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180 Cards in this Set
- Front
- Back
Most common supratentorial mass (tumor)
a) Gliomas b) Menigiomas c) Pituitary adenomas |
Gliomas
|
|
Common brain metastasis sites include
a) Breast b) Colorectal c) kidney d) lung e) melanoma |
"Because Katy Likes Men"
Breast Colorectal kidney lung melanoma |
|
What does Hypoxemia do to cerebral blood vessels & ICP
a) dilate b) constrict c) ↑ ICP d) ↓ ICP |
dilate
↑ ICP (open vessels increases amount of blood in brain) |
|
Hypercapnia does what to cerebral blood vessels & ICP
a) dilate b) constrict c) ↑ ICP d) ↓ ICP |
dilate
↑ ICP |
|
How is vasogenic edema treated? _____________
TEST ? |
Steroids
|
|
T/F In a compliant brain as there is a change in volume there will be minimal effect on intracranial pressure
|
True
the opposite is true in a brain that is less compliant (aka STIFF) it would only take a very sm. ↑ or ↓ in volume to make a BIG change in pressure |
|
A blood brain barrier that is disrupted and allows water, electrolytes, large hydrophyllic molecules in leads to what type of edema
a) vasogenic b) osmotic c) cytoxic |
vasogenic
osmotic edema is caused by a ↓ in osmolality cytotoxic by ischemia |
|
When ICP ↑'s in what order do the components of the skull shift
match Brain ............................1st Blood ...........................2nd CSF .............................3rd |
CSF..........................1st
Blood.........................2nd Brain..........................3rd |
|
Where is CBF regulated?
_______________ TEST ? |
ARTERIOLE LEVEL
|
|
Pressure gradient across the vessel is a result of
a) Cerebral Perfusion Pressure (CPP) b) PaCO2 c) PaO2 d) both a & b e) both a & c TEST ? |
Cerebral Perfusion Pressure (CPP)
PaCO2 |
|
T/F CPP autoregulation keeps CBF constant when changes in CPP or MAP are detected
|
True
a pt with chronic HTN may cause a shift to the right of the autoregulation curve from 50 - 150 to 60 - 170 for example |
|
T/F Autoregulation alters cerebral vasomotor tone (CVR) and remains intact for CPP values of 50 - 150
|
True
|
|
Cerebral ischemia develops @
a) CBF < 50 ml b) CBF < 35 ml c) CBF < 20 ml |
CBF < 20 ml
|
|
Tissue perfusion decreases when
a) CPP < 50 mmHg b) CPP < 35 mmHg c) CPP < 20 mmHg |
CPP < 50 mmHg
|
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What is the only thing that you as a CRNA can do to increase CPP
___________________ |
↑ MAP
|
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What are 5 ways a CRNA can ↓ ICP
a) drainage b) hyperventilation c) ↓ CMRO2 d) hypothermia d) ↑ HOB TEST ? |
drainage
hyperventilation ↓ CMRO2 hypothermia ↑ HOB |
|
T/F if CPP is maintained between 50 - 150 CBF will be maintained @ 50ml/100g/min
|
True
|
|
PaCO2 and CBF
a) have a linear relationship b) inverse relationship |
linear
when PaCO2 is 20 - 80 mm Hg |
|
PaO2 & CBF
a) have a linear relationship b) inverse relationship |
inverse relationship
LOOK IT SAYS OXYGEN (PaO2) nml PaO2 60 mmHg if hyperoxic = ↓CBF if hypoxic = ↑ CBF |
|
ICP & CBF
a) have a linear relationship b) inverse relationship |
inverse relationship
IF BP IS CONSTANT! |
|
T/F Autoregulation takes 30 - 120 seconds to take effect
|
TRUE
Rapid fluctuations in MAP cause undesirable effects on CVR, CBF, ICP |
|
Which of the following agents are cerebral vasoconstrictors
a) Brevital b) STP c) Propofol d) Etomidate |
Brevital
STP Propofol Etomidate these drugs also leave autoregulation & vessel reactivity to PaCO2 intact |
|
Cerebral Vasoconstrictors
a) ↓ CMRO2 b) decrease CBF c)decrease CBV d) decrease ICP |
↓ CMRO2
decrease CBF decrease CBV decrease ICP |
|
Does Ketamine ↑ CBF without ↑ CMRO2
TEST ? |
Yes, BUT only @ anesthetic doses @ sub-therapeutic doses it ↑ CBF & glucose metabolism
|
|
T/F Burst Suppression causes a parallel ↓ in CBF & CMRO2
|
True, decrease is dose dependent until reach flat EEG
|
|
Etomidate
a) has mild effect on MAP b) inhibits adrenal cortisol secretion for 24 - 48 hours c) can cause myoclonic sz d) can cause vomiting |
has mild effect on MAP
inhibits adrenal cortisol secretion for 24 - 48 hours can cause myoclonic sz can cause vomiting |
|
Propofol
a) can cause burst suppression b) ↓ CMRO2 c) has no effect on CMRO2 d) causes peripheral vasodilation e) ↑ ICP |
can cause burst suppression
has no effect on CMRO2 causes peripheral vasodilation ↑ ICP (this is related to peripheral vasodilation) |
|
What drug category is the GOLD Standard for burst suppression?
