Abg vs vbg

[MountainEM]

Hello everyone,

MS3 here hoping to go into EM and currently on a FM inpatient rotation.

I went to ACEP a few weeks ago and one of the lecturers was arguing that VBG could be just as good as ABG for most things. (decreased pain for pt, cost, time, not much difference in the values besides po2)...

so we were in a acid-base lecture the other day and I brought up the topic in the form of a question and bammm.. "well, maybe you can give us a lecture on that," says the attending...

so, any landmark papers people can remember about ABG vs VBG?
Does VBG suffice in most cases?
any stories? case scenerios?
when does VBG not cut it?
Is this a current debate in EM?

any info would be great.
cheers
d

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[GeneralVeers]

VBG is useful for DKA and on patients whom you want to know the pH. Typically a normal VBG pH is 7.30 to 7.35, whereas an ABG has a pH of 7.35 to 7.40.

VBG is not useful for managing vent settings or determining if someone is hypoxic.

 

[Venko]

You can use a VBG for ventilator management excepting adjusting FiO2. The CO2 and acid base status is usable information to determine ventilation for the patient.

 

[GeneralVeers]

You can use a VBG for ventilator management excepting adjusting FiO2. The CO2 and acid base status is usable information to determine ventilation for the patient.

Yes, but why bother? Typically we don't (as ER physicians) change vent settings to manage CO2, in fact it can be harmful.

 

[southerndoc]

Yes, but why bother? Typically we don't (as ER physicians) change vent settings to manage CO2, in fact it can be harmful.

Huh? You don't get gases 30 mins after intubating someone to see if you need to increase/decrease their rates or tidal volumes???

 

[Venko]

Yes, but why bother? Typically we don't (as ER physicians) change vent settings to manage CO2, in fact it can be harmful.

Maybe we're doing it wrong, but if our patients are gonna wait on a vent in the ED, we have found the VBG helpful to make adjustments to the rate and tidal volume (as SouthernDoc explains). The ventilation of the patient depends on these two factors in my experience. Oxygenation is something I have yet to be able to obtain from a VBG, however, so adjusting the FiO2 being provided is difficult. I would imagine we are having a situation of miscommunication as opposed to a true disagreement on the medicine and appreciate your follow up here.

Sincerely,
ThymeLess

 

[docB]

I like VBGs. I don't get near as many ABS as the older docs in my group. I strongly feel that the intubate/don't intubate decision is a clinical one. When I do get ABGs it's usually because I've got someone who's altered and Im trying to sort out primary respiratory with CO2 retention vs. hepatic encephalopathy, etc. That and the ever present "The HMO doctor won't admit the breather without an ABG on the chart." silliness.

 

[GeneralVeers]

Let me clarify. When dealing with patients intubated for primary respiratory causes like COPD, CHF, etc, oxygenation is what needs to be managed. It can be harmful to modify the vent settings to chase pCO2 unless the pO2 is adequate. Additionally lowering the pC02 (i.e. increasing VT or rate) can increase pressures causing barotrauma or PTX.

In short, unless they are in extreme respiratory acidosis, or they're going to be extubated in the ER I'm not going to change the vent settings based on the CO2.

 

[southerndoc]

In short, unless they are in extreme respiratory acidosis, or they're going to be extubated in the ER I'm not going to change the vent settings based on the CO2.

This is counterintuitive to common teaching, and I hope your intensivists are happy with this. They wouldn't go for it in my hospital (although most of my patients have an ICU bed ready before time is needed to draw an ABG).

If you don't correct a rising pCO2 with even a mild acidosis, the inadequate tidal volume will cause the acidosis to worsen. Even worse, a very high pCO2 can worsen hypoxemia.

What you are suggesting is the equivalent of withholding IV fluids in all patients because of the rare 1 in a million that might have undiagnosed CHF and might go into failure with a fluid bolus. Yes, barotrauma does happen, but not that frequently. Even brittle COPD'ers can tolerate changes in their tidal volumes and rates. Sometimes you even need to reduce them if you are breathing too fast or too much for them, but from what you are saying, you don't even reduce settings.

