Increased intracranial pressure

[leviathan]

So I'm going to be teaching a class on head + spinal injuries, and I realized I don't really understand the mechanism behind Cushing's response in increased intracranial pressure. I really hate just memorizing facts and I'd like to get a better understanding of what is actually going on underneath to cause Cushing's. If anyone has any knowledge on the subject, I'd love to find out.

Soooo....By what mechanism does mean arterial pressure increase after an increase in intracranial pressure (IICP)? In other words, what feedback mechanism or receptors are involved that react to the ICP, and then how does it raise the BP (ie., increased stroke volume, or increased vasoconstriction, etc.)? Also if someone has IICP, is it more advantageous to reduce the MAP and risk poor cerebral perfusion, or to leave the BP alone and risk the problems associated with hypertension?

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[bartleby]

Your questions are really too detailed to answer in this forum, and Rosen's should answer most of them, so I'll spare you. But I will address your last point. Since cerebral perfusion pressure is MAP-ICP, you can really screw somebody by dumping his/her pressure and causing resultant ischemia. If you're worried about elevated ICP, it's the simple things which are going to help in the ED such as elevating the head of the stretcher or normalizing the pCO2 by intubation if the patient is acutely hypercarbic. If more aggressive measures are needed, they should be undertaken in the ICU setting with a ventriculostomy in place so you at least have some hard data to work with.

 

[leviathan]

Your questions are really too detailed to answer in this forum, and Rosen's should answer most of them, so I'll spare you. But I will address your last point. Since cerebral perfusion pressure is MAP-ICP, you can really screw somebody by dumping his/her pressure and causing resultant ischemia. If you're worried about elevated ICP, it's the simple things which are going to help in the ED such as elevating the head of the stretcher or normalizing the pCO2 by intubation if the patient is acutely hypercarbic. If more aggressive measures are needed, they should be undertaken in the ICU setting with a ventriculostomy in place so you at least have some hard data to work with.

Ah, too bad I don't have Rosen's then....I'll have to stop by a hospital library and look for this stuff to quench my knowledge thirst. Do you think I'd look a little too keenerish though, a pre-med taking out a 1500 page book on EM? Would this stuff be covered in an EMT-P textbook by any chance? Regardless, thanks for what info you did offer.

 

[DropkickMurphy]

Who would know you're a premed unless you tell them? Couldn't be any worse than my owning my own copy of Rosen. And no it probably would not be adequately covered in a paramedic textbook. Remember that most of those are written at a very basic level (one of my EMS instructors said a sixth grade reading level is the standard for many community college textbooks) so you're not going to get the depth you're looking for.

By the way, why are you teaching if you don't understand? Seems like a bad idea to have someone who doesn't fully understand the subject matter (which you admittedly don't) try to educate others on it. JMHO....

 

[leviathan]

By the way, why are you teaching if you don't understand? Seems like a bad idea to have someone who doesn't fully understand the subject matter (which you admittedly don't) try to educate others on it. JMHO....

Exactly why I'm trying to get a better understanding. However, I'm teaching to a group of people taking a first-responder course, and all they need to know is the causes of increased intracranial pressure, the signs and symptoms (including Cushing's response), and how to help alleviate the IICP. Still, it's my own philosophy to understand things to a much deeper level than what is required for the class to know, and also just for personal curiosity. And I already know "why" it occurs (increasing MAP to increase CPP, and then bradycardia from a baroreceptor reflex), but I cannot seem to find anyone who knows the "how" it is occuring.

 

[DropkickMurphy]

I would suggest asking a neurosurgeon or consulting a neurotrauma textbook.

 

[leviathan]

I would suggest asking a neurosurgeon or consulting a neurotrauma textbook.

