# Types of Shock and other charts



## EMT91 (Mar 3, 2012)

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!


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## EMT91 (Mar 3, 2012)

Anyone?


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## adamjh3 (Mar 3, 2012)

Your book should have a nice chart outlining S/S of different types of shock


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## EMT91 (Mar 3, 2012)

adamjh3 said:


> Your book should have a nice chart outlining S/S of different types of shock



If it did, I would not be asking for one.


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## Veneficus (Mar 3, 2012)

http://www.amazon.com/Physiologic-B...1382/ref=sr_1_2?ie=UTF8&qid=1330820750&sr=8-2


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## adamjh3 (Mar 3, 2012)

Bizarre. Even my EMT book had one. What book is your class using? 

Also, first result on google


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## EMT91 (Mar 3, 2012)

adamjh3 said:


> Bizarre. Even my EMT book had one. What book is your class using?
> 
> Also, first result on google



That one is kinda what I am looking for. I am going to have to condense it though. and Brady Prehospital Care 9th


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## STXmedic (Mar 3, 2012)

Are you putting one together for a class?


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## Veneficus (Mar 3, 2012)

adamjh3 said:


> Bizarre. Even my EMT book had one. What book is your class using?
> 
> Also, first result on google



The stages of shock in that document are not entirely accurate. Particularly the pathophys parts.

There are 4 classes of shock which have various physio/pathophysio responses along with signs and symptoms and responses to various treatments.


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## EMT91 (Mar 3, 2012)

PoeticInjustice said:


> Are you putting one together for a class?



Kind of. Its not an assignment, but its something I find useful.


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## EMT91 (Mar 3, 2012)

Veneficus said:


> The stages of shock in that document are not entirely accurate. Particularly the pathophys parts.
> 
> There are 4 classes of shock which have various physio/pathophysio responses along with signs and symptoms and responses to various treatments.



I am mainly looking for the vitals, what happens to the bp, pr, rr.


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## Veneficus (Mar 3, 2012)

EMT91 said:


> I am mainly looking for the vitals, what happens to the bp, pr, rr.



But if you learn something right the first time, you have no need to learn it again 

If you plan to advance in a healcare field, time spent now pays dividends later.


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## STXmedic (Mar 3, 2012)

EMT91 said:


> I am mainly looking for the vitals, what happens to the bp, pr, rr.



So you're not interested in the major physiologic differences between them?


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## EMT91 (Mar 3, 2012)

PoeticInjustice said:


> So you're not interested in the major physiologic differences between them?



At this juncture in my education, no.


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## STXmedic (Mar 3, 2012)

EMT91 said:


> At this juncture in my education, no.



Ever thought of being in accounting? Don't they use charts? And I think people's lives don't depend on the knowledge of what's in the charts... Just sayin'


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## EMT91 (Mar 3, 2012)

PoeticInjustice said:


> Ever thought of being in accounting? Don't they use charts? And I think people's lives don't depend on the knowledge of what's in the charts... Just sayin'



....I find it easy to learn from charts. I thought I could find one here.


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## ffemt8978 (Mar 3, 2012)

As has been pointed out, there are various causes, types, and effects of shock so no one chart will be accurate or complete.


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## adamjh3 (Mar 3, 2012)

Veneficus said:


> The stages of shock in that document are not entirely accurate. Particularly the pathophys parts.
> 
> There are 4 classes of shock which have various physio/pathophysio responses along with signs and symptoms and responses to various treatments.



Hm... After reading this I flipped back through my paramedic text to see if I could refresh myself on this. Unfortunately, it's laid out almost identically in my book. 

Stop showing me how inadequate my paramedic program is, k thx. :rofl:


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## Anjel (Mar 3, 2012)

EMT91 said:


> That one is kinda what I am looking for. I am going to have to condense it though. and Brady Prehospital Care 9th



I have that book. And yes there is a chart. 

Read your book and make your own chart.


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## Rettsani (Mar 3, 2012)

ups......

