# PaO2



## skyemt (Mar 30, 2008)

Ok...

so, i understand that an SPO2 reading of 90 correlates with a PaO2 reading of 60... and that this is a critical level to remain above...

i want to check my understanding of why... is this the point on the oxygen desaturation curve, where below this point, desaturation occurs swiftly?

is this level of PaO2 the proverbial cliff?

i would like to expand my understanding here, if i am off...
as i learn about this, it seems that the focus would be to do everything you can to prevent that PaO2 from dropping below 60...

i realize my understanding may be rudimentary, but i would like to learn more...
comments welcome...


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## JPINFV (Mar 30, 2008)

SpO2 isn't quite that simple. It's more of a measure of the saturation of RBCs than a measure of PaO2. That said, the level of O2 carried in solution is very small. 

(bracketed units need number. Unbracket units are for book keeping)

```
PaO2=((0.003mL O2/100mmHg PO2)[PO2]) + (([g Hb]/100mL)(1.34mL O2/g HB)SaO2).
```
So, each gram/100mL of hemeglobin carries 400 times the amount of oxygen as each 100mL of plasma. A normal patient has somewhere around 15g Hb/100ml (12-18 is normal range).

So, a anemic patient can have an honest saturation of 100% yet still be hypoxic.


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## skyemt (Mar 30, 2008)

JPINFV said:


> SpO2 isn't quite that simple. It's more of a measure of the saturation of RBCs than a measure of PaO2. That said, the level of O2 carried in solution is very small.
> 
> (bracketed units need number. Unbracket units are for book keeping)
> 
> ...



true, but an SpO2 reading of 90 does correlate to a PaO2 reading of 60, if you take out the rare exceptions (anemia, sickle cell, CO, etc..)


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## VentMedic (Mar 30, 2008)

skyemt said:


> true, but an SpO2 reading of 90 does correlate to a PaO2 reading of 60, if you take out the rare exceptions (anemia, sickle cell, CO, etc..)



For the SpO2 to be 90% and the PaO2 to be 60 mmHg, you are assuming the oxyhemoglobin curve is in normal position. The position of this curve may shift rightwards (lower saturation for given PaO2) or leftwards (higher saturation for a given PaO2). 

http://www.utmb.edu/ERC/selfstud/pulseoximetry/curve.htm

http://www.ccmtutorials.com/rs/oxygen/page06.htm

To further this discussion you would have to get into tissue oxygenation and SvO2 monitoring to adequately grasp the big picture.

http://www.ccmtutorials.com/rs/oxygen/page04.htm

*ALL ABOUT OXYGEN*
http://www.ccmtutorials.com/rs/oxygen/index.htm

http://dwb.unl.edu/Teacher/NSF/C14/C14Links/www.mtsinai.org/pulmonary/ABG/PO2.htm

http://kcweb.nhmccd.edu/programs/respcare/O2.ppt

Good schematic :  Pathophysiology of Oxygen Delivery in Respiratory Failure
http://www.chestjournal.org/cgi/content/full/128/5_suppl_2/547S/F1

*SvO2*
http://www.lakesidepress.com/pulmonary/books/physiology/chap6_3.htm

http://signavitae.com/index.php?option=com_content&task=view&id=19&Itemid=6


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## VentMedic (Mar 30, 2008)

One more very important thing to consider is A-a gradient. 

If delivering 100% O2 via NRBM or ventilator and the SpO2 is 90%, the PaO2 could be 60 mmHg and the PAO2 may calculate to >450 depending on the barometric pressure.   This gives you a very large A-a gradient.  The SpO2 could even be 100% with a large A-a gradient and considerable work of breathing.   

You will still have a very sick patient even with 100% SpO2. 

See V/Q mismatching in ALL ABOUT OXYGEN from previous post.

Similar principles will also apply when using ETCO2.


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## MSDeltaFlt (Mar 30, 2008)

Man, it's people like Vent that make me look like someone who belongs on the short bus.  Just look at all the research Vent provides you with just about every possible question.

