Published Nov 17, 2005
epiphany
543 Posts
Hi:
Can anyone help me with this contradiction I have encountered, in what happens with ICP pts?
I have learnt that ICP patients hyperventilate (central neurogenic hyperventilation) and this expels CO2, and thus constrict the vessels to make more room for the cranial pressure. And then, I read that the body also responds the opposite - poor CPP will cause increased bp and dilate the vessels. So what really happens? dilation or constriction?
Thanks for any help.
RoxanRN
388 Posts
Hi:Can anyone help me with this contradiction I have encountered, in what happens with ICP pts?I have learnt that ICP patients hyperventilate (central neurogenic hyperventilation) and this expels CO2, and thus constrict the vessels to make more room for the cranial pressure. And then, I read that the body also responds the opposite - poor CPP will cause increased bp and dilate the vessels. So what really happens? dilation or constriction? Thanks for any help.
Both..... it's a form of feedback loop. The constricted vessels cause a decrease in the CPP which in turn, in an attempt to perfuse itself, the brain centers increase BP and decrease the MAP (widening of the pulse pressures).
papawjohn
435 Posts
ICP Pts?!
Hey Epiphany
Pretty simple idea to get in your head as you analysis of your neuro Pt--that LOW pCO2 is interpreted by the brain as roughly equivalent to HIGH pO2. (Well--they both happen when we hyperventilate don't they?)
So if the CNS has all the oxygen it needs--and it needs a lot!!!--it's happy to share. How does it share? By constricting the carotid/vertibral arteries!!
So if our brain injured Pt (on the vent) needs to have the circulation to his brain diminished....to lower his ICP....we can 'fool' his brain by hyperventilating him (with the vent) to lower his pCO2--and the carotids and vertibrals will somewhat constrict.
There are a few brain-damaged Pts that have 'kausmal' resps on their own--and Neuro ICU nurses tend to say--"he's self-hyperventilating'." I dunno the truth of that---but it seems to 'work' from the nurse's point of view.
If the pt is breathing slowly and very deeply--he probably is getting his pCO2 treated intrinsically and--without obvious pathology--most ICU nurses would just observe this and document the neuro-signs and vital signs that come with it.
Did that answer your question?
Papaw John
gwenith, BSN, RN
3,755 Posts
Hyperventilation only works to vasoconstrict for a short time. After a while the vessles dilate again - this is whay we no longer hyperventilate our patients - we usually "run" them at the low end of normal PCO2. Doing this also allows you to keep the hyperventilation trick up your sleeve in case of sudden ICP rise.
thanks for all your input, and giving me a picture of what's going on.
Hey Gwineth!!!
Gosh, if you look like your logo, girl......
I'm sailing my boat for Australia tomorrow....
Anyhow. You are of course correct, that hyperventilation is a transient way of lowering ICP. I remember several adrenalin-charged nights where I "bagged" my neuro-trauma Pt until the NeuroSurgeon could arrive to put in a ventriculostomy to replace the Camino that had showed the ICP going higher than biology allowed.
Keysnurse2008
554 Posts
Keep in mind hyperventilating a patient is only good for 30 minutes afetr that you are just asking for them to blow off too much co2 and then you have another crisis,,,,,bc ....along with the pco2 being a crisis low your ph and bicarb will adjust also.So hyperventilating will help blow off co2...but it is only safe and effective for 30 minutes.
mwbeah
430 Posts
hyperventilation aims at keeping the pco2 down to 30-25 mm hg so that cbf falls and cerebral blood volume is reduced and thereby reducing the icp. prolonged hyperventilation should be avoided and becomes in- effective after about 24 hrs. in addition it causes hypo tension due to decreased venous return . it is claimed a pco2 under 20 results in ischemia, although there is no experimental proof for the same.
the present trend is to maintain normal ventilation with pco2 in the range of 30 - 35 mmhg and po2 of 120 - 140 mmhg. when there is clinical deterioration such as pupillary dilatation or widened pulse pressure, hyperventilation may be instituted (preferably with an ambu bag) until the icp comes down.
http://www.thamburaj.com/intracranial_pressure.htm
ZASHAGALKA, RN
3,322 Posts
And I can remember the days when we used end tidal CO2 monitors to ensure that our CO2 was low enough.
I remember an RT bagging the heck out of a vented head once on the way down for an emergency ventric (old days - now we just do 'em at the bedside) and the neuro surgeon asked 'what the heck are you doing?'
'Blowing off the CO2'
'Well stop!'
But that pt came back on, you guessed it, end tidal CO2 monitoring w/ a high vent rate and parameter orders to keep the CO2 low.
That RT complained about that for years.
LOL.
(But isn't it amazing just how many things we do because it "helps" only to find out years later after much research that we were spitting in the wind. Shoot, look at Swans - we've gone from 'everybody has one' to whenever we get one, some new ICU nurse still needs to be inserviced on them.)
~faith,
Timothy.
Hindsight here....this patient was vented right? Bc...if not....then he/she is just going to tire soon and will head towards resp failure.Patients cant keep up the pace of tachypnea for long.They are human...and tire out.So hyperventilating? Does it work? yes....Is it a "short term fix?"-yes. Do you have to be very careful..yes...yes you do. You might lower that Pco2...which does result in constriction...but also think beyond that...how is that body going to adjust? If the benefit outweighs the risk...then thats great.Its just a good idea to have a baseline ABG of course to use as your reference of how his/her body is responding.Just a safety thing. You might lower that ICP...but what if you have them so acidotic that your dealing with high lactic acid..low low ph....really way off bicarb and base excess'.Look at the whole scenario..hope this helps.You might lower that ICP..but now he/she is potentially Multisystem organ failure.So...now he/she is neuro intact...but mad as h*** bc he is on dialysis and on a multi organ transplant list.LOL...said in humor but with a very serious undertone..
pixieelb
3 Posts
I'm skilled (nearly drilled) to attentive check bloodgas analyses after modification of active ventilation. Because Hyperventilating (otherwise Hypoventilating) may activate a vicious circle inside human body. A long during constriction at the wrong place anywhere inside body could be even fatal in refer of outcome as a dilation!
Once a competent doc told me:"Essential to say the worst case and biggest challenge is to handle a polytraumatic pt, in associate of a massive lung and brain injury. You have to understand biochemical processes to ensure a proper therapy. Because no brain activity without oxgen and otherwise no lung activity without brain input. It's like unsecured walking on a wire on top of trees.The primary injury in combination of the result of intensive care support influence the outcome. We can only intervene in intensive care support, so let us do it in the best way we're able."
Carpe diem or domestic tongue..."Hilbechilbi jede Tag"
Hey Pixeelb
You're of course completely correct that trauma with multi-system failure is the biggest challenge in our profession. At least, nothing I've ever done comes close. If the Pt is so unstable that hyperventilating is dangerous they oughta have a Ventricular drain so we can directly control the ICP.
By the way, here in the American South we know that 'carpe diem' means 'Go fishing every day'. But my German vocabulary fails me these days--studied it in College over 30yrs ago. What kinda fishin' is 'hilbechilbe every day'?
Gosh, Switzerland--I love this computer for puttin' an ol' redneck boy in touch with the world.