 

[kungfufishing]

I use VBG most of the time. I use ABG when they are on the vent or occasionally when fishing in the altered patient. In my practice I find that oxygenation of the intubated patient is rarely a problem whereas I do tweak the vent due to hypercapnia sometimes.

 

[KidDr]

I use VBG most of the time. I use ABG when they are on the vent or occasionally when fishing in the altered patient. In my practice I find that oxygenation of the intubated patient is rarely a problem whereas I do tweak the vent due to hypercapnia sometimes.

In a lot of the pediatric patients we end up intubating in the ED, ventilation is their primary problem. A VBG is more than adequate to figure out if they're ventilating well, though I agree with docB--the decision to intubate is a clinical one and shouldn't be based on VBG results. But for getting a baseline gas in a critically ill kids, I think a VBG is more than adequate. If oxygenation is an issue, or if it's a cardiac kid, the PICU will place an art line later (though many intubated PICU kids are managed just fine with serial VBGs alone and never get an art line). It's rare that an ABG would be done in the ED (it's not exactly easy to do an art stick on an infant).

I think VBGs can also be useful in unknown ingestions, kids with altered mental status, and bad asthmatics and bronchiolitics (not so helpful as a single VBG, but our pulmonologists and PICU people sometimes like to follow trends after they're admitted).

 

[GeneralVeers]

Just talked to my colleagues and they do not use VBG to manage ventilator either.

The pulmonary literature always talks about changing vent settings to manage acidosis, but this is not something I've seen done acutely in the ER (except by the pulmonologist).

Typically once intubated and oxygenation improves, the pH of the patient improves as well without chasing down the pCO2.

 

[GeneralVeers]

Here's a quote from the only website I could find (someone stole our ER Tintinalli). http://homepage.mac.com/lawhusick/pds/id45.htm

While it's aimed at pulmonologists and does address lowering volumes to compensate for low pH, here is the excerpt I was getting at:

· In ARDS, high VT causes alveolar damage; Limit VT (~5-6 ml/kg ideal body weight) to keep plateau pressure < 30. May allow permissive CO2 retention and lower pH.
· In COPD or asthma, high VE may cause autopeep. Autopeep should be measured before increasing VE. Aim for pH ~7.35, not for normal PCO2; minimize autopeep; keep plateau pressure < 30 and allow permissive CO2 retention.

 

[MountainEM]

thanks for the discussion folks...

also found an interesting links that I have been using to find literature:

http://www.emedmag.com/html/pre/fea/features/038120044.asp

as well as uptodate, pubmed, etc, etc

seems like the case is closed on using VBGs for DKA?

Ma et al2

This was a prospective observational study of 200 patients with suspected diabetic ketoacidosis to determine whether arterial blood gas results influenced management decisions and to compare arterial and venous pH samples. In the study population, arterial blood gas results changed 2 (1%) final diagnoses (ie, pneumonia with hypoxia, sleep apnea with hypercarbia), altered treatment in 7 (3.5%) patients, and changed disposition in 2 (1%) patients to hospital admission. Of the 7 cases where treatment was changed, 5 cases were based on the pH, resulting in a change in the route of insulin administration. The remaining 2 patients had either a low Po2 (supplemental O2 was applied) or a high Pco2 (bilevel positive airway pressure therapy was started). Emergency physicians made the final disposition decision without arterial blood gas results in 47 (97.9%) of 48 patients with confirmed diabetic ketoacidosis and did not alter this decision after reviewing the arterial pH results. Venous pH correlated well with arterial pH (r=.951), with typical values only slightly lower by 0.015.

The authors concluded that arterial blood gas results rarely influenced the final diagnosis, treatment plan, or final disposition in patients with suspected diabetic ketoacidosis. Although the number of confirmed diabetic ketoacidosis cases was small, the pH was most useful in changing the initial management. The venous pH may serve as an accurate substitute for arterial pH.