I just did a Google search and it seems like the actual mechanism is not well understood, though there are assumptions it is just vasoconstriction. I suppose that would make sense, as HR certaintly doesn't rise, and correct me if I'm wrong but there are no adrenergic receptors that are selective to only increasing stroke volume and not heartrate with it....soooo if BP is going up from a nervous response you'd either have increased stroke volume AND heartrate, or increased TPR and in this case it must be the latter.

 

[DropkickMurphy]

I'd recommend signing up for the TraumaList mailing list (www.trauma.org) and posting this question to the subscribers who include some of the really heavy hitters in the field of trauma. Surely someone on that list would be better positioned to answer your question, direct you to someone who could, or quite possibly make you wish you'd never asked.

 

[BKN]

I just did a Google search and it seems like the actual mechanism is not well understood, though there are assumptions it is just vasoconstriction. I suppose that would make sense, as HR certaintly doesn't rise, and correct me if I'm wrong but there are no adrenergic receptors that are selective to only increasing stroke volume and not heartrate with it....soooo if BP is going up from a nervous response you'd either have increased stroke volume AND heartrate, or increased TPR and in this case it must be the latter.

I think you probably won't get an answer from a bunch of relentlessly pragmatic ER docs. However, you may well be right that the mechanism is not well understood at the cellular level. One problem with your theory is that it assumes the CNS is responding normally to receptors. If you are an undergrad you may have studied normal physiology, but not yet been exposed to pathology and pathophysiology. Cushing's response is a late finding (shortly before death). The response is mediated by the medulla which is the part of the brain being most squeezed. The medulla is dying and does not repsond as in normal conditions.

At a gross level, perhaps the book to find is an old one: the diagnosis of stupor and coma by Plum and Posner. It'll be a tough read at your level, but if you deal with chapter two (the overview) and specifically pay attention to the discussions of central and uncal brainstem herniation you may get something out of it.

 

[leviathan]

I think you probably won't get an answer from a bunch of relentlessly pragmatic ER docs. However, you may well be right that the mechanism is not well understood at the cellular level. One problem with your theory is that it assumes the CNS is responding normally to receptors. If you are an undergrad you may have studied normal physiology, but not yet been exposed to pathology and pathophysiology. Cushing's response is a late finding (shortly before death). The response is mediated by the medulla which is the part of the brain being most squeezed. The medulla is dying and does not repsond as in normal conditions.

Very good point, BKN. I know some pathophysiology / pathology from EMS education, but again certaintly not to the level that would be explaining this mechanism.

At a gross level, perhaps the book to find is an old one: the diagnosis of stupor and coma by Plum and Posner. It'll be a tough read at your level, but if you deal with chapter two (the overview) and specifically pay attention to the discussions of central and uncal brainstem herniation you may get something out of it.

I see multiple holdings of that book at my university library, I'll have to check it out after the long weekend. Thanks.

 

[bartleby]

If you can snag a user account from your local med school or even stop by and use one of their computers in the library, they probably have access with a service called MDconsult.com which has the full text of Rosen's available online.

While it's great that you're poking around for your own edification, don't forget your target audience and keep to basic concepts.

 

[leviathan]

If you can snag a user account from your local med school or even stop by and use one of their computers in the library, they probably have access with a service called MDconsult.com which has the full text of Rosen's available online.

While it's great that you're poking around for your own edification, don't forget your target audience and keep to basic concepts.

Yeah, I think I'd scare everyone away if I started bringing up all of this. I was teaching them oxygen therapy before and had some pretty confused faces when explaining the DO2 equation.

 

[AlexCCRN]

Yeah, I think I'd scare everyone away if I started bringing up all of this. I was teaching them oxygen therapy before and had some pretty confused faces when explaining the DO2 equation.

Remembering years ago, having been through this myself as a medic, I think it was most useful to focus on etiology, basic mechanisms, s/s - early to late, and management and/or prophylaxis. It might be fun for you but EMS level providers aren't prepared to appreciate the medical pathophysiology. They want to know they identified and treated appropriately. Then you might direct them to resources to follow in their spare time.

