Stupid med student asks how to use Fick equation in practice

[Per4mer8]

I'm basically trying to figure out the actual use of the Fick equation. Can it be used intraoperatively to estimate CO? For example say I don't have a PAC in the patient, could I just get an ABG and a Venous gas (to calculate my a-v O2 content) and then calculate oxygen consumption and solve for CO? If I had a PAC i feel like the Fick equation is a moot point because the PAC can get me CO/CI by thermodilution right? So basically it boils down to how do I calculate oxygen consumption? I know I would use the difference between inspired 02 and etO2 and then some equation using gas flow rate, tidal volume, and/or minute ventilation but haven't been able to make it work myself. (my guess is inspired O2-etO2 x MV but can't find any concrete equation anywhere)

Sorry if this is an asinine and likely academic question. I understand that if your patient required monitoring of CO you'd probably have a PAC/TEE etc.

---

Members don't see this ad.

 

[pgg]

I'm not sure if I've ever once plugged actual #s into the Fick equation, but I think it sometimes provides a useful framework for thinking about why your patient's SvO2 is what it is. (And it was a recurring topic on every ITE that I took and my written boards, so know the formula when you sit down to take the boards.)

SvO2 = SaO2 - VO2/CO x Hb x 1.36


(FiO2 - EtO2) x MV = minute O2 consumption, try doing the math sometime in the OR, you may be surprised at how close to 3-4 cc/kg/min it works out to in most every adult and 5-6 cc/kg/min in peds, just like the books say.

So if you assume a peripheral venous O2 sat equals SvO2 then sure you could calculate a CO, but
a) they're not equal; in the patients where you're really interested in the #s they're likely even more unequal
b) what are you really going to do with the # except say 'oh neat'?


I like physics and saying 'oh neat' from time to time.

If milmd was around he'd be by shortly to say something about fleas and mental masturbation.

 

[Per4mer8]

Thanks for putting the time into explaining the use (or non-use in actual practice). I just came across the equation and it's application in my study text and it kept saying it could be used to calculate CO but in the same section said you would use the PAC to sample MvO2 and I thought "if I have a PAC why calculate using Fick?" (I know the computer uses a variation of Fick to do it's thermodilution calculation).

Thanks

 

[bullard]

In practice, I've used Fick much like Marino talks about in ICU book: by using it as a transfusion trigger.

Assume you have an anesthetized patient with a PAC and TEE having some kind of cardiac surgery, who is oxygenating well, and the VO2 is stable (which is a reasonable assumption in a anesthetized, paralyzed, mechanically ventilated patient), and if you know the cardiac output is OK (by looking at the right heart in the field and/or the left heart by TEE), then a decrease in SVO2 reflects a decrease in hemoglobin.

Of course, in the real world, you'd probably be doing the case without a PAC. But I think it's this application that shows up on boards.

We used continuous SVO2 monitors during liver transplants in residency and it helped in terms of deciding whether to hang more PRBCs versus FFP.

 

[fabfive5]

As mentioned by Bullard, one can use the theory of the Fick Equation via the PAC CCO and SvO2 in hear room and liver room. It's amazing to see the SvO2 trend upward back towards the normal 75% when giving blood.

 

[Per4mer8]

As mentioned by Bullard, one can use the theory of the Fick Equation via the PAC CCO and SvO2 in hear room and liver room. It's amazing to see the SvO2 trend upward back towards the normal 75% when giving blood.

Ok, read the section in Marino dealing with this and it makes sense conceptually. While anemia doesn't affect SaO2 it will affect SvO2 because less Hgb but same O2 demand requires increased extraction. Here's where i'm at now.

VO2 = Q x 13.4 x Hb x (SaO2-SvO2) ;

the graph shows a maximum O2 extraction of SvO2 = 50% before dysoxia occurs and your VO2 declines (fig 11.4). But if you plug in the numbers for SvO2, as SvO2 declines you're multiplying by a larger number therefore giving a larger VO2. And this makes sense in the fact you are consuming more oxygen. The only way your VO2 drops below the magic 100mL/min/m2 is if a.) CO falls and/or b.) your Hb drops. So correct me if I'm wrong, if you are monitoring CO and it remains stable while SvO2 drops you know it has to be because of a drop in Hb (or decreased SaO2)?

Sorry for carrying this on.

 

[fabfive5]

Ok, read the section in Marino dealing with this and it makes sense conceptually. While anemia doesn't affect SaO2 it will affect SvO2 because less Hgb but same O2 demand requires increased extraction. Here's where i'm at now.

VO2 = Q x 13.4 x Hb x (SaO2-SvO2) ;

the graph shows a maximum O2 extraction of SvO2 = 50% before dysoxia occurs and your VO2 declines (fig 11.4). But if you plug in the numbers for SvO2, as SvO2 declines you're multiplying by a larger number therefore giving a larger VO2. And this makes sense in the fact you are consuming more oxygen. The only way your VO2 drops below the magic 100mL/min/m2 is if a.) CO falls and/or b.) your Hb drops. So correct me if I'm wrong, if you are monitoring CO and it remains stable while SvO2 drops you know it has to be because of a drop in Hb (or decreased SaO2)?

Sorry for carrying this on.

The main way your body counteracts anemia is INcreased CO to offset the decreased in Hb and to keep the VO2 the same. Imagine what would happen if your body decreased VO2 in response to anemia...your CO would have to sky rocket. Not intuitive is it? It make way more sense when you actually SEE it happen in the OR...giving blood and seeing the CCO drop to normal and the SvO2 increase to normal.

Also remember that the DISSOLVED O2 in the blood (PaO2) doesn't matter too much with regards to CaO2 (= 1.34HbxSaO2 fraction + PaO2x0.003) and therefore doesn't matter too much with your VO2.

The Fick Principle is usually calculated like this:

CO = O2 Uptake / ([Arterial O2] - [Venous O2])

CO = VO2 / (Ca - Cv) <---> VO2 = (CO)(Ca - Cv)

CO = VO2 / [(1.34HbxSaO2 fraction + PaO2x0.003) - (1.34HbxSvO2 fraction + PaO2x0.003)]

As you can see, Hb is the main determinant, b/c that's where the O2 is bound and carried.

All this stuff is dyamic. What will be asked is what the MAIN determinants of CO, VO2, and CaO2.

At a resting state, Hb seems to be the main one. When activity or CAD/HTN/RAS/ESRD/ESLD....etc., are involved, then it's much much more complicated.

 

[pgg]

So correct me if I'm wrong, if you are monitoring CO and it remains stable while SvO2 drops you know it has to be because of a drop in Hb (or decreased SaO2)?

No. Eg, sepsis - high CO state, low SVR, poor tissue O2 extraction ... could have normal or high SvO2 but that doesn't mean everything's cool with the patient, or that Hb or O2 sat is to blame.

Cirrhosis.
Cyanide poisoning.

Without looking at the patient, you can't assume that VO2 is either constant or appropriate.

 

[MTGas2B]

In fellowship we would use the fick equation for pulmonary hypertension patients coming in for vasodilator trials and titrations.

So, the patients would go to the cath lab and have a PA catheter placed. (It was much less headache to just have cardiology do it under flouro, these are like awake outpatients) then the come back to the unit and we shoot baseline numbers. We would assume a constant VO2 and use the changes in mixed venous O2 to calculate changes in cardiac output. After getting baseline numbers we would start or increase their treprostinil (aka Remodulin) or for the old timers still on epoprostenol (aka Flolan) we would increase their dose. When we saw suitable increases in CO would stop and discharge them, usually the next morning. Or if they were starting, they would get a catheter place and then go home. It was fun physiology.