ACE Review - Neuro Flashcards
Questions
Answers
does age increase risk of stroke for non neuro cases
yes, 62 or older
do heart problems increase risk of stroke for non neuro cases
yes, MI within 6 months
do kidney problems increase risk of stroke for non neuro cases
yes, hx of ckd or dialysis imply pt w vascular dz
do pt with pulm problems increase risk of stroke for non neuro cases
yes, copd and smoking increases risk
does obesity increase risk of stroke for non neuro cases
actually no, bmi higher decreases risk of stroke
who has a higher risk of stroke for non neuro cases. akd vs dialysis pt
acute kidney disease pt
what metabolic disease predisoe pt to periop stroke
htn
in pt with sub arach hemorrhage…what 3 things predict m&M
degree of bleed, action to correct bleed, presence of vasospasm
what is the greatest predictor of vasospasm in sub arch hemorrhage
the degree of bleeding
what is pseudotumor cerebri
it is increased ICP secondary to decreased resorption of csf
what anesthestic technique is contraindicated in pseudotumor cerebri
non
can spinals be done in psuedotumor cerebri
actually it is one of the treatments
who is at increased risk for recall under general anesthesia
patients with long history of substance abuse, alcohol use, chronic opiod/ benzo use,
why dose substance abuse have increased of recall
their cyp450 are increased and thus metabolism of anesthetic agents
what kind of surgeries predispose pt to recall
pt who cannot tolerate low bp or high anesthetics…like cardiac or c-section
how does neuromusclar blocking drugs increase rate of recall
bc monitoring movement under ga can help us indicate low anesthesia…paralysis prevents this assessment
what is core temperature
brain temperature
does measureing bladder temperature over or underestimate core temp
it underestimates core…core could actually be colder than what bladder temp shows
where can u measure core temp
distal esoph, pa cath, tympanic, nasopharynx
what does general anesthesia do to the threshold of thermoregulation
it decreases the threshold
does “decreasing” threshold for thermoregulation make sense?
yes it does…decreasing threshold means that the temperature at which shivering and other mechs for temp maintanence is dropped to a lower temp…thus you wont shiver until you are reallllly cold
by how much does GA decrease the threshold for thermogenesis
2-3 degrees celcius
is agitation post op considered post op delerium
yes…it is a hyperactive variant
Is agitation required for diagnosis of delerium
no
is depression a risk factor for postop delerium
yes
what kind of surgery has the highest risk for postop delerium
hip surgery
does post op delerium increase mortality
yes
most common risk factor for post op delerium
pre-existing cognitive dysfuction
what things can be done to prevent post op delerium
prevent hyothermia. And avoid certain drugs
what is the diagnosis of delerium
acute onset, flux in mental status, innattention, and disorganized thinking vs abnormal behavior
why are the hyoactive delerium patients higher chance of mortality than the hyperactive delerium variant
because diagnosis is more difficult to be made in the hypoactive delerium pt…so treatment is done later
during craniotomy, what angle puts the patient at risk for venous air embolism
angle greater or equal to 15 degrees
how dose cvp affect risk for venous air embolism
when cvp is low in pressure, higher chance to get Venous air embolism
what is the treatment for venous air embolism
multiorifice central cath
where should the multiorifice central cath be placed to get venous air emboism
at the svc and atrial junction
for neuro case, what is the most sensitive detector for venous air embolism
tee
for neuro case, what is the 2nd most sensitive detector of venous air embolis
precordial doppler
what do you hear on stethoscope when you have a venous air emboism
mill whill murmur
what is the first line treatment for venous air embolism
decrease head height, flood surgical field, apply bone wax, occlude the offending vessel
in a neurosurg pt that develops diabetes insipidus, what Is the most common lab
decreased urine specific gravity/hypOosmolar urine
what is the lab value in diabetes insipidus for Na and osmolarity
hypernatremia, hyperosmolar
how to treat diabetes insipidus
free water replacement slowly, vasopressin q4hrs till intranasal desmopressin can be used
how to decrease icp in a emergency neuro decompression case
increase rr to decrease co2, 1g/kg mannitol, head up,
can you repeat mannitol for further decrease in icp
most likely, serum osm increased already and wont aid any more…
what is risk for repeat mannitol
hyperkalemia
what is risk of further hyperventilation beyond etco25
this will not only decrease icp, it will put pt at risk for ischemia
if rr mannitol and head raise still not bring icp down, what other tx can be done to decrease icp
barbituate/propofol bolus, ventriculostomy
if pt has a lumbar drain in already for an emergency decompressive craniotomy, should you use it
not the best choice on multiple choice exam…it can be used, but too rapid drain may cause herniation
how does propofol and barbs cause decrease icp
since the brain is still coupled, decreasing the cmro2 will decrease o2 demand and thus decrease flow to the brain
what is adverse effect of prop and thiopental (barb) usage
it may decrease bp, aka map, aka cerebral perfusion pressure
what can be used other than prop or thiopental
etomidate which also decreases icp
what adverse effect dose using etomidate cause
it can actually cause hypertension and adrenal suppression
does GBS have decreased or hyper reflexia at dtr
decreased dtr
do gbs patients present with fever?
