Surviving sepsis: Question from a student

[Josh1]

Hi all,

I'm a medical student and have some (possibly stupid) questions about the surviving sepsis guidelines:

1. I don't understand the blood transfusion aspect: Suppose the patient has a normal hematocrit, won't this be overtransfusion? We are already assuming they're on 100% O2 I suppose.


2. I actually don't understand what SvcO2 measures, What are the normal values? Is the low SvcO2 saying that when it's that low the tissues are extracting so much oxygen you need blood even though your hematocrit might be fine?
Actually that whole arm of the surving sepsis guidline is somewhat confusing as to the reasoning behind it (why are inotropes the next step?)

If someone could walk though this for me (I mean by explaining the reasoning behind each step) it would be a great help. Thanks for helping me out!

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[PMPMD]

Hi all,

I'm a medical student and have some (possibly stupid) questions about the surviving sepsis guidelines:

1. I don't understand the blood transfusion aspect: Suppose the patient has a normal hematocrit, won't this be overtransfusion? We are already assuming they're on 100% O2 I suppose.


2. I actually don't understand what SvcO2 measures, What are the normal values? Is the low SvcO2 saying that when it's that low the tissues are extracting so much oxygen you need blood even though your hematocrit might be fine?
Actually that whole arm of the surving sepsis guidline is somewhat confusing as to the reasoning behind it (why are inotropes the next step?)

If someone could walk though this for me (I mean by explaining the reasoning behind each step) it would be a great help. Thanks for helping me out!

SvO2 (and ScvO2, to a lesser extent) is a marker of global oxygen balance (delivery and consumption). It depends on SaO2, cardiac output, hemoglobin, and oxygen consumption (modified Fick equation). Normal SvO2 is 60-80%.

To improve SvO2, you can increase CO, Hgb, SaO2, or decrease VO2. Increasing CO above normal with dobutamine actually worsened outcomes according to one study, and showed no improvement in others. VO2 can be decreased with mechanical ventilation and sedation. SaO2 can be treated in the usual way Transfusion in this setting would be the remaining variable.

 

[Josh1]

What is the difference between ScvO2 and just SvO2? Is it just how they are measured?
Thanks for your help, I'm still new at this

 

[PMPMD]

What is the difference between ScvO2 and just SvO2? Is it just how they are measured?
Thanks for your help, I'm still new at this

SvO2 is true mixed venous oxygen saturation, and is measured from a pulmonary artery catheter (PAC). The term mixed refers to the blood from SVC and IVC mixing as it passes through the right heart. This is why SvO2 is thought to represent global oxygen balance. The use of these devices in critical care is somewhat controversial, and they have fallen out of favor in many ICUs. This is due to the very real risks of placing and maintaining PACs, and the questionable benefits obtained. ScvO2 is central venous oxygen saturation, and is measured from a central line (eg internal jugular, subclavian, femoral). While this reduces the risk compared to a PAC, it is not truly global since the tip of the catheter is usually in the cavoatrial junction, SVC or IVC. Therefore, complete mixing of blood hasn't occurred.

 

[PMPMD]

To go back to your original question, the recommendation for transfusion from the Surviving Sepsis Guidelines was 2C, which is code for "weak evidence".

 

[Josh1]

Hey, thanks a lot for your response. I know this must be common knowledge for practicing physicians. I appreciate the teaching.
I assume the inotropes are just another mechanism to increase CO and thus O2 delivery to tissue then. I guess there is no real hard reason for putting them after transfusion.

 

[PMPMD]

Hey, thanks a lot for your response. I know this must be common knowledge for practicing physicians. I appreciate the teaching.
I assume the inotropes are just another mechanism to increase CO and thus O2 delivery to tissue then. I guess there is no real hard reason for putting them after transfusion.

You are correct that inotropes are used to increase oxygen delivery. They are used only to bring CO/CI from low to normal, not supranormal. And they should be started after appropriate volume resuscitation.

There are indications for dobutamine in the managament of septic shock, but the evidence is not great.

Endotoxin is not only a vasodilator, but also a negative inotrope, which contributes to low CO in some of these patients.

 

[Xerxes1729]

I was under the impression that what distinguished mixed venous from central venous was the former including the outflow of the coronary sinus, not the mixing of blood from the SVC and IVC, since the venous return from the heart is pretty maximally extracted.

 

[leviathan]

I was under the impression that what distinguished mixed venous from central venous was the former including the outflow of the coronary sinus, not the mixing of blood from the SVC and IVC, since the venous return from the heart is pretty maximally extracted.

The blood from your upper body is not necessarily going to have the same extraction of oxygen as the blood from your lower body. Hence a central cath sitting in your SVC is not mixing with IVC blood and isn't as accurate. You're also right that there is further mixing of blood from the heart which as you said extracts much closer to 100% of the oxygen content in its blood supply, versus ~20-25% normal extraction elsewhere.

 

[jdh71]

Hi all,

I'm a medical student and have some (possibly stupid) questions about the surviving sepsis guidelines:

1. I don't understand the blood transfusion aspect: Suppose the patient has a normal hematocrit, won't this be overtransfusion? We are already assuming they're on 100% O2 I suppose.


2. I actually don't understand what SvcO2 measures, What are the normal values? Is the low SvcO2 saying that when it's that low the tissues are extracting so much oxygen you need blood even though your hematocrit might be fine?
Actually that whole arm of the surving sepsis guidline is somewhat confusing as to the reasoning behind it (why are inotropes the next step?)

If someone could walk though this for me (I mean by explaining the reasoning behind each step) it would be a great help. Thanks for helping me out!

According to early goal directed therapy and the surviving sepsis guidelines, if you're already at or more than 30 hematocrit, you are at your hemoglobin goals, so if the SvO2 is <70, then the ionoptrope. Also, keep in mind that high SvO2, as in >80, doesn't mean good things . . . either the endotoxin load is so bad it's disturbing electron transport at the mitochondrial level, or . . . the tissue is dead and therefore is not extracting anything.

 

[europeman]

Hi Josh.

In my opinion, one of the most important things to do when serially assessing a septic patient is trending lactate clearance.

Also, I hate transfusions (unless for severe hemorrhagic shock). While theoretically, transfusing increases oxygen delivery, often the blood/hemaglobin you are giving a patient (especially if you are at a big/tertiary hospital... those places have the crappiest/oldest blood) is old and has less 2,3-BPG (bisphosphoglycerate) and therefore has a much greater affinity for oxygen.

Thus, the older and crappier the blood you give, the HIGHER your Sv02 will become... and that's not a reflection of better oxygen DELIVERY, rather ,it's a reflection of more oxygen on hemoglobin, in great part as I just alluded to before, because it's stuck on there and can't help you physiologically 'cuz there is no 2,3 BPG.

In short, it helps your labs values, but not the patient.