Now I know you're in school, and I do not want to contradict anything your instructor(s) may or may not teach you.

I say that because I'm more of a philosophical teacher, student, and provider.  Vent's right.  Roughly the majority of pts you will encounter with a curve that is not in midline position would probably be your medicals with advanced age and/or disease.  Your young, healthy trauma's might present with a more midline curve.  

But can you garrantee that in the prehospital arena?  Naw. 

Generally speaking, when your PaO2 gets less than around 60 torr, the body's organs begin to feel the effects of a decreased oxygenation environment.  If this gets bad enough for long enough, cells begin to die.  When they die, they don't come back.  We've all heard to term "anoxic brain injury".  This is how it happens.  You usually have about 4-6 minutes, according to the American College of Surgeons, to get them adequately oxygenated. 

Because what are you going to do if the curve shifts to the left?  Give 'em O2.  What about when it shifts to the right?  Give 'em O2.  What about a 22 yo rollover ejection?  You guessed it.  Give 'em O2.

Now, sky, it sounds like you are getting a handle on all of this.  Keep up the good work.  Good luck.


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## VentMedic (Mar 30, 2008)

MSDeltaFlt,

I know Egan and Shapiro are still close to your heart. 

I am glad to see some asking about the "whys" and not just recipes.


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## MSDeltaFlt (Mar 30, 2008)

VentMedic said:


> MSDeltaFlt,
> 
> I know Egan and Shapiro are still close to your heart.
> 
> I am glad to see some asking about the "whys" and not just recipes.



Thanks, Vent.  There's a philosophical theorum written I don't know how many years ago by I can't remember who that goes something like this:

"If you understand the 'why', then the 'what' and the 'how' will make sense."

Ever since I started applying that, I started learning things a lot faster and more easily.


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## skyemt (Mar 30, 2008)

MS and Vent,

thank you very much for the replies!

i am trying to get a handle on this...

if i were to be honest, it is a bit like pandora's box... every time i grasp a concept, it leads to more questions, then i realize more how much i don't know!

i would like to understand more practical applications of this to prehospital care... obviously, and understand of this physiology can help in the critical time before the PaO2 drops below 60... of course, i won't know that in the field...

also, the shift in the curve equates to more time/less time basically?

i did not get a chance to go through all the links vent posted, i will, and then probably have more questions.

since i got my basic cert, i have spent much of the time learning, and learning that i didn't (and don't) very much about A/P...

but... one chapter at a time... lol

thanks again for the help!


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## skyemt (Mar 30, 2008)

JPINFV said:


> SpO2 isn't quite that simple. It's more of a measure of the saturation of RBCs than a measure of PaO2. That said, the level of O2 carried in solution is very small.
> 
> (bracketed units need number. Unbracket units are for book keeping)
> 
> ...



as a corollary, it's my understanding that cyanosis (not sure if it goes for both peripheral and central, or just peripheral) develops when 5g hb/100ml desaturates... 

if that is correct, that means that an adult could de-saturate 1/3 of there hemoglobin before becoming cyanotic, and a child closer to 1/2... 

would this not make cyanosis a VERY late and ominous sign of hypoxia/hypoxemia?


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## Ops Paramedic (Mar 30, 2008)

There is not to much more that can be said, there is a lot of info here.  Allow me to maybe add...

The O2 dissociation curve that the SPo2 monitor uses to spit out a value that you can read from the display is obtained from tables/values that are programmed into the monitor.  The clever guys with the white coats got these values from performing test on healthy adults.  As mentioned, your patient , will most likely not fall into this category.  Is it then wrong to use the SPo2??  Not at all, it the best we've got and adds value to the overall presentation of the patient to you.

It is also important to know all the false positives and negatives, as well as the mechanical working of the device.  This will help you to to truely interpret the value you see on the display.  Something you are highly unlikely to find in the manual of textbook:  "Treat the patient, not the monitor"  (Not saying you aren't)!!


