There has been considerable controversy over the use of sodium bicarbonate as a buffer to correct acidosis during cardiac arrest and there is little research to support its use (Bar-Joseph et al. 2002). Initial support for its routine use has diminished (Gazmuri 1999). Blood gas analysis is often unavailable quickly and in any case, arterial blood gases do not reflect intracellular values. In some cases, administration of sodium bicarbonate may worsen intracellular acidosis. Additionally, some degree of acidosis increases cerebral blood flow, so normalisation of values may hinder cerebral protection (Resuscitation Council UK 2000). However, acidosis reduces cardiac contractility (Adgey 1998) and so small dosages (50mmol intravenously; 50 ml of 8.4% solution) can be given in the following circumstances.
• Severe acidosis - pH <7.1 or BE <-10. This may exist prior to the cardiac arrest.
• Cardiac arrest associated with hyperkalaemia (raised potassium levels).
• Cardiac arrest associated with tricyclic antidepressant (for example, dothiepin, imipramine) overdose.
• Sodium bicarbonate causes tissue damage if the cannula extravasates; a large vessel such as the external jugular vein is a preferred route for administration.
• A flush with 0.9% saline must follow sodium bicarbonate infusion.
• If given with calcium chloride, calcium carbonate is precipitated.
• The tracheal route must always be avoided.
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