PaO2

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...
 
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.
 
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.
Click to expand...
 
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...
 
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?
 
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?
Click to expand...


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.
 
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??
 
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
 
Sickle Cell - Rt shift. Oops. Thanks, Vent.
 
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?
 
skyemt said:
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)
Click to expand...

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.
Click to expand...
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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