|
Barbitruates
|
|
T/F Peripheral vasodilation causes an ↑ ICP?
|
True
|
|
Opioids
a) effect coupling of CBF & CMRO2 b) do NOT effect coupling of CBF & CMRO2 c) have no effect on AutoRegulation d) have no effect on CO2 sensitivity of cerebral vessels |
do NOT effect coupling of CBF & CMRO2
have no effect on AutoRegulation have no effect on CO2 sensitivity of cerebral vessels |
|
T/F Opioids can cause a short term ↑ ICP and reflex cerebral vasodilation with a ↓ MAP
|
TRUE
|
|
T/F NTG, Nipride, & nicardipine all ↑ ICP
|
True, but we still use them.....
|
|
Do β-blockers interfere with coupling (CBF & CMRO2)
|
NO
|
|
Theophylline
a) constricts cerebral vessels b) dilates cerebral vessels c) ↑ CSF production d) ↑ risk of sz |
constricts cerebral vessels
↑ CSF production ↑ risk of sz |
|
Which of the following volatile anesthetics cause cerebral vasodilation
a) desflurane b) sevoflurane c) isoflurane d) Nitrous e) all of the above TEST ? |
desflurane
sevoflurane isoflurane Nitrous |
|
A MAC > 2 causes
a) flat EEG b) has no effect on EEG c) ↓ CMRO2 d) has no effect on CMRO2 |
flat EEG
↓ CMRO2 but could never run a pt @ that MAC for a long period of time! |
|
PaCO2 cerebral vessel reactivity & autoregulation are impaired or abolished @ what MAC
a) > 0.5 b) > 1 c) > 1.5 |
> 1 MAC
|
|
T/F a MAC of <1 causes a CBF that is lower than when pt is awake, but has no effect of cerebral blood volume (CBV)
|
True
|
|
Nitrous increases/decreases CBF, CMRO2, ICP
|
INCREASES
the effect is limited to the basal ganglia, thalamus, insula |
|
Prevention of ↑ ICP, Brain Bulk & Tension would include
a) euvolemia b) neck alignment c) mannitol d) β-blockers |
euvolemia
neck alignment (prevents venous pooling in brain) mannitol β-blockers (prevents SNS) (also sedation/local before noxious stimuli, a stable BP / HR, Hyperventilation) |
|
The Vasodilatory Cascade Model states a ↓ CPP causes
a) ↑ CBV b) ↓ CBV c) ↑ ICP d) ↓ ICP |
↑ CBV ("gates" are open dilated)
↑ ICP (more blood could cause a high pressure) a ↓ CPP means less "tone" in cerebral vessels so they dilate |
|
The Vasoconstriction Cascade Model states a ↑ CPP causes
a) ↑ CBV b) ↓ CBV c) ↑ ICP d) ↓ ICP |
↓ CBV ("gate" is closed so less blood comes in)
↓ ICP (less blood means less pressure) a ↑ CPP means more "tone" in cerebral vessels so they constrict |
|
T/F the vasoconstriction model is dependent on coupling being intact
|
True
meaning that as CBF increases so will CMRO2 |
|
Coupling of CBF & CMRO2 occurs @ _______________
TEST ? |
CBF of 50ml/100g/min
CMRO2 of 4ml/100g/min |
|
Hypocapnia (ETCO2)
a) vasodilation b) vasoconstriction c) ↑ ICP d) ↓ ICP e) ↑ CBF f) ↓ CBF |
vasoconstriction
↓ ICP ↓ CBF this effect is only good for 24 hours |
|
Hypercapnia (ETCO2)
a) vasodilation b) vasoconstriction c) ↑ ICP d) ↓ ICP e) ↑ CBF f) ↓ CBF |
vasodilation
↑ ICP ↑ CBF |
|
Mannitols effects are seen for how long?