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## skyemt (Mar 30, 2008)

OK guys, i am actually starting to get a grasp of this! i think!

so, with regards to the disassociation curve...

the problem is twofold... as the partial pressure drops, and the patient begins to de-saturate... the disassociation curve also moves to the right, due to work of breathing, hypercarbia, and acidosis... leading to a crash of the patient! IF I AM UNDERSTANDING THIS CORRECTLY...

a main goal of prehospital care would then be slow the shifting of the curve rightwards as much as possible...

a shift in the curve leftwards is desirable, and achieved with lower metabolic rates and lower core temperatures... then, probably no accident that hypothermia treatments for cardiac resuscitation are proving beneficial... basically, a big shift in the curve to the left!

sorry for the punctuation marks, but seems like light bulbs going on all around me...

if i am off track, please advise!


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## skyemt (Mar 30, 2008)

ok... a bit more...

when we give someone O2 via NRB, basically, we are increasing the partial pressure of O2 at the alveolar level...

in a healthy person, due to the flatness of the curve at high partial pressures, you will not see a big increase in SaO2...

however, in a diseased person who is experiencing a "rightward shift" of the disassociation curve, there will be a greater improvement in the SaO2...

is that correct?

also, with regards to JP's earlier statements... if someone is anemic, therefore less Hb... what Hb is present will still bind O2 normally, leading to the high SaO2 readings... however, due to there being less quantity of oxyhemoglobin in the blood, the overall O2 available to offload will be lower, hence the lower PaO2 for that given higher SaO2...

am i understanding this correctly?

thanks...


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## VentMedic (Mar 31, 2008)

The pulse oximeter doesn't know about the Oxyhemoglobin curve.  The pulse ox measures the hemoglobin and gives the percentage of oxygenated Hb. The principle of pulse oximetry is based on the red and infrared light absorption characteristics of oxygenated and deoxygenated hemoglobin. Oxygenated hemoglobin absorbs more infrared light and allows more red light to pass through. Deoxygenated hemoglobin absorbs more red light and allows more infrared light to pass through.

Of course PaO2 is just a one part of the picture. Notice also that the units is pressure as in mmHg.  That confuses many people. 

The lakepress website has some of the most useful information since it is also exerts from a book for ABG interpretation. 
http://www.lakesidepress.com/pulmonary/ABG/PREFACEnew.htm

*Sky, the link below will answer the questions from you last posts.* You are on the right track.   For practical example: CaO2 is a big factor athletes strive for by increasing their Hb by illegal and/or dangerous ways.  Altitude training is better but takes times.    Babies with congenital cyanotic heart defects will have a higher Hb/HCT level as will some patients who have chronic lung diseases with very low PaO2 levels. 

http://www.lakesidepress.com/pulmonary/ABG/PO2.htm

http://www.lakesidepress.com/pulmonary/ABG/MixedAB.htm

http://www.lakesidepress.com/pulmonary/ABG/bicarbgap.98.htm

http://www.lakesidepress.com/pulmonary/ABG/bicarbgapx.98.htm

*Good site with advice for new doctors:*
http://www.lakesidepress.com/pulmonary/books/house/rules-a.html

EXAMPLE:

*15 Rules on Oxygen Therapy -- What Every House Officer 
Should Know *

http://www.lakesidepress.com/pulmonary/books/house/rules-a.html#15rules



> 12. High FIO2 doesn't affect COPD hypoxic drive.
> The reason a high FIO2 may raise PaCO2 in a patient with COPD is not because the extra oxygen cuts off the hypoxic drive. Modest rise in PaCO2 occurs mainly because the extra oxygen alters V/Q relationships within the lungs, creating more physiologic dead space.





> 14. Face masks cannot deliver 100% oxygen unless there is a tight seal.
> So-called non-rebreather face masks can deliver an FIO2 up to around 80%. It is a mistake to label a patient with any loose-fitting face mask as receiving an "FIO2 of 100%." (Again, 100% oxygen can only be delivered with a ventilator or tight-fitting face mask.)



