Types of Shock and other charts

[Brandon O]

That excuse sounds a heck of a lot like the one given for why we should give oxygen to MI patients. One or two little blood cells might queeze through so we should make sure everything blood cell has as much O2 as possible.

And that was a coherent and logical belief at the time. It's just that after exploring the issue empirically, we found that any such benefit seemed to be minimal, and was outweighed by adverse effects of the oxygen.

We start with what makes sense, then we do the research to confirm or disconfirm it. Where is the evidence disconfirming the use of oxygen for shock states? And no, I don't feel you can broadly apply the studies on MI, stroke, etc. to shock, because those are cases of fundamentally localized ischemia (little to no flow) rather than systemic hypoxia (present but inadequate flow).

Here are a few further thoughts:

If your view (which as I said remains arbitrary at this point, not evidence-based) is that we should titrate to 94%, consider that pulse oximetry is often unreliable in shock states, that managing trauma patients often taxes our ability to closely monitor such numbers, and most of all that clinically obvious signs of hypoxia may not be present at meaningful levels of hypoxemia. Imagine a hypovolemic patient with 95% saturation. Is he hypoxemic in any ordinary context? No. Is he likely to present with gross signs of dyspnea, cyanosis, or the like? No. But could his oxygen delivery be improved, at a time when oxygen delivery is going to determine his survival, by increasing his saturation to 100% (or "100%+" via increased PaO2)? I don't know, but it's far from implausible, and you haven't demonstrated to me that this intuitively true possibility is empirically false. Further imagine that he continues to deteriorate, his respirations diminish in adequacy, and his sat begins to drop. At what point will you allow him oxygen? Are you going to be ready to immediately apply it when we cross that threshold? (Bear in mind that non-invasive pulse oximetry has a lag time of a minute or two.)

My original point is not that throwing oxygen on all our shocky patients is definitely valuable, or a top priority. My point was that right now, the weight of evidence (i.e. little either way) seems to favor doing it, because it makes some physiological sense, lots of practical sense, and there's little in the literature that goes against that.

I never thought I'd be on the conservative side of this argument, but come on, guys; it does harm rather than good to progressive care when we take too many liberties with the body of evidence.

 

[EMT91]

Well...at least I sparked a good discussion.

 

[Rettsani]

Well...at least I sparked a good discussion.

Why have you not discussed the topic with us ?
I think it's very lazy, to ask a question about a Topic and not work on the answer. This is a wrong way to learn.

 

[EMT91]

Because my knowledge of this is very limited thus far, and it went in a different direction than its purpose. Not to mention, I am sick.

 

[Handsome Robb]

A bit off topic of shock but on topic for the hyperoxia. Yes, it's from JEMS, it popped up on my facebook feed earlier when there was absolutely nothing going on in my urgent care rotation today.

http://www.jems.com/behind-the-mask

In the "Benefits of O2" section it *very* briefly mentions supplemental o2 in hypoperfusion scenarios.

 

[JPINFV]

A bit off topic of shock but on topic for the hyperoxia. Yes, it's from JEMS, it popped up on my facebook feed earlier when there was absolutely nothing going on in my urgent care rotation today.

http://www.jems.com/behind-the-mask

In the "Benefits of O2" section it *very* briefly mentions supplemental o2 in hypoperfusion scenarios.

First, reading articles written at a 5th grade level is not good for my cortisol levels.

Next, I love when articles get basic science wrong...

"The mitochondria are the powerhouses of the cells, containing enzymes that gradually break down fats, sugars and proteins into single carbon compounds that release a small amount of energy each time."

You mean like... glycolysis which occurs in the cytosol? What happens in the mitochondria is not the breakdown of sugars and proteins, but the further processing of the components of said breakdown in order to produce intermediate substances that shuttle electrons to the electron transport chain, in order to pump protons across the membrane. Also, I'm not fully sure I agree with the characterization of oxygen as a cofactor since it's involved directly in the chemical reaction in a way that modifies it (it's no longer molecular oxygen when it gets done), as well as not being regenerated in the cell (i.e. NAD+ or FADH+)

"The red blood cells aren’t really cells, because they don’t contain mitochondria, nuclei, Golgi apparatus or all the other things that make cells cells. They’re better thought of as little bags of hemoglobin."