Gokel et al3

This was a prospective study comparing venous blood gas and arterial blood gas values in patients with uremia, patients with diabetic ketoacidosis, and normal control subjects. Venous and arterial blood gas samples were obtained from 152 patients (100 uremia, 21 diabetic ketoacidosis, 31 normal control subjects). All samples were analyzed for pH and HCO3. On average, venous pH was 0.05 lower than arterial pH. In the small number of patients with diabetic ketoacidosis, the mean arterial pH was 7.15±0.15, whereas the mean venous pH was 7.10±0.15. In patients with uremia, the mean arterial pH was 7.17±0.14, whereas the mean venous pH was 7.13±0.14. In normal control subjects, the mean arterial pH was 7.39±0.02, whereas the mean venous pH was 7.34±0.02. The authors concluded that venous pH correlated well with arterial pH and could be reliably used to evaluate the acid-base status in patients with uremia and diabetic ketoacidosis, even in this small sample. The venous pH was slightly lower (approximately 0.05) than arterial pH.

Brandenberg and Dire4

This was a prospective study to determine whether venous blood gas results could accurately replace arterial blood gas results in the initial emergency department evaluation of a convenience sample of patients with suspected diabetic ketoacidosis. Forty-four episodes of diabetic ketoacidosis with complete arterial blood gas and venous blood gas data were analyzed. Venous blood gas sampling was performed during line placement, and all samples were taken before treatment. The mean arterial pH was 7.20±0.14 compared to a venous pH of 7.17±0.13, with an average difference of 0.03 (r=0.9689).

The authors concluded that venous pH reliably correlated with arterial pH in patients with suspected diabetic ketoacidosis.

Hale and Nattrass5

This was a small prospective study that compared arterial capillary blood gas results with finger capillary blood gas results in patients presenting with diabetic ketoacidosis. Twenty patients with diabetic ketoacidosis had samples analyzed for pH, HCO3, and Pco2 approximately 2 hours after treatment was initiated. The mean arterial pH was 7.07±0.15, compared with the mean capillary pH of 7.04±0.15, with a mean difference of 0.03 (r=0.89). The mean Pco2 and HCO3 values also significantly correlated between the arterial and capillary samples, although the capillary values were slightly higher than the arterial values.

The authors concluded that compared with arterial blood gas samples, capillary blood samples could reliably determine the acid-base status in patients with diabetic ketoacidosis.

...

 

[Venko]

Dr. Veers,

Thank you for your follow up on this conversation. I think it may be a misinterpretation of the data you are providing. COPD is primarily a disorder of ventilation (nearly identical to asthma). These patients are usually profoundly acidotic by the time of intubation. It is agreed, that intubation should be made on clinical grounds, but post intubation ventilator setting adjustments should be made on two separate goals: oxygenation & ventilation. It is very true, that one should not aim for perfect pH, and should avoid autopeep, breath stacking etc. These can surely cause harm. In my experience, the patients that I'm intubation are at pH of 7.1 or even lower. At these levels, there is a profoundly different outcome without adjusting for it. In the attempts to adjust for this, the clinician should take great care not to allow breathstacking, barotrauma, or other malady. There are plenty of means by which to adjust for this and still assist the patient in correcting their acidosis. You are right that oxygenation is not to be overlooked. At our institution, both oxygenation and ventilation are targeted goals for every vented patient regardless of cause if they are SIMV mode or other clinician directed setting (as opposed to patient directed setting). I am currently away from our hospital and cannot provide you with the data, but I recall Marino's text (the ICU book) among other critical care texts noting this. What you have listed above, is true, that if the pH is 7.35 (which is just outside of normal) would be harmful for many patients. COPD folks often live with a baseline acidosis and we shouldn't overcorrect this. They have physiologic norms which are different than most folks including oxygenation. Many of them require some hypoxia to keep their respiratory drive going (granted not important on vented patients as much)...but it just goes to show that correcting to normal isn't the goal. All I and SouthernDoc are getting at is that ventilation management is a key part of all vented patients' care; to overlook acidosis (often profound) would be a mistake in my best estimation (which admittedly lacks the experience that you are bringing to the table as you are an attending and I am a resident). I will try and find more resources when I return to the hospital, but these are my thoughts on this issue...thank you again for your followup.

Sincerely,
ThymeLess

 

[MountainEM]

Validity of venous blood gas analysis for diagnosis ofacid-base imbalance in children admitted topediatric intensive care unitNemat Bilan, Afshin G. Behbahan, A. J. KhosroshahiWorld J Pediatr. 2008 May;4(2):114-7.


