Cerebral O2 supply and Demand Flashcards
awerness =
functioning of the cerebral cortex
RAS
reticular activating system in the brainstem
arousal and consciousness = LOC
functional levels of the NS 1-2-3
- spinal cord (lowest)- automatic motor responses like reflexes
- Brainstem and subcortical level (second) - BB, RR, HR, equilib, primative emotions
- cortical level (highest) - cognition, thinking, info, memory - outer layer of cerebrum
meninges of the brain
skull - epidural space - dura - subdural - arachnoid - subarachnoid - pia - brain
where are the vessels and CSF in brain?
arachnoid space
what CN do we assess
II- optic and III - oculomotor = pupil reflex
V- trigeminal and VII facial = corneal
IX - glosopharyngeal and X vagus = gag and cough
what is ipsilateral and contralateral
ipsilateral - same side, anything above neck
contralateral - opp side, anything below neck
Decordicate =
toward core / abnormal flexion
Decerebrate =
accelerate fly /abnormal extension
where do the motor tracts cross?
in the medulla oblongata
contralateral
where is temp regulation
what does hyperthermia cause
hypothalamus
Increased in cerebral O2 requirements and metabolic rate and CO2 production
What can HTN and hypotension mean
HTN- rising ICP
Hypo- neurogenic shock in cervical spine injuries
what is Cushings Triad
- Bradycardia
- HTN with wide PP
- Bradypnea (often irreg)
from advanced increase in ICP
the brains last gasp!
late findings and irriverse damage
tentorium
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
what can happen to the brain tissue when there is herniation?
It can push the brain mater toward other structures
- Uncal - through tentorium toward hindbrain (cerebellum)
- Central - up to down
- Cingulate - from right to left hemisphere
types of stroke
Ischemic - thrombolic 80% - atherosclerosis
Embolic - 20% from elsewhere in the body
- A. FIB!!!!!
Hemorrhagic - aneurysms
most common SAH and ICH
The most common artery? what does it feed?
MCA - middle cerebral artery
Feeds: frontal, temporal, parietal lobes, basal ganglia, internal capsule
changes: personality, intellect, eye changes, speech, paralysis, weakness
stoke management 1st …
Head CT first to rule out ischemic or hemorrhagic
If Ischemic then?
you have 4.5 hrs to start t-PA (thrombolytic agents)
contraindications to starting t-PA
- recent MI
- GI hemorrhage
- previous stroke or head inj within 3 months
- BP > 180/110?
Stroke and BP
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
ischemic penumbra
zone of injury but still viable tissue that surrounds core of infarct
what is a choroid plexus
line the lateral 3 and 4th ventricles of the brain that hold the CSF
What is the CSF for and how much is produced
shock absorber
500cc/day
125-150 cc any given time
Where is CSF absorbed?
in the arachnoid villi and returned to the venous system
what is EVD
External Ventricular Device
when is an EVD warranted?
- hydrocephalus - excess production, malabsorption of CSF through arachnoid
- Meningitis/ Encephalitis - can = malabsorption of CSF through arachnoid
- Tumors around the 3/4th vents
- closed head injury IICP
- Subarachnoid hemorrhage = malabsorption of CSF
what is closed system EVD
not open to drain. stop cock pointing up
where is the EVD inserted and what does it do?
into lateral vents
measures the ICP and allows for ICP drainage
where do you level the EVD
Foramen Monroe
nurses role for EVD
- 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
why do you mntn HOB at 30?
for proper venous return
who is at greatest risk for SAH?
- women 3:2
- > 40yo
- premenopausal/hormonal?
- undiagnosed HTN
- “worse headache of my life”
what happens if severe hemorrhage?
ICP will reach MAP in subarachnoid space and there would be a tamponade effect
If the EVD is patent, what will you see?
SCF oscillating in the tubing
what creates both a pressure gradient and a safety valve?
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
what would happen if you raise the HOB above the 30?
SCF would drain faster than wanted. could = rapid collapse of vents
what is normal drainage amount?
5-15 cc
if > 30cc re-zero and watch. if keeps increasing notify MRP
always ____ before moving the PT
turn EVD off. then re-zero and turn back on
what are the surgical procedures for aneurysm
clipping or coiling
complications of aneurysms
- 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
what is vasospasm
post-aneurysm repair
decreased CPP
- wall thicken, lumen narrows, vascular reactivity impaired
- signs similar to stroke
- transcranial doppler and catheter angio
how to prevent vasospasm?
Triply H
- Hypervolemia expansion (CVP 8-10) with admin of crystalloid or colloid
- Hemodilution (HCT 32-35%)
- 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
how else can you prevent vasospasm?
