Published Nov 18, 2003
You are reading page 2 of Question about Cushing's
The reason for a lowered diastolic is release of vasoactive agents (Lysosomes I think) from ischemic brain cells. This lowering of the diastolic can be seen in terminal shock when you are not perfusing the brain and these vasoactive substances are released.
Thanks gwenith. This info will serve as a good starting point for more digging.. :)
Did anyone read my post????
I did read your post earle. Thanks for googling and posting that info.
Thanks to everyone for all of the info on Cushing's triad! Our professor asked us to find the rationale for increased systolic BP in the client with IICP and none of my textbooks could answer this question. This is my first time on this site but it won't be my last!!! Once again, thanks for all the help!
Generally, as the ICP rises and results in cushing's response, the pulse pressure widens. Systolic goes up, diastolic goes down. I am wondering- what causes the diastolic pressure to drop? Thanks for any ideas...
though i doubt the original posters need this information anymore i thought i'd contribute in case someone in the future is looking through this.
The Cushing Reaction is "an increase in systemic blood pressure in response to an increased intracranial pressure". The physiology behind the reaction is:
Increased intracranial pressure --> collapses arteries --> pCO2 increases --> Central chemoreceptors activated --> increase blood pressure (hoping to reperfuse the arteries)
This reaction occurs in any hypoxic situation, but it is technically only a "Cushing Reaction" if the hypoxic situation is due to an increase in cranial pressure...because in any other situation the increase in blood pressure serves to re-perfuse the brain...But in the situation of an increased cranial pressure, the increased blood pressure actually worsens the situation by further compressing the adjacent arterioles. Thus a "Cushing Reaction" is usually a bad thing, its the brain trying to fix something but making it worse.
In practice, in what situations does an increase in cerebral pressure occur? Usually either very rapid tumor growth, or more commonly, a head injury resulting in hematoma.
It is the hematoma in the situation you are thinking about when you describe the decrease in diastolic pressure. The sympathetic discharge would attempt to increase both the systolic & diastolic pressure, but remember, diastolic pressure would be compromised by any arteriovenous fistulas or arterio-CSF fistulas that are created during the trauma, not to mention any external blood loss experienced by the subject.
The trauma preceeds the sympathetic response, thus the diastolic pressure goes down first. The brain increases sympathetic tone, the blood leaves the heart, travels primarily to the brain (all other pathways being constricted), once at the brain--rather than entering a capillary as it should, the arterioles & capillaries are TORN and RUPTURED and the blood enters an ever widening cystic cavity, the hematoma. This hematoma is the middle-ground between the arteries (high systolic pressure) and the veins (much lower pressure), and while blood does accumulate in the hematoma, a lot of it also drains out into the veins & CSF--this is what keeps your diastolic pressure decreased.
A similar cardiovascular profile can be seen ANY time you have communication between the arteries & veins, as sometimes occurs in patients months after major surgeries--when the vasculature regrows, they might grow into each other. Patients present with huge pulse pressures and increased veinous pO2. The communication decreases the diastolic pressure, its a sort of...shunt.
In the case of the tumor, your diastolic pressure would remain increased, but that would be one FAST growing tumor
gwenith, BSN, RN
Do you have a link or a reference for any of this?
Here is what one educator says on this particular subject (found on another web discussion concerning this very topic).
"I disagree with your assertion that the diastolic pressure does not rise as part of the Cushing response to an acute rise in intracranial pressure. The increase in peripheral vascular resistance, which occurs in response to increased sympathetic tone, causes a tendency for diastolic pressure to rise, along with systolic pressure. You are correct in saying that the pulse pressure is often increased, but this results from a disproportionate rise in systolic pressure due to increased left ventricular stroke volume, as a consequence of increased sympathetic tone and increased circulating levels of catecholamines."
You can check out his CV here: http://medicalsciences.med.unsw.edu.au/medsciences.nsf/RI-All/8900146?OpenDocument
I have never seen nor heard of a drop in Diastolic BP with the hypertension, I have seen the large increase in SBP with an elevation of the DBP.
The pulse pressure does widen because of the large increase in SBP when compared the increase in DBP. For example, 120/80 turns into 190/110 then your pulse pressure changes from 40 to 80.
Could someone clarify: Does Cushing's Triad really consist of four elements: HTN, Bradycardia, irregular respirations and widening pulse pressures?
Here is what one educator says on this particular subject (found on another web discussion concerning this very topic). "I disagree with your assertion that the diastolic pressure does not rise as part of the Cushing response to an acute rise in intracranial pressure. The increase in peripheral vascular resistance, which occurs in response to increased sympathetic tone, causes a tendency for diastolic pressure to rise, along with systolic pressure. You are correct in saying that the pulse pressure is often increased, but this results from a disproportionate rise in systolic pressure due to increased left ventricular stroke volume, as a consequence of increased sympathetic tone and increased circulating levels of catecholamines."You can check out his CV here: http://medicalsciences.med.unsw.edu.au/medsciences.nsf/RI-All/8900146?OpenDocumentI have never seen nor heard of a drop in Diastolic BP with the hypertension, I have seen the large increase in SBP with an elevation of the DBP. The pulse pressure does widen because of the large increase in SBP when compared the increase in DBP. For example, 120/80 turns into 190/110 then your pulse pressure changes from 40 to 80.JMTOT,Mike
You know...there are things you see as "early signs- elevated sbp/elevated dbp" and then there are the "common late signs"......and one of the common late signs associated with Cushings is a widening pulse pressure. You see it postbleed ...usually 24-48 hours post bleed in like Grade 5 sah patients.Its not an immediate kinda response like you might see in the OR's...but ...its more like what the physicians and nurses will see 24-48 hours post bleed.You have widenning pulse pressure ...and its an ominous sign to watch out for.About the only thing to do to help(if the bleed has already been secured) is to slowly cool them down to medically induced hypothermic temps of 93-96 degrees and do burst suppression -pentobarb coma or even megadose with propofol(not the best choice..but as a last resort) to induce a burst suppressed state......keep em cold...and slow down the cerebral metabolic activity to almost a standstill, cross your fingers,....and hope your interventions work.But.....widening pulse pressure is a very common...ominous...late sign of cushings.Been there, done that, watched it happen for years and years.It isnt pretty......