VBG can be used instead of ABG in some diseases:

such as respiratory distress syndrome, neonatal
sepsis, renal failure, pneumonia, diabetic
ketoacidosis and status epilepticus, but in

other diseases such as neonatal seizure,
shock,congestive heart failure and congenital
heart diseases, ABG is preferable and must
not be replaced by VBG.


..have not read the study because I could not gain access but sounds interesting...not sure of the quality

 

[Venko]

thanks for the discussion folks...

also found an interesting links that I have been using to find literature:

http://www.emedmag.com/html/pre/fea/features/038120044.asp

as well as uptodate, pubmed, etc, etc

seems like the case is closed on using VBGs for DKA?

Ma et al2

This was a prospective observational study of 200 patients with suspected diabetic ketoacidosis to determine whether arterial blood gas results influenced management decisions and to compare arterial and venous pH samples. In the study population, arterial blood gas results changed 2 (1%) final diagnoses (ie, pneumonia with hypoxia, sleep apnea with hypercarbia), altered treatment in 7 (3.5%) patients, and changed disposition in 2 (1%) patients to hospital admission. Of the 7 cases where treatment was changed, 5 cases were based on the pH, resulting in a change in the route of insulin administration. The remaining 2 patients had either a low Po2 (supplemental O2 was applied) or a high Pco2 (bilevel positive airway pressure therapy was started). Emergency physicians made the final disposition decision without arterial blood gas results in 47 (97.9%) of 48 patients with confirmed diabetic ketoacidosis and did not alter this decision after reviewing the arterial pH results. Venous pH correlated well with arterial pH (r=.951), with typical values only slightly lower by 0.015.

The authors concluded that arterial blood gas results rarely influenced the final diagnosis, treatment plan, or final disposition in patients with suspected diabetic ketoacidosis. Although the number of confirmed diabetic ketoacidosis cases was small, the pH was most useful in changing the initial management. The venous pH may serve as an accurate substitute for arterial pH.

Gokel et al3

This was a prospective study comparing venous blood gas and arterial blood gas values in patients with uremia, patients with diabetic ketoacidosis, and normal control subjects. Venous and arterial blood gas samples were obtained from 152 patients (100 uremia, 21 diabetic ketoacidosis, 31 normal control subjects). All samples were analyzed for pH and HCO3. On average, venous pH was 0.05 lower than arterial pH. In the small number of patients with diabetic ketoacidosis, the mean arterial pH was 7.15±0.15, whereas the mean venous pH was 7.10±0.15. In patients with uremia, the mean arterial pH was 7.17±0.14, whereas the mean venous pH was 7.13±0.14. In normal control subjects, the mean arterial pH was 7.39±0.02, whereas the mean venous pH was 7.34±0.02. The authors concluded that venous pH correlated well with arterial pH and could be reliably used to evaluate the acid-base status in patients with uremia and diabetic ketoacidosis, even in this small sample. The venous pH was slightly lower (approximately 0.05) than arterial pH.

Brandenberg and Dire4

This was a prospective study to determine whether venous blood gas results could accurately replace arterial blood gas results in the initial emergency department evaluation of a convenience sample of patients with suspected diabetic ketoacidosis. Forty-four episodes of diabetic ketoacidosis with complete arterial blood gas and venous blood gas data were analyzed. Venous blood gas sampling was performed during line placement, and all samples were taken before treatment. The mean arterial pH was 7.20±0.14 compared to a venous pH of 7.17±0.13, with an average difference of 0.03 (r=0.9689).

The authors concluded that venous pH reliably correlated with arterial pH in patients with suspected diabetic ketoacidosis.

Hale and Nattrass5

This was a small prospective study that compared arterial capillary blood gas results with finger capillary blood gas results in patients presenting with diabetic ketoacidosis. Twenty patients with diabetic ketoacidosis had samples analyzed for pH, HCO3, and Pco2 approximately 2 hours after treatment was initiated. The mean arterial pH was 7.07±0.15, compared with the mean capillary pH of 7.04±0.15, with a mean difference of 0.03 (r=0.89). The mean Pco2 and HCO3 values also significantly correlated between the arterial and capillary samples, although the capillary values were slightly higher than the arterial values.