no…this is uncommon…fever usually means another diagnosis and not gbs
what is gbs
guillan barre syndrome - a autoimmune polyradiculopathy
how does gbs present
after 3 weeks of infxn, has symmetrical rapid progressive neuropathy/weakness
what are 2 common manifestations of gbs
decreased dtr and facial weakness
what labwork is done to test for gbs
csf shows high protien and normal wbc aka not infectious
how long does gbs last
days …up to 4 weeks
when do you see evelated protien in gbs pt
it may show up 2 weeks after onset of weakness
what usually precedes gbs weakness
diarrhea or uri
besides virus, what other things might cause onset of gbs
vaccinations for influenza, hepatitis, polio, and rabies
what is the most common symptom other than weakness found in gbs pts
pain!!! Occurs in 89% of pts
what is the cause for pain of gbs during the acute phase
the inflammation of nerves
what is the cause for pain of gbs during the late phase
regeneration of sensory nerves
pain treatment for gbs associated pain
carbamazepine, corticosteriods, gabapentin, opiods
does bowel constipation and urine incontinence present with gbs pt
no
what are the 3 phases of gbs
acute, plateau, recovery
what is the acute phase
weakness, ascending, bilateral, symmetrical, rapidly progressive
when is acute phase the max weakness
at 2 weeks
how long can acute phase last
4 weeks
what is the plateau phase
the pt has unchanged variables
how long does plateau last
several weeks to several months
how long does recovery last
depends on severity of weakness, variable, but is usually several months
what factors put pt at risk for not being able to walk or walk without assistance s/p gbs event
rapid onsent, age greater than 60, prolong plateau, and hx of vent dependancy
what are indications to intubate gbs pt
pna, weak resp muscles, inable to handle secretions (aspiration risk)
what is recommended to follow for pt with gbs daily
daily assessment of vital capacity
what is the vital capacity when we need to intubate gbs pt
vital capacity less than 15cc/kg
do steriods help gbs
iv steriods have not shown aid and oral steriods had shown actual worsening of pt outcome
does interferon beta 1 alpha treat gbs
no, that is for multiple sclerosis pt
what are 2 effective treatments of gbs pt
plasma exchange and IVIG
is plasma exchange same as exchange transfusion
no they are not the same
how is plasma exchange helpful for gbs
it has decreased the need for vent assistance, decrease time to walk, and decrease disabilities
during pregnancy, is there a increase in prevalence of intracranial pathology
no, for most tumors, av malformation, it is the same between pregnant and non pregnant patients
what has an increase in growth response during pregnancy for intracranial lesions
meningiomas…they grow in response to elevated estrogen and progesterone levels
what is the concern for intracranial mass during pregnancy
must handle intracranial hypertension and seizures
can mannitol and lasix be used for neuro surge for intracranial lesions in pregnant patients
yes…but only at certain doses 0.2g/kg to 0.5g/kg
what can mannitol cause the fetus
hyperosmolarity in the baby
what does hyperosm of mannitol given in pregos to the baby
hyperosm will cause decrease in fetal lung fluid, decrease fetal urine flow, and over all dehydration
main complication of intracranial mass in prego
seizure that can lead to death. These pt must have anticonvulsant meds
what is concern of anticonvulant given to pregos
levels are altered 2ndry to hepatic metabolism, protien and blood volume changes
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What is the cause for neurogenic pulmonary edema
Increased intracranial pressure
How does increased intracranial pressure cause neurogenic pulmonary edema
The brain ischemia Promotes increase catecholamines to increase cerebral perfusion pressure
What is the result of increasing catecholamines in NPE
There is a constriction of the pulmonary vasculature and systemic vasculature
What happens to cardiac output
Decrease because there is a decrease in left ventricle contractility
How often does NPE happen in neurotrauma
20%
When does nPE occur
First few hours
What are the causes of. NPE
Increased capillary permeability because of inflammatory factors when the blood brain barrier is dismantled, decreased left ventricle outflow, increased pulmonary vascular resistance
How do you treat NPE
Decrease ICP
How can you decrease ICP
Evacuate hematoma, Decompressive craniotomy, ventricular drain, hyperosmolar treatment
If a patient is tachycardic and hypertensive can use a beta blocker in NPE
It is not recommended
His permissive hypercapnia suggested and NPE
Is contraindicated because elevated CO2 will cause increase in cerebral bloodflow thus increased ICP
Where should the multiorifice cath be placed
At the junction of the svc and atrium
What is the EKG sign of correct cvc placement
Biphasic p waves
can pa02 influence cerebral blood flow
yes
at what values does pao2 influence cerebral blood flow
pa02 of 60 or less
what does pao2 of 60or less do to cerebral blood flow
it increases cerebreal blood flow
what does hypothermia do to cerebral blood flow
decrease cbf
what does chronic hypertension do to cerebral blood flow
it shifts the cerebral autoregulation curve to the right
cerebral blood flow…what increases cbf…hyper or hypoxemia
hypoxemia
cerebral blood flow…at what PaO2 doese cbf increase
PaO2 less than 60
Mannitol. What happens with rapid infusion.
Transient increase in icp
Mannitol. What happens with slow infusion,
Decrease in ICP and improved brain oxygen delivery and blood flow
Mannitol. When should it be stopped
When serum osm is greater than 310 or when Na is greater than 150.
Mannitol. What is lost in mannitol diuresis
Na K and Mg
venous air emolism. what are the most sensitive tests for this
tee is the most…but almost as equal is precordial doppler
venous air embolism. what is the most neuro surgery to get it
posterior fossa tumor excision
venous air embolism. what happens to fractiion expired nitrogen
increase
venous air embolism. what happens to PaO2
decrease
venous air embolism. what happens to etco2
decrease
venous air embolism. what happens to pulmonary artery pressure,
increase
venous air embolism. what happens to paco2
increase…builds up in blood bc cant vent out
venous air embolism. what happens to cvp
increase
venous air embolism. what should be first done
drop head, flood field, apply pressure to jugular viens
venous air embolism. how should volume be resuscitated
it should increase to apply cvp pressure to improve cardiac output forward flow
venous air embolism. what position is supposedly suppose to help
durants left lateral decubitus position
venous air embolism. what is durants position suppose to do
it is suppose to decrease right ventricular outflow obstruction
venous air embolism. a paradoxial vae occurs…why
bc there is some form of vsd or asd
venous air embolism. what to do to treat paradoxical vae
use hyperbaric oxygen
cerebral blood flow. what is dexemetomidines effect on cbf on normal autoregulatoin pressures
at increasing doses, it decreases cbf and decreases cmro2
cerebral blood flow. what is esmolol effect on cbf at normal autoregulatoin pressures
no effect
cerebral blood flow. what is epinephrine effect on cbf at normal autoregulation pressures
it increases cbf
cerebral blood flow. what is phenylephrine effect on cbf at normal autoregulation pressures
no effect
icp. what is the gold standard for monitoring icp
intraventricular drain catheter
icp. what are the benefits of an intraventric cath
it can be rezeroed while in place and can be a mode of therapy for elevated icp
icp. what are the disadvantages of intraventric cath
highest rate of infection, difficult placement, risk for damaging paranchyma
icp. what is a subarachoid bolt
it is a bolt that sits outside of the brain in the subarachnoid space
icp. what is the advantage of the subarachnoid bolt
less infection risk and less risk to damage brain paranchyma
icp. what is the disadvantage of a subarachnoid bolt
it may not be as accurate as brain matter may occlude the lumen
neuromonitoring. lumbar surgery. what kind of monitoring is more common
SSEP…bc lumbar surgery is mainly @ cauda equina level…and SSEP is enough to monitor both sensory and motor…bc if ssep is affected…motor most likey is affected too…there is no anterior spinal chord for surgery to affect seperately.
