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Systems: Neurology AB > Clinical Aspects of Cerebral Perfusion and ICP > Flashcards

Clinical Aspects of Cerebral Perfusion and ICP Flashcards

1
Q

What percentage of CO does the cerebral blood flow account for?

A

15%

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2
Q

What is the normal cerebral blood flow?

A

Normal cerebral blood flow averages 55 to 60 mL/100 g brain tissue per minute

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3
Q

What is the normal blood flow of grey matter?

A

Grey matter the blood flow is 75 mL/100 g/ minute

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4
Q

What is the normal blood flow of white matter?

A

White matter it is around 45 mL/100 g/ minute

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5
Q

When does ischaemia occur?

A

Ischemia at 20 mL/100 g/minute

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6
Q

When does permanent damage usually occur?

A

Permanent damage usually results when the blood flow drops below 10 mL/100 g/minute

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7
Q

What is the most significant factor determining cerebral blood flow at any given time?

A

Most significant factor that determines cerebral blood flow at any given time is the cerebral perfusion pressure (CPP)

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8
Q

What is the CPP?

A

CPP is the effective blood pressure gradient across the brain

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9
Q

What is CPP equal to?

A

CPP = MAP − ICP

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10
Q

How does the ICP affect the cerebral perfusion?

A

Increased ICP causes the cerebral perfusion pressure to decrease

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11
Q

What factors regulate cerebral blood low under physiological conditions?

A
  • CPP
  • Concentration of arterial CO2
  • Arterial PO2
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12
Q

What is cerebral autoregulation?

A

The ability to maintain constant blood flow to the brain over a wide range of CPP (50-150 mm Hg) is calledcerebral autoregulation

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13
Q

What is the cerebral autoregulatory response to low CPP?

A

The cerebral arterioles dilate to allow adequate flow at the decreased pressure

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14
Q

What is the cerebral autoregulatory response to high CPP?

A

The cerebral arterioles constrict

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15
Q

When does the cerebral autoregulatory system fail?

A

Under certain pathological conditions cerebral blood flow cannot always be autoregulated

  • CPP exceeds 150 mm Hg, such as in hypertensive crisis, the autoregulatory system fails
  • Exudation of fluid from the vascular system with resultant vasogenic edema
  • Certain toxins such as carbon dioxide can cause diffuse cerebrovascular dilatation and inhibit proper autoregulation
  • During the first 4 to 5 days of head trauma, many patients can experience a disruption in cerebral autoregulation
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16
Q

What is cerebral oedema a prominent cause of?

A

Cerebral edema is a prominent cause of subacute to chronic intracranial hypertension

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17
Q

What is intracranial hypertension?

A

State of increased brain volume as a result of an increase in water content

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18
Q

What type of cerebral oedema are steroids effective in?

A

Extracellular oedema

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19
Q

What type of cerebral oedema is mannitol effective in?

A
  • Extracellular oedema
  • Intracellular oedema
  • ? Interstitial oedema
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20
Q

What is the blood brain barrier?

A
  • A barrier composed of astrocytic foot process wrapping around a capillary endothelium composed of tight junctions
  • This means not all substances that are carried in the blood can reach the neural tissue
21
Q

What do endothelial tight junctions present barrier to in the brain?

A

Endothelial tight junctions are the barrier to the passive movement of many substances in order to protect the sensitive neural tissue from toxic materials

22
Q

By what mechanisms can material be transported naturally across endothelial cells?

A
  • Lipid-soluble substances can usually penetrate all capillary endothelial cell membranes in a passive manner
  • Amino acids and sugars are transported across the capillary endothelium by specific carrier-mediated mechanisms
23
Q

What is the Monro-kellu doctrine?

A

The craniums is a rigid structure:
-When a new intracranial mass is introduced, a compensatory change in volume must occur through a reciprocal decrease in venous blood or CSF to keep the total intracranial volume constant

24
Q

What is complicance?