The authors concluded that compared with arterial blood gas samples, capillary blood samples could reliably determine the acid-base status in patients with diabetic ketoacidosis.

...

Excellent work! I'm sorry that we monopolized your thread to discuss ventilator management. As you can see, each group has data and each group is passionate. I am not near my hospital to be able to do any meaningful searches for you, but if you are still in need, when I get back Wednesday I can try and help find data for you. Otherwise, I wish you the best of luck on your quest to advance the use of the VBG in place of the ABG.

Sincerely,
ThymeLess

 

[MountainEM]

thanks thymeless 🙂

debate on, I love it👍
d

 

[southerndoc]

Just talked to my colleagues and they do not use VBG to manage ventilator either.

The pulmonary literature always talks about changing vent settings to manage acidosis, but this is not something I've seen done acutely in the ER (except by the pulmonologist).

Typically once intubated and oxygenation improves, the pH of the patient improves as well without chasing down the pCO2.

Do they use an ABG to manage it though? I would be highly surprised if your colleagues just tube 'em and forget 'em. That's how I'm interpreting your philosophy. If their sat is fine, all is ok by you.

ARDS is usually not a problem in the ER. It's more of a long-term problem, so you are unlikely to see it (but can sometimes) in the ER. Therefore, it shouldn't affect the vast majority of your vented patients until they've been in the ICU for days to weeks.

Nobody should be chasing pCO2 by itself (unless it is high enough to cause hypoxemia, which can and does occur). Acidemia and alkalosis are key components in interpreting pCO2 (as mentioned in my first post which you replied to indicating you didn't obtain ABG's to tweak vent settings).

I hope I'm misinterpreting your response.

 

[GeneralVeers]

Do they use an ABG to manage it though? I would be highly surprised if your colleagues just tube 'em and forget 'em. That's how I'm interpreting your philosophy. If their sat is fine, all is ok by you.

It depends. Typically our intubated patients are in the ER long enough for the first ABG (they go up to the unit after that). I usually decrease the FiO2 as necessary to get them close to 40%. I don't immediately correct for CO2 as often their pH and bicarb will improve with oxygenation. In the rare case where the patient is in the ER long enough to require a second or pH I get an ABG, because if I'm going to change the vent for pH reasons I'm going to make sure that oxygenation is good before doing anything else. Hence I wouldn't use a VBG. I would only change the vent settings to address pH if it remains low, and the patient has been adequately oxygenated for some time, hence I would need an ABG again.

ARDS is usually not a problem in the ER. It's more of a long-term problem, so you are unlikely to see it (but can sometimes) in the ER. Therefore, it shouldn't affect the vast majority of your vented patients until they've been in the ICU for days to weeks.

True.

Nobody should be chasing pCO2 by itself (unless it is high enough to cause hypoxemia, which can and does occur). Acidemia and alkalosis are key components in interpreting pCO2 (as mentioned in my first post which you replied to indicating you didn't obtain ABG's to tweak vent settings).

I hope I'm misinterpreting your response.

We are in agreement. I always get ABGs after intubation. I said I wouldn't get a VBG to change vent settings. Perhaps I should have been more specific.

 

[MountainEM]

so in an intubated patient can you can you get a pulse ox and a VBG then?

 

[Venko]

so in an intubated patient can you can you get a pulse ox and a VBG then?

Its note quite the same, but its close...

 

[MountainEM]

" In physiologic terms, ABG composition reflects the relationship between ventilation and perfusion and thus is an important reflection of overall pulmonary function. In clinical practice, respiratory insufficiency can be broken down into two categories—namely, ventilatory failure (inadequate clearance of CO2, or hypercarbia) and oxygenation failure (inadequate plasma oxygenation, or hypoxemia). Arterial blood gas analysis has long been used to diagnose and quantify the severity of either or both of the above conditions in patients with apparent respiratory distress.

