When do I transfuse?

[RxBoy]

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Every attending, every book, and every surgeon seem to have there own transfusion strategy. The literature is even more diverse. 7th edition Miller even confesses there is no real protocol and clinical judgement trumps all.

Hemoglobin lab values themselves are misleading. Case being take a patient with a hgb of 10 gm/dl, bleed them 2 liters and immediately redraw the hgb after it will still be 10 gm/dl because the concentration has not changed. It only changes when extravascular volume shifts to intravascular volume (which takes some time) or more commonly we flood them with fluids to unmask the true hgb content (new concentration).

I know that PRBCs provides 2 things oxygen carrying capacity and volume. Volume you can cover without blood. It got me thinking....

Has anyone been in a long case with a moderate but constant rate of blood loss (say 400 cc/hour) and seen the patient desat strictly due to decreased hemoglobin content? Assuming you cover volume with fluids and kept FiO2 at 100% how fast did the patient's saturation tank?

I am just curious to know how much time I would have if I was behind on hemoglobin but kept up with volume.

 

[pgg]

Has anyone been in a long case with a moderate but constant rate of blood loss (say 400 cc/hour) and seen the patient desat strictly due to decreased hemoglobin content? Assuming you cover volume with fluids and kept FiO2 at 100% how fast did the patient's saturation tank?

O2 sat is not dependent upon Hb. O2 content is, but that's not what a pulse ox measures.

 

[PMPMD]

Every attending, every book, and every surgeon seem to have there own transfusion strategy. The literature is even more diverse. 7th edition Miller even confesses there is no real protocol and clinical judgement trumps all.

Hemoglobin lab values themselves are misleading. Case being take a patient with a hgb of 10 gm/dl, bleed them 2 liters and immediately redraw the hgb after it will still be 10 gm/dl because the concentration has not changed. It only changes when extravascular volume shifts to intravascular volume (which takes some time) or more commonly we flood them with fluids to unmask the true hgb content (new concentration).

I know that PRBCs provides 2 things oxygen carrying capacity and volume. Volume you can cover without blood. It got me thinking....

Has anyone been in a long case with a moderate but constant rate of blood loss (say 400 cc/hour) and seen the patient desat strictly due to decreased hemoglobin content? Assuming you cover volume with fluids and kept FiO2 at 100% how fast did the patient's saturation tank?

I am just curious to know how much time I would have if I was behind on hemoglobin but kept up with volume.

The most commonly cited transfusion thresholds I hear are hemoglobins of 7 for most patients, and 10 for active myocardial ishemia. I believe these come from the TRICC study by Hebert.

The spo2 shouldn't necessarily drop with anemia if cardiac output is maintained, although oxygen content, delivery and the mixed venous sat may drop with hgb.

Usually pts tolerate this situation in the OR because they're on moderately high fio2 (60%), and have decreased o2 utilization from GA and NMB.

There have definitely been patients in our ICU who refuse transfusion for religious reasons and get down to much lower hemoglobins than would be typically allowed in the OR, and they maintain their sat.

 

[RemyMcswain]

I liked Marino's explanation in the ICU book. It makes sense to me and I read a literature review in "Critical Care" recently that essentially argued the same point; that SvO2 can be used as a transfusion trigger in certain circumstances.

 

[RxBoy]

O2 sat is not dependent upon Hb. O2 content is, but that's not what a pulse ox measures.

Ok replying to this is going to totally derail what I was originally asking.

I understand what you are saying, but I guess a question for you would be is there an instance where Sp02 would be 100% even though your oxygen content is severely diminished (excluding the obvious carbon monoxide poisoning or an extreme leftward shift of the oxy-dissocation curve).

I would assume as hgb decreased and your organs continued to utilize oxygen, the amount of 02 combining with hemoglobin would not be able to be maintained and hence your saturation would decrease.

 

[BobBarker]

When people bleed to death they go tachy, tachy, tachy with st changes, suddenly brady then quickly asystole. You would lose your pulse ox just before the brady death spiral due to lack of perfusion.

 

[RxBoy]

The most commonly cited transfusion thresholds I hear are hemoglobins of 7 for most patients, and 10 for active myocardial ishemia. I believe these come from the TRICC study by Hebert.

The spo2 shouldn't necessarily drop with anemia if cardiac output is maintained, although oxygen content, delivery and the mixed venous sat may drop with hgb.

Usually pts tolerate this situation in the OR because they're on moderately high fio2 (60%), and have decreased o2 utilization from GA and NMB.

There have definitely been patients in our ICU who refuse transfusion for religious reasons and get down to much lower hemoglobins than would be typically allowed in the OR, and they maintain their sat.

The TRICC trial was aimed at the critical care population and I guess following those guidelines would be one strategy. An alternate question would be assuming you had standard ASA monitors and not following any hgb protocols, would there be any vital signs (or mix of VS) that would require a transfusion as opposed to fluids for survival?