*First, the base ...*

The shock is a life-threatening disorder of the circulation. It is based on a mismatch between the circulating blood volume at the circulatory  and  the actually required circulating blood volume. The cardiac output is reduced. Due to this reduced performance of the circulation, the oxygen supply to organs and tissues affected

*
Three causes can lead to shock:*
- Reduction in blood volume
- Reduction of cardiac output
- Dysregulation of blood vessels peripheral
(For example, the neuro-shock  or vasovagal syncope)

*
Altogether we distinguish six types of shock.*
- Hypovolemic shock
- Cardiogenic shock
- Neurogenic shock
- Vasovagal syncope as a special form of the Neurogenic shock
- anaphylactic shock
- Septic - toxic shock

*
 Hypovolemic shock*
The hypovolemic shock develops in a blood or plasma loss from about 20% (for an adult, this corresponds to approximately 1 liter), based on the total amount of blood of the Patient. Due to the onset of loss of blood regulation mechanisms of the organism results the corresponding one sign.

As the body tries to compensate for blood loss, the pulse rate rises to around the 100 / minute. Systolic blood pressure at the same time falls below 100 mm Hg. 

The peripheral blood vessels constrict so far, so that  only the life Important organs such as brain, lung and heart are sufficient blood supply. This process is called centralization. For longer-lasting centralization leads to metabolic changes in cells with accumulation of acidic metabolites in the blood (acidosis). Furthermore, leading to disturbances of capillary flow with clumping of blood cells. The lack of oxygen, the metabolic changes and the disruption of capillary blood flow leading to reduced performance and has completely failure of the liver, kidney, lung and brain and finally to circulatory collapse. 

Through the centralization results in further signs of shock...

The pulse becomes more rapid, and because of the falling blood pressure progressively get weaker. Due to the lack skin blood circulation, the patient will be very pale. The skin is cold, sweaty and  the patient is shaking and freezes. Initially, the patient is usually restless, nervous and afraid. Later, he becomes increasingly impassive until enters the unconsciousness.

*cardiogenic shock*
Severe disorders of cardiac activity as a result of a heart attack or heart disease, get to a lead  reduction in cardiac output and thus to a cardiogenic shock.

At a heart attack the patient often has pain,  radiating into the left arm, upper abdomen, back or jaw. Because of respiratory distress the patient attempts to raise the upper body. Heart rate changes such as bradycardia, tachycardia and an irregular heartbeat are possible. At the same time decreases the blood pressure. An apparent stasis of the neck veins develop as a result of underperformance of the right heart, thereby forming as result a stasis of backflow blood into the  leading veins to the heart .... 


My English is cruel...

The general risks similar to those of hypovolemic shock. In the case of acute heart disease is always to expected to that the Patient get a cardiac arrest. The patient must never be stored flat or in the shock position.
The sick, weak performance heart would not be able to cope with increased backflow of blood. 

The weakening of the left heart causes a backflow of blood into the pulmonary circulation. The result is the cardiac pulmonary edema.


*Neurogenic shock*

The Neurological shock occurs as a result of traumatic brain and spinal injuries.

Here, a disorder of the central vascular regulation leads to a reduction in peripheral vascular resistance  (the vessels are wide  ​​) and hence the relative lack of volume.


*vasovagal syncope*

The Vasovagal syncope is a special form of neurological shock.
As a result of psychological factors, fear, joy, and pain occurs after a transient excitation of the sympathetic nervous system, an excessive vagal stimulation.

Consequence is a vasodilatation, bradycardia and cardiac force reduction. By the fall of the blood level decreases the blood backflow to the heart. The cardiac output decreases and the brain is not receiving enough oxygen. 

Paleness and a short loss of consciousness are the result. 


*anaphylactic shock
*

The Anaphylactic shock is the result of a hypersensitivity reaction of the body, for example, medicines, insect venom, foods, pollen, infusions, etc.
This result is a histamine-mediated dilation of the capillaries. By changes in capillary plasma occurs from the vascular system. This creates a lack of volume. In addition,occurs a bronchial spasm on.  To the general shock  Symptoms, occur  skin changes such as itching, skin redness, blisters, hives, and eyelid edema.


*Septic - toxic shock*

The Septic Toxic shock is caused by the endotoxins of bacteria in the vascular system. Through the formation of very small blood clots in the capillary leads to among other circulatory disorders. Often, long time no drop in blood pressure can be seen. The skin is warm and rosy. The patient has a fever.

I hope you understand what I wrote....
.....

I could write you all the answers ..
But it would be nicer if you try you in a reply ....

What were your activities in which kind shock?


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## EMT91 (Mar 3, 2012)

Thank you!


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## 325Medic (Mar 4, 2012)

What he said..

325.


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## bw2529 (Mar 4, 2012)

I'm a basic student, and we haven't covered shock yet, but from my understanding...