A close correlation between arterial and venous PCO2 that would decrease dependency on an ABG does not exist. However, a venous PCO2 value that predicts significant arterial hypercarbia might be useful. In a study published in 2002 by Kelly, a venous PCO2 level above 45 mm Hg predicted an arterial PCO2 above 50 mm Hg (the designated value for significant hypercarbia) with a sensitivity of 100% and specificity of 57%. In this study, a venous PCO2 value above 45 mm Hg detected all cases of significant arterial hypercarbia (negative predictive value, 100%) and reduced the requirement for arterial blood sampling in 41% of cases.

Venous PO2 values do not provide any significant reflection of arterial PO2 levels and are therefore a poor surrogate to quantify oxygen delivery to target tissues. However, the widespread availability of pulse oximetry makes it an attractive alternative. A 2001 study by Witting of more than 700 emergency department patients showed that an oxygen saturation level of 96% or less on room air predicted a PO2 below 70 mm Hg with a sensitivity of 100% and a specificity of 54%. "

When Is Venous Blood Gas Analysis Enough?

Emerg Med 38(12):44-48, 2006



I am having trouble at the moment of remembering when 02 sats do not really reflect oxygenation.... but the above is interesting in this discussion

 

[southerndoc]

so in an intubated patient can you can you get a pulse ox and a VBG then?

I decrease FiO2 based on pulse oximetry.

I manage tidal volume and respiratory rate based on pH and pCO2. I can usually figure out when it's a respiratory acidosis and will correct it as necessary (i.e., hypoxemia inducing a lactic acidosis, which one would expect to have an acidotic pH with a low bicarb and/or increased anion gap plus an elevated lactic acid).

I get ABG's more frequently than VBG's because it's easier to get RT to draw them. Plus, in the very near future, our ABG's will include arterial lactic acid assays.

 

[MountainEM]

I decrease FiO2 based on pulse oximetry.

I manage tidal volume and respiratory rate based on pH and pCO2. I can usually figure out when it's a respiratory acidosis and will correct it as necessary (i.e., hypoxemia inducing a lactic acidosis, which one would expect to have an acidotic pH with a low bicarb and/or increased anion gap plus an elevated lactic acid).

I get ABG's more frequently than VBG's because it's easier to get RT to draw them. Plus, in the very near future, our ABG's will include arterial lactic acid assays.

thanks southerndoc...

why is it easier to get ABGs? I thought they were the pain in the butt to get?
I also thought that lactic levels could be drawn off both? do the VBG studies you have already have lactate? apparently venous and arterial lactic acid levels may be correlated..

" Based on the available evidence, the correlation between arterial and venous lactate values appears to be quite close. A 1996 study by Younger of 48 emergency department patients in whom concurrent arterial and venous blood gas analyses were performed demonstrated that an abnormally elevated venous lactate level (1.6 mmol/L or greater) was 100% sensitive and 89% specific in predicting elevated arterial lactate levels. A 2000 study by Lavery bolstered these results, demonstrating a close correlation between arterial and venous lactate levels in a population of 375 hypovolemic trauma patients. A venous lactate level above 2 mmol/L predicted an elevated injury severity score, ICU admission, and length of stay. " (same article)

Lastly, can you do VBGs right in the ED or do they get sent to a lab? ABGs?
thanks

 

[southerndoc]

By hospital politics, venous lactates must be done in the laboratory. Arterial lactates can be done by respiratory (they use their own machines). ABG's are done by respiratory. VBG's are drawn by the nurse.

If it's a DKA'er and I want to get a VBG with the initial blood draw, then I do it. If it's after IV access has been obtained, then I get respiratory to do an ABG.

 

[Apollyon]

By hospital politics, venous lactates must be done in the laboratory. Arterial lactates can be done by respiratory (they use their own machines). ABG's are done by respiratory. VBG's are drawn by the nurse.

If it's a DKA'er and I want to get a VBG with the initial blood draw, then I do it. If it's after IV access has been obtained, then I get respiratory to do an ABG.

What's funny/ironic is that you can run a VBG through an ABG machine (just adjust some parameters), and you get your gas (and a stat panel, too). I just LOVE politics!

 

[kungfufishing]

I wish we had an istat machine. I still have to wait for our lactates, and worse a "stat" potassium turns around just like a regular potassium...

