vicinihil

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So this confuses me...

In Goljan pp 566 blue box (3rd 3d)...he says that to prevent cerebral edema, you hyperventilate the patient to cause alkalosis which vasoconstricts because acidosis and hypoxemia--> vasodilation--> cerebral edema

In Costanzo BRS Phys she says: "When the brain is ischemic, the Pco2 increases and the chemoreceptors in the vasomotor center respond by INCREASING SYMPATHETICS to heart and blood vessel--> constriction--> increase TPR and MAP (aka Cushing's)"

Is it just me or these two seem to conflict each other. I may not be thinking correctly since it's almost midnight but I just want to get an answer for sure. Does acidosis and hypoxemia --> constriction of vessels or dilation of vessels?

Thanks!
 

vicinihil

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ok so I figured it out....

Cerebral circulation is more dependent on the METABOLITES that are produced than sympathetic response

Because the metabolite CO2 --> vasodilation, therefore the overall effect of increase in Pco2 due to hypoxemia is vasodilation--> cerebral edema
 

hartbot

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Yea, it seems like there is never all or none in medicine like what we were taught in high school. Kinda like ATII constricting the efferent arteriole when you are volume depleted.

Follow up question: I get how elevated sympathetics in the cushings reflex cause HTN and bradycardia, but what is the cause of the respiratory depression?
 
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The reflex begins when some event causes increased intracranial pressure (ICP). This increases the hydrostatic pressure of cerebrospinal fluid to the point that it meets and gradually exceeds mean arterial pressure (MAP). As the ICP exceeds the MAP, the cerebral arterioles become compressed, diminishing blood supply to the brain, a condition known as cerebral ischemia. Central chemoreceptors in the medulla sense the ischemia in the form of decreased pH and increased pCO2. The central chemoreceptors respond with a swift and potent activation of the sympathetic nervous system. (It is important to note that both the sympathetic system and the parasympathetic system are both activated but the sympathetic stimulation is much greater than the parasympathetic stimulation and renders the response of the parasympathetic system to be almost nonexistent.)
The sympathetic response activates alpha-1 adrenergic receptors within the arteries, causing vasoconstriction. This constriction raises the total peripheral resistance of blood flow and elevates blood pressure causing hypertension in an attempt to restore perfusion to the ischemic brain. The sympathetic stimulation also increases heart contractility and cardiac output.
Meanwhile, baroreceptors in the carotid arteries detect the increase in blood pressure and trigger a parasympathetic response via vagal stimulation, thereby inducing bradycardia. Bradycardia may also be caused by increased ICP impinging on the vagal nerve, mechanically stimulating a parasympathetic response. An irregular respiratory pattern is typically the result of herniation or increased pressure on the brainstem.
The Cushing reflex is complex and seemingly paradoxical. Commonly, the central chemoreceptors of the brain and the baroreceptors of the carotid sinuses work together to increase or decrease blood pressure, but in the Cushing reflex, the two sensors are receiving mixed signals. Thus, even in the presence of sympathetic stimulation from the brain, which would normally produce tachycardia, there is in fact bradycardia.