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Figure 3.9 Bicarbonate isopleths (diagonal lines; the bicarbonate level is constant along the lines). It can be seen that, if the bicarbonate level and PCO2 are known, the pH can be calculated. Indeed, if any two of the three values of bicarbonate, pH and PCO2 are known then the other value can be calculated. These values are yoked together. A change in ventilation will move the arterial point up or down an isopleth as shown, changing pH (bicarbonate level does not change). A pure metabolic disturbance (before any respiratory response) changes the bicarbonate level, moving from one bicarbonate isopleth to another and changing pH.
Acid/base disturbances
The three variables pH, PCO2 and bicarbonate are yoked together as just described. Analysis of their values provides information on the acid/base balance of the body and the broad nature of its cause. It may also provide information about the chronicity of an abnormality.
Changes in the acid/base status caused by changes in PCO2 (hyper‐ or hypoventilation) are termed respiratory. Changes in acid/base status caused by changes in bicarbonate are termed metabolic. A disturbance in one system tends to prompt a compensatory response in the other. When needed, the respiratory system responds promptly, and changes are evident within seconds to minutes. The metabolic system, largely regulated via renal excretion, is much slower, taking between hours and days to equilibrate. In respiratory disturbances, therefore, the degree of correction achieved by the metabolic system can tell us something about the duration of the abnormality.
As a general principle, physiological compensatory mechanisms don’t overcompensate; in fact, they often stop just short of total correction. This is a useful fact to remember when trying to interpret a blood gas result that displays both respiratory and metabolic changes. If the pH is in the normal range, it may be difficult to determine which is the primary abnormality and which the compensatory response. Look again at the pH. If the pH is towards the higher end of the normal range, the primary abnormality is probably an alkalosis; if at the lower end then the primary disturbance is an acidosis.
In reading the following examples of acid/base disturbance, refer to the diagrams in Figs 3.9 and 3.10.
Respiratory acidosis (acute): pH reduced, PCO2 raised, bicarbonate normal
A reduction in alveolar ventilation causes an increase in arterial PCO2. The pH falls. In the short term, there is insufficient time for metabolic (renal) correction, so the bicarbonate concentration remains almost unchanged. This pattern is seen where there is a sudden reduction in ventilation, such as obstruction of the airway, overdose of sedative drugs or acute neurological damage.
Respiratory acidosis (chronic): pH normal (lower half of normal range), PCO2 raised, bicarbonate high
If underventilation, from whatever cause, is sustained beyond a few days, renal tubular reabsorption of bicarbonate will achieve a significant elevation in plasma bicarbonate level, which will correct the acidosis caused by the underventilation. This can be caused by any process that results in sustained hypoventilation (commonly seen in COPD).
Respiratory alkalosis (cases are usually acute, as the causes are rarely sustained): pH raised, PCO2 reduced, bicarbonate normal
Alveolar hyperventilation causes a fall in PCO2 and a corresponding rise in pH. Bicarbonate concentration is virtually unchanged. This pattern is seen in any form of acute hyperventilation, including pulmonary embolism, acute severe asthma, anxiety‐related hyperventilation, salicylate poisoning and Covid‐19 pneumonia.
Metabolic acidosis: pH reduced, PCO2 reduced, bicarbonate reduced
The primary disturbance is generally an increase in acid. This has an effect on the equation
Figure 3.10 Acid/base disturbances. The oval indicates the normal position, the shaded areas indicate the directions of observed ‘pure’ or uncomplicated disturbances of acid/base balance. Bicarbonate levels are omitted for clarity. Letters (a)–(d) are referred to in the section on mixed disturbances.
H+ + HCO3 − ⇌ H2O + CO2, pushing it to the right. The CO2 produced is removed by increased ventilation and the net result is a lowering of plasma bicarbonate. In practice, the fall in pH causes further respiratory stimulation, so that CO2 is promptly blown off, and the pH changes are therefore much less dramatic than they would have been. The arterial point moves in the direction indicated in Fig. 3.10. This respiratory compensation is an inevitable accompaniment of metabolic acidosis – acute and chronic – unless there is some other factor limiting ventilatory function or responsiveness.
This pattern is seen in diabetic ketoacidosis, renal tubular acidosis, acute circulatory failure, sepsis and other forms of lactic acidosis.
Metabolic alkalosis: pH raised, PCO2 high normal or slightly raised, bicarbonate raised
An increase in bicarbonate concentration causes a rise in pH. To compensate, ventilation is reduced in order to accumulate CO2. This occurs despite the inevitable fall in PO2. For this reason, however, scope for correction is limited; the compensatory fall in alveolar ventilation is modest and correction in pH may not be complete.
This pattern is seen where there has been administration of excessive alkali, loss of acid through vomiting or reabsorption of bicarbonate (e.g. in hypokalaemia).
Mixed disturbances
Mixed respiratory and metabolic disturbances are common. There are usually a number of possible explanations, so it is essential to consider all the clinical details before interpreting the acid/base data. Fig. 3.10 shows the situations that may arise in complex acid/base disturbances.
Fig. 3.10a (low pH, normal PCO2, low bicarbonate) indicates a mixed metabolic and respiratory acidosis. The metabolic disturbance is perhaps obvious and the respiratory component can be deduced, as the PCO2 is higher than might have been suspected had this been a pure metabolic problem. This pattern could arise in a number of different clinical scenarios, such as a patient with acute severe pulmonary oedema with low cardiac output and ventilatory compromise or a patient in renal failure given a narcotic sedative suppressing ventilatory response to acidosis. Blood gas results should be interpreted in light of clinical data.
Fig. 3.10b could represent the situation soon after a cardiac arrest, where severe lactic acidosis exists and ventilation has been insufficient.
Fig. 3.10c could represent the situation in severe aspirin poisoning, where aspirin‐induced hyperventilation has been complicated by aspirin‐induced metabolic acidosis.
Fig. 3.10d could represent