I think most of us in this discussion, at least the attendings, are recent graduates. This means that for the most part, we probably have similar training and knowledge bases regarding this kind of thing. I think we are all aware that you CAN use a VBG for most of the applications you would use an art gas for, that permissive hypercapnea happens, how acidosis works, that oxygenation is good and too much CO2 is bad, unless you are allowing that to happen because their lungs are so screwed up you have to. I think most of this comes down to personal habit and hospital environment politics and ease of use.

 

[southerndoc]

Hospital politics are too much sometimes. I remember one hospital at one point requiring docs to send down the Hemoccult cards because it was a "lab test" under Joint Commission standards and therefore the lab had to do it.

After receiving quite a few cards with a "hunk of stool" smeared in them, the lab finally gave up.

No, I was not part of these shenanigans. Although it was an amusing story to hear of stool "overflowing from the Hemoccult card" from one of the docs involved. Of course he said as soon as the tube left the station heading toward the lab, he was already on the phone with them asking about results. He would wait on the phone until they received the tube and make them guaiac it while he was on the phone with them so he could get instantaneous results like he would at the bedside.

 

[docB]

Hospital politics are too much sometimes. I remember one hospital at one point requiring docs to send down the Hemoccult cards because it was a "lab test" under Joint Commission standards and therefore the lab had to do it.

After receiving quite a few cards with a "hunk of stool" smeared in them, the lab finally gave up.

No, I was not part of these shenanigans. Although it was an amusing story to hear of stool "overflowing from the Hemoccult card" from one of the docs involved. Of course he said as soon as the tube left the station heading toward the lab, he was already on the phone with them asking about results. He would wait on the phone until they received the tube and make them guaiac it while he was on the phone with them so he could get instantaneous results like he would at the bedside.

2 of the hospitals I work at do this. It's very annoying.

 

[Jeff698]

We have iStat machines in our department. When someone comes by and asks how they differ from the lab, I tell them it's just like the lab but slower.

Sadly, it often takes longer to get the iStat results because of logistics. Sigh....

Our teaching hospital went through the guiac nonsense while I was in residency (hopefully they've come to their senses by now). They removed all guiac developer from the floors. Talk about a black market for the stuff. If you were a medical student and wanted an A, the best plan was to always have a bottle in your coat pocket.

Take care,
Jeff

 

[deleted59964]

my town has two tertiary hospitals. one uses ABGs routinely, the other VBG + SpO2. the VBG + SpO2 hospital does just fine managing vents.

i never really got the need to know the PaO2 - Oxygen is transported (almost exclusively) bound to Hb anyway so I care far more about SpO2

 

[leviathan]

my town has two tertiary hospitals. one uses ABGs routinely, the other VBG + SpO2. the VBG + SpO2 hospital does just fine managing vents.

i never really got the need to know the PaO2 - Oxygen is transported (almost exclusively) bound to Hb anyway so I care far more about SpO2

The problem lies in the accuracy of a pulse oximeter in determining SaO2. Maybe the units have improved over the years, though.

 

[Stitch]

my town has two tertiary hospitals. one uses ABGs routinely, the other VBG + SpO2. the VBG + SpO2 hospital does just fine managing vents.

i never really got the need to know the PaO2 - Oxygen is transported (almost exclusively) bound to Hb anyway so I care far more about SpO2

This is what we use in general, and my understanding is that the SpO2 is pretty well correlated to PaO2, at least over 90%. The only caveats to using pulse ox is if you suspect carbon monoxide poisoning (shows up as 88% I think), or if the person is very anemic for some reason then your reading may not be accurate. Otherwise we're managing most vent changes with VBGs.

I also worry about PaO2 in newborns who may be developing pulmonary hypertention or have some other congenital heart lesion, so in those babies an ABG is absolutely necessary if it's on your differential. They usually look pretty crappy though.

 

[southerndoc]

This is what we use in general, and my understanding is that the SpO2 is pretty well correlated to PaO2, at least over 90%. The only caveats to using pulse ox is if you suspect carbon monoxide poisoning (shows up as 88% I think), or if the person is very anemic for some reason then your reading may not be accurate. Otherwise we're managing most vent changes with VBGs.

