Hyperventilation and ICP.

[Singh]

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Hyperventilation is commonly used to treat head-injured patients. By inducing cerebral vasokonstriction, one can reduce ICP. The danger of this is of course a reduction in CBF.

According to the equation: CPP = MAP - ICP, a decrease in ICP increases CPP.

My question is: Is it possible to have a reduction in CBF at the same time as an increase CPP?

Thanks for any response!
Best regards, Singh.

 

[DenRock]

I would say it is possible to have reduced CBF while increasing CPP. Think of the difinitions of each term. CBF is simply a volume/time thing. CPP like you stated is simply MAP - ICP or CVP whichever is highest. Think of the patient that has high blood pressure but low cardiac output.

 

[VentdependenT]

an embolism or a thrombus comes to mind

 

[jetproppilot]

Hyperventilation is commonly used to treat head-injured patients. By inducing cerebral vasokonstriction, one can reduce ICP. The danger of this is of course a reduction in CBF.

According to the equation: CPP = MAP - ICP, a decrease in ICP increases CPP.

My question is: Is it possible to have a reduction in CBF at the same time as an increase CPP?

Thanks for any response!
Best regards, Singh.

The practice of hyperventilation has questionable efficacy. Although transiently effective in reducing ICP, readjustment of brain pH occurs within 24 hours...so then when PaCO2 is normalized, one can see a dramatic increase in CBF, CBV, and consequently ICP.

Additionally, its seemingly a problematic maneuver...if cerebral ischemia is felt to be present for whatever reason, it seems decreasing CBF may not be a good idea.

Most importantly, at least to my knowledge, the only prospective, well controlled studies on hyperventilation for TBI have shown a poorer outcome.

 

[threepeas]

Hyperventilation is commonly used to treat head-injured patients. By inducing cerebral vasokonstriction, one can reduce ICP. The danger of this is of course a reduction in CBF.

According to the equation: CPP = MAP - ICP, a decrease in ICP increases CPP.

My question is: Is it possible to have a reduction in CBF at the same time as an increase CPP?

Thanks for any response!
Best regards, Singh.[/QUOT

there is no physiologically benefical scenario that could be induced by manipulating the parameters in the question. the only time we hyperventilate is if the ICPs are so high that we cant manipulate the CPP with volume or pressors into a favorable range, ie last ditch effort and usually an ominous sign. numerous studies have shown that hyperventilation can be harmful to the patient. dont let old school thinking pressure you into doing it. make sure you have a swan ganz in to maximize volume, use pitressin to manage SIADH, pressors, elevated HOB, barbs, paralytics, mannitol, fentanyl (not morphine or demerol), maximize ABG, ventriculostomy, and say a prayer if you choose. i have seen a simple thing mismanaged too much so that is why i am throwing my 2 cents in. i am sure someone else has some good advice on the subject though.

Congress of Neurological Surgeons website has some info:

http://www.neurosurgeon.org/education/medStudCur/curriculum.asp?inPage=a3

 

[Singh]

Thanks for your replies!

I think what's confusing me is the fact that a decreased cerebral flow (CBF)can give increased perfusion pressure (CPP). Usually one would think that these two change in the same direction, since a decreased amount of blood in the blood vessels (=CO) in the brain will cause the pressure to fall (BT = CO * TPR). Since this isn't the case, it must mean that hyperventilation increases TPR in the brain by inducing vasoconstriction, thus increasing pressure. Is this how it is?

Is this situation equivalent to the situation where you induce periferal vasoconstriction to increase blood pressure, yet the amount of blood reaching these periferal tissues in reduced?

Man, this is confusing me now

 

[nitecap]

Yeah But CPP= map-ICP or CVP

taking CVP if the central venous pressure is lower you have better cerbral venous drainage which will decrease the ICP but maintain good CPP.

 

[BKN]

Thanks for your replies!


Is this situation equivalent to the situation where you induce periferal vasoconstriction to increase blood pressure, yet the amount of blood reaching these periferal tissues in reduced?

Man, this is confusing me now

In fluid dynamics, flow is inversely propotional to the fourth power of the radius of the pipe. Increasing resistance drops flow but doesn't necessarily change pressure at all. The screwy medical thinking that increasing resistance increases pressure is left over from the use of sympathomimetics which affect both the pump and the pipes. You can give norepinephrine to a patient in shock and see an increase in the pressure, but the actual C.O. usually falls and the tissue is more ischemic than ever.