As BLS, I don't believe I'd treat any differently based on the type of shock, EXCEPT anaphylactic or diabetic.

I'd place the pt. on the gurney, elevating their legs (pillows or whatever), keep them warm, put them on high flow oxygen (NRB), call ALS and when we intercept with them assist starting a line. Any form of shock is a priority call and we're going to load and go. Their best chance for survival is getting to definitive care as quickly as possible.

For anaphylactic... if the patient has their own prescribed epi I can assist in the administration (so long as it isn't expired, it is the patient's, etc). We also carry epi which we can administer but it is an absolute online and ALS must have been dispatched (either on the initial or as per our request). If we do intercept with ALS, they must ride with us if epi has been administered (they cannot release it to BLS).

For diabetic (know Hx), I can administer oral glucose or any other available sugar (non-diet soda, etc). BGL is a BLS skill in my state, but it is not in my agency.

That is my limited understanding, would definitely be interested in hearing any feedback.


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## JPINFV (Mar 4, 2012)

bw2529 said:


> As BLS, I don't believe I'd treat any differently based on the type of shock, EXCEPT anaphylactic or diabetic.


Hypoglycemia is not a form of hypoprofusion ("shock"). 



> I'd place the pt. on the gurney, elevating their legs (pillows or whatever), keep them warm, put them on high flow oxygen (NRB), call ALS and when we intercept with them assist starting a line. Any form of shock is a priority call and we're going to load and go. Their best chance for survival is getting to definitive care as quickly as possible.


I'm not going to get nit picky on the lack of evidence supporting trendelenburg for hypoprofusion besides pointing out that the studies done are small, poor and quality, but consistent with showing no benefit from trendelenburg. 

As far as "definitive care," for shock it isn't necessarily the hospital as paramedics can use a variety of interventions to help support the patient's cardiovascular status. Getting to the hospital is important, but getting competent paramedics to the patient is also important. Depending on the type of shock, this is one of the few times where saline can save lives.


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## DesertMedic66 (Mar 4, 2012)

JPINFV said:


> I'm not going to get nit picky on the lack of evidence supporting trendelenburg for hypoprofusion besides pointing out that the studies done are small, poor and quality, but consistent with showing no benefit from trendelenburg.



Which is why I am extremely surprised that my county actually went away with trendelenburg, seeming how we have a horrible rep for EMS lol


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## Rettsani (Mar 4, 2012)

The treatment of shock is very simple ...

For this requires that you need only a look at the shock cascade. 

--> Decrease in cardiac output -
-> blood pressure drops 
--> Compensatory counter regulation including catecholamine mediated by sympathetic activation and stress response: Increase in heart rate, constriction of peripheral vessels = Centralization to ensure the circulation of the heart and brain influx of fluid from the interstitial space into the vascular system.

-> Later failure of the counter-regulation 
-> vascular atony 
-> Migration of fluid from the vasculature into the interstitial space
-> Gain of hypovolemia
-> Hypoperfusion of the organs
-> stasis - capillary damage - microthrombi formation 
-> Propagation of the clotting activity of the entire organism
-> Depletion of clotting potential, with increased bleeding tendency
-> Gain of hypovolemia
-> tissue hypoxia
-> anaerobic metabolism
-> metabolic acidosis

*Consequence of the cascade of shock*

-> Acute renal failure
-> heart failure
-> Adult Respiratory Distress Syndrome
-> liver failure
-> Decompensation of the circulation
-> death

Task of any shock treatment should be the shock to stop or prevent cascade.

-> Shock position in hypovolemic shock or vasovagal syncope
-> Upper body elevated in cardiogenic shock or anaphylactic ( except for cardiogenic shock)
-> Flatness in neurogenic shock
-> Stop bleeding in trauma
-> Administration of low molecular infusions

so and now you are to write to it .......^_^


->I am a Cruel EMT or whatever.


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## triemal04 (Mar 4, 2012)

JPINFV said:


> I'm not going to get nit picky on the lack of evidence supporting trendelenburg for hypoprofusion besides pointing out that the studies done are small, poor and quality, but consistent with showing no benefit from trendelenburg.


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.


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## Veneficus (Mar 4, 2012)

triemal04 said:


> 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.



Different things work for different reasons on different patients.

Everyone like to point out studies that show "statistically" significant benefits and drawbacks, but rarely are they profound. 

Numbers needed to treat and harm are seldom reported. 

