ICP Flashcards

1
Q

outline the MOnro Kelli hypothesis and describe what happens past the point of compensation

A

The Monro-Kellie hypothesis states that sum of the volumes of the brain (CSF, brain tissue and intracranial blood) is constant as it is in a fixed volume in the cranium. E.g. an increase in one causes a decrease in the other. The principal buffers are CSF, and to a lesser extent, blood volume (in the venous compartment especially). These can compensate for a short period of time, the point of decompensation is illustrated below (around 10 mmHg). Once these compensatory mechanisms are exhausted, further increases in volume result in large rises in ICP.

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2
Q

what are the 4 most characteristic features of raised ICP

A

headache, vomiting and papilloedema

progressive deterioration in conscious level (GCS)

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3
Q

why is raised ICP headache classically worse in morning/wake from sleep

A
  • lying flat - rise in ICP
  • resp depression whilst asleep - inc CO2
  • dec CSF absorption?
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4
Q

what will exacerbate an ICP headache

A

anything that further increases ICP eg coughing and sneezing

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5
Q

when does vomiting tend to occur

A

in morning with headache

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6
Q

when does papilloedema develop?

A

may take several days

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7
Q

what can be seen int eh eye due to an acute and severe rise in ICP

A

fundal haemorrhage

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8
Q

what is a cingulate herniation

A

brain tissue forced under falx cerebri

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9
Q

what is an uncal herniation

A

uncus (medial part of temporal lobe) herniates inferior to the tentorium cerebelli

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10
Q

what is the clinical syndrome assoicated with an uncal herniation

A

progressively imaired consciousness, dilated ipsilateral pupil (CNIII) and contralateral hemiplegia

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11
Q

tonsillar herniation

A

cerebellar tonsils herniate down through teh foramen magnum

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12
Q

outline the relation between CPP and ICP

A

CPP = MAP - ICP

Normally, cerebral blood flow is maintained at a constant level by cerebrovascular autoregulation. If this autoregulation is impaired, changes in MAP or ICP can have direct effects on cerebral blood flow.

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13
Q

what physiological response can inc ICP have

A

reflex bradycardia - cushings triad

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14
Q

outline cushings triad

A
  • compresses the arteriole, this decreases cerebral blood flow to the point of cerebral iscahemia
  • This activates the sympathetic response, which causes vasoconstriction of blood vessels (hypertension) and an increase in heart rate
  • Baroreceptors in the aortic arch detect this and trigger a parasympathetic response via CNX, induces bradycardia. Cushing’s ulcers develop in the stomach due to increased production in stomach acid.
  • Both HTN and raised ICP compress the respiratory centre at the brain stem causing irregular breathing
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15
Q
A
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