The idea of using hyperventilation for head njury was to restrict flow and decrease cerebral edema. It actually didn't make sense for two reasons: The CO2 autoregulation only worked in uninjured vessels. The injured ones had the same blood supply and leaked at the same rate or higher than before and why in in the world would making tissue more ischemic be a good idea? As other posters have said, there is no evidence hyperventilation helps brian injury and some that it harms.

 

[Idiopathic]

No, simply because one is dependent on the other. (CPP and CBF, that is)

 

[canjosh]

Maybe you guys could give some direction to a paramedic. I've been one for awhile, and we were taught to hyperventilate when I went to school. I've noticed that practice falling out of favor in the minds of many Emergency Medicine types, but others still think old school and blast away at a rate of damn near 30. From an anesthesia/ccm perspective, what do you guys believe are the best things that can be done for the early TBI...in the field and/or ED. Sedate/paralyze, elevate HOB, hypothermia, massive crystalloid infusions, inotropes, withhold fluids?...remember we've gotta keep it simple and don't have access to your kick arse invasive monitors. Thoughts?

 

[Idiopathic]

I think that the main idea to consider for the acute team is that hyperventilation is certainly something that can be used, especially when other rx options are limited and you are unsure of the nature/extent of the damage. The physiology still works in uninjured tissue, and in my mind, its kind of like the self breast exam. Until it is shown to harm the patient, it is a reasonable acute therapy. With that said, I think the literature bears out that long term hyperventilation, or even hyperventilation in a controlled setting is essentially worthless.


I believe the current trauma rx reccomendations are to hyperventilate to PaCO2 of 25, or to normocapnia. Preventing CO2 retention is obviously of greater import than ridding the individual of physiologic CO2 levels.

As far as the rest, airway, pressure and volume maintenance are the most important concerns, I would assume.

 

[VentdependenT]

I think that the main idea to consider for the acute team is that hyperventilation is certainly something that can be used, especially when other rx options are limited and you are unsure of the nature/extent of the damage. The physiology still works in uninjured tissue, and in my mind, its kind of like the self breast exam. Until it is shown to harm the patient, it is a reasonable acute therapy. With that said, I think the literature bears out that long term hyperventilation, or even hyperventilation in a controlled setting is essentially worthless.


I believe the current trauma rx reccomendations are to hyperventilate to PaCO2 of 25, or to normocapnia. Preventing CO2 retention is obviously of greater import than ridding the individual of physiologic CO2 levels.

As far as the rest, airway, pressure and volume maintenance are the most important concerns, I would assume.

I think the brain compensates for hyperventilation after 24 hours (maybe less, can't recall). So after that time its effect is useless as a cerebral vasoconstrictor.

You can always run a nitro drip to drop MAP and just toss the hyperventilation thing to the curb. High narcs low agent (Agent will vasodilate).

 

[jetproppilot]

I think that the main idea to consider for the acute team is that hyperventilation is certainly something that can be used, especially when other rx options are limited and you are unsure of the nature/extent of the damage. The physiology still works in uninjured tissue, and in my mind, its kind of like the self breast exam. Until it is shown to harm the patient, it is a reasonable acute therapy. With that said, I think the literature bears out that long term hyperventilation, or even hyperventilation in a controlled setting is essentially worthless.


I believe the current trauma rx reccomendations are to hyperventilate to PaCO2 of 25, or to normocapnia. Preventing CO2 retention is obviously of greater import than ridding the individual of physiologic CO2 levels.

As far as the rest, airway, pressure and volume maintenance are the most important concerns, I would assume.

Dude,

thats a Michael Roizen like post.

You da man. 👍

 

[MAC10]

Thanks for your replies!

I think what's confusing me is the fact that a decreased cerebral flow (CBF)can give increased perfusion pressure (CPP). Usually one would think that these two change in the same direction, since a decreased amount of blood in the blood vessels (=CO) in the brain will cause the pressure to fall (BT = CO * TPR). Since this isn't the case, it must mean that hyperventilation increases TPR in the brain by inducing vasoconstriction, thus increasing pressure. Is this how it is?

Is this situation equivalent to the situation where you induce periferal vasoconstriction to increase blood pressure, yet the amount of blood reaching these periferal tissues in reduced?