(Yes, doctors commonly use the FiO2 and Percentage of FiO2.  interchangeably.  New computer charting systems help them out when they forget the decimal point in some documentation.) 

And now my favorite: *ARDS*

http://www.ardsnet.org/

http://www.aafp.org/afp/20020501/1823.html


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## MSDeltaFlt (Mar 31, 2008)

Sky, I hope you're using this for class.  To be totally honest with you, I do not even contemplate the dissociation curve whatsoever prehospital.  It's pretty cool in the ER when you are trying to get a game plan for the ICU, great in the ICU when their oxygenation doesn't want to work right despite conventional means, and makes you look pretty smart to the cute nurses you want to impress.

You don't want the curve to shift at all.  You want it where it belongs: in the middle.

But if someone's critical on a 911 call due to either trauma or severe SOB, I'm going to give them pretty much the same thing.  It also happens to be the same thing my protocols tell me to give: Oxygen.  I don't care what the curve is doing.

Vent may agree.  Vent may not agree.  That's just what's going on in my mind when I'm critically thinking.


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## JPINFV (Mar 31, 2008)

I agree on the "well, it really doesn't matter street level due to education, environment, tools, end goal (reach the hospital with a patient who is hopefully in a better situation than when they were found). On the other hand, its rather refreshing to see people who want to increase their education past "blood goes round and round and you need oxygen, so all patients get a NRB at 15LPM regardless of their complaint (stubed toe, needs ride to the store next to the hospital, etc). Oh, look, here's the short bus to take me to work!" (we've all worked with that provider)

I'm all for increased education, be it formal (class room) or informal (internet forum) as long as the provider understands the limitations of its application to the environment and restrictions that we find ourselves in. It's also helpful to understand that a pink patient with an SpO2 of 100 is not necessarily not hypoxic.


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## VentMedic (Mar 31, 2008)

MSDeltaFlt said:


> But if someone's critical on a 911 call due to either *trauma or severe SOB*, I'm going to give them pretty much the same thing.  It also happens to be the same thing my protocols tell me to give: Oxygen.  I don't care what the curve is doing.



It is sad when physical assessment and listening to what the patient is saying takes the back seat to a pulse oximeter that will give a teddy bear a 99% SpO2 if the ceiling light catches it just right.

Not all patients will need a NRBM but again that depends on the assessment. 


If a patient has a minute volume requirement of 22 L/Min and the NRBM is providing 15 L/Min, how well are you meeting that pt's demands?

Is the NRBM actually "high flow"?


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## Ops Paramedic (Mar 31, 2008)

This thread is on the go!

Now add Maternal Hb to the picture, and that our aim/use for the SPo2 monitor might be to measure oxygenated/deoxygenated Hb, it measures the percentage of saturated Hb.  Thus reminding you of Carbon monoxide which has a higher affintiy for Hb than O2, yet you can still get a good (Negative) reading, in the presence of hypoxemia.

To vent:  I often come across people refering to Fi02 as a percentage, i think it is more a lack of understanding.  So you say it is a new thing??  I can't grasp the concept, as Fio2 is: Fraction of inspired oxygen.  I am by no means a mathematician (and stand to be corrected), but how can a fraction be denoted as a percentage??  Its most probibly a podantic concept to try and get across, as we understand in anycase what is meant when Fio2 is refered to as a percentage!!


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## skyemt (Mar 31, 2008)

Vent and others, i will study further and be back with another post...
thank you!

MSDelta, you have provided me with a first on this site!!

of course, my protocols say to give O2 and get to the hospital with a better patient as well... so am i likely to consciously consider the disassociation curve in the field? maybe, maybe not...

after countless posts saying to me that the education standard is too low, and that if i don't really fully understand the physiology i have no real business doing this or that, you actually bring it back and say that the knowledge doesn't matter, and that i should just give O2 and go!!!!!

right on brother, there will be many who are pleased to see your post!

i, however, am not one of them... if i understand exactly what is going on on the physiologic level, then i am better able to assess and treat the patient... who knows, it may even help me treat a patient one day...


