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7520 Final > Cerebral O2 supply and Demand > Flashcards

Cerebral O2 supply and Demand Flashcards

1
Q

awerness =

A

functioning of the cerebral cortex

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2
Q

RAS

A

reticular activating system in the brainstem

arousal and consciousness = LOC

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3
Q

functional levels of the NS 1-2-3

A
  1. spinal cord (lowest)- automatic motor responses like reflexes
  2. Brainstem and subcortical level (second) - BB, RR, HR, equilib, primative emotions
  3. cortical level (highest) - cognition, thinking, info, memory - outer layer of cerebrum
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4
Q

meninges of the brain

A

skull - epidural space - dura - subdural - arachnoid - subarachnoid - pia - brain

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5
Q

where are the vessels and CSF in brain?

A

arachnoid space

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6
Q

what CN do we assess

A

II- optic and III - oculomotor = pupil reflex

V- trigeminal and VII facial = corneal

IX - glosopharyngeal and X vagus = gag and cough

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7
Q

what is ipsilateral and contralateral

A

ipsilateral - same side, anything above neck

contralateral - opp side, anything below neck

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8
Q

Decordicate =

A

toward core / abnormal flexion

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9
Q

Decerebrate =

A

accelerate fly /abnormal extension

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10
Q

where do the motor tracts cross?

A

in the medulla oblongata

contralateral

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11
Q

where is temp regulation

what does hyperthermia cause

A

hypothalamus

Increased in cerebral O2 requirements and metabolic rate and CO2 production

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12
Q

What can HTN and hypotension mean

A

HTN- rising ICP

Hypo- neurogenic shock in cervical spine injuries

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13
Q

what is Cushings Triad

A
  1. Bradycardia
  2. HTN with wide PP
  3. Bradypnea (often irreg)

from advanced increase in ICP
the brains last gasp!
late findings and irriverse damage

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14
Q

tentorium

A

hard structure, fold in the dura mater that separates the cerebellum from cerebrum

If there is vol expansion above the tentorium, the brain gets pushed through the tentoria and compress CN III

Brain stem can get pushed in (coning) can = death

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15
Q

what can happen to the brain tissue when there is herniation?

A

It can push the brain mater toward other structures

  1. Uncal - through tentorium toward hindbrain (cerebellum)
  2. Central - up to down
  3. Cingulate - from right to left hemisphere
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16
Q

types of stroke

A

Ischemic - thrombolic 80% - atherosclerosis

Embolic - 20% from elsewhere in the body
- A. FIB!!!!!

Hemorrhagic - aneurysms
most common SAH and ICH

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17
Q

The most common artery? what does it feed?

A

MCA - middle cerebral artery

Feeds: frontal, temporal, parietal lobes, basal ganglia, internal capsule

changes: personality, intellect, eye changes, speech, paralysis, weakness

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18
Q

stoke management 1st …

A

Head CT first to rule out ischemic or hemorrhagic

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19
Q

If Ischemic then?

A

you have 4.5 hrs to start t-PA (thrombolytic agents)

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20
Q

contraindications to starting t-PA

A
  • recent MI
  • GI hemorrhage
  • previous stroke or head inj within 3 months
  • BP > 180/110?
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21
Q

Stroke and BP

A

you want a high BP before starting t-PA so that you have higher ICP to increase blood flow to brain during ischemic events help decrease cerebral ischemia. But manage if > 220/120

particular important to protect ischemic penumbra

after t-PA started you want to decrease BP to < 180/105

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22
Q

ischemic penumbra

A

zone of injury but still viable tissue that surrounds core of infarct

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23
Q

what is a choroid plexus

A

line the lateral 3 and 4th ventricles of the brain that hold the CSF

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24
Q

What is the CSF for and how much is produced

A

shock absorber

500cc/day
125-150 cc any given time

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25
Q

Where is CSF absorbed?

A

in the arachnoid villi and returned to the venous system

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26
Q

what is EVD

A

External Ventricular Device

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27
Q

when is an EVD warranted?

A
  1. hydrocephalus - excess production, malabsorption of CSF through arachnoid
  2. Meningitis/ Encephalitis - can = malabsorption of CSF through arachnoid
  3. Tumors around the 3/4th vents
  4. closed head injury IICP
  5. Subarachnoid hemorrhage = malabsorption of CSF
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28
Q

what is closed system EVD

A

not open to drain. stop cock pointing up

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29
Q

where is the EVD inserted and what does it do?

A

into lateral vents

measures the ICP and allows for ICP drainage

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30
Q

where do you level the EVD

A

Foramen Monroe

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31
Q

nurses role for EVD

A
  • Assess color, clarity, amount CSF
  • document
  • HOB 30 deg
  • ensure prescribed drip chamber level (norm 20)
  • secure drain - clamp and string
  • level and zero
  • infection - aseptic technique
  • C/S cell count - Q3days check policy
  • Assessments reg and prn to detect worsening and changes
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32
Q

why do you mntn HOB at 30?

