Cushing Reaction ?

[Ludacris]

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So this is how I think it works:

Increased ICP -> Compression of cerebral vessels -> Decreasing cerebral blood flow -> Brain ischemia -> Increase PCO2 -> Detected by the Vasomotor center in medulla to increase sympathetic outflow to the heart & blood vessels -> Increase in MAP (Hypertension), which Increases cerebral blood flow

Then the Increased MAP is sensed by baroreceptors -> Increased afferents to the Medulla -> Increased Parasympathetic efferents and Decreased sympathetic efferents -> Bradycardia & Respiratory depression (?)

Is that how it works and produces the Cushing Triad of HTN, Bradycardia, and Respiratory depression?

 

[WashMe]

So this is how I think it works:

Increased ICP -> Compression of cerebral vessels -> Decreasing cerebral blood flow -> Brain ischemia -> Increase PCO2 -> Detected by the Vasomotor center in medulla to increase sympathetic outflow to the heart & blood vessels -> Increase in MAP (Hypertension), which Increases cerebral blood flow

Then the Increased MAP is sensed by baroreceptors -> Increased afferents to the Medulla -> Increased Parasympathetic efferents and Decreased sympathetic efferents -> Bradycardia & Respiratory depression (?)

Is that how it works and produces the Cushing Triad of HTN, Bradycardia, and Respiratory depression?

Well when FA talks about Cushing's, it says that the increased pressure leads to increased vagal (parasympathetic) outflow. Wikipedia says that the bradycardia is driven by both (1) reflex bradycardia following increased sympathetic-driven vasoconstriction (HTN) and (2) a direct increase in vagal outflow by mechanical compression/stimulation.

That takes care of the bradycardia and HTN I guess. As far as the respiratory depression, maybe it's due to compression of the medullary respiratory center or something. Not sure.

Also, Curling's ulcer is seen as a result of the increased vagal output. I don't know why it isn't generally mentioned as part of the triad... maybe it's less acute.

 

[Ludacris]

Cool, thanks!

 

[fahimaz7]

I thought that the Curling issue was a matter of cerebral hypoxia, secondary to the increased ICP shutting putting pressure on the incoming vasculature and reducing it's flow. Since the brain doesn't like being hypoxic, it increased the blood pressure to try and get more perfusion, which only makes the ICP worse. It's the increased BP that causes a reflexive bradycardia (by increasing vagal tone).

 

[WashMe]

I thought that the Cushing issue was a matter of cerebral hypoxia, secondary to the increased ICP shutting putting pressure on the incoming vasculature and reducing it's flow. Since the brain doesn't like being hypoxic, it increased the blood pressure to try and get more perfusion, which only makes the ICP worse. It's the increased BP that causes a reflexive bradycardia (by increasing vagal tone).

meh who knows... at least the compression is responsible for the respiratory depression. whether or not there's increased vagal output from compression is probably not that important.

 

[fahimaz7]

Apparently the cushing's issues (breathing and the ulcers) correct themselves as soon as the ICP is brought down.

 

[JMTX]

not that this is a relevant question anymore, but the reason Cushing's Ulcer and Cushing's triad/reaction are linked is due to the Vagus nerve and ECL cells in the GI system - if you increase vagal stimulation, you're ganna get gastrin too.