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## skyemt (Mar 31, 2008)

VentMedic said:


> One more very important thing to consider is A-a gradient.
> 
> If delivering 100% O2 via NRBM or ventilator and the SpO2 is 90%, the PaO2 could be 60 mmHg and the PAO2 may calculate to >450 depending on the barometric pressure.   This gives you a very large A-a gradient.  The SpO2 could even be 100% with a large A-a gradient and considerable work of breathing.
> 
> ...



i assume then, conversely, that up in the mountains the A-a gradient is inherently lower, leading to mild hypoxia in even healthy individuals??

we are using NRB or other mechanical ventilations to artificially raise the A-a gradient to saturate the hemoglobin with O2... however, this does nothing to fix the underlying pathology of the patient... is that what you are saying Vent??


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## skyemt (Mar 31, 2008)

ok... Rome wasn't built in a day...

SCRATCH LAST POST... wayyy off....

so, normal A-a means healthy person,
increased A-a means sick patient, not diffusing gas from alveolar spaces to arterial blood...

sounds similar to the rise in venous pressure when blood is not being effectively pumped out by the right side of the heart...


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## MSDeltaFlt (Mar 31, 2008)

Now hold on a second.  I never said "knowledge doesn't matter", but maybe I did use a poor choice of words.  On further recall, I do take the curve into account, I just have been doing for so long that's it's become second nature to me.  I apologize for confusing you.  I did it again, I"m sorry.  I told you to keep me in check, gut Good Lord, I didn't realize I needed that much checking:huh:.  

The theory behind it all is, in my opinion, at least as important as the applications.  The big picture.  The why you would do something.  If the curve does anything, what will you do?  Yes, give O2.  But is that all?  Absolutely not.  Healthcare is holistic care.  You treat the pt as a whole.  A shift to the left or a shift to the right will change your game plan.

" rightward shift, by definition, causes a decrease in the affinity of hemoglobin for oxygen. This makes it harder for the hemoglobin to bind to oxygen (requiring a higher partial pressure to achieve the same oxygen saturation), but it makes it easier for the hemoglobin to release bound oxygen. Conversely, a leftward shift increases the affinity, making the oxygen easier for the hemoglobin to pick up but harder to release."

Your sickle cells would be your left shift, however (Vent, correct me if I'm wrong), your hypovolemias would be your right shifts.


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## VentMedic (Mar 31, 2008)

Exactly skyemt!

High gradients result from impaired diffusion or, more commonly, by ventilation-perfusion inequality of the "shunting" variety. A normal A-a gradient is less than 10 mmHg. The age (years) / 4 + 4 is another conservative estimate of a normal gradient.

Alveolar Gas equation which takes barometric pressure into consideration
PAO2 = ( FiO2 * (760 - 47)) - (PaCO2 / 0.8)

A-a gradient = PAO2 - PaO2

******************

A patient’s condition may deteriorate considerably before there’s a dramatic change in SpO2.  Everything we do in Critical Care medicine is about optimizing the delivery of blood to the tissues as a means of maintaining homeostasis and promoting healing, and in the end it is the oxygen content of blood that is more important than the partial pressure of oxygen.

A patient may have an SpO2 of 100% and a decent ABG on 2 L NC but have a lactate level of 4.0 which places them on a Sepsis protocol in the hospital. If their BP is unstable with any signs of respiratory difficulties or wavering SpO2, they may get a ventilator.  For the next several hours or until the lactate starts to drop, by our protocol we will do whatever we can to the ventilator to maintain the SpO2 (or SaO2 if drawing ABGs) at 97% or above while also monitoring the continuous SvO2 reading from the central line.  Various pressors and fluid will be used to maintain BP MAP >65.    

Looking at just ABGs to measure respiratory distress is also a common mistake made by some who don't look at the "distress".  Pts can sometimes keep themselves alive and compensate very nicely...until they tire.   We used to get a pre-intubation ABG on everyone. Then, we realized how silly it was if the person was FTD (fixin' to die) and the values may be deceiving anyway.     

