bozhenka
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1. Hypercapnia dilate cerebral resistance vessels and hypocapnia constrict it. Mechanical hypeventilation to a PaCO2 of 20 to 25 mm Hg reduces cerebral blood flow by approximately 40 to 45% and normal adult cerebral blood volume from 50 mL to 35 mL.
This mechanism suffies to retard the progression of cerebral herniation and to use it in sudden increases in intracranial pressure
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| ELM
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Thank you bozhenka!
Your explanation is true for mechanical ventilation...but what about if we make patient just hyperventilate them on their own?...then it's reverse huh?.....hypocapnia----> dilate cerebral vessels---> increased IC pressure??? I guess when we see this in contest it's talking about ventilator then.
What about my other q? :?
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| bozhenka
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hypocapnia constrict cerebral vessels and this mechanism work for both machanical and own hyperventilation. What are they distinguish from each other?
hypocapnia----> constrict cerebral vessels---> decrease IC pressure
With regard to your second question - I didn't find any info about using alcohol in fat embolism. :-(
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| ELM
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Douh.......silly me :cry: .... I guess i slept too long last night....but i am still sleepy! :lol: Thanks for waking me up! :lol: :lol:
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| drvic
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alcohol is no longer used for fat embolism. initial rationale was that it will dissolve the large fat globules in the bloodstream and prevent obstruction of vessels. but the Clinical utility has not been consistently demonstrated. Its listed among the treatments that are NOT useful (in CMDT)...
plus it would knock out the patient's sensorium...will have difficulty in assessing sensorium if the patient has developed cerebrovascular occlusion due to fat embolism....
regards
drvic
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| miky
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1. How hyperventilation decreases the intracranial pressure? What is the mechanism
I wouldn't hyperventilate a pt with increased ICP - there is always a risk of barotrauma - besides, there are more effective measures to decrease ICP instead. First, try to use that "miraculous" device that monitor ICP - thus you know how much you have to reduce the ICP. I would use Manitol or Dexamethasone first.
2. Why we use alcohol (perhaps IV) in fat embolism? How is that work? ( Few other indications of alcohol use in medicine are Ethylene glycol piosoning and Spasticity (used intrathecally) worth to mention)
ethyl alcohol (a lipoprotein lipase inhibitor) used as an intravenous infusion.hastens metabolism of intravascular lipids, but at the cost of forming more free fatty acids which may further damage pulmonary capillary endothelium. Its use is therefore controversial and probably best avoided.
:roll:
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| ELM
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I appretiated everybodies contribution here!
BUT...
guys......my q was what is the working mechanism of alcohol in fat embolism? It didn't say anything about if it's still on practice or not!
Also again Miky......i asked how Hyperventilation decreases IC pressure....not what can i use first or second or how can i manage high IC pressure!
I thank you all!
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| drvic
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i would agree with miky regarding the management part...
would use mannitol, dexa, steroids, head elevation to 30 degrees
to achieve reduction in ICP(latter after ruling out cervical spine injury of course)
as far as the mechanism goes - its pretty straightforward and has been mentioned by others in their posts -
hypocapnia -> cerebral vasoconstriction -> reduced ICP...
this mechanism applies for all -
whether a patient is hyperventilating voluntarily
or is being made to do so during mechanical ventilation...
and works in patients with severe head injuries too...
but the effect is very short lived...
works mostly for vasogenic cerebral edema...
therefore its used for pts who have acute increase in ICP (sec to head injury for eg) with signs s/o of imminent/ongoing herniation....
in these (usually intubated) patients hyperventilation can be used as initial mx...
should be pretty easy to understand.
next comes mechanism of alcohol, dr miky again did the job well in his last post...
alcohol inhibits lipoprotein lipase(LPL), which is inc in pts with fat emb
(that's why levels of LPL are used as a screening test for suspected FE!).
so then, why should we inhibit LPL, u will ask?
coz otherwise it will hydrolyze all TGs into FFAs
-> the latter in large quantities are extremely histotoxic to pulmonary cap
-> will cause neutrophil chemotaxis, sludging and platelet aggregation
-> pulmonary microthrombi
-> V/Q mismatch
-> if extensive and if it occurs throughout the lungs, patient deteriorates
-> ranging from asymptomatic hypoxemia to frank PE to ARDS.
so inhibiting LPL is theoretically useful (or it should be!)... but then real life is different from what is theoretically possible....
alcohol simply isn't effective enough in fat embolism
because LPL levels rise significantly only 5-8 days after onset of FE...
but by then, my dear friend, its already too late...
you have already lost the battle by then in most cases...
regards
drvic
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