Types of Shock and other charts

[Brandon O]

I need to have a chart or know what the vitals do in the different types of shock as well in basilar skull fracture. I also would like to make a general request for charts/quick guides/flowcharts/algorithms that relate to EMT Basic stuff, please.

Thanks!

Although somewhat lengthy, this might be helpful.

http://emsbasics.com/2011/12/14/understanding-shock-introduction/

 

[JPINFV]

What exactly would the point be of doing either?

In theory, autotransfusion of the blood from the legs or legs+abdomen to the core would increase venous return, which increases preload, which increases cardiac output per Starlings law.

 

[Veneficus]

In theory, autotransfusion of the blood from the legs or legs+abdomen to the core would increase venous return, which increases preload, which increases cardiac output per Starlings law.

Starling was given too much credit...

Except that the venous system is expandable, so adding blood volume increases vascular volume and does not equate to venous return to the heart.

It was a similar improper utilization of Starling's law in hemorrhage. systolic BP measures pressure out (including water), not blood returning.

 

[Aidey]

In theory, autotransfusion of the blood from the legs or legs+abdomen to the core would increase venous return, which increases preload, which increases cardiac output per Starlings law.

Oh, I understand the theory. My issue is that it is a theory that a whole bunch of people swear by that has very little evidence showing that A. It happens in sufficient levels to be measurable and B. Those levels affect systemic perfusion and C. The increased systemic perfusion is sustained long enough to actually help the patient.

It strongly reminds me of the radial pulse = a systolic BP of 70mm/hg thing.

And frankly, if we're going to push autotransfusion by elevating the legs, why not just reintroduce MAST pants? Those at least reduce the size of the 'container', unlike elevating the legs.

What I would like to see (aside from a controlled study evaluating the basic premise) is a study evaluating autotransfusion in hypovolemic shock with the bleeding controlled and pressors administered.

 

[bw2529]

What exactly would the point be of doing either?

Again, my background is that I am an EMT-B student who has not yet covered shock in class. But to answer your question, in my limited understanding, the idea would be to encourage blood flow to the heart and brain, and away from less essential organs such as the lower extremities.

 

[Aidey]

I'm going to disabuse you of a few things right now.

Your textbooks are at least 5-10 years behind. While you must following the outline of the class in order to pass the tests it is very very important to remember that what is in the book is generally not current practice. Do not blindly accept what the book (or your instructor) says. It is important to obtain information from a variety of evidence based sources.

1. Supplemental oxygen is not actually necessary for everyone. NRBs are definitely not necessary for the vast majority of patients. You will have the ability to assess your patient's respiratory status, use it, and titrate oxygen as needed. Current practice is that patient's with an SpO2 above 94% do not need supplemental oxygen. That includes people complaining of chest pain, shortness of breath*, and who present with stroke symptoms or the various forms of shock.

2. Raising the legs is, well, useless. If full trendelenburg doesn't accomplish anything only raising the legs isn't likely to do anything different. The patient would likely benefit more from being in a position of comfort, which for most people is NOT lying flat.

True trendelenburg positioning (legs up and head down) causes negligible affect.
Trendelenburg is probably not a good position for hypotensive patients.
Invasive monitoring of patient's in Trendelenburg and modified trendelenburg showed no statistical change in cardiac output or perfusion.
Did not improve cardiac performance.
The slight change in BP cause absolutely no change in oxygenation status.
The PASG is better at improving perfusion in hypovolemic dogs than trendelenburg

*This is in absence of other clinical signs and symptoms of hypoxia. Just because someone SAYS they are SOB doesn't mean they automatically need to be treated with oxygen. Plenty of people with abd pain say they are SOB, and it is because they aren't breathing deeply because taking a deep breath aggravates the pain. That is just one example of many I can think of.

 

[Brandon O]

Current practice is that patient's with an SpO2 above 94% do not need supplemental oxygen. That includes people complaining of chest pain, shortness of breath*, and who present with stroke symptoms or the various forms of shock.

Since you mentioned evidence-based care, I assume you're referring to the AHA guidelines here. These make little mention of oxygen treatment for systemic shock.

I know some of the EGDT/Surviving Sepsis/etc. pathways for septic shock mention a target SpO2, although I don't really think that was rigorously derived either. But otherwise I think you're stretching the evidence a little.

 

[Maine iac]

http://resusme.em.extrememember.com/?p=5959


The REAL Shocked Patient- Dr. Cliff Reid

 

[Aidey]

Nope. Hyperoxygenation has been proven detrimental in multiple studies for multiple different types of patients. At this point if people want to continue to advocate oxygen for anyone who does not have hypoxemia* the burden of proof lies on them to show it is beneficial.


*And some types of histotoxic hypoxia.

 

[Handsome Robb]

Why does everyone keep equating Trendelenburg's with what actually get's done? There is a difference between simply raising the legs while the body stays flat and actually tilting the entire body so that the head is lower than the feet.

As far as studies looking at passive leg raising, there are quite a few, mostly looking at something besides it's direct usefullness, but all do point out that it works, though possible only transiently. Didn't see any that pointed out any major drawbacks, though I'm not saying there aren't any.

To the OP: Perhaps if you made your own chart you'd learn a lot more than if you simply copied someone else's work.

I agree. I've personally watched a pt gain 15-20 pts SBP with the "legs up" positioning our stretcher allows. Is is transient, it seemed like it but then again the pt was actively bleeding into their abdomen. In other patients I've seen their mental status improve as well as their SBP and stay that way although we are talking about short transport times (to the tune of <10 minutes in most cases). I know n=1 with a stupid EMT-I as the attendant but I like to think that I have a little better grasp on the medicine than the average intermediate, but I'm also 3 months from graduating medic school and am totally finished with the didactic portion. I've read the studies and took the time to read the ones Aidey posted as well so I have seen both sides of the argument. I may get lynched for saying it but my protocol still says use it if the patient will tolerate it so I do use it unless it's contraindicated but most, it not all, of those patients who it is contraindicated in end up being my medic's call not mine.

edit: our TC still uses true trendelenburg as well. All of what I said is based on my experiences so take it with a grain of salt.

