Acid-base Balance

Arterial blood pH is normally closely regulated to between 7.35 and 7.45. Maintaining the pH within these limits is achieved by bicarbonate, other buffers, the lungs and the kidneys. Primary changes in bicarbonate are metabolic and primary changes in carbon dioxide are respiratory.

• In the absence of any significant respiratory disease or hyperventilation it can be assumed that the primary cause is metabolic.
• In general the kidneys compensate for respiratory causes and the lungs compensate for metabolic causes. Therefore hyperventilation may be a cause of respiratory alkalosis or a compensatory mechanism for metabolic acidosis.

• pH: to determine whether acidaemia or alkalaemia are present. Arterial pH is not required in the assessment of metabolic acidosis or metabolic alkalosis and serum bicarbonate is adequate in these situations. Arterial pH is required in situations where it is not clear whether the cause is metabolic or respiratory, or when there is a mixed disturbance of acid-base balance.
• Carbon dioxide: If raised with acidosis then the acidosis is respiratory. If decreased with alkalosis then the alkalosis is respiratory. Otherwise any change is compensatory.
• Bicarbonate: increased with metabolic alkalosis and decreased in metabolic acidosis. Otherwise the change is compensatory (i.e. normal or raised in respiratory acidosis; normal or decreased in respiratory alkalosis).
• Standard bicarbonate: calculated from arterial blood gas values to indicate what the bicarbonate would be if the carbon dioxide excretion were normal. It therefore allows assessment of whether there is a metabolic component of any decrease in the level of bicarbonate.
• Chloride: high chloride associated with metabolic acidosis is usually due to impaired renal handling of acid, e.g. renal tubular acidosis.

• In plasma, the sum of the cations (sodium plus potassium) is normally greater than that of the anions (chloride plus bicarbonate) by approximately 14 mmol/l (normal range 10-18 mmol/l). This is known as the anion gap.
• The anion gap exists because there are more unmeasured anions (mostly albumin, but others include lactate and sulphate) than cations (includes calcium and magnesium).
• Metabolic acidosis is generally divided into those with high and those with normal anion gap.

Respiratory effects deep sighing respiration (Kussmaul breathing) is a common feature of acidosis (hyperventilation in an attempt to remove carbon dioxide) but may take some hours to appear. Causes of metabolic acidosis include:

• Increased anion gap:
  • Lactic acidosis: shock, infection, hypoxia
  • Urate (renal failure)
  • Ketones (diabetes mellitus, alcohol)
  • Drugs or toxins: salicylates, metformin, ethylene glycol, methanol
• Normal anion gap (due to loss of bicarbonate or ingestion hydrogen ions):
  • Renal tubular acidosis
  • Diarrhoea
  • Addison's disease
  • Pancreatic fistulae
  • Drugs or toxins: acetazolamide, ammonium chloride

Causes of metabolic alkalosis include:

• Vomiting
• Potassium depletion, e.g. diuretics
• Burns

Causes of respiratory acidosis:

• Any upper or lower respiratory tract or neuromuscular cause of respiratory failure

Respiratory alkalosis results from hyperventilation:

• Anxiety
• Central nervous system: e.g. stroke, meningitis
• Altitude
• Pregnancy

Treatment is of the underlying condition.

• Cardiovascular effects: acidosis reduces cardiac contractility and both acidosis and alkalosis predispose to arrhythmias.
• Nervous system effects: severe acidosis often causes impaired consciousness ranging from mild drowsiness to coma.