a) 1 hour b) 2 - 3 hours c) 4 - 5 hours |
2 - 3 hours
(↓ brain edema) remember mannitol ↑'s osmolality it also ↓'s Na, K, and can cause hypervolemia (which is bad for CHF pt) |
|
What is the max amount of CSF that should be pulled off when trying to ↓ ICP
a) 20 ml b) 30 ml c) 40 ml d) 50 ml |
50 ml
10 - 20 ml usually pulled off @ any one time |
|
T/F Hypovolemia & Hypoxia cause cerebral vasodilation
|
TRUE
|
|
T/F CMRO2 reflects brain activity it does NOT reflect basal met activity of neurons
|
True,
there is a ceiling effect for reduction of CMRO2 with burst suppression |
|
T/F 1 MAC with N2O / volatile = ↑ CMRO2 & CBF than with a volatile alone
|
True
|
|
T/F One of the most important pre-op activities by a CRNA should be doing & charting a neuro check
TEST ? |
TRUE
|
|
Where do you level an aline in a crani?
TEST ? |
@ TRAGUS of the ear b/c it's closest to the COW
|
|
T/F after the dura is opened the ICP = atm pressure, so this follows that CPP = MAP
|
TRUE!!!
|
|
The most common sign of deterioration post-op crani is
a) ↓ LOC b) focal neuro deficit c) a sudden drop in BP |
↓ LOC
focal neuro deficit |
|
T/F Most feared complication in a crani post-op is hemorrhage which usually occurs within 6 hours
|
True
|
|
Treatment of an ACUTE Hematoma
a) is same as for a space occupying lesion b) same as for an AVM |
is same as for a space occupying lesion
Surgical decompression is the ONLY thing that can save this pts life |
|
You see blood in the CSF what might you expect to see on the EKG
a) T-wave elevation b) T-wave inversion c) widened QRS d) flipped p wave |
T-wave inversion " the T-wave is catching the blood that is falling from brain")
|
|
Steroids are an appropriate drug to use in treatment of cranial hemorrhage? yes/no
|
NO!!! actually associated with ↑ mortality in pt with head trauma
|
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T/F after an intracranial hematoma is evacuated you would expect to see a loss Cushings effect?
|
True, will get SEVERE HOTN (opposite of cushings => HTN, Brady, irreg resp)
|
|
What is Queckenstedt’s maneuver?
|
a way to assess if there is stenosis present & blockage of CSF drainage Bil. jugular compression will cause ↑ CSF pressure (this is an outdated technique)
|
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T/F the Middle Cerebral artery carries 60% of ipsilateral carotid artery blood flow
|
True,
|
|
T/F Pinning is the most stimulating part of a crani
|
True
|
|
T/F To help with brain edema, ↑ ICP, ↑ CBV r/t masses below tentorium you can Hyperventilate, give steroids, burst suppress etc
|
False!! these maneuvers are only effective in SUPRATENTORIAL masses
there is nothing you can do below tentorium |
|
Your pt is experiencing one sided paralysis, memory deficit/mental changes & seizures, where would the mass be located
a) frontal b) temporal c) parietal d) occipital |
Frontal
"the thinker" picture hand on forehead (frontal) as statue is trying to "think" |
|
Your pt is having difficulty with language skills, and an occasional seizure where would the mass be located
a) frontal b) temporal c) parietal d) occipital e) cerebellum |
temporal ("temp"/occasional)
|
|
Your pt is having seizures, speech disturbances & has lost the ability to write where would the mass be located
a) frontal b) temporal c) parietal d) occipital e) cerebellum |
parietal
|
|
Your pt is exhibiting blindness on one side & having seizures where would the mass be located
a) frontal b) temporal c) parietal d) occipital e) cerebellum f) brain stem |
occipital
|
|
Your pt c/o headache, vomiting and has uncoordinated movement/walking where would the mass be
a) frontal b) temporal c) parietal d) occipital e) cerebellum f) brain stem |
cerebellum
|
|
Your pt is vomiting, has uncoordinated movement/walking and trouble with speech where would the mass be
a) frontal b) temporal c) parietal d) occipital e) cerebellum f) brain stem |
brain stem (symptoms are similar to cerebellum with the addition of SPEECH problems)
|
|
Why does the posterior fossa mass present unique challenges
a) smaller space b) positioning is difficult c) many vessels in the area d) need to maintain CV/Resp status |
smaller space
positioning is difficult many vessels in the area need to maintain CV/Resp status |
|
Why would you want to get an Echo on a pt who will be in the sitting position for crani?
