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Posted

I understand that the baroreceptor reflex is responsible for the bradycardia in Cushing's, but can the bradycardia also be due to compression of the vagal nerve when the brain herniates, esp. with profound bradycardia?

Posted

:shock:

Hardcore....

You have me thinking, i will have to go and do some reading. I would think that the ICP causing the herniation would be sufficient for a vagal stimulus, even without the herniation actually happening.

Mind you i have a hang over from the work christmas party last night, i will sober up and do some reading.

Posted

The short answer here is simply yes.

For those who don't know, what we're basically talking about here is the so-called Cushing's reflex, which occurs when the intracranial pressure rises and compresses intracranial blood vessels (we're mostly talking veins here, arteries are more muscular and don't compress that easily). The body's natural response to this is to raise blood pressure to forcefully push the blood up to the brain (ischemia in the brain triggers the pressor center to stimulate the heart through the sympathetic nervous system).

Now, the baroreceptor in the carotid sinus will detect this sudden raise in blood pressure and respond by lowering heart rate (parasympathetic reflex from the depressor center through the vagus nerve).

What you will commonly see in those patients is extremely high blood pressure (220+ in systolic BP is common in those cases), but low heart rate (bradycardia).

This is the commonly accepted model of how this works, and is known as the Cushing's reflex. Another model is what the OP described, physical intracranial pressure on the vagus nerve. If I remember correctly, this model is described as Cushing's response (as opposed to reflex, the word "reflex" indicating that it as a pressor/depressor center thing, where the "response" does not).

I think most physiologists agree that what happens is a little of both.

Posted

I have heard a couple of different explanations.

-The stimulation of baroreceptors by elevated B/P as described above.

-I have also been told that actual pressure and ischemia of the brain stem causes the changes. Some people think that the bradycardia may be independent of the blood pressure.

In any case, bradycardia is most often a very late sign.

Take care,

chbare.

Posted

Yeah, what he said :cry:

Is there a differentiation between cushings reflex and cushings triad?

Cushing triad is listed (at least in my text book) as consisting of hypertension, widening pulse pressure, bradycardia and irregular respiratory pattern (which i am assuming is some kind of medullary breathing pattern?) How they get 4 signs and call it a "triad" i dont know :? Is the "reflex" specifically the raising of MAP and the "triad" a sum of the signs of the "reflex"?

wow, that was so incoherent :shock:

Posted

I have seen both terms used interchangeably.

The changes in breathing can be anything from Apnea to Biot's to Cheyne-Stokes. Different locations of lesions and type of herniation can effect the type of breathing pattern. For example, Biot's has an association with pontine or medullary dysfunction.

-Three general concepts fall under the umbrella of Cushing's Triad. I think the confusion comes from how the three concepts are described.

1) Heart Rate

-slows down

2) Respirations

-changes

3) Blood pressure

-elevated

-widened pulse pressure

Take care,

chbare.

Posted

Ahh cheers chbare. Thats tied it up nicely for me.

Posted

The respiratory pattern described in Cushings reflex or triad (in which the triad is usually the late sign, causing the full pattern) is usually central neurogenic hyperventillation or Biott's respiratory pattern. Deep, irregular breathing pattern (not to be confused with Kussmaul's) respiration's.

R/r 911

Posted

I've never understood why the baroreceptor reflex only slows the heart rate. You'd think that in order to lower the BP, it would both lower the HR and also vasodilate.

This thread is quite old. Please consider starting a new thread rather than reviving this one.

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