**ABG MASTERCLASS-I BY DILEEP RAMAN**

**A 19 year-old-male, with Insulin dependent Diabetes, presented with cough, and malaise. ( FiO2 0.21, Albumin 4, Pb 760 mmHg)**

**pH 7.10, PaCO2 10, PaO2 112, HCO3- 4,**

**Sat 94%, Na+ 140, K+ 4.1, Cl- 105**

**Total CO2 5, Glu 845, Cr 1.1**

When discussing ABGs one must not forget the trinity; OXYGENATION, VENTILATION AND ACID-BASE BALANCW

For me the story must start with oxygenation - why - because without it every story ends. the cardinal rule - hypoxia kills but hypercarbia happens. Therefore diagnose at treat hypoxia early. Here our unfortunate lad is breathing room air at sea level (Pb -760 mmHg). Here you invoke the Alveolar gas equation (one of the BIG 4 pulm onary equations ). The gradient is 25 . Now you have to know what is is his gradient for his age. It turns out that it is around 8.

**PAO2= PiO2- PaCO2/R where PiO2 = (Pb-PH**2

**O) x FiO2**

**The formula for expected A-a gradient for age is, A-a gradient = (age/4)+ 4**

Things brings us close to our first relevant point.

A young pt with a cough who at first glance appears to have a normal PaO2 has a problem with oxygenation. He has an abnormal Aa gradient indicating that he has one of 3 pathologies. Shunt, VQ mismatch or diffusion impairment. So he may have a pneumonia for example. Also note that if this pt was 90 yrs old this would be a normal gradient and essentially all the 3 causes could be ruled out. But here you CAN rule out some interesting causes. for eg hypoventilation -Why? because hypoventilation will not cause a wide Aa gradient.

This can be very useful for people dealing with neuromuscular blockers . If you guys have a pt that is hypoxic pos t op that has a norm al Aa gradient, you do not need to worry about pneum onia or PE but should rather start looking for a reversal agent.

So why is the PaO2 of 112 "abnormal" even though most people would be happy with it? it is because according to the gas equation the space left out by blowing out CO2 should have been taken up by oxygen and the PaO2 should have been slightly higher. This is a subtle point but hopefully gets the message across . The message being check the poor lad for some pulmonary problem - ? Pneumonia.

**Quick bedside shortcut is expected PaO2 in mmHG is 500 x FiO2 (in decimals )**

Even though temperature seems to play a critical role, correction for temperature is not mandatory on a blood gas m achine. The correction factors are of dubious clinical relevance at best. For eg in hypothermia patients it is not known if correction is really helpful as the pt itself is 33oC. So it may actually cause harm. Just calibrating to 37o C on the machine is fine in most instances.

When analyzing the rest of the ABG the very FIRST thing to do is to check external and internal consistency. There is no point in proceeding further without this step.

Here is where we meet the next important equation - the henderson-hasselbach. We can simplify this greatly to the following:

**[H+]= 24 x PCO2/[HCO3-]**

Key point: Now when calculating this use the bicarb that is measured directly from the serum chemistry - CO2 provided in the question. Why? becaus e if you use the ABG bicarb it will not show external validity.

Ie. basically you are testing if your calculated bicarb in the ABG is the same as the measured bicarb in the serum . The ABG only measures PaO2, pH and PaCO2. everything else is calculated.

So 24 x 10/4 = 60. this is the approximate H+ ion concentration. A concentration mentioned previously was around 50 slightly lower that what I would have thought. but it may be because the calculated bicarb was used.

The so called rule of 80 tells you the expected pH. it is 80-60 = 20. this will be the last 2 digits of the pH. Ie expected pH is around 7.20. but we have 7.1. Why the discrepancy. This is because at extremes of pH rule of 80 starts to fail (as do all short cuts).

Before you start looking at numbers we should consider normal values. All of you can look up normals and you will find answers in ranges. Ranges are good for most situations as there are various ranges for norm als . But if you want to be a purist for ABG interpretation you have to go by fixed numbers to get a definite

answer. This is a theoretical point and may have no clinical relevance. but to analyze in detail forget ranges temporarily. pH 7.4, PCO2 - 40, bicarb - 24, AG - 12. these are the numbers most people use as definite break points.