TEST ? |
Need to r/o PFO to avoid paradoxical air embolism
about 3 out of 35 (adults) people have a PFO |
|
Where is the precordial steth/doppler placed on a crani in the sitting position?
TEST ? |
On the RIGHT side @ 3 - 6 intercostal space
|
|
Which position are you most likely to see a VAE in? WHY?
a) sitting b) lateral c) supine d) prone TEST ? |
sitting
b/c operative site is above the heart |
|
Name two things you can do to help decrease the incidence of a VAE in a sitting crani
TEST ? |
AVOID HOTN
USE PEEP |
|
T/F the greater the pressure gradient between cerebral veins & Right Atrium & the lower the CPP => greater chance for air to enter venous openings @ crani site
|
TRUE
|
|
Which type of embolism enters the body thru a PFO
a) VAE b) paradoxical AE |
paradoxical Air Embolism
this is an arterial air embolism |
|
Advantages of the sitting position
include a) ↓ airway pressure b) ↑ ability to Hyperventilate c) easy diaphragmatic excursion d) ↓ risk of VAE |
↓ airway pressure
↑ ability to Hyperventilate easy diaphragmatic excursion |
|
Contraindications for sitting position include (choose any that apply)
a) intracardiac defects b) Severe Hypovolemia c) Lesion vascularity d) Pulm. AV malformation e) Severe Hydrocephalus TEST ? |
intracardiac defects
Severe Hypovolemia Lesion vascularity Pulm. AV malformation Severe Hydrocephalus (also cachexia ? why) |
|
Physiologic changes in the sitting position include
a) ↑CO b) ↓ CO c) ↓ venous return d) ↑ CPP e) ↓ CPP f) ↑ vital capacity g) ↑ FRC |
↓ CO
↓ venous return ↓ CPP ↑ vital capacity ↑ FRC |
|
T/F There is a 100% chance of pneumocephalus in the sitting position
|
True
|
|
Complications in the sitting position include (choose any that apply)
a) HOTN b) Cerebral / Cervical spine Ischemia c) Dysrhythmias d) VAE e) Paradoxical air embolism |
HOTN
Cerebral / Cervical spine Ischemia Dysrhythmias VAE Paradoxical air embolism |
|
Risk of retinal artery thrombosis, ischemic optic neuropathy and venous pooling are most likely in which position
a) sitting b) lateral decubitus c) prone d) supine |
prone
|
|
T/F There is a decrease chance for a VAE in the prone position
|
True
|
|
The risk of a Venous Air Embolism (VAE) is increased by how much in the sitting position
a) 5 - 10 % b) 10 - 20% c) 20 - 40% d) > 50% TEST? |
20 - 40%
|
|
The consequences of a VAE are dependent on (choose any that apply)
a) rate of air entry b) volume of air entry c) presence/absence of PFO |
rate of air entry
volume of air entry presence/absence of PFO interesting to note that use of N2O can increase the volume of air entrained |
|
Clinical signs of a VAE include
(choose all that apply) a) ↓ ETCO2 b) ↓ SaO2 c) HOTN d) Hypoxemia e) slight ↑ in PaCO2 TEST ? |
↓ ETCO2
↓ SaO2 HOTN Hypoxemia slight ↑ in PaCO2 (r/t pulmonary dead space) |
|
What is the most sensitive internal monitor for VAE?
TEST? |
TEE
(inject 5cc agitated NS via CVP,watch to see where the tiny bubbles go [ie PFO] listen for difference in doppler tone) |
|
What is the most sensitive external monitor for VAE?
TEST? |
Precordial doppler
|
|
You suddenly hear a "mill wheel" sound coming from the precordial doppler, what the HECK do you do?
TEST? |
Tell surgeon to flood field with saline
D/C N2O FiO2 100% Aspirate air via CVP |
|
Would increasing CVP in a pt with a VAE be helpful or harmful?
|
Helpful, could help keep air from moving forward
give IVF bolus, apply jugular compression, use PEEP) |
|
The most likely mechanism of Paradoxical Air Embolism is
a) Right → Left cardiac shunting b) Left → Right cardiac shunting |
Right → Left cardiac shunting through PFO
20 -30% of population has a PFO |
|
When doing interventional neuroradiology it is important to
a) have pt completely immobile b) have NO post tetanic twitch c) be prepared for hemorrhage & vascular occlusion d) ask surgeon for a 30 minutes heads up |
have pt completely immobile
have NO post tetanic twitch be prepared for hemorrhage & vascular occlusion ask surgeon for a 30 minutes heads up |
|
What drug is often used to help to reduce incidence of vasospasm during Interv. Neuro Radiology procedure?
|
Transdermal NTG
|
|
What drug class can be used as prophylaxis against cerebral ischemia during Interv. Neuro Radiology procedure?
|
Calcium Channel Blockers
|
|
Protamine administration may be contraindicated in
a) prior vasectomy b) fish allergy c) recent steroid use d) insulin allergy |
prior vasectomy (antiprotamine antibodies can develop in these pts)
fish allergy (protamine found in the sperm of fish) recent steroid use insulin allergy (some insulin made from protamine) |
|
Hyperventilation is used to
a) treat intracranial hypotension b) treat intracranial hypertension c) provide brain relaxation after turning bone flap d) help decrease the amount of retraction on the brain |
treat intracranial hypertension
provide brain relaxation after turning bone flap help decrease the amount of retraction on the brain |
|
During a hemorrhagic crisis in Neuro procedure what would you do?
a) stop heparin & reverse with protamine b) Lower the MAP c) Burst Suppress d) FiO2 @ 100% e) cool to 33 -34 degrees |
stop heparin & reverse with protamine 1mg/100 units Heparin
Lower the MAP Burst suppress FiO2 @ 100% cool to 33 -34 degrees |
|
T/F Versed & Fentanyl have been implicated in inducing transient focal motor deterioration/altered language & spatial functions in pts who have had recent ischemic attacks
|
True, but no one know why
|
|
Would you want your pt who is coming in for a coiling or stent placement for an aneurysm to be anticoagulants prior to procedure?
|
Yes, they are needed to prevent thromboembolic complications during & after the procedure
|
|
Triple H Therapy is used to prevent & Treat cerebral vasospasm what does Triple H Therapy include
a) Hypertension b) Hyperventilation c) Hemodilution d) Hypervolemia e) Hypotension TEST ? |
Hypertension
Hemodilution Hypervolemia |
|
T/F Cerebral Vasospasm is a protective mechanism in pts who have had a subarachnoid hemorrhage (SAH)
|
True,
1 out of 4 will have vasospasm |
|
Highest risk of death r/t Re-rupture of an aneurysm occurs within how many weeks of initial SAH?
a) within 2 weeks of rupture b) within 6 weeks of rupture c) within the first 6 months |
within 2 weeks of rupture
|
|
Vasospasm occurs
a) in 30% of all pts with SAH b) in 75% of all pts with SAH c) in 3 -14 days d) first 24 hours |
in 30% of all pts with SAH
in 3 -14 days |
|
T/F With a SAH free blood irritates the blood vessels, they clamp down and can lead to stroke
|
True
|
|
During Carotid Occlusion Test
Hyper/Hypo tension improves quality of the test |
Hypotension
this test is done to assess the consequences of carotid occlusion prior to surgery CAUTION, the surgeon will inject NTG WITHOUT TELLING YOU! |
|
Brain AVM's
a) space occupying lesion b) non- space occupying lesion |
NON- SPACE OCCUPYING
they are a PART OF THE BRAIN |
|
T/F Nidus is the large tangle of vessels with multiple feeding & draining veins found in an AVM
|
True
|
|
Deliberate Hyper/Hypo tension may help ↑ safety with Cyanoacrylate Glue delivery
|
HYPOTENSION
|
|
Dural Arterovenous Fistulas
a) capillary bed only b) artery & vein no capillary bed c) artery & vein & capillary bed |
artery & vein no capillary bed
|
|
When anticoagulating a pt prior to a coiling or stent placement in neuro the PTT should be
a) 2 -3 times baseline b) 3-4 times baseline c) normal |
2 -3 times baseline
|
|
T/F Heparin 70 units/kg is used to prolong baseline 2 - 3x
|
True
|
|
Vein of Galen Malformation
a) uncommon b) presents in infants c) is an intracranial AV Shunt d) s/s include heart failure, Sz, hydrocephalus |
uncommon
presents in infants is an intracranial AV Shunt s/s include heart failure, Sz, hydrocephalus |
|
Schlerosing agents such as 95% ETOH are used to treat Craniofacial Venous malformations, you see your SaO2 monitor go REALLY low are you concerned?