 

[Melclin]

Again, my background is that I am an EMT-B student who has not yet covered shock in class. But to answer your question, in my limited understanding, the idea would be to encourage blood flow to the heart and brain, and away from less essential organs such as the lower extremities.

http://www.cjem-online.ca/v6/n1/p48

This is a nice little review article of some of the issues involved. While its great to read this stuff and then apply it to some extent in the real world, remember that you may still have to simply wrote learn whatever they're teaching in class before you can get accredited and on the road in the first place.

 

[Rettsani]

It is interesting, that you discuss Trendelenburg. For us, this type of patient positioning in the ambulance is no longer taught, in school and EMS Training, even if we can perform it with our hydraulic stretcher table.


Here is taught:


Hypovolemischer shock
- Classical shock position
- warmth preservation
- Wound care
- Volume therapy

Contraindication Classical shock position:
- Spinal injury
- Traumatic brain injury
- Open and blunt abdominal trauma
- Aortenanurysma / rupture


cardiogenic shock
- Upper body elevated
- warmth preservation
- Specific drug therapy of coronary heart disease


neurogenic shock
- Flat Storage
- warmth preservation
- Specific medical treatment and drug therapy


vasovagal syncope
- Classical shock position
- warmth preservation
- If necessary volume therapy / specific drug therapy


anaphylactic shock
- Upper body elevated or Classical shock position according to the patient situation
- warmth preservation
- Specific Drug therapy of allergic reaction
- If necessary Volume therapy

 

[Brandon O]

Nope. Hyperoxygenation has been proven detrimental in multiple studies for multiple different types of patients. At this point if people want to continue to advocate oxygen for anyone who does not have hypoxemia* the burden of proof lies on them to show it is beneficial.


*And some types of histotoxic hypoxia.

I have yet to see any reliable study demonstrating this for hypovolemic shock. I'm the first to push for progressive, evidence-based care, but in this case the treatment makes sense prima facie (it's primarily a failure of oxygen delivery, so increasing oxygen in the remaining volume should help, if only slightly), and there's little in the literature showing otherwise. If you know of anything good, toss out some cites and let's munch on them.

"Multiple studies for multiple different types of patients" is not a class, and does not allow universal generalization across entirely different types of disease. Let's not get overly generous throwing out the bathwater here.

 

[Veneficus]

I have yet to see any reliable study demonstrating this for hypovolemic shock. I'm the first to push for progressive, evidence-based care, but in this case the treatment makes sense prima facie (it's primarily a failure of oxygen delivery, so increasing oxygen in the remaining volume should help, if only slightly), and there's little in the literature showing otherwise. If you know of anything good, toss out some cites and let's munch on them.

No.

Oxygen binding and heme explains very well why.

so does this book.


http://www.amazon.com/Physiologic-B...1382/ref=sr_1_2?ie=UTF8&qid=1331044565&sr=8-2

which also cites its sources.

Then for some extra reading, you can look up free radical formation and IGG and C3B fixation of damages RBCs.

For icing on the cake, you can even research neutrophil activation on lung parenchyma and the renal medula during shock and hyperoxygenation.



Your statement seems rather basic for your knowledge?

 

[Aidey]

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 no, that isn't a class of patients. It wasn't meant to be. But all humans who are not hypoxemic is a class, albeit a big one. There is enough evidence that oxygen is harmful that at this point it is pretty safe to extrapolate the available data to cover anyone who is not hypoxemic. People have been homeostasing breathing 21% O2 for a while now. Why start altering one of the basic facts of our biology if it isn't necessary?

EDIT - Vene, you would be amazed how many MDs I get into this debate with. I almost told one particularly annoying ED doc that the plural of anecdote is not data after he said he would continue to put every chest pain pt on O2 no matter what their SpO2 was because he had seen it work occasionally, but I decided against it.

 

[Veneficus]

People have been homeostasing breathing 21% O2 for a while now. Why start altering one of the basic facts of our biology if it isn't necessary?.

For a real brain teaser, humans only need environments of 11% oxygen, so you really have a 10% reserve in normal air.

EDIT - Vene, you would be amazed how many MDs I get into this debate with. I almost told one particularly annoying ED doc that the plural of anecdote is not data after he said he would continue to put every chest pain pt on O2 no matter what their SpO2 was because he had seen it work occasionally, but I decided against it.

I most certainly would believe it. I see it all the time.

 

[Veneficus]

No.

Oxygen binding and heme explains very well why.

so does this book.


http://www.amazon.com/Physiologic-B...1382/ref=sr_1_2?ie=UTF8&qid=1331044565&sr=8-2

which also cites its sources.

Then for some extra reading, you can look up free radical formation and IGG and C3B fixation of damages RBCs.

For icing on the cake, you can even research neutrophil activation on lung parenchyma and the renal medula during shock and hyperoxygenation.



Your statement seems rather basic for your knowledge?

and I forgot to add about reperfusion injury.

 

[Aidey]

That is a good point, but people still compensate in lower oxygen atmospheres by increasing RBC production.

 

[Veneficus]

That is a good point, but people still compensate in lower oxygen atmospheres by increasing RBC production.

I think you are confusing lower partial pressure with percent concentration.

 

[Aidey]

*Facepalm* I am.

I haven't had my coffee yet this morning.