It's a huge topic for prehospital - it was impressed upon me how essential our role was in improving the pts outcome. Time is tissue

 

[leviathan]

Remembering years ago, having been through this myself as a medic, I think it was most useful to focus on etiology, basic mechanisms, s/s - early to late, and management and/or prophylaxis. It might be fun for you but EMS level providers aren't prepared to appreciate the medical pathophysiology. They want to know they identified and treated appropriately. Then you might direct them to resources to follow in their spare time.

It's a huge topic for prehospital - it was impressed upon me how essential our role was in improving the pts outcome. Time is tissue

I usually avoid all the stuff that I find interesting because I know the same doesn't apply to THEM . However, I found that explaining what factors affect oxygen delivery was important to explain why giving a high FiO2 is only beneficial for certain situations...for example why our protocol is to use only a simple face mask in cardiogenic shock, rather than a non-rebreather. I know when I first got into EMS, it was never explained to me and I felt pretty sketchy about giving low FiO2, say to someone with a possible MI.

 

[12R34Y]

I usually avoid all the stuff that I find interesting because I know the same doesn't apply to THEM . However, I found that explaining what factors affect oxygen delivery was important to explain why giving a high FiO2 is only beneficial for certain situations...for example why our protocol is to use only a simple face mask in cardiogenic shock, rather than a non-rebreather. I know when I first got into EMS, it was never explained to me and I felt pretty sketchy about giving low FiO2, say to someone with a possible MI.

huh?

people in shock generally get high flow O2 via NRB if in shock in the prehospital setting. Regardless of the sort. sometimes it takes us floating a swan and a bunch of time before we can differentiate between septic shock and cardiogenic shock and hypovolemic shock in the MICU as evidenced by my last patient I had a couple of days ago in the unit. Doubtful I want to have a medic deciding what type of shock a patient has UNLESS it is obvious that it is hypovolemic (ie trauma) or anaphylaxis (ie. stung by a bee and lost a blood pressure).

I've never heard of doing a simple face mask for cardiogenic shock in the field? could you elaborate. I'm just curious more than anything else. thanks!

later

 

[leviathan]

huh?

people in shock generally get high flow O2 via NRB if in shock in the prehospital setting. Regardless of the sort. sometimes it takes us floating a swan and a bunch of time before we can differentiate between septic shock and cardiogenic shock and hypovolemic shock in the MICU as evidenced by my last patient I had a couple of days ago in the unit. Doubtful I want to have a medic deciding what type of shock a patient has UNLESS it is obvious that it is hypovolemic (ie trauma) or anaphylaxis (ie. stung by a bee and lost a blood pressure).

I've never heard of doing a simple face mask for cardiogenic shock in the field? could you elaborate. I'm just curious more than anything else. thanks!

later

Sure. Basically, our CURRENT protocol indicates to use an NRB / high FiO2 ONLY in the case of multi-trauma or smoke inhalation/CO poisoning. Everyone else who does not fit into these categories, but who we think would still benefit from oxygen receives a SFM.

Using an SFM includes for a protoypical patient with a suspected MI who is shocky...we would just give SFM because we assume the shock is cardiogenic in nature, and so increasing the FiO2 won't make a heck of a lot of difference to the outcome as of course the shock is from cardiac output failure and not SaO2 (right?).

I certaintly don't agree with the protocols, so don't shoot the messenger here...but for whatever reason, the medical officers involved in creating these protocols decided to do it this way. I remember back when I was learning this stuff for the first time myself, I had a scenario on my exam with a patient who was cyanotic and severely SOB with wet lungs and a history of CHF...I tried to use a NRB for what I assumed was pulmonary edema, but I was told that I had to use SFM because the patient was not multi-trauma or suspected CO poisoning...rather stupid, in my opinion.

 

[bartleby]

I don't know about where you work, but unless the person is a COPD'er who is not severely hypoxic, the choice to use an NRB versus a SFM is about the last thing I'd give a medic crap about.