I also worry about PaO2 in newborns who may be developing pulmonary hypertention or have some other congenital heart lesion, so in those babies an ABG is absolutely necessary if it's on your differential. They usually look pretty crappy though.

CO poisoning will show an SpO2 of 100%. The pulse oximeter measures bound v. unbound hemoglobin and cannot differentiate what the hemoglobin is bound to. Since CO has a very high affinity for hemoglobin (250 times that of oxygen), the pulse oximeter will read 100% even if the patient is profoundly hypoxemic with a pO2 of nearly 0.

 

[Stitch]

CO poisoning will show an SpO2 of 100%. The pulse oximeter measures bound v. unbound hemoglobin and cannot differentiate what the hemoglobin is bound to. Since CO has a very high affinity for hemoglobin (250 times that of oxygen), the pulse oximeter will read 100% even if the patient is profoundly hypoxemic with a pO2 of nearly 0.

You are right, thanks. There was a Board prep question which had the patient satting at 88%, and the explanation stated that PO2 of 88% should make you think of CO poisoning.

 

[WilcoWorld]

You are right, thanks. There was a Board prep question which had the patient satting at 88%, and the explanation stated that PO2 of 88% should make you think of CO poisoning.

Are you sure it wasn't methemoglobinemia? That should cause a pulse ox reading of 85%.

 

[Stitch]

Are you sure it wasn't methemoglobinemia? That should cause a pulse ox reading of 85%.

ah yes, that's probably it. Brain fart. 😛

 

[paiute]

my town has two tertiary hospitals. one uses ABGs routinely, the other VBG + SpO2. the VBG + SpO2 hospital does just fine managing vents.

i never really got the need to know the PaO2 - Oxygen is transported (almost exclusively) bound to Hb anyway so I care far more about SpO2

PaO2 is useful for seeing how well the lungs are functioning. The aveolar (A)-arterial (a) O2 difference is the calculation you can make: PAO2-PaO2=P(inspired)O2-(P (end tidal) CO2/0.8)-PaO2

 

[deleted59964]

PaO2 is useful for seeing how well the lungs are functioning. The aveolar (A)-arterial (a) O2 difference is the calculation you can make: PAO2-PaO2=P(inspired)O2-(P (end tidal) CO2/0.8)-PaO2

Fair enough - if you want an Aa gradient.

But mostly you can just go - geez he's on 60% O2 and his sat is 93% - lungs cant be workin too well.


I'm not saying I'd never want an ABG - just that routine use of ABGs is causing unnecessary pain for patients most of the time. (moot point if you've got an art line)

 

[poresofkohn]

But mostly you can just go - geez he's on 60% O2 and his sat is 93% - lungs cant be workin too well.

>
You'd be amazed at how many people can't think like that.
>
In my hospital, lab or RT draws the VBG and we (RT) run them. If a Pt is in mild distress we'll get a VBG with any other labs that get drawn. If the Pt is in extremis, we'll just get an ABG. As far as managing the ventilator, it's left soley up to us. Occasionally we'll see an intubated Pt who's acid/base status normalizes after correcting a lactic acidosis or repurfusing / oxygenating the kidneys, however the vast majority of our vented Pt's are ventilatory failure. Many of which have obstructive disease and can be difficult to wean, so I usually place an A-line.

 

[leviathan]

CO poisoning will show an SpO2 of 100%. The pulse oximeter measures bound v. unbound hemoglobin and cannot differentiate what the hemoglobin is bound to. Since CO has a very high affinity for hemoglobin (250 times that of oxygen), the pulse oximeter will read 100% even if the patient is profoundly hypoxemic with a pO2 of nearly 0.

PO2 should still be virtually normal in a CO poisoning patient, no? PO2 refers to plasma concentration of O2. Their SaO2 will be nearly 0 though depending on the severity of exposure.

 

[southerndoc]

PO2 should still be virtually normal in a CO poisoning patient, no? PO2 refers to plasma concentration of O2. Their SaO2 will be nearly 0 though depending on the severity of exposure.

Sorry, I think it got lost in translation. I was basically saying that the SpO2 would be 100% even if the patient was dead (therefore having a pO2 of 0).