Step 1: So based on that this is this is acidemia.

Step 2: The bicarb is low - therefore is at least a metabolic acidosis (diagnosis #1)

Step 3 - see if compensation is appropriate. Apply formula used above for met acidosis -

**Winters formula. PCO2= 1.5 x [HCO3-] + 8 ± 2**

Expected PCO2 is around 12-16. The patients measured PCO2 is 10. Which means there may be a very mild resp alkalosis (diagnosis #2) but this is not definite as the difference of 2 is within the error margin of these bedside tests. So if one were to say there is no resp alkalosis you would not be wrong.

**Other rough formulae for other disorders-**

Respiratory Acidosis : for every increase of 10 in PCO2 : pH decreases by 0.08 (If acute) and 0.03 (if chronic) and the [HCO3-] increases by 1 m eq/L ( if acute) and 4 meq/L (if chronic)

Respiratory Acidosis : for every increase of 10 in PCO2 : pH decreases by 0.08 (If acute) and 0.03 (if chronic) and the [HCO3-] increases by 1 m eq/L ( if acute) and 4 meq/L (if chronic)

**Metabolic alkalosis: PCO2= 0.9 x [HCO3-] + 9 ± 2**

Respiratory alkalosis : For every decrease of 10 in PCO2: pH increases by 0.08 (if acute) and 0.03 (if chronic) and the [HCO3-] decreases by 2 m eq/L (if acute) and 5 meq/L (if chronic)

Respiratory alkalosis : For every decrease of 10 in PCO2: pH increases by 0.08 (if acute) and 0.03 (if chronic) and the [HCO3-] decreases by 2 m eq/L (if acute) and 5 meq/L (if chronic)

Step 4 - Calculate AG.it may be easier to use 12 as your cut off for normal but I also like another technique for assessing the role of Albumin. I use the same at bedside.

**Serum Albumin X 3 is the expected AG for that patient. So you can avoid using the normal 12 if you use this method.**

So here pts alb is 4 and thus his expected gap is 12.

One point. you may be tempted to correct the sodium for hyperglycemia to calculate the AG - DONOT do this . All the electrolytes are equally diluted so correcting Na+ alone will raise the gap erroneously. So best to leave it as is.

Here AG is 31. So diagnosis #3 is Anion gap metabolic acidosis

Step 5. The fall in bicarb from a normal of 24 is 24-4 =20. So delta bicab is 20 and delta AG ( measured - normal = 31-12 = 19).

This means that the fall in bicarb is almost matched by the rise in the gap. The difference is only 1. This falls in the gray zone. One cannot conclusively say if there is met alkalosis or coexistant non gap acidosis here. For eg if the bicarb was 10. the delta bicarb would be 14. In that case even though AG went up by 19 the the bicarb fell only by 14 meaning that there is slightly more bicarb around - ie alkalosis.

Step 6 involves urine analysis which we can skip for now

CONCLUSION:

So given this info I can only conclude that it is AG metabolic acidos is with mild (debatable) resp alkalemia. The metabolic alkalos is part is not discernible with certainty with these numbers .

**ABG MASTERCLASS-II**

**Basic arterial blood gas analysis**

**A 64 year-old-female presented with lethargy and swollen feet.**

pH 7.40, PaCO2 38, PaO2 72, HCO3- 24, Sat 95% on RA, Na+ 149, K+ 3.8, Cl- 100, Total CO2 24, Cr 8.7

How would you characterize her state of oxygenation, ventilation and acid-base balance?

pH 7.40, PaCO2 38, PaO2 72, HCO3- 24, Sat 95% on RA, Na+ 149, K+ 3.8, Cl- 100, Total CO2 24, Cr 8.7

How would you characterize her state of oxygenation, ventilation and acid-base balance?

To check the expected pH (not at extremes of pH) we use the rule of 80. First calculate the expected [H+] e.g here it is 38. Substract this value from 80... we get 42. So 42 will be the last 2 digits of the pH i.e 7.42 and here the pH is 7.40. So quite near.

Diagnosis #1 - Hypoxia with wide Aa gradient

Diagnosis #2 - Anion gap acidosis without acidemia

Diagnosis #3 - Metabolic acidosis without alkamemia

Rise in AG= 25-12= 13, delta AG= 13, delta HCO3-=0, therefore delta gap=13- 0= +13

She had really abd AKI on CKD and was vomiting a lot.

Acidemia and acidosis are different. 7.4 means no acidemia but can have acidosis or alkalosis hidden.

- Get used to looking at normal pH with hidden disorders.

- Looking for anion gap even if bicarb is normal.

1. Would look at the clinical picture first. Very rarely does it help in finding a diagnosis. An example is asymptomatic mild RTA or mild primary Resp alkalosis. But if all normal then it is unlikely that anything serious is going on. More like a rule out test that a rule in.

2. Acidosis is based on the direction of the metabolic abnormality. Acidemia is based on the pH alone. Sodium does not affect pH in the simplified bicarbonate model. But according to the Stewart model hypernatremia with high chloride will cause acidosis. But Again looking at the pH is the only direct way to tell.

**ABG MASTERCLASS-III**

A 28 year-old-male presented to the ED profoundly confused.

pH 7.35, PaCO2 20, PaO2 120, HCO3 15, Sat 98% on room air, Na+ 140, K+ 4.1. Cl- 100

Total CO2 12, albumin 4

How would you characterize his state of oxygenation, ventilation and acid-base balance?

Expected pCO2 = 1.5 x HCO3- + 8 (+/- 2)

Exp PCO2 = 1.5 x 12 + 8 = 26 (=/-2) i.e 24-28

But we have pCO2 of 20; so it's outside the compensation range.

So there is met acidosis. secondary resp alkalosis but also a primary resp alkalosis that is driving the PCO2 lower that what it should be - so definitely a primary resp alk also exists.

Diagnosis #1 - Met acidosis - anion gap

Diagnosis #2 - primary resp alkalosis

AG is 28 against an expected of 12. Is there a hidden met alkalosis or non gap acidosis?

If you go by the ABG calculated bicarb, there may be a slight met alk. Drop in bicarb is 9 (24-15) but rise in gap is higher. So slight alkalosis. But if you use the measured bicarb, the total co2, the delta is almost equal. So no underlying met alkalosis.

**DIAGNOSIS**

#1 Anion gap metabolic acidosis

#2 Respiratory alkalosis (that goes beyond compensation and is a primary disorder here.

And its definitely salicylate overdose. This was a case of Aspirin over dose. The primary resp alkalosis was the major clue. Hence it is very important to consider if the resp alk is just compensatory or a true primary disorder. If compensatory only the pH would have been lower and the PCo2 higher - hence the importance of actually calculating the expected PCO2.

MUDPILES ( ANION GAP METABOLIC ACIDOSIS CAUSES)

MUDPILES ( ANION GAP METABOLIC ACIDOSIS CAUSES)

Methanol

Uremia

Diabetic Ketoacidosis

Paraldehyde

Infection

Lactic Acidosis

Ethylene Glycol

Salicylates

**GOLD MARK**has been suggested for use by nephrologists. This acronym represents

Glycols (Ethylene Glycol and Propylene Glycol )

Oxoproline

L-lactate

D-lactate

Metanol

Aspirin

Renal Failure

Ketoacidosis

Another mnemonic

**CUTE DIMPLES**includes Cyanide, Uremia, Toluene, Ethanol, Diabetic ketoacidosis, Isoniazide, Metanol, Propylene Glycol, Lactic acidosis, Ethylene Glycol, Salicylates).

Easiest mnemonic is

**KULT**: Ketones, Uremia, Lactate and Toxins, because these are the most common causes of a High Anion Gap Metabolic Acidosis (HAGMA).

The mnemonic for the (rare, in comparison) toxins is

**ACE GIFTs**: Aspirin, Cyanide, Ethanolic ketosis, Glycols (ethylene and propylene), Isoniazid, Ferric iron, Toluene.