Question about arterial blood gases

[rachelthehobbit]

Hi, can anyone help me interpret this ABG?

pH 7.44 (7.34-7.45)
paCO2 32 (32-36)
PaO2 67 (75-100)
HCO3 21 (20-26)
BE -2 (-3 - +3)
SaO2 92%

This patient has idiopathic pulmonary fibrosis (chronic presentation).

My hypothesised mechanism (can someone please give me the thumbs up or tell me where i've gone wrong if so?):

Due to the disease process, the patient has developed insensitivity to the CO2 drive - because she has had chronically high CO2. As a result, she has switched to the hypoxic drive.

Because she has decreased surface area and increased thickness of membrane, it is more difficult for gas to be exchanged. This has lead to low PO2. Due to the hypoxic drive, she is now hyperventilating to increase her PO2. However, this hyperventilation is not adequate to raise her PO2 to normal, hence the low PO2 and SaO2.

Because CO2 diffuses more easily across the membrane than O2, the increased hyperventilation causes this patient to blow off an excess amount of CO2.

The loss of CO2 causes respiratory alkalosis in this patient.

This respiratory alkalosis is compensated by the kidneys ie metabolic compensation. The resorption of bicarb is decreased so that more of it is lost in the urine. In this way, the pH is normal (though in the high range of normal).

***

Is this correct? i'm only just getting my head around ABGs.

Also, can anyone explain Base excess to me or pointme to a good place to find out about it? I'm pretty confused atm so i can't tell the diff between compensated metabolic acidosis and respiratory alkalosis, and resp acidosis and metabolic alkalosis...

Also, is what i said about hypoxic drive etc true? Or is that an incorrect cause for the hyperventilation?

Any help much appreciated

Cheers.

---

Members don't see this ad.

 

[MirkoCrocop]

we're in path to avoid this type of question. medicine forum!

 

[yaah]

I'm just flattered that someone picked the path forum to post this. Normally the majority of random visitors we get are here to post about dead bodies.

Basically, the only thing I really know about blood gases is that there shouldn't be bubbles in them and we can also reject them if they weren't received on ice. But your reasoning sounds ok. You tell the difference between compensated vs not compensated by those silly annoying equations (you know, like pH should change by 0.08 for every 10 point change in pCO2, or whatever the numbers are). I think I have to know those for boards but I am putting off learning the actual numbers, since at most it would be one question.

Whether hypoxic drive is an appropriate trigger, I dunno, to be honest.

 

[djmd]

I'm just flattered that someone picked the path forum to post this. Normally the majority of random visitors we get are here to post about dead bodies.

Basically, the only thing I really know about blood gases is that there shouldn't be bubbles in them and we can also reject them if they weren't received on ice. But your reasoning sounds ok. You tell the difference between compensated vs not compensated by those silly annoying equations (you know, like pH should change by 0.08 for every 10 point change in pCO2, or whatever the numbers are). I think I have to know those for boards but I am putting off learning the actual numbers, since at most it would be one question.

Whether hypoxic drive is an appropriate trigger, I dunno, to be honest.

The parts of my brain that used to be able to do this are badly atrophied..
But... Yaah point about that the equation is key..

This patient (or case) strikes me as one of those mixed acid/base cases.. pH should never be compensated back to normal... So you have to figure is this mild resp alk or sometime more complicated

Make sure there isn't an anion gap acidosis... check the equation for the level of pH vs pCO2... (usually I used the sections in the Washington manual or whatever that other pocket Internal Medicine book was)

 

[mlw03]

i think the OP is about right; part of the reason it's a tougher problem is that technically the values fall mostly within normal limits. i was taught that for chronic resp alkalosis, for every 10 decrease in PCO2, you get a 5 decrease in bicarb. so that seems about right. but i'd be reluctant to call this an acid-base disorder at all because the pH is at the upper limit of normal.

i never really understood base excess, sorry.

i do agree that the hypoxemia is the stimulus for the patient's hyperventilation. chronic lung disease can cause hypoxemia, which is a potent respiratory stimulus.

