blood gases are analysed as a respiratory acidosis, the bicarbonate will be found to be lower than appropriate for the level of PCO2 and the base excess will be negative. If analysed as a metabolic acidosis, the PCO2 will appear inappropriately high. In patients with chronic respiratory acidosis, superimposed metabolic acidosis may reduce the bicarbonate only to a level appropriate for an acute respiratory acidosis.However a negative base excess suggests that the problem is a combined chronic respiratory acidosis and metabolic acidosis, not an acute respiratory acidosis.

Metabolic acidosis and alkalosis

This diagnosis is difficult to make as the pH may be normal, alkalaemic or acidaemic depending on the relative magnitude of the primary disorders. The arterial blood gases are not diagnostic as they can fall within the range expected for either metabolic alkalosis or acidosis or be in the normal range and recognition depends largely on the clinical setting and history. The most common cause is metabolic alkalosis due to vomiting superimposed on diabetic or alcoholic ketoacidosis. Ingestion of large amounts of citrate antacid for the gastric discomfort accompanying DKA or alcoholic ketoacidosis may also result in this acid-base disturbance. If the acidosis is of high anion gap type the presence of a high anion gap may be a clue to a hidden metabolic acidosis. However a high anion gap is not unequivocal evidence of metabolic acidosis. It may be moderately increased and occasionally may be >25 mmol/L in metabolic alkalosis. Increase in unmeasured anions in metabolic alkalosis is due principally to increased albumin anions. Release of protons by albumin acting as a buffer increases the number of anions per molecule. Plasma albumin concentration may also be increased by associated volume depletion.

Metabolic alkalosis and respiratory acidosis

In patients with chronic respiratory acidosis due to pulmonary disease, a metabolic alkalosis is often superimposed by treatment with diuretics, steroids or ventilation. This is important to recognize as metabolic alkalosis will reduce the acidaemic stimulus to breathe.

Metabolic alkalosis with respiratory alkalosis

Causes: