Raised intracranial pressure?

[Singh]

I'm having a hard time understanding the pathophysiology of raised ICP:

Ok, to start with we all know that:

CPP = MAP - ICP

and

CBF = CPP/CVR


In order to keep a constant CPP, the MAP is kept high and the pt. is hyperventilated to increase CVR and thereby increase the CBF. My question is, will the increased CBF not increase the ICP and hence reduce CPP?

Another thing is: Raised ICP will decrease CPP. Decreased CPP will reduce CBF, unless there is a compensatoric decrease in CVR aswell. But then why are patients hyperventilated when hyperventilation increases CVR?

The alternative would be not to hyperventilate patients. What would this cause? ICP would raise because of more blood intracranially, and therefore CPP and CBF would fall. But the CVR would fall too, increasing the CBF.


I am very confused! Is there something I have misunderstood? Any relevant comments appreciated.

Singh

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[SoulRFlare]

Edit-I'm an idiot
sorry for the incorrect response

 

[cremaster2007]

I'm having a hard time understanding the pathophysiology of raised ICP:

Ok, to start with we all know that:

CPP = MAP - ICP

and

CBF = CPP/CVR


In order to keep a constant CPP, the MAP is kept high and the pt. is hyperventilated to increase CVR and thereby increase the CBF. My question is, will the increased CBF not increase the ICP and hence reduce CPP?

Another thing is: Raised ICP will decrease CPP. Decreased CPP will reduce CBF, unless there is a compensatoric decrease in CVR aswell. But then why are patients hyperventilated when hyperventilation increases CVR?

The alternative would be not to hyperventilate patients. What would this cause? ICP would raise because of more blood intracranially, and therefore CPP and CBF would fall. But the CVR would fall too, increasing the CBF.


I am very confused! Is there something I have misunderstood? Any relevant comments appreciated.

Singh

CO2 is a cerebral vasodilator..........you hyperventilate to lower CO2 which vasoconstricts and decreases CBF. Hyperventilation is not as popular as it once was and the new recommendations is to keep the pCO2 30-35. Hyperventilation is also a short term answer to a long term problem. It buys you time to treat with something more permanent ie ventriculostomy, 3%, mannitol, etc.

 

[Jackofknives]

You put way too much emphasis on the cardiovascular system and total neglected acid-base and the respiratory system, which act in concert to give a coordinated response.

Increased intra cranial pressure is often a result of cerebral edema or herniation secondary to tumor, ischemia and trauma. This in turn would compress cerebral arteries and compromise perfusion. As the neuronal tissue are not sufficiently supplied with oxygen, neurons switch to anaerobic metabolism and produce excessive amount of acid – local metabolic acidosis. Hydrogen ion is a vasodilator metabolite, however, more importantly, it is the most potent stimulant of the chemosensitive area in the medulla which excite other portion of the respiratory center and render hyperventilation.

So I doubt that the purpose of hyperventilation is a compensatory response to the elevated ICP but rather a counter-indicated response as a result of the brain being fooled to believe that the entire body is hypoxic, because the expansion and compression of the thorax does not have a significant effect on the cerebral vascular system. You as a physician should give the pt high pCO2 to breath in order to prevent respiratory alkalosis.

When it goes really bad, Cheyne-Stokes breathing may occur and death will ensue shortly.

 

[Vermian]

You put way too much emphasis on the cardiovascular system and total neglected acid-base and the respiratory system, which act in concert to give a coordinated response.

Increased intra cranial pressure is often a result of cerebral edema or herniation secondary to tumor, ischemia and trauma. This in turn would compress cerebral arteries and compromise perfusion. As the neuronal tissue are not sufficiently supplied with oxygen, neurons switch to anaerobic metabolism and produce excessive amount of acid – local metabolic acidosis. Hydrogen ion is a vasodilator metabolite, however, more importantly, it is the most potent stimulant of the chemosensitive area in the medulla which excite other portion of the respiratory center and render hyperventilation.

So I doubt that the purpose of hyperventilation is a compensatory response to the elevated ICP but rather a counter-indicated response as a result of the brain being fooled to believe that the entire body is hypoxic, because the expansion and compression of the thorax does not have a significant effect on the cerebral vascular system. You as a physician should give the pt high pCO2 to breath in order to prevent respiratory alkalosis.

When it goes really bad, Cheyne-Stokes breathing may occur and death will ensue shortly.

Okay - first of all - I want to add an initial correction to the above. Elevated intracranial pressure is not always equal to cerebral edema or herniation. Cerebral edema can lead to elevated ICP, and herniation is a result not a cause. Start by looking at the Kellie-Monroe principle. The intracranial vault is composed of three things - brain, blood (in vasculature), and CSF. Any derangement of these three things can be compensated for to a degree. After the limit is reached, increased ICP and then herniation ensue. Yes, there was a lot of emphasis placed on the cardiovascular system, and there is some role in the emergent setting for hyperventilation. However, hyperventilation is short lived, and it does cause vasoconstriction, thus limiting CBF. Still, you need to search for the graph of cerebral volume versus ICP - then you will see that there is compensation to a point then the curve sharply rises. Also, look at the graph for CPP versus SBP, there are compensatory mechanisms there, as long as auto-regulation is taking place. There are a lot of things that affect ICP. In the hospital setting, one must assess which is the most likely cause - mass, edema, increased CBV, - you get the idea. Treatment of elevated ICP can then be geared toward this entity. Good luck.

 

[NSGYRes]

I finished my residency in neurosurgery last year. So let me answer this question intelligently.

First, you are overanalizing it. It is true that these equations are accurate.

CPP = MAP - ICP

CBF = CPP/CVR

The problem in your thought is you are thinking in extremes. Fortunately, there is an amazing autoregulation system in the brain that essentially creates a stable CBF regardless of blood pressure, ICP, etc. So, 99% of the time, it is irrelevant what you do or what is happening to the patient because autoregulation is functioning and CBF is maintained.

When autoregulation falls apart, these concepts come more into play. Then it is a balancing act... and as you deduced... doing too much of one thing can have bad consequences based on the above equation.

One way to lower your ICP is to decrease the VOLUME in your head. Remember, Your head is an enclosed space... and as you increase the volume the pressure rises... the only way to decrease the pressure is to decrease the volume. High pressure is bad because you can heriate through the main opening in the skull (foramen magnum) resulting in death... Also, if you intracranial pressure is high enough you can get to the point where your CPP is effectively zero. If you have a CPP of zero... it is irrelevant what your CVR is... because your CBF will still be zero. Generally, CBF of zero = death

So... how do we decrease the volume in your head?
1) reduce cerebral edema (water content) in your head. This can be accomplished through osmotic therapy (hypertonic saline, mannitol) or in the case of vasogenic tumor edema from treatment with steroids
2) reduce CSF volume in head (ventriculostomy)
3) decrease blood in your head (ie, decrease the total volume of circulating blood in the head) INDUCED hyperventilation to lower PCO2 and blow off Hydrogen ions. L-type calcium channels when stimulated allow calcium ion influx into vascular smooth muscle cells and thus contraction of those muscle cells which equals vasoconstriction. Hydrogen ions compete and inhibit L-type calcium ion channel function. Ie... acidic environment = less L-type calcium ion channel opening, which equals less vasoconstriction overall... acidic environment = relative vasodilation. Contrarily... if you get rid of the hydrogen ions (hyperventilation) the L-type calcium channels on the vascular smooth muscle cells function better and there is more vasoconstriction. Therefore less acidic environment (hyperventilation) = vasoconstriction. IF all of the blood vessels in your head are all vasoconstricting more overall than earlier... you will have less blood flowing into your head and therefore have a lower ICP.

The problem with this concept is... when taken to extreme... if you vasoconstrict too much... there will be less oxygen carrying blood going to the head and you will get neuronal ischemia... which if left unchecked can cause stroke, worsened cerebral edema, and increased ICP. So... the treatment of hyperventilation for high ICP's works well in moderation temporarily... but severe hyperventilation over a long period of time induces a vasoconstrictive ischemia which is very bad.

As a side note... other ways to decrease your ICP... increase the volume capacity of the head (surgical decompressive craniectomy, expansive duraplasty).

You can also decrease metabolic demand, increase venous drainage, and others.

 

[spearman]

Excellent treatise and instructive for all.

However, the critical fallacy in Singh's understanding of the pathophysiology of raised
ICP, as stated, was apparently produced by his simple misuse of the equasion CBF = CPP/CVR. He stated correctly that hyperventilation increases CVR but followed incorrectly that such should also increase the CBF. On the contrary, if CVR increases the CBF should correspondingly decrease due to the inverse relationship.

Had he understood the simple inverse relationship of the two moieties (CBF and CVR)
then he would not become so confused..., and would probably not ask the question
that generated this thread.