neuromonitoring. what is more sensitive to volatiles
MEP is more sensitive to volatiles
neuromonitoring. how does volatile sensitivity help select between modes of neuromonitoring
since MEP are more sensitive to volatiles…SSEP is better used to monitor and not worry about false positives caused by anesthesia…so at lumber sites…SSEP is good enough to monitor both sensory and inferred motors
neuromonitoring. at what level of the spinal chord is it best to monitor ssep and mep seperately
at or above L1 level
neuromonitoring. what do volatiles do to ssep
decrease amplitude and increased latentcy
neuromonitoring. what is latentcy
it is the time from stimulus to response in neuromonitoring
neuromonitoring. between mep and ssep, when is tiva more recommended
if MEP is used, it highly rec that TIVA is used bc only MAC of 0.25 is recommended when MEP is monitored
neuromonitoring. what is more sensitive to hypoperfusion. mep or ssep
there are more MEP synapses compared to SSEP and hypoperfusion and hypoxia affects MEPS the most
neuromonitoring. what the goal hg when spinal cord surgery is done and MEP is being monitored
attempt to keep Hg above 10
subarachnoid hemorrhage. what is the diagnostic test of choice
ct head non contrast
subarachnoid hemorrhage. what are the risk factors for older patients
smoking, hypertension, etoh abuse
subarachnoid hemorhage. what are the risk factors for young patients
cocaine abuse
subarachnoid hemorrhage. what increases the chances of ct scan detecting the sah
the greater the symptoms, the greater likely hood of detecting sah
subarachnoid hemorrhage. what is the next step after ct scan is ordered
consult neurosurgery service
subarachnoid hemorrhage. what is the next step after ct scan is ordered and neurosurg notified..
ct arteriogram for confirm diagnosis and treatment
subarachnoid hemorrhage. what is the greatest risk for these pt
rebleeding
subarachnoid hemorrhage. what are risk factors rebleeding
pt w/ small vessel disease: uncontrolled htn, renal disease, atrial fib, heart failure, cad
subarachnoid hemorrhage. what about the initial hemorrhage puts the pt at increased risk for rebleeding
increase time to treatment, increased size of initial hemorrhage, posterior circulation locaiton of previosu hemorrhage,
suarachnoid hemorrhage. what percent of pt will rebleed if no intervention is done
4% of patients
subarachnoid hemorrhage. what symptoms can tell you that there is intracranial hypertension
hypertension with bradycardai, altered mentation, posturing
subarachnoid hemorrhage. what interventions can u do during acute increase in intracranial htn
mannitol, lasix, acute brief hyperventilation,
subarachnoid hemorrhage. what neuroprotection can u do
glucose control and anticonvulsants
subarachnoid hemorrhage. what is prefered, tiva vs volatile anesthetics
tiva, bc volatiles increase cbf and thus increase intracranial htn
subarachnoid hemorrhage. how is bp maintained
normotension is prefered. during temp aneurysm clip, moderate htn can be used.
subarachnoid hemorrhage. what do wide swings in bp mean
possibly rebleeding.
subarachnoid hemorrhage. should u use hypothermia
as of now no data to support decrease in mortality
Neuro monitoring. What are considered changes in amplitude or latentcy
50 percent decrease in amplitude or 30 percent increase in latentcy
Neuro monitoring. Does nitrous oxides cause change in neuromonitoring
Yes.