 

[SexPanther]

I liked Marino's explanation in the ICU book. It makes sense to me and I read a literature review in "Critical Care" recently that essentially argued the same point; that SvO2 can be used as a transfusion trigger in certain circumstances.

Agree with this. If you don't have a PAC, a central venous O2 from a IJ or scl line can be used as a surrogate with the knowledge that trends are better than a single number in time.

I also like to use lactate as a marker of tissue dysoxia and change to anaerobic metabolism, especially in those case I don't have a central line.

A PCV of 20 with a lactate of 1.0 and/or SvO2 of 75% means no transfusion (generally) in my mind.

 

[RxBoy]

When people bleed to death they go tachy, tachy, tachy with st changes, suddenly brady then quickly asystole. You would lose your pulse ox just before the brady death spiral due to lack of perfusion.

Hmm... So this would result from a hypovolemia -> decreased cardiac output -> hypoperfusion to organs -> death. But wouldn't volume correct the cardiac output (assuming at baseline it was a healthy heart) until you became hypoxic?

 

[RxBoy]

Agree with this. If you don't have a PAC, a central venous O2 from a IJ or scl line can be used as a surrogate with the knowledge that trends are better than a single number in time.

I also like to use lactate as a marker of tissue dysoxia and change to anaerobic metabolism, especially in those case I don't have a central line.

A PCV of 20 with a lactate of 1.0 and/or SvO2 of 75% means no transfusion (generally) in my mind.

Thank you... nice answer. I should start sending lactate labs with my ABGs, it would offer a much better overall picture especially in the setting of mild acidosis.

 

[BobBarker]

Sorry, forgot about the whole dilutional replacement component of the question. My earlier post is what happens in the GI bleeder who you cant keep up with.

 

[pgg]

Ok replying to this is going to totally derail what I was originally asking.

I understand what you are saying, but I guess a question for you would be is there an instance where Sp02 would be 100% even though your oxygen content is severely diminished (excluding the obvious carbon monoxide poisoning or an extreme leftward shift of the oxy-dissocation curve).

I would assume as hgb decreased and your organs continued to utilize oxygen, the amount of 02 combining with hemoglobin would not be able to be maintained and hence your saturation would decrease.

As Hb decreases, extraction % will go up (the heart is kind of a special case because extraction % is already high there under normal circumstances), and venous O2 sat will drop, but your arterial O2 sat will be unchanged.

Even with a Hb of 3, arterial blood will be 100% saturated.

As pointed out by BobBarker, the measured SpO2 isn't likely to change until the ischemic heart starts struggling and hypotension / decreased perfusion ensues.

 

[RxBoy]

As Hb decreases, extraction % will go up (the heart is kind of a special case because extraction % is already high there under normal circumstances), and venous O2 sat will drop, but your arterial O2 sat will be unchanged.

Even with a Hb of 3, arterial blood will be 100% saturated.

As pointed out by BobBarker, the measured SpO2 isn't likely to change until the ischemic heart starts struggling and hypotension / decreased perfusion ensues.

Thank you for the reply, makes sense. So Sp02 would be a very a poor indicator regarding transfusion because it would be an extremely late finding, one so late that not only are you behind but you're pretty much doomed.

So tachycardia with normotensive/or later hypotensive findings should start thinking about transfusion as you fluid resuscitate. Then follow Sv02, lactate levels, or hemoglobin trends because their changes will come much earlier then Sp02 changes. Clears up a lot. Puts it all in clinical context. Thank you.

 

[Idiopathic]

i dont know where to begin with this thread except to say that transfusion, for me, is strictly a way to prevent/minimize end-organ damage.

By the time you see SpO2 changes your patient has problems that you probably cant recover from.

All volume depletion is not necessarily best treated with transfusion. Lactate can be valuable in your assessment. Know your patients risk factors (age, reanl/cardiac/vascular disease) and realize that oxygen content is markedly decreased in the setting of anemia.

 

[Idiopathic]

A PCV of 20 with a lactate of 1.0 and/or SvO2 of 75% means no transfusion (generally) in my mind.

Realizing, of course, that you are on the edge here, conceptually...uncommon for these three to coexist.

 

[etherdreams]

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[etherdreams]

TRICC trial doesn't apply to patients who are actively bleeding.

 

[fakin' the funk]

Thank you for the reply, makes sense. So Sp02 would be a very a poor indicator regarding transfusion because it would be an extremely late finding, one so late that not only are you behind but you're pretty much doomed.

Anemia alone cannot cause arterial desaturation.

However you can have arterial desaturation from anemia (or low cardiac output) if there is a big enough shunt going on as well. Even the normal 5% shunt can cause desaturation if the CO is low enough.

Play with the Fick equation and solve for SaO2.

 

[SexPanther]

Realizing, of course, that you are on the edge here, conceptually...uncommon for these three to coexist.

Of course. Written that way to illustrate my point.