Epidemiological diagnosis and treatment is one tool in the bag, medicine is not one size fits all, the patient you are treating doesn't care and it doesn't matter if the treatment works in 10, 20, 30, or 90% of patients. 

He only cares what works for him.

There are indications for both passive leg raising and lowering. The key is to know when.

I agree with JP though, the use of elevating the legs while keeping the body flat, does not work by the mechanism originally postulated and isn't likely to work very well for acute treatment of hypovolemic shock.


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## triemal04 (Mar 4, 2012)

Veneficus said:


> Different things work for different reasons on different patients.
> 
> Everyone like to point out studies that show "statistically" significant benefits and drawbacks, but rarely are they profound.
> 
> ...


Depends I think.  I agree with the first part; even studies that have a wide margin for showing a specific effect can still be interpeted differently, depending on how the information is looked at.  For the ones I referenced, none that I've seen really said that a passive leg raise was a good treatement, just that it was a good indicator that the patient would respond to fluid, and caused an increase in cardiac output and aortic blood flow; close to what a 500cc bolus of saline did for them.

The don't say anything about if that was sustained or not, or if there were any drawbacks to the increase.

I'm not saying that lifting the legs is the best treatement for hypovolemic shock, or even neccasarily a good, or long lasting one.  Just that it's what is more commonly done than actually placing someone in Trendelenburg's, it doesn't have all the drawbacks, and can be beneficial for some.


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## Veneficus (Mar 4, 2012)

triemal04 said:


> Depends I think.  I agree with the first part; even studies that have a wide margin for showing a specific effect can still be interpeted differently, depending on how the information is looked at.  For the ones I referenced, none that I've seen really said that a passive leg raise was a good treatement, just that it was a good indicator that the patient would respond to fluid, and caused an increase in cardiac output and aortic blood flow; close to what a 500cc bolus of saline did for them.
> 
> The don't say anything about if that was sustained or not, or if there were any drawbacks to the increase.
> 
> I'm not saying that lifting the legs is the best treatement for hypovolemic shock, or even neccasarily a good, or long lasting one.  Just that it's what is more commonly done than actually placing someone in Trendelenburg's, it doesn't have all the drawbacks, and can be beneficial for some.



I was thinking more along the lines of surgical positioning than actual hemodynamics.


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## JPINFV (Mar 4, 2012)

triemal04 said:


> 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.




1. Because I'm including the studies that do just look at passive leg raising.

2. Because if trendelenburg, an intervention that would also move blood in the abdominal cavity doesn't work, then passive leg raising, which would recruit much less blood and spread it out over a wider area, is also not going to work.


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## Veneficus (Mar 4, 2012)

JPINFV said:


> 1. Because I'm including the studies that do just look at passive leg raising.
> 
> 2. Because if trendelenburg, an intervention that would also move blood in the abdominal cavity doesn't work, then passive leg raising, which would recruit much less blood and spread it out over a wider area, is also not going to work.



Stop it with your scientific reasoning


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## triemal04 (Mar 4, 2012)

JPINFV said:


> 1. Because I'm including the studies that do just look at passive leg raising.
> 
> 2. Because if trendelenburg, an intervention that would also move blood in the abdominal cavity doesn't work, then passive leg raising, which would recruit much less blood and spread it out over a wider area, is also not going to work.


Unfortunately it would appear that passive leg raising does work, though probably only transiently.  And since it lacks some of the problems associated with dropping the patient's head...not a definitive treatement, but, depending on the situation, also not as potentially harmful as trendelenburg's.


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## JPINFV (Mar 4, 2012)

Oh, and also I'm not talking about something where it's just barely off of the critical P value ([soapbox] P values as a dividing line is stupid and useless [/soapbox]). I'm talking "Let's measure 15 people who just gave blood. Oh look only 1 person saw a mild increase in blood pressure."


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## Veneficus (Mar 4, 2012)

JPINFV said:


> Oh, and also I'm not talking about something where it's just barely off of the critical P value ([soapbox] P values as a dividing line is stupid and useless [/soapbox]). I'm talking "Let's measure 15 people who just gave blood. Oh look only 1 person saw a mild increase in blood pressure."



Holy $hit!!!

Somebody finally gets it!!!

Pass the word.


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## JPINFV (Mar 4, 2012)

Veneficus said:


> Holy $hit!!!
> 
> Somebody finally gets it!!!
> 
> Pass the word.




You would love my epidemiology professor in grad school.


