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Delta Ratio

The delta ratio is used to quantify the relationship between changes in the anion gap and bicarbonate in metabolic acidosis. It is calculated as the increase in anion gap divided by the decrease in bicarbonate. A delta ratio of 1 indicates that all buffering occurred extracellularly by bicarbonate, but in reality 50% occurs intracellularly. This causes the anion gap to increase more than the bicarbonate decreases, resulting in a delta ratio greater than 1 in high anion gap metabolic acidosis. The delta ratio can help distinguish between normal anion gap versus high anion gap acidosis and provide insight into the underlying etiology.

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286 views2 pages

Delta Ratio

The delta ratio is used to quantify the relationship between changes in the anion gap and bicarbonate in metabolic acidosis. It is calculated as the increase in anion gap divided by the decrease in bicarbonate. A delta ratio of 1 indicates that all buffering occurred extracellularly by bicarbonate, but in reality 50% occurs intracellularly. This causes the anion gap to increase more than the bicarbonate decreases, resulting in a delta ratio greater than 1 in high anion gap metabolic acidosis. The delta ratio can help distinguish between normal anion gap versus high anion gap acidosis and provide insight into the underlying etiology.

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gasman2003
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Delta Ratio PY = the increase in Anion Gap/the decrease in HCO3- if one molecule of metabolic acid (HA) is added to the

ECF and dissociates, the one H+ released will react with one molecule of HCO3- to produce CO2 and H2O (buffering). - the net effect will be an increase in unmeasured anions by the one acid anion A- (ie anion gap increases by one) and a decrease in the bicarbonate by one. - if all the acid dissociated in the ECF and all the buffering was by bicarbonate, then the increase in the AG should be equal to the decrease in bicarbonate so the ratio between these two changes (which we call the delta ratio) should be equal to one. - the delta ratio quantifies the relationship between the changes in these two quantities. - the above assumptions about all buffering occurring in the ECF and being totally by bicarbonate are not correct. - 50% of the buffering for a metabolic acidosis occurs intracellularly. This amount of H+ from the metabolic acid (HA) does not react with extracellular HCO3- so the extracellular [HCO3-] will not fall as far as originally predicted. The acid anion (ie A-) however is charged and tends to stay extracellularly so the increase in the anion gap in the plasma will tend to be as much as predicted. - overall, this significant intracellular buffering with extracellular retention of the unmeasured acid anion will cause the value of the delta ratio to be greater than one in a high AG metabolic acidosis.

Sources of error
(i) calculation requires measurement of 4 electrolytes, each with a measurement error (ii) changes are assessed against 'standard' normal values for both anion gap and bicarbonate concentration.

Interpretation
< 0.4 - hyperchloraemic normal anion gap acidosis - the reason here is that the acid involved is effectively hydrochloric acid (HCl) and the rise in plasma [chloride] is accounted for in the calculation of anion gap (ie chloride is a 'measured anion'). - the result is that the 'rise in anion gap' (the numerator in the delta ratio calculation) does not occur but the 'decrease in bicarbonate' (the denominator) does rise in numerical value. - the net of both these changes then is to cause a marked drop in delta ratio (commonly to < 0.4) 0.4 - 0.8 - consider combined high AG & normal AG acidosis BUT note that the ratio is often < 1 in acidosis associated with renal failure

Jeremy Fernando (2010)

1 - 2 - usual for uncomplicated high-AG acidosis. - lactic acidosis: average value 1.6 - DKA more likely to have a ratio closer to 1 due to urine ketone loss (esp. if patient not dehydrated) > 2 - a high delta ratio can occur in the situation where the patient had quite an elevated bicarbonate value at the onset of the metabolic acidosis. - such an elevated level could be due to a pre-existing metabolic alkalosis, or to compensation for a pre-existing respiratory acidosis (ie compensated chronic respiratory acidosis).

Jeremy Fernando (2010)

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