Neuro monitoring. Do narcotics affect neuromonitoring.
No u dumb fuck. That’s why we use it in tiva
Neuromonitoring. Does ketamine cause any effect
It increases amplitude. And possible at low doses helps with interpretation of monitoring
Icp. Of barbiturate mannitol and hyperventilate. What is the best at lowering icp.
Mannitol
Icp. Mannitol. How fast should it be given.
Within 30 minutes.
Icp. Mannitol. When do u see its effects.
15 minutes.
Icp. Mannitol. When is its peak effect.
1 hour
Icp. Mannitol. How long does it last.
6 hours.
Icp. Mannitol. How should it be monitored.
Keep the serum osmolarity 300-320
Icp. Mannitol. What happens when serum osm. Gets above 340
Hypovolemia and electrolyte disturbance bc excess diuresis
Awake craniotomy. What is the kind of sedation preferred for this case.
Moderate sedation. With propofol.
Awake craniotomy. When should sedation be stopped.
30 minutes before cortical mapping so it does not interfere with the mapping.
Awake craniotomy. What helps awake approach be successful
Local anesthestics to provide comfort.
ect. what is a good duration of seizure activity to help improve depression
greater than 25 seconds
ect. what is the first hemodynamic change
bradycardia because of parasympathetic discharge.
ect. what is the danger for bradycardia
in some cases, parasympathetic overtone is so great you get asystole
ect. what is given prophylactically to prevent the parasympathetic discahrge
glycopyrroalte
ect. does glycopyrrolate affect the seizure
no
ect. what can be done if pt in previous ect does not reach long enough seizure duration
give iv caffeine or theophylline
ect. what about anesthesia ventilation and oxygenation can effect the duration of seizure
hypercapnea and hypoxemia may decrease the duration of seizure
ect. how should you treat the second hemodynamic effect of ect
sympathetic discharge (tachycardia and htn) should be treated with labetalol
autonomic hyper-reflexia. when the bladder is stimulated…what is the afferent limb
the dorsal collumns, spinothalamic track, and a massive sympathetic discharge
autonomic hyper-reflexia. what happens normally if the spinal cord is intact and you get the afferent signals
the sympathetic discharge would cause htn and the carotid barorecptors would see this and send out vagal responses and inhibitory signals to ablate the sympathetic vasoconstriction
autonomic hyer-reflexia. what are the bp above and below the transection
hypo above, hyper below
autonomic hyper-reflexia. what is the treatment
nitroglycerine to bring down the bp below the transection. so that that strong vagal response will no persist and cause asystole
autonomic hyper-reflexia. what is the catecholeamine causing the htn
noreepi
subarachnoid hemorrhage. what is the most common cause of death after first bleeding event
vasospasm
subarachnoid hemorrhage. what is triple h therapy
hypertension, hypervolemia, hemodilution
subarachnoid hemorrhage. what is the goal of hypervolemia
get cvp above 8 or wedge pressure of 15 or greater
subarachnoid hemorrhage. triple h. what is the mechanism of hypervolemia
it increases cardiac output
subarachnoid hemorrhage. triple h. what is the goal for hemodilution.
to keep the hematocrit around 30.
subarachnoid hemorrhage. triple h. when should hypertension be induced.
when hypervolemia and hemodilution is reached
subarachnoid hemorrhage. vasosopasm. what are risk factors for vasospasm after a bleeding event
previous big bleeding, history htn, old, hydrocephalus, female, smoker
subarachnoid hemorrhage. when can vasosopasm happen
up to 14 days out
subarachnoid hemorrhage. how urgent is it to operate on vasospasm
emergency
subarachnoid hemorrhage. how is diagnosed
frequent neuro exam. cerebral angiogram, transcranial doppler
guillain-barre. what is the moa
viral infection. (cmv, gbs) or bacterial infection. antigens mimic myelin sheath, autoimmune attack schwan cells. ascending paralysis
gulillan-barre. can you use succ
contraindicated
gullian-barre. can you use nondepol mm block
not contraindicated, but may be more sensitive
gullian-barre. are epidurals contraindicated
no