Man, this is confusing me now

Think of pressure and flow seperatly. If you have an increase in vessel pressure ie with an alpha agent such as phenylephrine, that constriction(smaller size) can result in less flow to the brain. You have to remember that the brains autoregulation protects it by maintiaing FLOW over a wide range of PRESSURES. If MAP is too low or high out of autoregulation range then flow to the brain will be compromised. Think of an IV, if you put a pressure bag on a 1000cc of LR and try to pump if through a 25g the water will come out a high pressure but lower flow than if you pump it through a 14g (low pressure flood).

One of my attendings always asks during major trauma. Which is more important pressure or flow to vital organs? Always flow. Thats why you dont treat that 60/30 bp and 110 HR with phenylephrine, you load um up with blood and fluid and make the heart work.

Hope that helped

 

[Sugar72]

I think the brain compensates for hyperventilation after 24 hours (maybe less, can't recall).

It's 6 hours (per Miller lite)! Not a lot of time, but probably still helpfull in the prehospital scenario.

 

[canjosh]

Thanks for the helpful info guys...this forum is the shiznit.

 

[Singh]

Think of pressure and flow seperatly. If you have an increase in vessel pressure ie with an alpha agent such as phenylephrine, that constriction(smaller size) can result in less flow to the brain. You have to remember that the brains autoregulation protects it by maintiaing FLOW over a wide range of PRESSURES. If MAP is too low or high out of autoregulation range then flow to the brain will be compromised. Think of an IV, if you put a pressure bag on a 1000cc of LR and try to pump if through a 25g the water will come out a high pressure but lower flow than if you pump it through a 14g (low pressure flood).

One of my attendings always asks during major trauma. Which is more important pressure or flow to vital organs? Always flow. Thats why you dont treat that 60/30 bp and 110 HR with phenylephrine, you load um up with blood and fluid and make the heart work.

Hope that helped

Thanks, that was a great help! I have never had Pressure and Flow-relationships explained like this (maybe because I used Berne & Levy for physio?).

If I understand your the example you discuss (low BP and high heartrate) correctly, then it indicates hypovolaemia, and there it would be wrong to give vasoconstrictors. In relation to this, I would like to ask you another question. When arterioles constrict (leading to a high MAP), does that mean that the capillaries are recieving less blood? And vice versa? I always thought that when BP goes down due to systemic vasodilatation, organs are deprieved of blood supply, but it seems like I misunderstood the whole thing... Or did I?

Thanks again.

 

[Singh]

It's 6 hours (per Miller lite)! Not a lot of time, but probably still helpfull in the prehospital scenario.

Are you sure about that man? I read 24 hrs too.

 

[Laryngospasm]

Are you sure about that man? I read 24 hrs too.

To quote and exact time is not realistic, to say "at six hours the effect of hypocapnia on CBF dissapears" is incorrect, first of all it would happen over a range of time not at a set point, second it may vary from individual to individual, third it may be affected in different ways by different drugs, fluids, positioning etc. There is a wide range of varying info on this from as short as four hours to 24-48, some studies on dogs etc. Recent info shows that it is likely less than 12 hours in humans. Also let it return to normal slowly so as to avoid an abrupt increase in CBF. Dont be so concrete in your thinking.

 

[Sugar72]

Are you sure about that man? I read 24 hrs too.

I'm not sure about much! My thinking at this point is much more amorphous than concrete.
"In volunteers, however, the effect of hyperventilation wanes with time, as evidenced by a return of cerebral blood flow to normal after about 6 hours."
Baby Miller 4th edition pg 446. The book references an article from Arch Neurol from 1970.
Could be out of date info - I'm not trying to spread disinformation!

 

[MAC10]

I'm not sure about much! My thinking at this point is much more amorphous than concrete.
"In volunteers, however, the effect of hyperventilation wanes with time, as evidenced by a return of cerebral blood flow to normal after about 6 hours."
Baby Miller 4th edition pg 446. The book references an article from Arch Neurol from 1970.
Could be out of date info - I'm not trying to spread disinformation!

..And I have read 6-24hrs.

I think the big point to take home is that hyperventilation appears to be only useful acutely for controlling ICP. Just something to remember when you pick up your neuro patient that has been hyerventilated in the ICU for the past coupla days.