Ops Paramedic, that is why computer some charting systems tell people the err of their ways.   You are also opening up fetal Hb and then there is HBO and altitude medicine.   There are many textbooks dedicated to each of these subjects after getting only mentioned in some of the textbooks only about ABGs.  

Many doctors also have their own theories about oxygen which they learned specifically for their specialty.  Wound care and limb reattachment doctors may love O2.   Neuro doctors may be minimalists worried about free radicals and want normal PaO2 if the SjvO2s are normal.  

Another one of my favorite PaO2 topics is cyanotic heart disease and various methods to keep the PDA open including reducing the FiO2 to 0.16.  

JPINFV brought up the topic of Nitric Oxide on another forum which is another area when Pulmonary HTN is involved.  Prostacyclins are also used in both neonates and adults.

Critical Care medicine changes and evolves constantly.   Healthcare professionals (RRTs, RNs, Dieticians, Pharmacologists, MDs) that work in progressive ICUs are required to read articles (like homework) and attend mandatory training on top of their regular CEUs.   Getting advanced degrees may also be expected to advance to the next tier of their clinical ladder.  We also have a saying in our ICUs that the team is only as strong as the weakest link.   You also won't find any Excelsior entry level RN graduates in our ICUs.   

For 30 years I had hoped EMS would adopt even a fraction of these standards for education and more EMT(P)s in the profession would develop a thirst for more knowledge to compliment the "skills".   If there are more out there like JPINFV and skyemt, the future of EMS may start to look a little brighter.   

**************************

MSDeltaflt, your continuing eduation for more knowledge is very clear by your posts and interests on this forum and others as well as your two licenses.  

This study has sickle cell going to the right on the curve.
*OXYGEN DISSOCIATION CURVES IN SICKLE CELL ANEMIA AND IN SUBJECTS WITH THE SICKLE CELL TRAIT*
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=438687&blobtype=pdf

Another study to the right:

*Accuracy of Pulse Oximetry in Sickle Cell Disease *

http://ajrccm.atsjournals.org/cgi/content/full/159/2/447



> We confirmed that RBCs from most patients with sickle cell disease have abnormally low oxygen affinity, resulting in far right-shifted oxyhemoglobin dissociation curves in vivo. Only a small fraction of the right shift could be explained by the normal Bohr shift (3). Because of the right-shifted curve, estimates of SO2 from blood gas data, based on assumed normal p50, are without value.
> 
> A right-shifted oxyhemoglobin dissociation curve is generally considered adaptive in anemia, allowing "unloading" of relatively large volumes of oxygen to tissues at relatively high PO2, which preserves a high driving pressure for diffusion of oxygen into poorly vascularized tissues and/or reduces the need for increased cardiac output. However, in sickle cell disease, to the extent that the well-preserved tissue PO2 discourages increasing cardiac output as a compensation for the low oxygen-carrying capacity of the anemic blood, venous blood becomes even more severely deoxygenated than in other forms of anemia. Hemoglobin polymerization depends on red cell concentrations of deoxyhemoglobin (14), so the right-shifted oxyhemoglobin dissociation curve may indirectly encourage polymer formation, sickling, and perhaps the consequent organ damage.


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## skyemt (Mar 31, 2008)

ok...

regarding PaO2... oxygen that binds to hemoglobin no longer exerts pressure... so PaO2 is really measuring the "extra" O2 dissolved in the blood, but doesn't really tell us the O2 content of the blood?

to know the real O2 content of the blood, we would need the PaO2, and we would need to know the amount of hemoglobin in the blood, and then the saturation of that hemoglobin (SaO2)?

so, if you have an idea of where the disassociation curve is, and a relative amount of hemoglobin present (nothing making it too low, or too high), then you can infer a true meaning to the SpO2?

if we believe the PaO2 (and SpO2) to be low, due to V/Q mismatch, then we need to increase the FiO2 in the hopes of raising the implied PaO2?

if the A-a is too high, implying poor diffusion across the alveolar capillary gradient, would increasing the FiO2 have an effect? seems like just adding more oxygen molecules would not change the fact of poor diffusion at the alveolar level... how do we fix that?

that is, if i am correct in my above assumptions...