- Nimodipine - CCB normal 60 mg Q4H can give 30mg Q2H
SE hypotension - Milrinone - phosphodiesterase inhibitor - vasodilating
- BP control : avoid nitro - elevate ICP
- IV labetalol (short 1/2 life), hydralazine, CCB’s
why give statins to mangage?
SAH
To improve endothelial function and increase eNOS (nitric oxide) : has vasodilator effect
What is the “closed box theory”
kelly-monroe
skull non-expandable/non-compressible
ICP = CBF + CSF + brain vol
what is a normal ICP
0-15 mmHg
how do you measure compliance
compliance = change in vol/ change in pressure
what is cerebral autoregulation
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
how much CBF do we need
50-54 mls/min
15 % CO
> 54 mls hyperemia = IICP
18-20 mls ischemia = decreased CBF and ICP
8-10mls = tissue death
what influences CBF ?
- viscosity of blood
- vessel diameter
- CPP (which is dependent on MAP)
CBF =
CBF = CPP
———
CVR
CVR ***
Influenced by?
how many types ?
Cerebral vascular resistance
Influenced by: vessel diameter and ICP
- Biophysical- stretch receptors in vessels constrict with BP /SBP high
- Chemical -
dilate if: increased Temp, CO2 or acidotic
constrict if: decreased CO2
CPP is dependent on ?
MAP
CPP= MAP- ICP
CPP: blood pressure gradient across brain
Normal 60-80
what happens if ICP increased ?
CBF decreases = tissue hypoxia, which causes hypercarbia and acidosis = cerebral vasodilation and cerebral edema
What increases ICP
- 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
decreased CBF=
ischemia
compression of brain pathways =
neurological dysfunction
brain shift or herniation =
death
what is vessel diameter influenced by?
autoreg and cerebral metabolic demand
how do you manage IICP?
reduce one of the 3 intercranial vol’s
how do you reduce brain vol?
- 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
how do you reduce blood volume? **
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
what two things do you need to know about dilantin
phenytoin
Needs a filter tubing and only use with NS NOT D5W bc this causes it to crystalize
how do you reduce Intracranial Vol
Goal: Normalize ICP while maintaining serebral oxygenation
- internal shunts (peritoneal shunt)
- EVD
- or change the size of the cranial vault (craniotomy)
what do you need to do to monitor ICP
- assess waveforms
- determine CPP = MAP-ICP
- determine cerebral compliance = change vol/change pressure
- immediate evaluation after interventions
- assess ICP with sedated / paralyzed PT
ICP wave has?
3 upstrokes
what does it mean if the P2 is higher than the P1?
non-compliant brain
what do you do if the ICP waveform disappears from the monitor?
- focus neuro assessment
- check stopcocks, tubing, transducer and placement
- no flushing
- check EVD fluctuation
- inform Dr
How often are you doing neuro exams?
Q1-4 H
when do you lose autoreg?
trauma PTs
how do you measure/monitor cerebral O2 supply or O2 extraction objectivly?
Jugular Bulb- single lumen central line toward head
what is a normal SjvO2
What is a normal CERO2
60-80%
25-35%
what does < 60% SjvO2 mean
What does > 80 % SjvO2 mean?
< 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)
what is CERO2?
Cerebral Oxygen Extraction Ratio
SaO2- SjvO2 / SaO2 x 100
= 25-35%
If CERO2 is < 24%
Is > 40%
< 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
what does mannitol work on?
decreases edema, works on brain tissue
sedation and analgesia
decreases cerebral O2 demand –> decreased CBF –> decrease CBVol
what does the EVD work on
decreases CSF
what does elevate HOB work on
CBF
what does reducing stimulation work on
CBV by decreasing O2 demand and CBF
If given CVP 9, MAP 70, ICP 22
what intervention ?
Make sure to calc CPP first. MAP-ICP (norm 60-80)
then decide intervention
How will vasopressors help CPP?
they will drive up MAP increasing CPP
how does increasing O2 supplementation increase Cerebral blood vol?
hypoxemia = vasodilates so increased O2 will vasoconstrict
what is diffuse axonal injury
neuron disconnection
shearing
what is index of suspicion
suspect occult injuries or complications to be present
until ruled out
secondary injuries
- inflam response
- reduced cerebral blood flow
- dysfunctional autoreg
- ischemia
- cereberal edema (24-48 hrs, peaks after 72)
- herniation syndrome - coning
- Diabetes Insipidus
- SIADH
exacerbating injuries (secondary)
- uncontrolled IICP
- Cerebral Ischemia
- Hypotension
- Hypoxia
- Infection
Diabetes Insipidus
secondary TBI
lack of ADH – so diuresing increased urine
= dehydrated
Serum NA is increased
SIADH
Secondary TBI
Too much ADH –> no/low urine output
= waterlogged
serum NA decreased
