Venous c02 and arterial pC02 inverse correlation

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RNtoMD87

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What would a worsening venous c02 while improving arterial pC02 indicate?

Chem profile says from 8/16-8/19 c02 trend from 31-42 mmol/L

Meanwhile, the initial ABG indicates 86mmHg pC02 on 8/16 and 69.4mmHg pC02 on 8/17 after a regimen of Lasix and BIPAP ventilation.

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It indicates that the patient's metabolic alkalosis worsened from diuresis (contraction alkalosis, loss of chloride), while his respiratory acidosis got better.
 
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Thank you. I'm a stepdown nurse, and this is something we didn't go too indepth with at school.

Appreciate the knowledge. His potassium is still doing well thankfully.
 
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“CO2” on a basic metabolic panel is a misnomer - it actually refers to bicarbonate (HCO3). The pCO2 on a blood gas (arterial or venous) is the partial pressure of carbon dioxide. They are not the same
 
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“CO2” on a basic metabolic panel is a misnomer - it actually refers to bicarbonate (HCO3). The pCO2 on a blood gas (arterial or venous) is the partial pressure of carbon dioxide. They are not the same

Actually it's not a misnomer as the way in which the test is run in the lab (or at least how it was run back in the day, methods have probably improved), results in the conversion of HCO3 to CO2 which is then ultimately measured on the assay. I don't know the specific mechanism of this test to be honest though. Never really cared that much to look it up.

Second important point is that blood gas machines only calculate the "bicarb" based on the pH and the PCO2, so that is not an actual number.
 
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Darn, I was hoping this was going to be a venous pCO2 vs. an arterial pCO2 thread. . . . . . .
Hah we could make one. I’d still learn a lot.

Honestly in my nursing practice I haven’t seen venous blood gases done, just ABGs.
 
Well in residency, I barely ordered any venous gases. Where I work now, its a lot harder to get ABGs outside of MICU or a rapid. I also just feel my RTs are just plain lazy. So for a non-ICU doc, I don't get many. There is at least one one study that suggests a pCO2 on a venous gas and pCO2 on ABG are pretty much the same, but lots of smart CCM/PCCM always believe, and I don't feel its been a problem.​
 
Second important point is that blood gas machines only calculate the "bicarb" based on the pH and the PCO2, so that is not an actual number.

Worth pointing out that, while this is true, this doesn't actually result in any measurement error ie your calculated bicarb will be essentially identical to your "assayed" bicarbonate.
 
Worth pointing out that, while this is true, this doesn't actually result in any measurement error ie your calculated bicarb will be essentially identical to your "assayed" bicarbonate.

Yes, under most conditions, but there can be times when it doesn't and a deviation between the two warrants further exploration.
 
Yes, under most conditions, but there can be times when it doesn't and a deviation between the two warrants further exploration.

Do you mind expanding on this? My understanding was that differences were tiny and only down to analytical error.
 
I would never order an ABG in a non-intubated patient without an arterial line if I had my way.

The intensivists I work with are like this. At most, we might do an art stick to roughly correlate PO2 and SpO2 plus get a baseline.

And hell, if you end up at a hospital where the RT's don't insert the arterial lines, they'll probably build a shrine to you in the break room.
 
The intensivists I work with are like this. At most, we might do an art stick to roughly correlate PO2 and SpO2 plus get a baseline.

And hell, if you end up at a hospital where the RT's don't insert the arterial lines, they'll probably build a shrine to you in the break room.
Seriously? Have they never heard of the oxygen-hemoglobin dissociation curve?
 
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Seriously? Have they never heard of the oxygen-hemoglobin dissociation curve?

They have, as have I. However, I also have occasionally posted incomplete and/or incorrect information on the internet. It happens, you understand. In my defense, I don't really work or function well during daylight hours, so excuse my terrible answer if you could. If you'll allow me to elaborate:

What I was (poorly) trying to convey is that we don't drawn many ABG's. Often, we'll draw one somewhere near the beginning of a patients saga with us to see what the PaO2 and SaO2 look like. We usually do this because our MICU teeters somewhere between a SNF and a holding chamber for the undead. The cachectic 85 y/o with sepsis from their indwelling foley, coupled with afib and an EF south of 25% maintaining a borderline BP on levophed is usually the average customer. Cut and paste for the other 15 beds. Our ****ty pulse ox probes really don't help either, and we have forbidden from using the good neo-probes by management, because budgets trump patient care, naturally. So the average waveform is usually some meandering and only borderline pulsatile line. As for actual correlation, it's usually to get an idea of the relationship between the PaCO2 and the EtCO2. Granted, most of our patients have severe obstructive disease so this isn't great either, but it's something?

So, assuming there's nothing causing anyone to be clinically suspicious, why harass these already tortured souls with around the clock ABG's?

Admittedly I'm only an RT, but from my perspective if I see that my patients RR, VT, VE, VCO2 and EtCO2 have remained mostly unchanged, that there haven't been any changes to their Cstat or pPlat, their CXR is unchanged, Tmax is stable, and there's nothing eye-catching on their routine morning labwork -- what exactly would I even be looking for on another ABG, and why would I want to draw another one? As a physician your knowledge on this matter obviously outstrips mine, so perhaps I'm missing something. Otherwise though, I'm a firm opponent of the "routine ABG" in the setting of otherwise total status quo.
 
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