 

[tardieu]

Hi, can anyone help me interpret this ABG?

pH 7.44 (7.34-7.45)
paCO2 32 (32-36)
PaO2 67 (75-100)
HCO3 21 (20-26)
BE -2 (-3 - +3)
SaO2 92%

This patient has idiopathic pulmonary fibrosis (chronic presentation).

My hypothesised mechanism (can someone please give me the thumbs up or tell me where i've gone wrong if so?):

Due to the disease process, the patient has developed insensitivity to the CO2 drive - because she has had chronically high CO2. As a result, she has switched to the hypoxic drive.

Because she has decreased surface area and increased thickness of membrane, it is more difficult for gas to be exchanged. This has lead to low PO2. Due to the hypoxic drive, she is now hyperventilating to increase her PO2. However, this hyperventilation is not adequate to raise her PO2 to normal, hence the low PO2 and SaO2.

Because CO2 diffuses more easily across the membrane than O2, the increased hyperventilation causes this patient to blow off an excess amount of CO2.

The loss of CO2 causes respiratory alkalosis in this patient.

This respiratory alkalosis is compensated by the kidneys ie metabolic compensation. The resorption of bicarb is decreased so that more of it is lost in the urine. In this way, the pH is normal (though in the high range of normal).

***

Is this correct? i'm only just getting my head around ABGs.

Also, can anyone explain Base excess to me or pointme to a good place to find out about it? I'm pretty confused atm so i can't tell the diff between compensated metabolic acidosis and respiratory alkalosis, and resp acidosis and metabolic alkalosis...

Also, is what i said about hypoxic drive etc true? Or is that an incorrect cause for the hyperventilation?

Any help much appreciated

Cheers.

For what it's worth: When I read your numbers and saw the brief history of IPF, before I read further, I thought it through and came to the exact same interpretation you did.

As far as if you need to know blood gas interpretation, as a CP board survivor, I can tell you this kind of scenario could very well be on the CP boards. They may give you the numbers and ask for the most likely diagnosis from a list of choices, etc. Per my recollection, a question like this would be on the gimmie side of the difficulty-obscurity scale (at least you've heard of blood gasses).

Base excess always seemed superfluous to me. It's basically a qualitative (?) indicator of how much base is needed to bring someone's pH back to physiologic neutral. So it just tells you if your acidotic or alkalotic, like pH. I'm sure there must be some subtle and vital wisdom in it that I've been missing all these years.

Sometime during the previous century, an intensive care doc gave me an algorithm for A/B problems that has always served me well. It's easiest to draw, and I'm reaching deep into the vault for this one, but I'll try to put it in step by step.


A. Premises:

1. It's all about the ratio of CO2 to bicarb, with CO2 reflecting the respiratory situation and bicarb the metabolic.

2. If CO2 is up or bicarb low - expect acidosis.

3. If CO2 is low or bicarb up - expect alkalosis.

4. If your expectations do not jive with the measured levels, some kind of compensation is going on.


B. Algorithm:

1. Check pH to see if you're acidotic, alkalotic or neutral

2. Check the CO2 / bicarb ratio -- NOTE: This is a qualitative check, NOT numeric, with the respective normals as your baseline.

A. Adidotic
i. CO2 up / bicarb normal = respiratory acidosis
ii. CO2 up / bicarb up = respiratory acidosis with partial metabolic compensation
iii. CO2 normal / bicarb low = metabolic acidosis
iv. CO2 low / bicarb low = metabolic acidosis with partial respiratory compensation

B. Alkalotic
i. CO2 normal / bicarb up = metabolic alkalosis
ii. CO2 up / bicarb up = metabolic alkalosis with partial respiratory compensation
iii. C02 down / bicarb normal = respiratory alkalosis
iv. C02 down / bicarb down = respiratory alkalosis with partial respiratory compensation

C. Neutral: It gets more complicated. If the C02 / bicarb ratio is normal – no problem. If they’re not normal then in order for pH to be neutral they have had to vary in the same direction, which means there’s been complete compensation. You have to look at other indicators to get an idea of the primary problem. Maybe that’s where base excess comes in, I don’t know.

Good luck.