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## Veneficus (Mar 4, 2012)

JPINFV said:


> You would love my epidemiology professor in grad school.



There is hope.


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## bw2529 (Mar 4, 2012)

JPINFV said:


> Hypoglycemia is not a form of hypoprofusion ("shock").



Fair enough.



JPINFV said:


> I'm not going to get nit picky on the lack of evidence supporting trendelenburg for hypoprofusion besides pointing out that the studies done are small, poor and quality, but consistent with showing no benefit from trendelenburg.



I never said trendelenburg. That would be slightly different. I said I would elevate the legs, by placing pillows etc under them to support them. 



JPINFV said:


> As far as "definitive care," for shock it isn't necessarily the hospital as paramedics can use a variety of interventions to help support the patient's cardiovascular status. Getting to the hospital is important, but getting competent paramedics to the patient is also important. Depending on the type of shock, this is one of the few times where saline can save lives.



Certainly, Paramedics are useful, but I'm not going to wait for them in these cases. If we can intercept, or if they were on the initial dispatch, awesome. If not, the hospital will be able to do everything a medic can and more.


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## Rettsani (Mar 5, 2012)




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## Aidey (Mar 5, 2012)

bw2529 said:


> I never said trendelenburg. That would be slightly different. I said I would elevate the legs, by placing pillows etc under them to support them.



What exactly would the point be of doing either?


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## Brandon O (Mar 5, 2012)

EMT91 said:


> 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/


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## JPINFV (Mar 5, 2012)

Aidey said:


> 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.


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## Veneficus (Mar 5, 2012)

JPINFV said:


> 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.


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## Aidey (Mar 5, 2012)

JPINFV said:


> 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.


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## bw2529 (Mar 5, 2012)

Aidey said:


> 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.


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## Aidey (Mar 5, 2012)

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.


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## Brandon O (Mar 5, 2012)

Aidey said:


> 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.


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## Maine iac (Mar 5, 2012)

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


The REAL Shocked Patient- Dr. Cliff Reid


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## Aidey (Mar 5, 2012)

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.


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## Handsome Robb (Mar 6, 2012)

triemal04 said:


> 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.


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## Melclin (Mar 6, 2012)

bw2529 said:


> 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.


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## Rettsani (Mar 6, 2012)

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


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## Brandon O (Mar 6, 2012)

Aidey said:


> 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.


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## Veneficus (Mar 6, 2012)

Brandon Oto said:


> 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?


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## Aidey (Mar 6, 2012)

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.


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## Veneficus (Mar 6, 2012)

Aidey said:
			
		

> 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.



			
				Aidey said:
			
		

> 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.


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## Veneficus (Mar 6, 2012)

Veneficus said:


> No.
> 
> Oxygen binding and heme explains very well why.
> 
> ...



and I forgot to add about reperfusion injury.


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## Aidey (Mar 6, 2012)

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


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## Veneficus (Mar 6, 2012)

Aidey said:


> 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.


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## Aidey (Mar 6, 2012)

*Facepalm* I am.

I haven't had my coffee yet this morning.


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## Brandon O (Mar 6, 2012)

Aidey said:


> 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.


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## EMT91 (Mar 6, 2012)

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


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## Rettsani (Mar 6, 2012)

EMT91 said:


> 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.


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## EMT91 (Mar 6, 2012)

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.


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## Handsome Robb (Mar 7, 2012)

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.


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## JPINFV (Mar 7, 2012)

NVRob said:


> 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?


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## Farmer2DO (Mar 7, 2012)

JPINFV said:


> 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.


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## systemet (Mar 7, 2012)

Brandon Oto said:


> 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.


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## Rettsani (Mar 7, 2012)

EMT91 said:


> 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.


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## Brandon O (Mar 7, 2012)

systemet said:


> 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.


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## systemet (Mar 8, 2012)

Brandon Oto said:


> 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)
> ...



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.


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## systemet (Mar 8, 2012)

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

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


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## Handsome Robb (Mar 8, 2012)

JPINFV said:


> 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...
> 
> ...



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.


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## JPINFV (Mar 8, 2012)

NVRob said:


> 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.


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## Handsome Robb (Mar 8, 2012)

JPINFV said:


> 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.


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## Melclin (Mar 8, 2012)

JPINFV said:


> 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...
> 
> ...



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.


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## Veneficus (Mar 8, 2012)

Melclin said:


> 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.


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## Brandon O (Mar 9, 2012)

systemet said:


> 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...


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