By that definition, neither are prokaryotes since prokaryotes lack internal membrane structures.


Rust? Really? Quick, how good is hemoglobin at binding oxygen when it's in its Fe3+ configuration. Yea...

"The odds ratio for death was 1.8 (95% CI 1.5–2.2) in the hyperoxia group compared with the normoxia group. This was even higher than the odds ratio for death in the hypoxia group."

Credit when credit is due for providing not only a useful statistic, but a confidence interval to boot! [golf clap]

"supplemental oxygen (often high-flow)"

Class, today's assignment is to look up the real definition of "high flow" in relation to respiratory therapies. Heck, even the National Registry uses the term "high concentration" on their skill sheets.


"Free radicals are oxygen atoms with a charge due to an unequal number of protons and electrons."

Congratulations, you've found the definition of the term "ion." For "free radicals," the correct definition includes use of the term "unpaired electron" (although "hippie" is acceptable in a political "science" course).

"much like pouring hydrogen peroxide into an open would"

Probably because H2O2 basically equates to "free radicals" in a discussion of biochemistry?

 

[Farmer2DO]

First, reading articles written at a 5th grade level is not good for my cortisol levels.

Next, I love when articles get basic science wrong...

Two big reasons I let my JEMS subscription go. I just wasn't getting anything out of it, and often times could point out where there were factual errors.

For "free radicals," the correct definition includes use of the term "unpaired electron" (although "hippie" is acceptable in a political "science" course).

OK, that made laugh.

 

[systemet]

Imagine a hypovolemic patient with 95% saturation. Is he hypoxemic in any ordinary context? No. Is he likely to present with gross signs of dyspnea, cyanosis, or the like? No. But could his oxygen delivery be improved, at a time when oxygen delivery is going to determine his survival, by increasing his saturation to 100% (or "100%+" via increased PaO2)? I don't know, but it's far from implausible, and you haven't demonstrated to me that this intuitively true possibility is empirically false.

Hi Brandon. I don't have empirical data for this, but the physiology can give some answers. If we consider arterial oxygen content:

CaO2 (ml/dl) = [SaO2 * Hgb(g/dl) * 1.36 ml 02(/g%)] + [pO2 * 0.003 (ml / mmHg dl)]

If we take a normal male patient, SaO2 = 0.99, Hgb = 15 g /dl, pO2 = 100 mmHg, we get arterial oxygen content of 20.5 ml / dl, of which 20.2 ml/dl is carried on bound hemoglobin, and 0.3 ml (or 1.5%) dissolved in the plasma.

If we make this person a little sick, e.g. Hgb = 10 g / dl, SaO2 = 94%, pO2 = 80 mmHg, we get a CaO2 of 12.5 ml/dl (0.24 ml, still ~ 1.5% in the plasma *** note that this almost completely represents the lost hemoglobin, the amount of dissolved oxygen is relatively unchanged).

Now we give supplemental oxygen via NRB, Hgb = 10 g / dl, SaO2 = 100%, pO2 = 300 mmHg (let's say). We get a CaO2 of 13.9 ( 0.9 ml or 6.5% dissolved in the plasma).

We have made an impact on the CaO2, of about 1.5 ml/dl, primarily from saturating the other 6% of unsaturated hgb, but we've also made an improvement by increasing the amount transported in the plasma.

Although our issue here, is likely to be oxygen delivery, versus oxygen content. This is a situation where we have elements of stagnant and hypemic hypoxia. While some tissue beds may be maximally extracting the delivered oxygen, e.g. the myocardium, the issue might be more one of cardiac output and local perfusion pressures. For regions that aren't being perfused, the decreased oxygen-carrying capacity of the blood circulating in other areas may be less of an issue.

Hypovolemia, or specifically anemia, is a situation where supplemental oxygen is going to have a bigger impact, as the relative contribution of dissolved O2 is much greater when your hemoglobin is depleted, but hyperoxygenation is not going to resolve issues of stagnant hypoxia. Furthermore it might worsen tissue perfusion secondary to hyperoxic vasoconstriction, free radical generation, or immune cell activation. I think there are other people here better qualified to talk about this than me.