I tried to use a NRB for what I assumed was pulmonary edema, but I was told that I had to use SFM because the patient was not multi-trauma or suspected CO poisoning...rather stupid, in my opinion.

 

[leviathan]

I don't know about where you work, but unless the person is a COPD'er who is not severely hypoxic, the choice to use an NRB versus a SFM is about the last thing I'd give a medic crap about.

Well it gets a bit worse, because I'm actually not working, I'm in a volunteer organization and doing this for free because I enjoy it. We work as first-responders for most major public events in my region (NHL + NBA games, concerts, etc). I won't name the organization because I respect them as a whole and don't want to give them a bad name, it's just some of their policies I disagree with...and apparently some emergency physicians in here are posting the same confusion with it, so it's probably not just that I'm a clueless pre-med.

I responded to an unconscious casualty at an event about a month ago, and the partner that responded with me (who was a higher up) gave me hell for checking for responsiveness by doing a sternal rub on a patient w/o c-spine precautions. Again, because it wasn't "part of protocol". I mean, is there something dangerous about doing it that I'm not aware of?

 

[12R34Y]

Yeah. someone is "shocky" need high flow Oxygen in the prehospital arena. Transport times are short generally and you cannot hurt anyone with it. You may however hurt someone without it.

Remember oxygen also works to decrease pulmonary vascular resistance which is a good thing for CHF'ers and heart patients.

i understand that you didn't make the protocols, but for your own edification O2 is good in the prehospital setting. Instead of having EMT's decide what type of shock someone is in.

later

 

[canjosh]

double post--sorry!

 

[canjosh]

Not debating high-flow O2 in shocky patients...but I do take issue with not being able to decide what type of shock the pt is in. 12R34Y, you seemed to use the words 'medic' and 'EMT' to mean the same level of care. Generally, when you say EMT you are referring to an EMT-Basic. When you say 'medic' generally you mean 'paramedic' which is an entirely different scope compared to the EMT-B. An EMT-B might be trained to recognize your example of anaphylaxis, but basically shock is shock to an EMT. Treat with O2, trendelenberg, keep the pt warm, and rapid transport. But a medic, or paramedic, absolutely must be able to come to some conclusion as to what type of shock the pt is in. That's why dopamine is carried in the field. If we couldn't determine, within reason, the nature of the pt's shock we would never have reason to carry an inotrope. We'd just give everybody with poor perfusion 2 liters of NS and call it a day. So, a paramedic MUST be able to at least make some assumptions about shock in order to treat appropriately. Where I worked 911 we had a cardiogenic shock protocol, a hypovolemic shock protocol, an anaphylaxis protocol, and a sepsis protocol. Neurogenic shock is also discussed in the realm of paramedicine; obviously field treatment is for all intents and purposes inconsequential to those pts. In other words, paramedics are expected to differentiate between the different types of shock--and to treat accordingly.

 

[leviathan]

i understand that you didn't make the protocols, but for your own edification O2 is good in the prehospital setting. Instead of having EMT's decide what type of shock someone is in.

later

Just to clarify, our protocols aren't making EMTs decide what type of shock a patient is in...protocols are plain and simple: if the patient is multi-trauma, or has CO poisoning, you give a NRB mask at high flow. Everyone else receives either a simple face mask or nasal cannula. I know for the ambulance service here, they use NRB for most patients and have tools such as pulse oximetry to guide their decisions in all cases.

