Disorders of acid–base balance

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1.5 Disorders of acid–base balance

Metabolic acidosis

A metabolic acidosis is any process, other than a rise in PaCO₂, that acts to lower blood pH. It may occur through accumulation of metabolic acids (excess ingestion, increased production or reduced renal excretion) or through excessive loss of base (HCO₃). Calculating the anion gap (see over) may help to establish the cause of a metabolic acidosis.

Metabolic acidosis is recognised on an ABG by low HCO₃ (and negative base excess (BE)). There is normally a compensatory increase in alveolar ventilation to lower PaCO₂. If respiratory compensation is overwhelmed, an acidaemia will result. Severity must be judged according to both the underlying process and the resulting acidaemia. An HCO₃ < 15 mmol/L (or BE < 10) indicates a severe acidotic process whereas a pH < 7.25 (H⁺ > 55) constitutes serious acidaemia.

The dominant symptom in metabolic acidosis is often hyperventilation (Kussmaul’s respiration) owing to the respiratory compensation. Other signs are fairly non-specific or related to the underlying cause. Profound acidaemia (pH < 7.15; H⁺ > 70) may lead to circulatory shock, organ dysfunction, and, ultimately death.

Specific causes of metabolic acidosis are discussed in greater detail in the relevant cases in Part 2.

In blood, positively charged ions (cations) must be balanced by negatively charged ions (anions) to maintain electroneutrality. But when the main cations (Na⁺ + K⁺) are compared with the main anions (Cl⁻ + HCO₃⁻), there appears to be a shortage of anions or an anion gap.

The gap is made up of unmeasured anions such as phosphate and sulphate and negatively charged proteins (these are difficult to measure).

A raised anion gap (>18 mmol/L) therefore indicates the presence of increased unmeasured anions, e.g. lactate, salicylate.

A note on … lactic acidosis

This common cause of metabolic acidosis occurs when tissues receive an inadequate supply of O₂ due to either hypoxaemia or impaired perfusion. Normal aerobic metabolism (which relies on O₂) is then replaced by anaerobic metabolism (which generates lactic acid). Lactic acidosis is therefore a marker of tissue hypoxia and a useful indicator of severity in a variety of conditions, including severe hypoxaemia or shock from any cause.

Metabolic alkalosis

A metabolic alkalosis is any process, other than a fall in PaCO₂, that acts to increase blood pH and is characterised by a rise in plasma HCO₃. Respiratory compensation (↑PaCO₂) occurs to limit the resulting alkalaemia but is limited by the need to avoid hypoxaemia.

Loss of H⁺ ions may initiate the process but the kidneys have huge scope to correct threatened alkalosis by increasing HCO₃ excretion. Factors that impair this response are therefore also necessary. The usual suspects are depletion of chloride (Cl⁻), potassium (K⁺) and sodium (Na⁺) ions – in most cases due to either sustained vomiting (Figure 17) or diuretic drugs.

Figure 17 Effect of vomiting on acid–base balance.

Respiratory acidosis

A respiratory acidosis is, simply, an increase in PaCO₂. Since CO₂ dissolves in blood to form carbonic acid, this has the effect of lowering pH (↑H⁺ ions).

Normally, lungs are able to increase ventilation to maintain a normal PaCO₂ – even in conditions of increased CO₂ production (e.g. sepsis). Thus, respiratory acidosis always implies a degree of reduced alveolar ventilation. This may occur from any cause of type 2 respiratory impairment (see section 1.3) or to counteract a metabolic alkalosis.

Respiratory alkalosis

A respiratory alkalosis is a decrease in PaCO₂ and is caused by alveolar hyperventilation. Primary causes include, pain, anxiety (hyperventilation syndrome), fever, breathlessness and hypoxaemia. It may also occur to counteract a metabolic acidosis.

Acute versus chronic respiratory acidosis

Since metabolic compensatory responses take days to develop, acute respiratory acidosis is almost always uncompensated, leading rapidly to profound and dangerous acidaemia. Indeed, an opposing metabolic alkalosis suggests that a respiratory acidosis must have been present for some time. In other words, the presence of metabolic compensation distinguishes chronic from acute type 2 ventilatory failure (see section 1.3).

Mixed respiratory and metabolic acidosis

This is the most dangerous pattern of acid–base abnormality. It leads to profound acidaemia as there are two simultaneous acidotic processes with no compensation. In clinical practice it is often due to severe ventilatory failure, in which the rising PaCO₂ (respiratory acidosis) is accompanied by a low PaO₂, resulting in tissue hypoxia and consequent lactic acidosis.

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