Acid-base balance: part II. Pathophysiology.
OBJECTIVE
To review the normal human acid-base physiology and the pathophysiology and management of acid-base disturbances in a two-part presentation.


METHODS
Articles and published peer-review abstracts and a review of studies reported from 1990 to 2000 and identified through a MEDLINE search of the English language literature on acid-base balance.


RESULTS
Acid-base disorders are usually classified as metabolic (non-respiratory) or respiratory, depending on whether the primary change occurs in the plasma bicarbonate or the carbonic acid (i.e. carbon dioxide) concentrations, respectively. Respiratory or renal compensatory changes usually occur to minimise the effect of the primary disturbance. A metabolic acidosis arises from an abnormal process that generates non-carbonic acid or an abnormal loss of HCO3- and may be identified by an increase or normal anion gap, respectively. The arterial blood gas usually reveals a pH < 7.36, PCO2 < 35 mmHg and 'calculated' HCO3- < 18 mmol/L. In general, a high anion gap acidosis is managed by treating the disorder generating the acid (thereby ceasing the acid production) and enhancing the clearance of the acid anion (e.g. by metabolism or excretion) thereby regenerating the HCO3- reduced by buffering. A metabolic alkalosis arises from an abnormal process generating excess HCO3-. The arterial blood gas usually reveals a pH > 7.44, PCO2 > 45 mmHg and 'calculated' HCO3- > 32 mmol/L. As the kidney has a large capacity to excrete HCO3-, management usually requires treatment of the processes that are generating as well maintaining the alkalosis. Respiratory acidosis and alkalosis are usually caused by a primary disorder of carbon-dioxide excretion, and correction of the pH disorder only occurs with correction of the primary disease process.


CONCLUSIONS
In man, acid-base disturbances are usually classified as either metabolic or respiratory. Correction of the underlying disorder is often all that is required to allow the body to metabolise or excrete the acid or alkali and return the buffer pair (HCO3- and PCO2) to normal.
McNamara
J
J
Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, South Australia.
Worthley
L I
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