 

[12R34Y]

Not debating high-flow O2 in shocky patients...but I do take issue with not being able to decide what type of shock the pt is in. 12R34Y, you seemed to use the words 'medic' and 'EMT' to mean the same level of care. Generally, when you say EMT you are referring to an EMT-Basic. When you say 'medic' generally you mean 'paramedic' which is an entirely different scope compared to the EMT-B. An EMT-B might be trained to recognize your example of anaphylaxis, but basically shock is shock to an EMT. Treat with O2, trendelenberg, keep the pt warm, and rapid transport. But a medic, or paramedic, absolutely must be able to come to some conclusion as to what type of shock the pt is in. That's why dopamine is carried in the field. If we couldn't determine, within reason, the nature of the pt's shock we would never have reason to carry an inotrope. We'd just give everybody with poor perfusion 2 liters of NS and call it a day. So, a paramedic MUST be able to at least make some assumptions about shock in order to treat appropriately. Where I worked 911 we had a cardiogenic shock protocol, a hypovolemic shock protocol, an anaphylaxis protocol, and a sepsis protocol. Neurogenic shock is also discussed in the realm of paramedicine; obviously field treatment is for all intents and purposes inconsequential to those pts. In other words, paramedics are expected to differentiate between the different types of shock--and to treat accordingly.

I appreciate your input. However, those on the board who know me realize that I have been a paramedic and worked for the last 7 years as one. I know am graduating medical school in 5 months and going into EM. I'll start with saying the obvious. I do in fact know the difference between EMT-B's and medics. having said that. Paramedics should not give anything other than high-flow O2 via NRB for any patient in shock of any type. Plain and simple.

I'm not for sure where you are in your training canjosh, but having been the ICU for a couple of months this year I can tell you that MICU attendings and pulmonary/critical care fellows spend sometimes all night trying to figure out what kind of shock someone is in? Sepsis, hypovolemic (ie. GI bleed) and cardiogenic shock can look super duper similar.

When you are dealing with the elderly ( which is who typically goes into shock) things get blurred very quickly and they don't follow the textbooks at all.

Case in point.........A couple of weeks ago a guy gets brought in the ED by medics and is being bagged from a nursing home. Unresponsive with history of VP shunt for hydrocephalus 2 weeks ago. Guy is hypotensive, cool, clammy, and has mottled extremities, tachycardic, afebrile, has a white count of 28 with 30% bandemia bla hblah blah blah.....

Is this sepsis? looks like it (has a white count with bands, recent neurosurgery, elderly, nursing home etc....) I intubate him, and put a cordis in his subclavian (lots of procedures on this guy). Get's his antibotics.

His Sv02 is like 25% (that's really really low). His cardiac index (ie CO) is 1.9 (cardiogenic shock).

Refractory hypotension, tachycardia with lots of runs of Vtach. Cardiac enzymes are all high. 12-lead shows non-specific stuff.

Bottom line.............the attending got called in the middle of the night to do mental gymnastics as to what kind of shock to call this. Wedge pressures were around 18 (doesn't help too much), but his heart isn't working worth a darn. CT head is okay.........you get my drift.

So if you are telling me that a paramedic (ie myself) can decipher between different types of shock in the elderly then you are much more highly trained them myself and our critical care department at my school.

So bottom line........high flow O2 is your friend in the pre=hospital setting.

later

 

[leviathan]

I appreciate your input. However, those on the board who know me realize that I have been a paramedic and worked for the last 7 years as one. I know am graduating medical school in 5 months and going into EM. I'll start with saying the obvious. I do in fact know the difference between EMT-B's and medics. having said that. Paramedics should not give anything other than high-flow O2 via NRB for any patient in shock of any type. Plain and simple.
later

Hey 12R34Y,
What good will giving high-concentration oxygen instead of a simple face mask do for a patient in shock? Isn't the purpose of oxygen to raise their saturation under cases of stress? It seems as if in most cases of shock, their SaO2 is going to be almost fine, so really, all they need is a standard mask, and giving extra O2 won't make a significant difference in their clinical outcome. In the case of hypovolemic shock, I can understand wanting to diffuse extra O2 into the actual blood plasma itself because of the loss of hemoglobin, but in other cases it doesn't seem like it will provide much benefit. Now obviously there is a good reason why protocol is to always use NRBs in shock, and so I'm probably missing something here..but I'd like to figure out where I'm going wrong in my thought process.