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## skyemt (Mar 31, 2008)

ok, perhaps if i am understanding...

to try answer my above question, i guess positive pressure ventilations would be needed to "force" the O2 across the gradient? with an increased FiO2?


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## VentMedic (Mar 31, 2008)

skyemt said:


> ok, perhaps if i am understanding...
> 
> to try answer my above question, i guess positive pressure ventilations would be needed to "force" the O2 across the gradient? with an increased FiO2?




Treat the underlying cause (antibotics if PNA, surgery, thoracentesis, chest tubes) maintaining BP MAP, improving cardiac output pharmacologically, FiO2 1.0, ARDSnet protocols running high PEEPs, HFOV (High Frequency Oscillatory Ventilator), seriously educated and skills professionals like RRTs, RNs and Intensivists at bedside....

The theory behind increased PEEP leads to lowering the FiO2 to get off the "oxygen clock" and below at least an FiO2 of 0.60 (0.50 for some literature).  That is unless the Sepsis issue is still in play and high saturations must be maintained.  If that is not the case PaO2 of 55 mmHg or > will be acceptable as well as a permissive rise in PaCO2 with NaHCO3 or preferrably THAM to buffer the pH.       

Now you can get into plateau pressures, static lung compliances... 

First, slow down a little, master the oxygen transport system....

Egan's Fundamentals of Respiratory Care is a great book which you can pick up earlier editions very reasonably.  I just added the pricey 9th to my library to replace the edition I used in RT school.


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## skyemt (Mar 31, 2008)

ok... just to backtrack a little (ok a lot!)...

as far as the oxygen delivery...

is it true that the O2 that enters the bloodstream will bind to the hemoglobin first? when that is saturated, then they float dissolved in the bloodstream?

PaO2, as sort of a reserve?

then the O2 offloads to the organs... do they come from the free floating O2 first, and then the bound O2 after the dissolved O2 is used up?

if that is the case, could someone still be saturated, but be on the verge of a major desaturation? is that the point on the curve where thing rapidly desaturate?

if so, then in a sick person, a high SpO2 could be a misleading number??


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## Ridryder911 (Mar 31, 2008)

I have purposely stayed out of this discussion and let you RT gang explain it. As I thought and presumed, both did great upon pointing out the basics. Vent as usual, my hat is off to you. Your emphasis on placing homeostasis should be the main point of good care in a unit. So many get wrapped up one one segment and fail to see the whole forest out there. 

I do not see many that pay attention to the lactate level as they should (especially in shock syndromes), in which many internist or intensivist do not emphasize and have to play or attempt to catch up later. As well so many wait to place the patient on a ventilator until the patient has exhausted their resources. Yes, we should attempt to prevent needless intubation and ventilator treatment, but as you eloquently described many await for the numbers to change and by that time the patient has already decompensated and has an uphill swim to survive. 

I am really glad you pointed out the emphasis on education levels in units. I admit I get irritated and amused of those that presume since they passed Paramedic school they automatically could work in a true CCU/ICU setting. Many assume that most nurses are those that they have been exposed to at a nursing home. Also there is well a vast difference in critical care and emergency medicine. 

I am precepting Paramedic students in an aggressive ICU. I plan on returning back for PRN work, and have to admit I have beads of sweat thinking of it, due to my absence in a couple of years. Hence.. the reason I am slowly getting re-exposed. The methods of care, routine equipment changes so radically unlike EMS which hardly ever evolves. 