|
Not really, it is a normal occurance when using 95% ETOH (like methyl. blue)
|
|
Risk of death / MI is higher in a pt who has an ASYMPTOMATIC ICA lesion and has a
a) carotid endarterectomy b) stenting & angioplasty |
carotid endarterectomy
WITHIN THE FIRST 30 DAYS |
|
Risk of death / MI is higher in a pt who has an SYMPTOMATIC ICA lesion and has a
a) carotid endarterectomy b) stenting & angioplasty |
stenting & angioplasty
r/t to the ↑ risk of pushing plaque out of carotid |
|
Abrupt correction of BP in an area that is chronically hypotensive d/t an embolic event
a) may overwhelm autoregulation b) cause hemorrhage/swelling c) is called Normal Perfusion Pressure Breakthrough |
may overwhelm autoregulation
cause hemorrhage/swelling is called Normal Perfusion Pressure Breakthrough |
|
Treatment of vasospasm may include
a) balloon angioplasty b) papavarine c) calcium channel blockers d) Triple H Therapy |
balloon angioplasty
papavarine (vasodilator) calcium channel blockers (vasodilators) Triple H Therapy |
|
Direct Thrombin Inhibitors
a) used in Heparin allergy b) inhibit free and clot bound thrombin c) monitored with APTT or ACT d) Lepirudin, Bivalirudin, Argantroban |
used in Heparin allergy
inhibit free and clot bound thrombin monitored with APTT or ACT Lepirudin, Bivalirudin, Argantroban |
|
Which of the following Direct Thrombin Inhibitors would you want to be careful when giving it to a patient with renal dz
a) Lepirudin b) Bivalirudin c) Argatroban |
Bivalirudin
"Bi" = 2 we have 2 kidneys |
|
Which of the following Direct Thrombin Inhibitors would you want to be careful when giving it to a patient with hepatic dz
a) Lepirudin b) Bivalirudin c) Argatroban |
Argatroban
|
|
Examples of Thienopyridine derivatives
a) ReoPro b) Ticlid c) Plavix d) ASA |
Ticlid
Plavix |
|
Example of a glucoproteinIIb/IIIa antagonist(s) is/are
a) ReoPro b) Ticlid c) Plavix d) ASA |
ReoPro
|
|
T/F There is no specific agent ot reverse direct thrombin inhibitors and antiplatelet drugs
|
True, but there has been some promise seen with DDAVP in regards to ASA, Ticlid
|
|
What procedure is the Gold standard for stroke prevention?
|
Carotid Endarterectomy
|
|
The brain
a) is devoid of oxygen stores b) is devoid of glucose stores c) makes it's own glucose |
is devoid of oxygen stores
is devoid of glucose stores |
|
Internal Carotids supply what % of blood to the brain
a) 20% b) 30% c) 50% d) 80% Test? |
80%
|
|
Vertebral Arteries supply what % of blood to the brain
a) 20% b) 30% c) 50% d) 80% Test? |
20%
|
|
CBF is dependent on ______& is autoregulated in response to brains metabolic requirement
|
CPP
CBF= CPP - CVR |
|
Formula for CBF
Test? |
CPP - CVR
or CBF= (MAP- ICP) - CVR Cerebral Vascular Resistance is a function of blood viscosity and vessel diameters KNOW |
|
T/F During a Carotid Endarterectomy Arterial Blood Pressure & Carbon Dioxide tension are the ONLY things we can control
|
True
|
|
CBF changes _______ml/100g/min for every 1 mmHg change in PaCO2
TEST? |
1 - 2 ml
within range of 20 - 80 mmHg |
|
Hypocapnia causes
a) vasodilation b) vasoconstriction |
Vasoconstriction
|
|
Vasoconstriction diverts blood to/from ischemic regions of the brain
|
To
ROBIN HOOD EFFECT |
|
Hypercapnia causes
a) vasodilation b) vasoconstriction |
vasodilation
INCREASES GLOBAL CBF (by decreasing CVR) STEALS BLOOD FROM ISCHEMIC AREAS |
|
Common Co-morbs found in pts who have Carotid Disease include
a) elderly b) CAD c) HTN d) COPD e) DM |
elderly
CAD HTN COPD DM |
|
Greatest benefit of carotid surgery in a pt with >50% occlusion is seen if done within how many weeks of ischemic event?
|
2 weeks
trouble is most of them have CAD so this makes it difficult |
|
Your pt has had a stroke with Right sided weakness/paralysis which side would you monitor the SaO2 on?
|
Left side
DO NOT monitor on same side as weakness there is up regulation of receptors on stroke side so will OVERDOSE muscle relaxants |
|
T/F During a CEA conversion from a Regional anesthetic to GA is 5x more likely when deep cervical blocks are done
|
True
|
|
Which volatile agent has been associated with post-op fever, wound infection, pneumonia, atelectasis, severe PONV
a) Halothane b) Nitrous Oxide c) Isoflurane d) Ethrane |
Nitrous Oxide
|
|
Traction on the carotid can be misinterpreted as high blood pressure and cause _________
|
Baroreflex parasympathetic response → HOTN, Bradycardia
|
|
Examples of cerebral protective drugs include
a) Barbs b) Etomidate c) Propfol d) Volatiles e) Benzo TEST? |
Barbs
Etomidate Propfol Volatiles Benzo also listed was Ketamine (but really, it ↑ 's ICP) |
|
T/F The awake pt is the most reliable & sensitive neurological monitor
|
True
|
|
Three most common complications after a CEA
a) Stroke b) MI c) Cranial nerve injury d) PE Test? |
Stroke
MI Cranial nerve injury |
|
Which is most likely to occur after a CEA
a) Stroke b) MI c) PE d) hoarseness TEST? |
Stroke
|
|
Which is most likely to cause death after a CEA
a) Stroke b) MI c) PE d) hoarseness TEST? |
MI
|
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Your pt has a hoarse voice after his CEA surgery you attribute it to
a) rough placement of ETT b) recurrent laryngeal nerve injury c) a result of the surgeon being so rough d) he just has a "frog" in his throat, tell him to clear it for goodness sake TEST ? |
recurrent laryngeal nerve injury
HOARSNESS IS INDICITIVE OF RECURRENT NERVE INJURY POST=OP |
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Your pt is exhibiting ispsilateral HA, Sz, face & eye pain, and has cerebral edema/hemorrhage what is causing this
a) Cushings Syndrome b) Takotsubo Syndrome c) Hyperperfusion Syndrome d) Normal Perfusion Pressure Breakthrough |
Hyperperfusion Syndrome
as a result of the brain no receiving so much blood Drastic increases in CBF sometimes up to 200% Takotsubo = "broken heart syndrome" |
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during a Carotid Endarterectomy which Cranial nerves are the most likely to become damaged
a) Hypoglossal b) vagus c) branches of the face nerve d) all of the above TEST? |
Hypoglossal
vagus branches of the face nerve note Superior & Recurrent laryngeals can also be injured |
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Dysphagia, Hoarseness, Absence of unilateral cord movement are all signs of
a) superior laryngeal injury b) recurrent laryngeal injury c) hypoglossal nerve injury TEST? |
recurrent laryngeal injury
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Once an aneurysm bleeds the risk of rebleeding is _______ for the next 2 weeks
a) 10% b) 20% c) 30% d) 40% |
20%
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In a Cerebral Aneurysm the goal for the CPP would be
a) <50 mmHg b) 60 - 80 mmHg |
60 - 80 mmHg
too high or low → further hemorrhage |
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With Cerebral Aneurysm what are the 3 events that can ↑ risk of rupture of aneurysm
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Induction
Clipping Emergence |
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ICP correlates with grading scale
a) Fisher Grades b) Hunt & Hess Grades |
Hunt & Hess Grades
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Hypovolemia correlates with which grading scale
a) Fisher Grades b) Hunt & Hess Grades |
Fisher Grades (looks @ CT results)
36-100% of pts with a Rupture (SAH) are hypovolemic |
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After a SAH you would not be surprised to see which lab values
a) hyperkalemia b) hypokalemia c) hypercalcemia d) hypocalcemia e) hypernatremia f) hyponatremia TEST? |
hypokalemia
hypocalcemia hyponatremia |
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Your SAH pt has elevated Troponin levels & is showing T-wave inversion & ST segment depression you suspect
a) cardiac problems b) consider this normal for SAH TEST? |
consider this normal for SAH
EKG changes occur in 40 - 100% of all cases |
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T/F Most changes in EKG after SAH are neurogenic rather than cardiogenic in nature
TEST? |
True
expect to see changes in EKG (ST, T-wave) also draw labs (Ca, K) |
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T/F Pulmonary changes such as edema, aspiration, hydrostatic pneumonia can be seen after a SAH
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True
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T/F In SAH vasospasm has a 13.5% overall mortality and morbidity rate
