Delta Ratio = 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.
WHEN TO USE
- can check delta ratio in the presence of a high anion gap metabolic acidosis (HAGMA) to determine if it is a ‘pure’ HAGMA or if there is coexistant normal anion gap metabolic acidosis (NAGMA) or metabolic alkalosis.
ASSUMPTIONS ABOUT BUFFERING ARE NOT CORRECT
- 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
- calculation requires measurement of 4 electrolytes, each with a measurement error
- changes are assessed against ‘standard’ normal values for both anion gap and bicarbonate concentration.
- hyperchloraemic normal anion gap metabolic acidosis (NAGMA)
- 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 HAGMA + NAGMA, BUT note that the ratio is often < 1 in acidosis associated with renal failure
1 – 2
- usual for uncomplicated HAGMA.
- 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)
- 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).
- Delta gap and delta ratio. Deranged Physiology
- Wrenn K. The delta (Δ) gap: An approach to mixed acid-base disorders Annals of emergency medicine 1990; 19(11): 1310-1313.
- Jones BJ, Twomey PJ. The anion gap revisited International journal of clinical practice 2009; 63: 1409-1412.
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of three amazing children.
On Twitter, he is @precordialthump.