 

[canjosh]

I appreciate your input. However, those on the board who know me realize that I have been a paramedic and worked for the last 7 years as one. I know am graduating medical school in 5 months and going into EM. I'll start with saying the obvious. I do in fact know the difference between EMT-B's and medics. having said that. Paramedics should not give anything other than high-flow O2 via NRB for any patient in shock of any type. Plain and simple.

I'm not for sure where you are in your training canjosh, but having been the ICU for a couple of months this year I can tell you that MICU attendings and pulmonary/critical care fellows spend sometimes all night trying to figure out what kind of shock someone is in? Sepsis, hypovolemic (ie. GI bleed) and cardiogenic shock can look super duper similar.

When you are dealing with the elderly ( which is who typically goes into shock) things get blurred very quickly and they don't follow the textbooks at all.

Case in point.........A couple of weeks ago a guy gets brought in the ED by medics and is being bagged from a nursing home. Unresponsive with history of VP shunt for hydrocephalus 2 weeks ago. Guy is hypotensive, cool, clammy, and has mottled extremities, tachycardic, afebrile, has a white count of 28 with 30% bandemia bla hblah blah blah.....

Is this sepsis? looks like it (has a white count with bands, recent neurosurgery, elderly, nursing home etc....) I intubate him, and put a cordis in his subclavian (lots of procedures on this guy). Get's his antibotics.

His Sv02 is like 25% (that's really really low). His cardiac index (ie CO) is 1.9 (cardiogenic shock).

Refractory hypotension, tachycardia with lots of runs of Vtach. Cardiac enzymes are all high. 12-lead shows non-specific stuff.

Bottom line.............the attending got called in the middle of the night to do mental gymnastics as to what kind of shock to call this. Wedge pressures were around 18 (doesn't help too much), but his heart isn't working worth a darn. CT head is okay.........you get my drift.

So if you are telling me that a paramedic (ie myself) can decipher between different types of shock in the elderly then you are much more highly trained them myself and our critical care department at my school.

So bottom line........high flow O2 is your friend in the pre=hospital setting.

later

Again, I don't disagree with high flow O2 in all 'shocky' patients. I'm all for giving the NRB to a blue COPD'er or anybody else for that matter. The statement that I was addressing was this one:
'Doubtful I want to have a medic deciding what type of shock a patient has UNLESS it is obvious that it is hypovolemic (ie trauma) or anaphylaxis (ie. stung by a bee and lost a blood pressure).'

In your MICU pt did you withhold treatment until you floated the Swan? No, you treated the best you could with the data you had at the time. A paramedic ought to be able to make an educated assumption about their pt's condition and treat accordingly. The same would be done in the ED. You don't place a Swan in the ED (not in ours anyhow), but you still treat shock by using some deduction and educated guessing. Like you said, the medicine guys can mentally masturbate all night long to either confirm or debunk the previous working dx and thereby determine the long term plan. So, basically I believe a paramedic must be able to arrive at a reasonable conclusion so that appropriate initial intervention can be performed. i.e. do we give more crystalloid, start inotropes, give blood, abx, etc. (in the ED, obviously). Agree?

 

[canjosh]

I omitted my background--paramedic x 7 years. Oh boy, I get to recert in another year--exciting. :|

 

[12R34Y]

Again, I don't disagree with high flow O2 in all 'shocky' patients. I'm all for giving the NRB to a blue COPD'er or anybody else for that matter. The statement that I was addressing was this one:
'Doubtful I want to have a medic deciding what type of shock a patient has UNLESS it is obvious that it is hypovolemic (ie trauma) or anaphylaxis (ie. stung by a bee and lost a blood pressure).'

