Isotonic (1.26%) sodium bicarbonate may be used to correct acidosis associated with renal failure or to induce a forced alkaline diuresis. The hypertonic (8.4%) solution is rarely required in intensive care practice to raise blood pH in severe metabolic acidosis. Bicarbonate therapy is inappropriate when tissue hypoperfusion or necrosis is present.

Administration may be indicated as either specific therapy (e.g. alkaline diuresis for salicylate overdose) or if the patient is symptomatic (usually dyspnoeic) in the absence of tissue hypoperfusion (e.g. renal failure).

The PaCO2 may rise if minute volume is not increased. Bicarbonate cannot cross the cell membrane without dissociation so the increase in PaCO2 may result in intracellular acidosis and depression of myocardial cell function.

The decrease in plasma ionised calcium may also cause a decrease in myocardial contractility. Significantly worse haemodynamic effects have been reported with bicarbonate compared to equimolar saline in patients with severe heart failure.

Convincing human evidence that bicarbonate improves myocardial contractility or increases responsiveness to circulating catecholamines in severe acidosis is lacking, though anecdotal success has been reported. Acidosis relating to myocardial depression is related to intracellular changes that are not accurately reflected by arterial blood chemistry.

Excessive administration may cause hyperosmolality, hypernatraemia, hypokalaemia and sodium overload.

Bicarbonate may decrease tissue oxygen availability by a left shift of the oxyhaemoglobin dissociation curve.

Sodium bicarbonate does have a place in the management of acid retention or alkali loss, e.g. chronic renal failure, renal tubular acidosis, fistulae, diarrhoea. Fluid and/or potassium deficits should be corrected first.


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