Cushings triad consists of Hypertension, Bradycardia, and hyperventilation in the presence of increased intracranial pressure. The widening pulse pressure that accompanies the hypertension is as a result of the increasing systolic pressure in an attempt to perfuse the brain, the only decrease in the diastolic that I have seen is after herniation and is not a component of cushings traid.
cushings triad consists of hypertension, bradycardia, and hyperventilation in the presence of increased intracranial pressure. the widening pulse pressure that accompanies the hypertension is as a result of the increasing systolic pressure in an attempt to perfuse the brain, the only decrease in the diastolic that i have seen is after herniation and is not a component of cushings traid.
as i said...it is a "late sign" commonly associated with cushings.please re-read my post.it is a late sign commonly seen associated with cushings triad.is it one of the trio?no...no it is not. do you commonly see it as a late "ominous- as i said" sign in like for example (as i stated above )with grade 5 sah patients? yes...you do. and you are correct these patients are the "high risk/high mortality" group of patients that are often trying to herniate.we make interventions like the medically induced hypothermia and burst suppression to "attempt" to reverse partial herniation and maintain "any" cerebral function.cushings triad is really a trio of "early warning signs" for those that work in the neuroicu.when your pulse pressure widens it is a late ominous sign that interventions have to be made immediately or else you will proceed on to tentorial herniation and all brain stem functions will fade....brain death.a widening pulse pressure is something to really watch for closely when you are seeing cushings...it is a late ominous sign.when i think of cushings i think of our common everyday neurocardiogenic shock type patients that pretty much are seen in any grade 4-5 sah patients, large hemmorragic strokes etc etc. these are things we see pretty much every day...and are "aware" of.....but it is seen in the majority of patients that we deal with.widening pulse pressures = either extension of the bleed, massive cerebral edema or another event that is pressing that patient towards the grim reaper(tentorial/tonsillar herniation).hope i havent confused you...on what i was saying.its just alot of our patient population has all the elements of cushings or they probably wouldnt be in the neuro icu...so i watch for the latter ominous signs and of course treat anything we can treat early.
No you didn't confuse me, but thanks for asking. I am however glad that we seem to agree that a decrease in diastolic blood pressure is not a component of cushings triad, but occurs after someone has herniated, be it supra, intra, or subtentorial. I am however confused as to why any patient in a NSICU, with a grade 4-5 SAH, a large hemorrhagic stroke, or for that matter any trauma patient with a GCS
no you didn't confuse me, but thanks for asking. i am however glad that we seem to agree that a decrease in diastolic blood pressure is not a component of cushings triad, but occurs after someone has herniated, be it supra, intra, or subtentorial. i am however confused as to why any patient in a nsicu, with a grade 4-5 sah, a large hemorrhagic stroke, or for that matter any trauma patient with a gcs thanks
addnurse...you know some hcf's really agressively monitor icp,,,and when that icp crawls over 20 and stays there they see "this" as the time to agressively treat the patients with things like mannitol, 3% nacl to get them hypernatremic and dry that brain out, some utilize that "20" golden marker as the time to medically induce hypothermia , pentobarb comas etc etc etc.. i think alot of it just has to do with "if" that hcf is teaching or nonteaching.nonteaching hcf's tend to less agressively manage and monitor icp...and often times.....sad to say....its probably out of ethics considerations. meaning...these patients....that have really high icps like in the 40's ( have seen them as high as 142 icp) how much brain function are they truly going to have post swelling?(younger ones have better results)...but unless this is a teenager...the chances of this patient having anything but some basic brainstem functions is almost nill.so....they have agressively treated them....so that they can be vegatative and vent dependant for life.can you see what i am saying?...in a teaching hospital...those residents are there to learn.in a nonteaching hospital...they have stronger ethical standards(at times) and look beyond just getting that icp below 50...like what is the long term prognosis.beneficience-, ethics, its all highly political and controversial.
i am interested though in one thing you said...cerebral svo2 monitoring.tell me more....are you talking about a device that actually is placed like an evd....or with an evd that acts as like a spo2 monitor?if so...does it come with your evd....what are your parameters of normal and crisis values?
also....widening pulse pressure doesnt mean someone has "already" herniated.....it usually means they are begining to...or have only partially herniated....and if treated aggressively...can often times be reversed.....but again.....unless this is a young teenager we are talking about you have only saved them for a vegatative-vent dependant life...which further and progressively traumatizes that family.so...its a highly ethical decision that needs to made jointly with the family and nsurgeon after....after....they have been told a truthful honest realistic cognitive rehab potential for the family to make the correct decision.
to be honest...most neuro icu nurses dont focus on cushings.they have to be pretty critical to meet admit criteria for a neuroicu....and that means that 99.999999% of them we see with the cushings triad.so,,...we know what weve got....we just look for the latter ominous signs like widening pulse pressure, anisocoria, overbreathing the vent to stop, icps to top and be maintained at over 20 as k e y signs to make needed interventions ...fast...depending on how aggressively that neurosurgeon and the "well informed family" want to treat the patient.hope this helps...
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