I am glad you did make reference to background education. Although, I have found those that do make it through the Excelsior type programs (let me emphasize "that do make it through") to be usually intelligent; they lack clinical exposure and a thorough nursing background to comfortably care for critical care patients. Again, what many that the read posts here fails to understand that not all EMS or Nursing programs are alike. Yes, one can obtain a license for entry level, that does not mean it is an open door. Even if one is hired, one may not be able to work and perform comfortably in such environments. Just because one is a great medic does not mean they will be a great ER or Critical Care Nurse, vice versa nursing to EMS. I know of great Critical Care nurses that are crappy ER nurses and again vice versa. Each area is of its own speciality and with this requires detailed education to really be proficient and to deliver great care. 

You and I are quite aware that we will never be allowed to or should even consider not having to learning continuously, we have demonstrated this after 30 years; that we still continue to study on a daily basis. This should be a a *major hint* to those that presume once they have obtained a license level then one can ease off. That is a wrong or poorly assumption, so if you are considering Paramedic or Nursing, realize you will continue to go to classes, school, take test, perform clinical skills test for the rest of your career life. If you do not like school, studying, reading, writing, taking tests, do not even consider the medical field and best to leave while you are ahead. 

Back to the original posts, I believe it is essential to understand the oxyhemoglobin curve and fully understand the changes associated with it. Ironically, one would not believe that it was tested over in detail on the old AHA ACLS courses in the late 70's and early 80's. Quite of bit of difference from the current course level being taught today. 

Hang in there Sky.. keep asking the questions and searching for the answers. The more confused one gets, ironically the better you will become because you will challenge statements to understand it more fully. There are many that never get to the point of questioning and take everything at face value, and only memorize which is shameful. 

Good luck, 

R/r 911


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## MSDeltaFlt (Apr 1, 2008)

Sickle Cell - Rt shift.  Oops.  Thanks, Vent.


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## skyemt (Apr 1, 2008)

ok... some things so far...

from the lung side of things, V/Q mismatch could be from:

R to L shunting (pneumothoraces, PE?)   or
diffusion defects (disfunctional alveoli, thickened alveolar walls, edema, etc)

if the V/Q mismatch occurs in a pt with ventilation issues (code, or exhausted from work of breathing), but has no diffusion defects or shunts, the pt can be effectively ventilated by BVM, with the reservoir to raise the FiO2, if we want to raise the PaO2.

if the V/Q mismatch occurs because of diffusion defects, as in CHF or COPD, continuos pressure ventilations (CPAP or BiPAP) will be more effective... splinting open the alveoli (preventing increased work of breathing and recruiting back collapsed alveoli), and also prevent further V/Q mismatch during the expiratory phase of ventilation by preventing the alveoli from collapsing, and being removed from the cycle.

am i on track here?


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## JPINFV (Apr 1, 2008)

skyemt said:


> ok... some things so far...
> 
> from the lung side of things, V/Q mismatch could be from:
> 
> ...



R to L shunting occurs when oxygenated blood enters the systemic circulation. Some of these are congenial (transposition of the great veins [yes, it is exactly how it sounds], septal defects) or normal (broncial circulation gets dumped into the pulmonary veins, and the patent ductus arteriosus (connection between the pulmonary artery and aorta) and patent foramen ovale (normal hole in the atrial septum) at birth (those should quickly close though). Vent might correct me (in class it was kinda of simplified to "we're just going to consider shunting to be no diffusion at all for that blood volume").


> if the V/Q mismatch occurs in a pt with ventilation issues (code, or exhausted from work of breathing), but has no diffusion defects or shunts, the pt can be effectively ventilated by BVM, with the reservoir to raise the FiO2, if we want to raise the PaO2.


Not quite. Shunting, yes, but diffusion is determined by surface area, thickness and the concentration gradient. Thus if you increase FiO2, you will also increase diffusion.


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## VentMedic (Apr 1, 2008)

Couple more links:

Great slide presentation for overview of hypoxia, A-a, shunts
http://www.anest.ufl.edu/ccm/Hypoxia_files/frame.html#slide0011.html

The blank index positions are CXRs with some come hypoxia causes. 

A-a gradient made simple:
http://www.madsci.com/manu/gas_aa.htm


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