A

for proper venous return

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33
Q

who is at greatest risk for SAH?

A
  • women 3:2
  • > 40yo
  • premenopausal/hormonal?
  • undiagnosed HTN
  • “worse headache of my life”
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34
Q

what happens if severe hemorrhage?

A

ICP will reach MAP in subarachnoid space and there would be a tamponade effect

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35
Q

If the EVD is patent, what will you see?

A

SCF oscillating in the tubing

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36
Q

what creates both a pressure gradient and a safety valve?

A

the difference in height btwen the Pt vents and drip chamber

the height of the drip chamber = the pressure inside the head (ICP). This pressure may be reached bfr SCF will drain into drip chamber

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37
Q

what would happen if you raise the HOB above the 30?

A

SCF would drain faster than wanted. could = rapid collapse of vents

38
Q

what is normal drainage amount?

A

5-15 cc

if > 30cc re-zero and watch. if keeps increasing notify MRP

39
Q

always ____ before moving the PT

A

turn EVD off. then re-zero and turn back on

40
Q

what are the surgical procedures for aneurysm

A

clipping or coiling

41
Q

complications of aneurysms

A
  • seizures
  • post-op watch for vasospasms (3-12 days post-op): might look like stroke
  • hydrocephalus (hotdogs): IICP d/t blood in CSF in arachnoid villi
42
Q

what is vasospasm

A

post-aneurysm repair
decreased CPP

  • wall thicken, lumen narrows, vascular reactivity impaired
  • signs similar to stroke
  • transcranial doppler and catheter angio
43
Q

how to prevent vasospasm?

Triply H

A
  1. Hypervolemia expansion (CVP 8-10) with admin of crystalloid or colloid
  2. Hemodilution (HCT 32-35%)
  3. HTN - induced 30% increase in MAP with vasopressors (levophed)

: SBP 180-200 if has been clipped

this is done to decrease viscosity and increase vol and flow of pressure through vasospastic area

44
Q

how else can you prevent vasospasm?

A
  1. Nimodipine - CCB normal 60 mg Q4H can give 30mg Q2H
    SE hypotension
  2. Milrinone - phosphodiesterase inhibitor - vasodilating
  3. BP control : avoid nitro - elevate ICP
    - IV labetalol (short 1/2 life), hydralazine, CCB’s
45
Q

why give statins to mangage?

A

SAH

To improve endothelial function and increase eNOS (nitric oxide) : has vasodilator effect

46
Q

What is the “closed box theory”

A

kelly-monroe

skull non-expandable/non-compressible

ICP = CBF + CSF + brain vol

47
Q

what is a normal ICP

A

0-15 mmHg

48
Q

how do you measure compliance

A

compliance = change in vol/ change in pressure

49
Q

what is cerebral autoregulation

A

in normal brain:
a regulatory hemostatic mechanism that ensures the maintenance of nearly constant CBF despite marked changes in MAP. constrict or dilation depending on MAP changes

CBF = CPP/CVR

50
Q

how much CBF do we need

A

50-54 mls/min
15 % CO

> 54 mls hyperemia = IICP

18-20 mls ischemia = decreased CBF and ICP

8-10mls = tissue death

51
Q

what influences CBF ?

A
  • viscosity of blood
  • vessel diameter
  • CPP (which is dependent on MAP)
52
Q

CBF =

A

CBF = CPP
———
CVR

53
Q

CVR ***

Influenced by?

how many types ?

A

Cerebral vascular resistance

Influenced by: vessel diameter and ICP

  1. Biophysical- stretch receptors in vessels constrict with BP /SBP high
  2. Chemical -
    dilate if: increased Temp, CO2 or acidotic

constrict if: decreased CO2

54
Q

CPP is dependent on ?

A

MAP

CPP= MAP- ICP

CPP: blood pressure gradient across brain

Normal 60-80

55
Q

what happens if ICP increased ?

A

CBF decreases = tissue hypoxia, which causes hypercarbia and acidosis = cerebral vasodilation and cerebral edema

56
Q

What increases ICP

A
  • hypercapnia = vasodilation
  • valsalva maneuver = Increased ICP, decreased venous return by compressing venous outflow> Give bowel care!
  • body positioning: HOB, neck neutral, ETT = venous outflow
  • shivering = increased O2 demand
  • noxious stimuli (light, noise, family, restraints) = increase metabolic demands
57
Q

decreased CBF=

A

ischemia

58
Q

compression of brain pathways =

A

neurological dysfunction

59
Q

brain shift or herniation =

A

death

60
Q

what is vessel diameter influenced by?

A

autoreg and cerebral metabolic demand

61
Q

how do you manage IICP?

A

reduce one of the 3 intercranial vol’s

62
Q

how do you reduce brain vol?