In your MICU pt did you withhold treatment until you floated the Swan? No, you treated the best you could with the data you had at the time. A paramedic ought to be able to make an educated assumption about their pt's condition and treat accordingly. The same would be done in the ED. You don't place a Swan in the ED (not in ours anyhow), but you still treat shock by using some deduction and educated guessing. Like you said, the medicine guys can mentally masturbate all night long to either confirm or debunk the previous working dx and thereby determine the long term plan. So, basically I believe a paramedic must be able to arrive at a reasonable conclusion so that appropriate initial intervention can be performed. i.e. do we give more crystalloid, start inotropes, give blood, abx, etc. (in the ED, obviously). Agree?

I'm not bashing medics (I am one and love EMS wholeheartedly), however my only point is that high flow O2 should be a no brainer for any patient in shock regardless of the etiology.

The other poster was implying that if it is cardiogenic shock then you just put them on a simple mask. Well, my point is that you may very well NOT know what kind of shock the 79 y/o nursing home patient is in (cardiogenic, septic, hypovolemic etc...) Like you said..........you can make educated guesses, but that's it. It's still a guess and I don't want to guess wrong. therefore you put them on highflow O2 and haul to the ED.

The difference in the ED is that the guessing is a tad better because you can look at their ABG, CXR, etc.... and see that there Pa02 is 500....Well, then you can go ahead and back down on the 'ole Oxygen at that point.

My whole point about not using a simple face mask on cardiogenic shock patients is that pulmonary edema increases the diffusion distance for oxygen causing an increase in alveolar-arterial oxygen distance. Hypoxia is a huge issue in cardiogenic shock. Peripheral vasoconstriction is also a huge compensatory response to cardiogenic shock causing poor peripheral perfusion rendering your pulse ox uselss oftentimes.

We all know (been well studied) that high flow O2 causes a significant decrease in pulmonary artery pressures (thus increasing right heart function) and decreases pulmonary vascular resistance and significantly increases your cardiac index!! that's HUGE in cardiogenic shock. This is extremely helpful and their protocol states to slap them on a simple mask for the few minutes they'll be in an ambulance.

i say just throw them all on high-flow O2 and go.

There was also a study out of east carolina that showed that paramedics and EMT's could not adequately assess hypoxemia based on clinical parameters alone. There were some 180 patients enrolled and 27 of them were hypoxemic and the medics/EMT's did not recognize it.

Many ambulance services still don't have pulse oximetry in the field.

If you've got one in the field and it says 100 percent and it is a good reading then go ahead and back off on the oxygen and make sure the sats don't drop.

nice discussion however,

later

 

[bartleby]

What is shock in the first place? Inadequate tissue perfusion. If your problem is carrying capacity, as you mentioned, you'll be able to improve delivery by dissolving O2 in plasma with a high Fi02. If it's delivery of blood, you'll improve matters by increasing the amount of oxygen delivered in each bit of blood delivered.

Hey 12R34Y,
What good will giving high-concentration oxygen instead of a simple face mask do for a patient in shock?

 

[leviathan]

What is shock in the first place? Inadequate tissue perfusion. If your problem is carrying capacity, as you mentioned, you'll be able to improve delivery by dissolving O2 in plasma with a high Fi02. If it's delivery of blood, you'll improve matters by increasing the amount of oxygen delivered in each bit of blood delivered.

Hmmm, but is the amount dissolved in blood significant enough to make a difference over someone with 100% SaO2? Good discussion in here BTW, I'm learning a lot!

 

[bartleby]

Ordinarily, only 3% of your oxygen carrying capacity comes from oxygen directly dissolved in plasma. But in certain situations, this can make a significant difference.

100% Oxygen saturation is only part of the story. The real determinant of how your tissues are doing is oxygen delivery. Imagine that you have two patients...both with sats of 100%. But one has a hematocrit (packed red cell volume) of 41% and the other is 15%, but one patient is able to deliver far more oxygen to their tissues than the other because oxygen delivery = cardiac output (stroke volume x heart rate) x oxygen content. Thus, lower oxygen content in blood equals lower peripheral delivery.

