The normal pH of arterial blood is 7.35–7.45. Normally hydrogen (H+ ) ions are buffered by two main systems:
· Proteins including haemoglobin comprise a fixed buffering system.
· Bicarbonate is a very important buffer, as it has both a gaseous and an aqueous phase:
CO2 ↔ CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3−
This means that bicarbonate buffering is a very powerful way of maintaining the body’s pH through both rapid and slow compensation:
· Rapid compensation takes place at the lungs, where CO2 can be blown off in response to acidosis. This reduces the amount of H2CO3 (carbonic acid) in the blood as shown by the equation and so acutely compensates for acidosis. Conversely, if pCO2 concentrations rise, e.g. in hypoventilation, then acidosis can result (respiratory acidosis).
· In long-term abnormalities of pH balance, this mechanism is inadequate because the body’s stores of bicarbonate become depleted. The kidney is able to compensate for this, by increasing its reabsorption of bicarbonate in the proximal tubule.
The arterial blood gas is used to assess acid–base status. The pH is first examined to see if the patient is acidotic or alkalotic. The pCO2 and bicarbonate are then examined to identify the cause of any acid–base disturbance and any compensation that may have occurred. Most arterial blood gas machines also provide the base excess. This is a calculated figure, which provides an estimate of the metabolic component of the acid–base balance. The base excess is defined as the amount of H+ ions that would be required to return the pH of the blood to 7.35, if the pCO2 were adjusted to normal. A normal base excess is –2 to +2. A more negative base excess signifies a metabolic acidosis (hydrogen ions need to be removed) and a more positive base excess signifies a metabolic alkalosis (hydrogen ions need to be added). The pO2 is examined separately to determine if there is respiratory failure.
There are four main patterns:
· Acidosis with high pCO2 defines a respiratory acidosis. If this is acute, there is no compensation (i.e. the bicarbonate levels are normal). In chronic respiratory acidosis renal reabsorption of bicarbonate will reduce the acidosis (partial metabolic compensation) or return the pH to a normal level (complete metabolic compensation). Causes include respiratory failure.
· Acidosis with low bicarbonate and negative base excess defines a metabolic acidosis. If the patient is able the respiration will increase to reduce carbon dioxide and hence return the pH to normal (partial or complete respiratory compensation). Causes of metabolic acidosis include salicylate poisoning, lactic acidosis or diabetic ketoacidosis. Alternatively failure to excrete acid or increased loss of HCO3− , such as renal tubular disease and diarrhoea. Hyperkalaemia may occur as an important complication particularly if there is also acute renal failure.
· Alkalosis with a low carbon dioxide defines respiratory alkalosis. This may result from any cause of hyperventilation including stroke, subarachnoid haemorrhage, meningitis, pyrexia, hyperthryoidism, pregnancy or anxiety. It is generally an acute condition and so little compensation occurs.
· Alkalosis with a high bicarbonate and a positive base excess defines metabolic alkalosis. It is rare and may be caused by loss of acid from the gastrointestinal tract (e.g. vomiting) or from the kidney (e.g. Cushing or Conn’s syndrome). Hypokalaemia may occur.
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