A
  • surgery: lesion, tumor, lobectomy, evacuate hematoma
  • Osmotic duiretics: mannitol (or 3% NS). Hypertonic in intravascular space shifts fluids
  • Lasix: decrease cerebral edema
  • Corticosteroids : dexameth or methylpred: decrease inflam
63
Q

how do you reduce blood volume? **

A

Goal: reduce ICP while mntning cerebral Oxygenation
- decrease anything that causes vasodilation

  • oxygenation: hypoxia = cerebral vasodilation
  • lasix: mntn CPP 60-80
  • positioning: to mntn venous outflow
  • controlled hyperventilation : decreasing Pa CO2 will constrict cerebral blood vessels = deceasing CBF (only after 24 hrs)
  • PEEP no more then 5 (decreases venous outflow from cerebral venous return, keeping blood in cranial vault. increased PEEP = increased intrathoracic pressure, deceased venous return/drainage from brain = increased ICP
  • can reduce systemic venous return and contribute to decreased preload and decreased CO which can decrease MAP and CBF
  • control: temp, pain, decrease stimulation, sedation and muscle relaxants, anti-convulsant
64
Q

what two things do you need to know about dilantin

A

phenytoin

Needs a filter tubing and only use with NS NOT D5W bc this causes it to crystalize

65
Q

how do you reduce Intracranial Vol

A

Goal: Normalize ICP while maintaining serebral oxygenation

  • internal shunts (peritoneal shunt)
  • EVD
  • or change the size of the cranial vault (craniotomy)
66
Q

what do you need to do to monitor ICP

A
  • assess waveforms
  • determine CPP = MAP-ICP
  • determine cerebral compliance = change vol/change pressure
  • immediate evaluation after interventions
  • assess ICP with sedated / paralyzed PT
67
Q

ICP wave has?

A

3 upstrokes

68
Q

what does it mean if the P2 is higher than the P1?

A

non-compliant brain

69
Q

what do you do if the ICP waveform disappears from the monitor?

A
  • focus neuro assessment
  • check stopcocks, tubing, transducer and placement
  • no flushing
  • check EVD fluctuation
  • inform Dr
70
Q

How often are you doing neuro exams?

A

Q1-4 H

71
Q

when do you lose autoreg?

A

trauma PTs

72
Q

how do you measure/monitor cerebral O2 supply or O2 extraction objectivly?

A

Jugular Bulb- single lumen central line toward head

73
Q

what is a normal SjvO2

What is a normal CERO2

A

60-80%

25-35%

74
Q

what does < 60% SjvO2 mean

What does > 80 % SjvO2 mean?

A

< 60 % = hypoxemic not enough supply or too much consumed (demand too high). So increase supply or decrease demand

> 80% = hyperemic too much supply or, not enough consumed (no demand)

75
Q

what is CERO2?

A

Cerebral Oxygen Extraction Ratio
SaO2- SjvO2 / SaO2 x 100

= 25-35%

76
Q

If CERO2 is < 24%

Is > 40%

A

< 24% would mean that more O2 is being consumed = higher cerebral tissue demand

> 40 % means that less is being consumed = less cerebral tissue is up taking the O2. Less demand

77
Q

what does mannitol work on?

A

decreases edema, works on brain tissue

78
Q

sedation and analgesia

A

decreases cerebral O2 demand –> decreased CBF –> decrease CBVol

79
Q

what does the EVD work on

A

decreases CSF

80
Q

what does elevate HOB work on

A

CBF

81
Q

what does reducing stimulation work on

A

CBV by decreasing O2 demand and CBF

82
Q

If given CVP 9, MAP 70, ICP 22

what intervention ?

A

Make sure to calc CPP first. MAP-ICP (norm 60-80)

then decide intervention

83
Q

How will vasopressors help CPP?

A

they will drive up MAP increasing CPP

84
Q

how does increasing O2 supplementation increase Cerebral blood vol?

A

hypoxemia = vasodilates so increased O2 will vasoconstrict

85
Q

what is diffuse axonal injury

A

neuron disconnection

shearing

86
Q

what is index of suspicion

A

suspect occult injuries or complications to be present

until ruled out

87
Q

secondary injuries

A
  • inflam response
  • reduced cerebral blood flow
  • dysfunctional autoreg
  • ischemia
  • cereberal edema (24-48 hrs, peaks after 72)
  • herniation syndrome - coning
  • Diabetes Insipidus
  • SIADH
88
Q

exacerbating injuries (secondary)

A
  • uncontrolled IICP
  • Cerebral Ischemia
  • Hypotension
  • Hypoxia
  • Infection
89
Q

Diabetes Insipidus

A

secondary TBI

lack of ADH – so diuresing increased urine
= dehydrated

Serum NA is increased

90
Q

SIADH

A

Secondary TBI

Too much ADH –> no/low urine output
= waterlogged

serum NA decreased

7520 Final (5 decks)

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