A
  • Change in volume observed for a given change in pressure

- dV / dP

25
Q

What is elastance?

A
  • Inverse of compliance
  • Change in pressure observed for a given change in volume
  • dP / dV
26
Q

What does elastance represent?

A

It represents the accommodation to outward expansion of an intracranial mass

27
Q

How can CSF be displaced from the ventricular system?

A

CSF can be displaced from the ventricular system through the foramina of Luschka and Magendie into the spinal subarachnoid space

28
Q

What happens when the venous system collapses?

A

The venous system collapses easily and squeezes venous blood out through the jugular veins or through the emissary and scalp veins

29
Q

What happens when the homeostatic compensatory mechanisms fail to resolve an increase in volume?

A

When the compensatory mechanisms have been exhausted, small changes in volume produce significant increase in pressure

30
Q

What keeps compliance flat in increasing cerebral volume?

A

The innate homeostatic pressure-buffering mechanism offered by displacement of CSF and venous blood keeps compliance flat until a “critical volume” is reached

31
Q

What happens once the ‘critical volume’ is reached?

A

After this critical volume, small volumetric changes result in precipitous increases in pressure, and intracranial hypertension naturally ensues

32
Q

What are A Lundberg waves?

A

Abrupt elevation in ICP for 5 to 20 minutes followed by a rapid fall in the pressure to resting levels
The amplitude may reach as high as 50 to 100 mm Hg

33
Q

What are B Lundberg waves?

A

Frequency of 0.5 to 2 waves per minute, are related to rhythmic variations in breathing

34
Q

What are C Lundberg waves?

A

Rhythmic variations related to waves of systemic blood pressure and have smaller amplitude

35
Q

What is Cushing’s reflex?

A

Vasopressor response

36
Q

What is the Cushing’s reflex triad?

A
  • Hypertension
  • Irregular breathing
  • Bradycardia
37
Q

What is the physiology behind Cushing’s triad?

A
  • Increased ICP more than MAP
  • Compression of cerebral arterioles
  • Decreased CBF, activation autonomic nervous system
  • Sympathetic response: alpha-1 adrenergic receptors -> Hypertension and tachycardia
  • Aortic baro-receptors stimulate vagus nerve -> Bradycardia
  • Bradycardia also due to mechanical distortion of medulla
38
Q

How should raised ICP be managed?

A
  • Head end elevation: facilitate venous return
  • Mannitol/ Hypertonic saline
  • Hyperventilation: decrease CBF (temporary measure)
  • Barbiturate coma: decrease cerebral metabolism, CBF
  • Surgical decompression
39
Q

What is brain tissue oxygenation monitoring?

A
  • Probe to monitor oxygenation of tissue

- Detect and treat low oxygenation, increasing CPP

40
Q

What is micro-dialysis?

A
  • Investigate brain metabolism
  • Implantation of specially designed catheters
  • To collect small-molecular-weight substances to help measure and identify neurotransmitters, peptides, and other substances
41
Q

What is the composition of oedema fluid in intracellular oedema?

A

Increased intracellular water and sodium due to failure of membrane transport

42
Q

What is the composition of oedema fluid in interstitial oedema?

A

CSF

43
Q

What is the extracellular fluid level in extracellular oedema?

A

Increased

44
Q

What is the extracellular fluid level in intracellular oedema?

A

Decreased

45
Q

What is the extracellular fluid level in interstitial oedema??

A

Increased

46
Q

What is the pathological lesion causing oedema in extracellular oedema?

A
  • Primary or metastatic tumour
  • Abscess
  • Late stages of infarction
  • Trauma
47
Q

What is the pathological lesion causing oedema in extracellular oedema?

A
  • Early stages of infarction

- Water intoxication

48
Q

What is the pathological lesion causing oedema in extracellular oedema?

A

Obstructive or communicating hydrocephalus

Systems: Neurology AB (51 decks)

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