Metabolic acid–base disorders

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Metabolic acid–base disorders

Metabolic acid–base disorders are caused by an increase in H+ production or a loss of H+ triggering compensatory mechanisms that result in the loss or gain of HCO3−. Direct loss or gain of HCO3− will also cause metabolic acid-base disorders. Primary metabolic acid–base disorders are recognized by inspecting the bicarbonate concentration (Fig 21.1). Respiratory compensation takes place quickly so patients with metabolic acid–base disorders will usually show some change in blood PCO2 because of hyperventilation or hypoventilation (Fig 21.2).

Metabolic acidosis

In a metabolic acidosis the primary problem is a reduction in the bicarbonate concentration of the extracellular fluid. The main causes of a metabolic acidosis are shown in Figure 21.3. These are:

The anion gap

The cause of a metabolic acidosis will nearly always be apparent from the clinical history of the patient, but occasionally knowledge of the anion gap may be helpful. This can be assessed by looking at the serum electrolyte results and calculating the difference between the sum of the two main cations, sodium and potassium, and the sum of the two main anions, chloride and bicarbonate. There is no real gap, of course, as plasma proteins are negatively charged at normal [H+]. These negatively charged amino acid side chains on the proteins account for most of the apparent discrepancy when the measured electrolytes are compared. The anion gap is thus a biochemical tool that is sometimes of help in assessing acid–base problems. It is not a physiological reality.

In practice, because the potassium concentration is so small and will vary by so little, it is generally excluded when calculating the anion gap. Thus:

image

In a healthy person, the anion gap has a value of between 6 and 18 mmol/L. When the bicarbonate concentration rises or falls, other ions must take its place to maintain electrochemical neutrality. If chloride substitutes for bicarbonate, the anion gap does not change. However, the anion gap value will increase in metabolic conditions in which acids, such as sulphuric, lactic or acetoacetic, are produced, or when salicylate is present.

Causes of metabolic acidosis

Metabolic acidosis with an elevated anion gap occurs in:

image Renal disease. Hydrogen ions are retained along with anions such as sulphate and phosphate.

image Diabetic ketoacidosis. Altered metabolism of fatty acids, as a consequence of the lack of insulin, causes endogenous production of acetoacetic and β-hydroxybutyric acids.

image Lactic acidosis. This results from a number of causes, particularly tissue anoxia. In acute hypoxic states such as respiratory failure or cardiac arrest lactic acidosis develops within minutes and is life-threatening. Lactic acidosis may also be caused by liver disease. The presence of a lactic acidosis can be confirmed, if necessary, by the measurement of plasma lactate concentration.

image Certain cases of overdosage or poisoning. The mechanism common to all of these is the production of acid metabolites. Examples include salicylate overdose where build-up of lactate occurs, methanol poisoning when formate accumulates, or ethylene glycol poisoning where oxalate is formed.

Metabolic acidosis with a normal anion gap is sometimes referred to as a ‘hyperchloraemic acidosis’ because a reduced HCO3− concentration is balanced by increased Cl− concentration. It is seen in:

Metabolic alkalosis

The causes of a metabolic alkalosis are shown in Figure 21.3. The condition may be due to:

image Loss of hydrogen ion in gastric fluid during vomiting. This is especially seen when there is pyloric stenosis preventing parallel loss of bicarbonate-rich secretions from the duodenum.

image Ingestion of an absorbable alkali such as sodium bicarbonate. Very large doses are required to cause a metabolic alkalosis unless there is renal impairment.

image Potassium deficiency. In severe potassium depletion, often a consequence of diuretic therapy, hydrogen ions are retained inside cells to replace the missing potassium ions. In the renal tubule more hydrogen ions, rather than potassium, are exchanged for reabsorbed sodium. So, despite there being an alkalosis, the patient passes an acid urine. This is often referred to as a ‘paradoxical’ acid urine, because in other causes of metabolic alkalosis urinary [H+] usually falls.

Clinical effects of alkalosis

The clinical effects of alkalosis include hypoventilation, confusion and eventually coma. Muscle cramps, tetany and paraesthesia may be a consequence of a decrease in the unbound plasma calcium concentration, which is a consequence of the alkalosis.

image Clinical note

A patient who has had prolonged nasogastric suction following surgery will lose gastric fluid in large quantities and may develop a metabolic alkalosis.

Case history 15

A 28-year-old man is admitted to hospital with a week-long history of severe vomiting. He confessed to self-medication of his chronic dyspepsia. He was clinically severely dehydrated and had shallow respiration. Initial biochemical results were:

Arterial blood gases:

image

Serum:

image

A random urine sample was obtained, and had the following biochemical results: osmolality 630 mmol/kg, Na+ <20 mmol/L, K+ 35 mmol/L, pH 5.

Comment on page 165.

Metabolic acid–base disorders

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