I don't think you're going to find any empirical evidence suggesting that restricting oxygen therapy in hemorrhagic shock results in improved outcomes. I don't think anyone's done these studies yet. If you go back and run these numbers with normal hemoglobin ranges for the desaturated patients, the relative contribution of the dissolved oxygen decreases greatly.

 

[Rettsani]

Because my knowledge of this is very limited thus far, and it went in a different direction than its purpose. Not to mention, I am sick.

It's not so bad. You know "Learning by doing " ? That means reading text and try to find a logical answer. Then write what you think and wait until someone tells you whether you have a wrong mindset. There are no wrong answers or questions. There are only stupid answers or wrong reaction. But i think that you need not fear. These are all just humans here like you and me.

I was sick last week to.

 

[Brandon O]

Hi Brandon. I don't have empirical data for this, but the physiology can give some answers. If we consider arterial oxygen content... (snip)

Good stuff, although we should remember that the oxygen per volume is only half of the issue -- the other half is cardiac output, which of course is what's actually challenged in the case of shock.

Although our issue here, is likely to be oxygen delivery, versus oxygen content. This is a situation where we have elements of stagnant and hypemic hypoxia. While some tissue beds may be maximally extracting the delivered oxygen, e.g. the myocardium, the issue might be more one of cardiac output and local perfusion pressures. For regions that aren't being perfused, the decreased oxygen-carrying capacity of the blood circulating in other areas may be less of an issue.

Although true, these problems are a constant for the issue at hand; they would presumably not be worsened (or improved, although you could imagine better pumping or vascular tone -- see the study below) by improved arterial oxygenation. The question is, all things being equal, are we better or worse with a little more oxygen in the blood?

(I suppose to really go out on a limb, you could posit that increased FiO2 in a slightly hypoxic patient could lead to decreased respirations, hence less ventilation, more retained CO2, and a beneficial shift in oxyhemoglobin affinity. But that's a stretch.)

Hypovolemia, or specifically anemia, is a situation where supplemental oxygen is going to have a bigger impact, as the relative contribution of dissolved O2 is much greater when your hemoglobin is depleted, but hyperoxygenation is not going to resolve issues of stagnant hypoxia. Furthermore it might worsen tissue perfusion secondary to hyperoxic vasoconstriction, free radical generation, or immune cell activation. I think there are other people here better qualified to talk about this than me.

In the end, as I hope I more or less communicated, I think this is the central question. There would presumably be some benefit and, based on the more recent literature, probably some harm. So the question is whether the harm or the benefit is more profound. (In the end I do suspect that it's not far from the middle no matter which way it falls -- which means that the practical considerations I mentioned may be the most relevant.)

I don't think you're going to find any empirical evidence suggesting that restricting oxygen therapy in hemorrhagic shock results in improved outcomes. I don't think anyone's done these studies yet.

Grudgingly, you make me dig. I'm going to sniff around a little more, because I do remember at least one or two more pertinent studies, but here's some rats for now:

http://www.ncbi.nlm.nih.gov/pubmed/10959021
http://www.ncbi.nlm.nih.gov/pubmed/19410357 (these appear to be the same study)

Conclusion: little effect either way, perhaps some benefit to a modest bump in FiO2.

 

[systemet]

Good stuff, although we should remember that the oxygen per volume is only half of the issue -- the other half is cardiac output, which of course is what's actually challenged in the case of shock.

Absolutely.

There would presumably be some benefit and, based on the more recent literature, probably some harm. So the question is whether the harm or the benefit is more profound. (In the end I do suspect that it's not far from the middle no matter which way it falls -- which means that the practical considerations I mentioned may be the most relevant.)

I agree, I don't think the risk or benefit has been defined. It seems reasonable to oxygenate to the point that the hemoglobin is maximally saturated, i.e. 98-100%, but not to continue piling on extra FiO2 to get to supraphysiologic pO2s (just my opinion).

Grudgingly, you make me dig. I'm going to sniff around a little more, because I do remember at least one or two more pertinent studies, but here's some rats for now:

http://www.ncbi.nlm.nih.gov/pubmed/10959021
http://www.ncbi.nlm.nih.gov/pubmed/19410357 (these appear to be the same study)

Conclusion: little effect either way, perhaps some benefit to a modest bump in FiO2.