On average, you deliver 1000 mL/min of oxygen to your tissues in a resting state, with 250 mL/min consumed by your various bits & pieces. There's plenty of slop in that system in your average vigorous young specimen. But consider the case of your local chronically ill nursing home player with a baseline hematocrit of 30% and depressed cardiac output on a good day. Throw a little urosepsis in the mix and you've got somebody with sats of 100% but O2 demands of 250 mL/min (likely significantly higher in the setting of sepsis) and supply of 200 mL/min. What can you do to improve delivery? You can improve cardiac output (i.e. flog a dying heart), and increase oxygen carrying capacity. All of a sudden, every little bit of help from oxygen dissolved in plasma counts, doesn't it?

 

[leviathan]

Ordinarily, only 3% of your oxygen carrying capacity comes from oxygen directly dissolved in plasma. But in certain situations, this can make a significant difference.

100% Oxygen saturation is only part of the story. The real determinant of how your tissues are doing is oxygen delivery. Imagine that you have two patients...both with sats of 100%. But one has a hematocrit (packed red cell volume) of 41% and the other is 15%, but one patient is able to deliver far more oxygen to their tissues than the other because oxygen delivery = cardiac output (stroke volume x heart rate) x oxygen content. Thus, lower oxygen content in blood equals lower peripheral delivery.

On average, you deliver 1000 mL/min of oxygen to your tissues in a resting state, with 250 mL/min consumed by your various bits & pieces. There's plenty of slop in that system in your average vigorous young specimen. But consider the case of your local chronically ill nursing home player with a baseline hematocrit of 30% and depressed cardiac output on a good day. Throw a little urosepsis in the mix and you've got somebody with sats of 100% but O2 demands of 250 mL/min (likely significantly higher in the setting of sepsis) and supply of 200 mL/min. What can you do to improve delivery? You can improve cardiac output (i.e. flog a dying heart), and increase oxygen carrying capacity. All of a sudden, every little bit of help from oxygen dissolved in plasma counts, doesn't it?

Very well explained, Bartleby!

After I read this, I did a search and found a great page which summarizes the effect of PO2 on plasma oxygen concentration. Most importantly, read the part in bold:

Oxygen in the blood are carried by two routes: bound by hemoglobin (Hb) and dissolved in the plasma
Calculate CaO2 allows us to know amount of oxygen in the blood.
CaO2 = (Hb x 1.39 x SaO2/100) + (PaO2 x 0.003)
For example, if Hb = 15 g/dl, SaO2 =100%, and PaO2 = 100 mmHg, then CaO2 = (15 x 1.39 x 1) + (100 x 0.003) = 20.85 + 0.3 =21.15 ml/dl
At 100% saturation, each gram of hemoglobin caries 1.39 ml of oxygen and normal blood contains about 15 gm of hemoglobin/dl
Notice that oxygen dissociative in the plasma has little impact upon CaO2 because it is only 0.3, and hemoglobin carry majority of the oxygen- 20.85
Majority of the oxygen are carried by hemoglobin
Clinically, it is better to provide hemoglobin (blood transfusion) than providing 100% oxygen to an anemic patient (see the equation)
Plasma oxygen
Only a small component of the total amount of oxygen dissolved in the plasma (0.3 ml/dl at 100 mm Hg PO2)
High inspired oxygen concentration can increase the amount of plasma oxygen modestly (1.8 ml/dl at 650 mm Hg PO2), which results in about a 10% increase in the total oxygen content of blood at normal hemoglobin levels
Anemia & reduced blood hemoglobin levels dramatically reduces the oxygen carrying capacity of blood, even with 100% oxygen saturation

http://www.cvm.okstate.edu/Courses/vmed5412/LECT003.ASP

Notice how they said at NORMAL hemoglobin levels, so presumably under conditions of anemia, the effect would be an even greater increase in DO2.

I can't wait until I'm in med school to learn all this scheiBe; it's so interesting. /insert nerd emoticon