Peer reviewed by Dr Steven Musca and Dr Patricia Hurune
55 year old male with known ESRF presented to hospital with shortness of breath after missing haemodialysis (HDx).
PMHx: CKD-5D (HDx 3x/wk via AV fistula), T1DM, HTN
VBG on presentation:
|VBG Parameter||Patient Value||Normal Range|
|pH||7.13*||7.31 – 7.41|
|pCO2||43mmHg||40 – 50|
|HCO3||14mmol/L*||22 – 26|
|Base Excess||-14.4mmol/L*||-2 to +2|
|Hb||101g/L*||120 – 160|
|Na||122mmol/L*||135 – 145|
|K||7.7mmol/L*||3.5 – 4.5|
|Cl||87mmol/L*||98 – 106|
|Glucose||>60.0mmol/L*||3.9 – 5.8|
Interpretation of blood gases
A common question for the CICM Second Part Examination is interpretation of a blood gas, with a request to comment on the specific abnormalities of the blood gas. Having a structure will ensure you don’t miss any important details in the exam or on your next ward round. In this blog post I’ll demonstrate a structure I use to help interpret blood gases.
My structure starts with the assumption that there is only one normal arterial blood gas (note: VBG values vary slightly):
pH = 7.4
pCO2 = 40mmHg
HCO3– = 24mmol/L
Any deviation from this is then described using the various rules for acute/chronic respiratory/metabolic acidosis/alkalosis. (See references 1 and 2).
NB: for this blog post we will be looking at VBGs only, and we will omit my usual first step of assessing adequacy of oxygenation and determination of A-a gradient (to be covered in a future post!)
Question 1. Describe the acid-base abnormalities on the above blood gas.
1a. Is there an acidaemia or alkalaemia?Click to see answer
There is an acidaemia (pH < 7.31 on VBG).
1b. Is the acidaemia explained by a respiratory or metabolic abnormality?Click to see answer
In this example the pCO2 is in the normal range for a VBG, which doesn’t explain the acidaemia. However, the HCO3 is < 22, which fits with a metabolic acidosis contributing to the acidaemia.
1c. Assess for compensation using ABG interpretation rulesClick to see answer
The expected pCO2 would be 1.5x[HCO3–] + 8 = 29; therefore, there is likely a respiratory acidosis, or inadequate compensation; however interpretation must be cautious from a VBG (rule applies for paCO2).
1d. For the metabolic acidosis, determine if the anion gap (AG) is high or normalClick to see answer
AG = Na – (Cl + HCO3)
Normal value = 12
This is a high anion-gap metabolic acidosis (HAGMA), with an AG of 122 – (87+14) = 21
1e. Determine the delta gap or delta ratioClick to see answer
This is done to determine if the acidosis is entirely due to the extra anions in the AG, or if there is also another cause contributing to the acidosis (i.e. a co-existing normal anion-gap metabolic acidosis – NAGMA)
Delta gap = (change in AG) – (change
where normal AG = 12, and normal HCO3 = 24
Delta gap < -6 implies there is a mixed HAGMA and NAGMA
Delta gap -6 to 6 implies there is only a HAGMA, with no co-existing NAGMA
Delta gap >6 implies there is a mixed HAGMA and a metabolic alkalosis
The delta gap is (21-12) – (24-14) = 9-10 = -1 suggesting only HAGMA
The delta ratio uses the same information, but is a ratio comparison
Delta ratio = (change in AG) / (change
<0.4 = NAGMA
0.4 – 0.8 = mixed HAGMA and NAGMA
0.8 – 2 = pure HAGMA
>2 = mixed HAGMA and a metabolic alkalosis
The delta ratio is 9/10 = 0.9 –> suggests pure HAGMA (see reference 3)
1f. Note other relevant featuresClick to see answer
There is a lactic acidosis, with a raised lactate of 4.4.
NB: although a raised lactate is one of the causes of a high anion-gap, the lactate of 4.4 mmol/L does not explain the whole increase in the AG from 12 (normal) to 21. There are 9mmol/L of “extra anions” so something else must also be contributing.
There is also anaemia, hyponatremia, a significant hyperkalaemia and hyperglycaemia.
This question is a good example of how to work through an approach to metabolic acidosis on a blood gas.
Question 2. What are the general causes of a HAGMA?Click to see answer
A common mnemonic for HAGMA is “Left Total Knee Replacement” or LTKR
LTKR – Lactic acidosis, Toxins, Ketones and Renal failure
As you can see – all of the above could be contributing to this case.
There are many potential causes of a lactic acidosis, and several possible toxins include ethylene glycol, methanol and pyroglutamic acidosis.
Question 3. What are some of the specific contributors in this case?Click to see answer
Lactic acidosis – shock/sepsis related?
Ketones – DKA
Renal failure – known ESRF
Question 4. The formal EUC comes back as below. Please comment on the abnormalities with a possible cause for each.
|Parameter||Patient Value||Normal Range|
|Na||121 mmol/L*||135 – 145|
|K||8.3 mmol/L*||3.5 – 2.0|
|Cl||82 mmol/L*||98 – 109|
|Urea||22.9 mmol/L*||2.1 – 7.1|
|Creatinine||465 umol/L*||49 – 90|
|ALT||36 U/L||35 – 50|
|GGT||168 U/L*||40 – 100|
|Glucose||74.0 mmol/L*||3.0 – 7.7|
Ketones: 5 mmol/L (on bedside fingerprick)Click to see answer
Hyponatraemia – possibly hypervolaemic due to missed haemodialysis (HDx), pseudohyponatraemia due to hyperglycemia
Hyperkalaemia, hyperphosphataemia – in setting of missed HDx
Renal impairment – known ESRF
Mildly deranged LFTs with obstructive pattern – ?possible trigger for DKA, or just part of illness
Hyperglycaemia, ketosis – T1DM with poor control DKA
Click to see answer
Question 5. The following ECG was taken. Comment on the abnormalities seen
HR approximately 60, sinus rhythm
Borderline right axis deviation
Increased PR interval (>0.2ms)
Mildly increased QRS duration (>0.12ms)
Widespread peaked T-waves, consistent with hyperkalaemia
Question 6. What would be your immediate management in this scenario?Click to see answer
Received IV Ca2+ (membrane stabilisation), salbutamol, dextrose-insulin, NaHCO3 and antibiotics in ED as well as some 0.9% saline volume resuscitation. Transferred to ICU for urgent HDx and a DKA insulin protocol which saw correction of the biochemical and ECG abnormalities. Discharged to ward 2 days later for ongoing titration of subcutaneous insulin.
Disclaimer: this is a fictional case for educational purposes that may contain de-identified patient data.
1) Brandis, K. Acid-base physiology, http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php, last accessed 15th August 2020
2) Foot, C. Steel, L. et al (2012) Examination Intensive Care Medicine, second edition, Elsevier Australia, pg 176
3) Nickson, C. Delta Ratio, Life in the Fast Lane, https://litfl.com/delta-ratio/, last accessed 15th August 2020
4) Yartsev, A. Delta gap and delta ratio, Deranged Physiology, https://derangedphysiology.com/main/cicm-primary-exam/required-reading/acid-base-physiology/Chapter%20705/delta-gap-and-delta-ratio, last accessed 20th August 2020