Yeah. I mean, there's the obvious caveat here that these are 200g rats, that are almost impossible to kill, with a very different physiology (e.g. resting heart rate 400 bpm), under halothane anesthesia.

I think you can read this both ways:

* It's pretty clear there's no benefit from higher FiO2 in terms of MAP or PTO2 during the hypotensive phase, i.e. before volume resuscitation, although the acidosis is improved. So this supports the idea that the stagnant hypoxia has to be treated first.

* The greater change in MAP during resuscitation suggests a benefit of supplemental oxygen -- but also represents an overresuscitation. So it makes you wonder if this would be clinically relevant data, if you were running a little rat trauma center If we volume resuscitated the FiO2=0.21 group to similar MAP, how would our other parameters change? Or conversely, if we goal-directed our resuscitation to a MAP of 90 for all groups, how would the data look?

* Their data doesn't shed a lot of light on the role of oxidative stress, with higher pO2s, but suggests that FiO2 = 0.4 has similar effects on hemodynamics to FiO2 = 1.0. So it could be argued that this either (1) represents a beneficial effect of O2, or (2) shows that beyond a certain point, there's no additional benefit to further increasing pO2, which might lead us to question the practice in the light of ongoing controvery regarding the risks of hyperoxia.

I don't think there's a clear answer yet. But it does seem like once you've fully-saturated the hemoglobin, it's hard to imagine that increasing the pO2 further is going to have large effects on DO2.

 

[systemet]

There's a bit of a discussion about hyperoxia in various shock states here as well:

http://www.medscape.com/viewarticle/741752

 

[Handsome Robb]

First, reading articles written at a 5th grade level is not good for my cortisol levels.

Next, I love when articles get basic science wrong...

"The mitochondria are the powerhouses of the cells, containing enzymes that gradually break down fats, sugars and proteins into single carbon compounds that release a small amount of energy each time."

You mean like... glycolysis which occurs in the cytosol? What happens in the mitochondria is not the breakdown of sugars and proteins, but the further processing of the components of said breakdown in order to produce intermediate substances that shuttle electrons to the electron transport chain, in order to pump protons across the membrane. Also, I'm not fully sure I agree with the characterization of oxygen as a cofactor since it's involved directly in the chemical reaction in a way that modifies it (it's no longer molecular oxygen when it gets done), as well as not being regenerated in the cell (i.e. NAD+ or FADH+)

"The red blood cells aren’t really cells, because they don’t contain mitochondria, nuclei, Golgi apparatus or all the other things that make cells cells. They’re better thought of as little bags of hemoglobin."

By that definition, neither are prokaryotes since prokaryotes lack internal membrane structures.


Rust? Really? Quick, how good is hemoglobin at binding oxygen when it's in its Fe3+ configuration. Yea...

"The odds ratio for death was 1.8 (95% CI 1.5–2.2) in the hyperoxia group compared with the normoxia group. This was even higher than the odds ratio for death in the hypoxia group."

Credit when credit is due for providing not only a useful statistic, but a confidence interval to boot! [golf clap]

"supplemental oxygen (often high-flow)"

Class, today's assignment is to look up the real definition of "high flow" in relation to respiratory therapies. Heck, even the National Registry uses the term "high concentration" on their skill sheets.


"Free radicals are oxygen atoms with a charge due to an unequal number of protons and electrons."

Congratulations, you've found the definition of the term "ion." For "free radicals," the correct definition includes use of the term "unpaired electron" (although "hippie" is acceptable in a political "science" course).

"much like pouring hydrogen peroxide into an open would"

Probably because H2O2 basically equates to "free radicals" in a discussion of biochemistry?

I will go back to lurking these threads when they get above my reading comprehension level then.

I'm the first to admit I don't understand physiology as well as i wish I did.

 

[JPINFV]

I will go back to lurking these threads when they get above my reading comprehension level then.

I'm the first to admit I don't understand physiology as well as i wish I did.

Sorry if you took it personally because it wasn't directed at you. It's just sad that something like that is published in what is supposed to be a leading EMS trade journal, especially with the inaccuracies involved.

 

[Handsome Robb]

Sorry if you took it personally because it wasn't directed at you. It's just sad that something like that is published in what is supposed to be a leading EMS trade journal, especially with the inaccuracies involved.

No worries. That was more my terrible attempt at sarcasm than anything.