TEST ? |
True
risk peaks @ end of 1 weeks |
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T/F The rationale for Triple H Therapy (Hypervolemia, Hemodilution & HTN) after a SAH is that ischemic brain areas have impaired autoregulation so CBF is dependent on CPP
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True, CPP is dependent on Vascular Volume & MAP
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Hypervolemic treatment of SAH includes
a) a CVP of 10 mmHg b) PAWP of 12 -20 mmHg c) infusion with 5% Albumin d) infusion with crystalloids e) Infusion with Hetastarch |
a CVP of 10 mmHg
PAWP of 12 -20 mmHg infusion with 5% Albumin infusion with crystalloids |
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T/F Hypervolemia & Hypertension together can cause vagal response
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True
Atropine 1mg IM is given q3 - 4 hrs to keep HR 80 - 120 this is part of the Triple H Therapy used for increased ICP |
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In an aneurysm that has been clipped what would be the max BP range
a) 160 - 200 mmHg b) 120 - 150 mmHg |
160 - 200 mmHg
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In an aneurysm that has not been clipped what would be the max BP range
a) 160 - 200 mmHg b) 120 - 150 mmHg |
120 - 150 mmHg
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T/F As Hct & viscosity of blood diminish CVR is reduced & CBF is ↑
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True
a Hct of 33% provides optimal balance between viscosity & O2 carrying ability |
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Papaverine can cause
a) Thrombocytopenia b) ↑ ICP c) pupillary dysfunction d) transient brainstem dysfunction |
Thrombocytopenia
↑ ICP pupillary dysfunction transient brainstem dysfunction |
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T/F patients with good SAH grades (Hunt & Hess) & low Fishers grade are less likely to vasospasm
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True
Vasospasm is not likely to occur after 12 days |
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When positioning pt after intubation for a crani consider that flexion of head does what to ETT
a) advances it b) pulls tube "out" |
advances it
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When positioning pt after intubation for a crani consider that extension of head does what to ETT
a) advances it b) pulls tube "out" |
pulls tube "out"
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T/F Desflurane in high concentrations can cause SNS stimulation
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True
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What MAC would you want during an aneurysm clipping
a) 0.5 b) 1.0 c) 1.2 |
0.5
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Mannitols
a) effect starts in 3-5 minutes b) effect starts in 7-9 minutes c) peaks @ around 45 minutes d) peaks @ around 90 minutes |
effect starts in 3-5 minutes
peaks @ around 45 minutes watch for ↑ osmolarity, ↓ Na, K, Cl |
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T/F Reduction of CSF Compartment can be achieved by drainage of CSF 5ml/min up to 20 -30 ml
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True
do this VERY SLOWLY (rapid withdrawal can cause reflex HTN) |
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T/F Reduction of cerebral blood volume can be achieved thru hyperventilation
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True,
HYPOCAPNEA CBF ↓'s 1 - 2 ml for every 1 mmHg in PaCO2 (in the 25-35 mmHg range) |
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Techniques for Brain Relaxation include
a) reverse t-berg (10 degrees) b) mannitol c) drainage of CSF d) hyperventilation TEST? |
reverse t-berg (10 degrees)
mannitol drainage of CSF hyperventilation |
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If the usual treatments to relax the brain don't work consider
a) hypoxemia / HTN b) venous obstruction c) d/c N2O d) HOB up e) STP |
hypoxemia / HTN
venous obstruction d/c N2O HOB up STP |
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T/F The Law of Laplace states
Wall tension = radius of aneurysm x MAP /2 |
True
T=R x P / 2 |
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Mild hypothermia
a) <33 degrees b) 34-35 degrees c) decrease excitatory neurotransmitter from ischemic cells d) metabolic suppression |
34-35 degrees
decrease excitatory neurotransmitter from ischemic cells metabolic suppression |
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Moderate hypothermia
a) <33 degrees a) 33 degrees b) 34-35 degrees c) decrease excitatory neurotransmitter from ischemic cells d) metabolic suppression |
33 degrees
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