Blood Gas of the Week #15
A 4-year old, castrated male domestic shorthair cat is presented after being found comatose in the owner’s house. He is an indoor/outdoor cat who roams freely at will. When he returned home this morning the owner thought he was more tired than usual, and when she came home to check on him at lunch found him laterally recumbent and non-responsive in a puddle of urine.
On presentation the cat is comatose with no evidence of trauma, tachypneic, is dribbling urine, has dilated fixed pupils, absent corneal, gag, and deep tendon reflexes. Occasional muscle fasciculations are also noted. Initial vital signs are as follows:
T 97F P 140 R 100 mm pink CRT 2s BCS 5/9 Weight 4.5kg BP 88/56 (66mmHg)
Over the subsequent 3 minutes IV access is established, blood is collected for analysis, the patient is intubated to protect his airway, and he is connected to your monitoring devices. The initial blood gas results return just as you finish hooking up the ECG. Interpret the blood gas:
Step 1: Evaluate the pH
This patient’s pH is 6.46 – critically low indicating a severe acidemia.
Step 2: Determine the primary process
Acidemia can be caused by a low bicarbonate or a high carbon dioxide. In this case both the bicarbonate and carbon dioxide are very low. Since the low bicarbonate is an acidifying process (and the low carbon dioxide is an alkalinizing process), the process represented by the bicarbonate is the cause of the low pH – this is a primary metabolic acidosis.
Step 3: Is there compensation?
The expected compensation process with a metabolic acidosis is a respiratory alkalosis – a low pCO2. This patient’s pCO2 19, which is much lower than the ‘normal’ value of 40.
The first-glance diagnosis is compensated metabolic acidosis. If you want to check mathematically to be sure the changes in the CO2 are all due to compensation and being minimally altered by a true respiratory problem, we can do that as well.
Step 4: Calculating the expected compensation
With a metabolic acidosis, for every 1 point decrease in the bicarbonate there should be a corresponding 0.7 point decrease in the CO2.
Our patient’s bicarbonate is 18 points lower than normal:
20 – 1.8 = 18.2 (we will round to 18)
This means there should be an approximately 13 point change in the carbon dioxide to compensate:
18 x 0.7 = 12.6 (we will round to 13)
The normal CO2 is about 40, so this means we expect the CO2 to be about 27 if our patient is compensating for his metabolic alkalosis
40 – 13 = 27
BUT there is a range for normal (both bicarbonate and CO2) that we need to account for, so generally we say that the range is the calculated value +/- 4. So for this patient the range for the CO2 would be about 63-71:
27 – 4 = 23 (low end of range)
27 + 4 = 31 (high end of range)
Our patient’s CO2 is 19 – quite impressively low, which falls outside our estimated range. Since it is outside the calculated range it is technically classified as a mixed acid-base disturbance characterized by severe metabolic acidosis and respiratory alkalosis. With this severe of a metabolic acidosis and a significant tachypnea, my opinion is you have to consider at least most of the pCO2 to be a compensatory response to the profound metabolic acidosis. In fact, this patient’s extreme ventilatory rate is probably the only thing keeping it alive for the moment.
The next steps in the blood gas analysis: defining the type of metabolic acidosis, and calculating the anion gap
So far on BGOTW we have concluded each case at this point – with the basic analysis of the blood gas. Beginning this week we are going to look further into what might be causing the changes on the blood gas, and how it relates to the initial presentation of the patient.
When using the traditional acid-base analysis approach (the approach presented above) metabolic acidosis is subdivided into two classes:
- High Anion Gap Metabolic Acidosis (HAGMA)
- Normal Anion Gap Metabolic Acidosis (NAGMA)
If we think all the way back to high school physics, we learned that there is a law of neutrality, which means that the sum of all the positive charges must equal the sum of all the negative charges no that the net difference between positive and negative is zero. For blood gas analysis this means that if we were able to measure absolutely everything in our sample fluid, the net electrical charge would equal zero. We can’t (clinically) measure everything that makes up a blood/plasma/serum sample. BUT we can measure the ions found in the greatest concentration in those samples – the things that are contributing the most to the electrical charge of the sample. The cations are sodium and potassium. The anions are chloride and bicarbonate. If you add these things up, the difference between the sum of the cations (sodium and potassium) and the anions (bicarbonate and chloride) is called the anion gap.
Anion Gap = [Na + K] – [Cl + HCO3]
In reality the ‘gap’ does not exist – the ‘gap’ is made up of all the negatively charged things that we don’t routinely measure. These are things like lactate, ketones, organic acids, etc (more on this in a minute). The normal anion gap is roughly 10-20 depending on the references and machines used. This is useful because there are a relatively limited number of things that can increase the anion gap, limiting our differential diagnosis.
Several mnemonics exist for the medically relevant ‘things’ that increase the anion gap. The most recently proposed (and arguably more clinically relevant, particularly for veterinarians) is GOLDMARK:
- Glycols (ethylene and propylene)
- Oxyproline (a metabolite of acetaminophen)
- L-Lactate
- D-Lactate
- Methanol
- Aspirin
- Renal failure
- Ketoacidosis
This patient has an anion gap of 31.8! A very high anion gap.
[138 + 5.6] – [110 + 1.8]
143.6 – 111.8
= 31.8
So the GOLDMARK list above is where our initial list of differential diagnoses come from. The patient presented here ingested ethylene glycol.