 

[Melclin]

First, reading articles written at a 5th grade level is not good for my cortisol levels.

Next, I love when articles get basic science wrong...

"The mitochondria are the powerhouses of the cells, containing enzymes that gradually break down fats, sugars and proteins into single carbon compounds that release a small amount of energy each time."

You mean like... glycolysis which occurs in the cytosol? What happens in the mitochondria is not the breakdown of sugars and proteins, but the further processing of the components of said breakdown in order to produce intermediate substances that shuttle electrons to the electron transport chain, in order to pump protons across the membrane. Also, I'm not fully sure I agree with the characterization of oxygen as a cofactor since it's involved directly in the chemical reaction in a way that modifies it (it's no longer molecular oxygen when it gets done), as well as not being regenerated in the cell (i.e. NAD+ or FADH+)

"The red blood cells aren’t really cells, because they don’t contain mitochondria, nuclei, Golgi apparatus or all the other things that make cells cells. They’re better thought of as little bags of hemoglobin."

By that definition, neither are prokaryotes since prokaryotes lack internal membrane structures.


Rust? Really? Quick, how good is hemoglobin at binding oxygen when it's in its Fe3+ configuration. Yea...

"The odds ratio for death was 1.8 (95% CI 1.5–2.2) in the hyperoxia group compared with the normoxia group. This was even higher than the odds ratio for death in the hypoxia group."

Credit when credit is due for providing not only a useful statistic, but a confidence interval to boot! [golf clap]

"supplemental oxygen (often high-flow)"

Class, today's assignment is to look up the real definition of "high flow" in relation to respiratory therapies. Heck, even the National Registry uses the term "high concentration" on their skill sheets.


"Free radicals are oxygen atoms with a charge due to an unequal number of protons and electrons."

Congratulations, you've found the definition of the term "ion." For "free radicals," the correct definition includes use of the term "unpaired electron" (although "hippie" is acceptable in a political "science" course).

"much like pouring hydrogen peroxide into an open would"

Probably because H2O2 basically equates to "free radicals" in a discussion of biochemistry?

I think the worst think about this article is the the language it uses and the demographic at which it obviously feels it must aim itself. Physiology aside, this really does read like a book aimed at kids about halfway through elementary school.

It may as well read, "Haemoglobin and his good friend the oxygen molecule played all the way to the ischaemic tissue. Hey Mr Haemoglobin, can I also be friends with the oxygen molecule, said the ischaemic tissue. Why, said the Haemoglobin, you sure can, because the pH is juuuuuuuust right".

At best, it feels like its aimed at a lay people, but I kinda feel like even an intelligent lay person would baulk at the language in this article, even if the actual physiology was beyond them.

One of the education chaps in our service regularly posts fantastic summaries of complex issues in simple terms. They are great examples of how you CAN discuss complex ideas and break them down in a way that people who haven't necessarily memorised Guyton's just yet can understand, but without feeding them total bulls**t. I don't have any issue with simplicity, but I do have an issue with infantile dialogue that knowingly replaces the complex truth with simple lies in the interest of brevity.

 

[Veneficus]

I don't have any issue with simplicity, but I do have an issue with infantile dialogue that knowingly replaces the complex truth with simple lies in the interest of brevity.

Get used to the idea, this is what US EMS education is.

 

[Brandon O]

There's a bit of a discussion about hyperoxia in various shock states here as well:

http://www.medscape.com/viewarticle/741752

My first thought was, gosh this is good. After page two I realized I've already read this before. I need a vacation.

Anyway, most pertinent: http://www.medscape.com/viewarticle/741752_8

Their focus is on hyperbaric hyperoxic treatment, which is probably somewhat relevant although not exactly. But there's normobaric hyperoxic stuff too. As always, the best material is in the cites.

More rats:
http://www.ncbi.nlm.nih.gov/pubmed/7742707
http://www.ncbi.nlm.nih.gov/pubmed/2044210

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1516320/

Kidneys: http://www.ncbi.nlm.nih.gov/pubmed/18400820

Mostly I think we're staying the course so far. Perhaps a bit of benefit, some harm, if you had to pick sides maybe a little more benefit, but mostly a wash. But we're not in a great place for data when the only studies with M&M-based outcomes are in rats, of course...