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156 Cards in this Set
- Front
- Back
Functions of CSF include
a) protection of brain b) nutrition c) control of chemical environment d) excretion of metabolites e) transport neurotransmitters |
protection of brain
nutrition control of chemical environment excretion of metabolites transport neurotransmitters |
|
The majority of CSF is produced
a) Epindymal cells b) Pia c) Choroid Plexus d) Foramina of Monroe |
Choroid Plexus (70%)
|
|
Another name for the 3rd Ventricle is
a) Foramina of Monroe b) Aquaduct of Sylvius c) Choroid Plexus d) Arachnoid villi |
Aquaduct of Sylvius
|
|
Intracranial absorption of CSF occurs via arachnoid villi at
a) Dorsal Nerve Root b) Superior Sagittal Sinus c) Foramina of Monroe |
Superior Sagittal Sinus
|
|
Spinal cord absorption of CSF occurs via spinal veins at
a) Dorsal Nerve Root b) Superior Sagittal Sinus c) Foramina of Monroe |
Dorsal Nerve Root
(spinal dural sinusoids) |
|
T/F absorption of CSF occurs thru fenestrations in the villi epithelium when CSF pressure exceeds that of the sinus pressure
|
True
|
|
Which of the following substances found in both the plasma & CSF has the same concentration in both areas
a) K b) Glucose c) Na d) Mg |
Na
|
|
All of the following is true regarding CSF production except
a) 0.35 - 0.40 ml/min b) totally replaced every 5 -7 hours c) 500 - 600 ml/day d) replaced on an as needed basis |
replaced on an as needed basis
|
|
Total CSF is
a) 300ml b) 150ml c) 500 ml |
150ml
|
|
CSF concentration is about ____% of plasma concentration
a) 30% b) 6% c) 60% d) 10% |
60%
|
|
T/F Glucose in CSF is autoregulated
|
True between 270 - 360 ml/dl
Requires active or passive transport process |
|
CSF concentration of protein is ____% of plasma concentration
a) 60% b) 6% c) 30% d) 70% |
6%
|
|
If ICP < 20mmHg and
CPP > 70 mmHg, CSF formation is a) decreased b) increased c) no change |
No change
|
|
If ICP increased OR
CPP < 70 mmHg, CSF formation is a) decreased b) increased c) no change |
decreased
|
|
If ICP increased AND
CPP < 70 mmHg, CSF formation is a) decreased b) increased c) no change |
decreased
AND so is CHOROID PLEXUS FLOW |
|
If ICP > 30 what happens to reabsorption of CSF
a) increases b) decreases c) no change |
increases (decreased resistance to reabsorption)
|
|
Trace the pathway of CSF
|
Lateral ventricles (2 – Foramina of Monroe) → 3rd ventricle (Aquaduct of Sylvius) → 4th ventricle (Aquaduct)
through Foramina of Luschka and Magendie→ subarachnoid space → Reabsorbed via arachnoid villi (superior sagital sinus or spinal dural sinusoids) |
|
Isoflurane
a) decreases CMRO2 b) increases CMRO2 c) has a variable effect on ICP d) all of the above |
decreases CMRO2
has a variable effect on ICP (can dec. ICP with hyperventilation, MAC 0.5) |
|
Which of the following should not be used on a pt with increased ICP
a) N2O b) Desflurane c) Isoflurane d) a & b |
N2O
Desflurane |
|
The ions in the CSF influence
a) HR, BP b) CBF c) cerebral metabolism d) autonomic & vasomotor reflexes |
HR, BP, autonomic & vasomotor reflexes
as well as RR , emotional states |
|
Acid- base balance of CSF & neural tissue influences
a) BP, HR b) Respiration c) autoregulation d) cerebral metabolism & CBF |
Respiration
autoregulation cerebral metabolism & CBF |
|
T/F Isoflurane inhibits excitatory neurotransmission
|
True
|
|
With a mild increase of CBF there is a pronounced ___________in CMRO2
a) increase b) decrease |
decrease in CMRO2
|
|
Barbs
a) increase CBF b) decrease CBF c) increase cerebral resistance d) decrease cerebral resistance |
decrease CBF
increase cerebral resistance |
|
What dose of Lidocaine prevents and increase in ICP & SNS
a) 5 mg/kg b) 3 mg/kg c) 1.5 mg/kg d) Lidocaine doesn't have any effect on ICP |
1.5 mg/kg
|
|
An intracranial mass causes
a) initial increase in ICP b) decrease in CBV c) decrease in CSF d) decrease in brain tissue volume |
initial increase in ICP
decrease in CBV decrease in CSF decrease in brain tissue volume |
|
T/F The initial increase in ICP with an intracranial mass is a compensatory mech that is diverting ICP thru Foraman Magnum down the spinal cord
|
True
|
|
What is the gold standard for monitoring & treating ICP? _________
|
Ventriculostomy
|
|
Which of the following components determines ICP
a) Blood b) Brain c) CSF d) all of the above |
Blood
Brain CSF |
|
Acid- base balance of CSF & neural tissue influences
a) BP, HR b) Respiration c) autoregulation d) cerebral metabolism & CBF |
Respiration
autoregulation cerebral metabolism & CBF |
|
Sux
a) increases CBF b) decreases CBF c) increases ICP d) decreases ICP |
increases CBF
increases ICP |
|
An intracranial mass causes
a) initial increase in ICP b) decrease in CBV c) decrease in CSF d) decrease in brain tissue volume |
initial increase in ICP
decrease in CBV decrease in CSF decrease in brain tissue volume |
|
T/F The initial increase in ICP with an intracranial mass is a compensatory mech that is diverting ICP thru Foraman Magnum down the spinal cord
|
True
|
|
What is the gold standard for monitoring & treating ICP? _________
|
Ventriculostomy
|
|
The initial response to an increased ICP is to _________________
|
Shift CSF into the spinal arachnoid villi
|
|
The most rapid maneuver to lower ICP is_________________________
|
Hyperventilation to a PaCO2 25 mmHg
DO NOT go below 25!! |
|
Intracranial HTN defined as
a) sustained ICP > 20 mmHg b) sustained ICP > 30 mmHg c) sustained ICP > 15 mmHg |
sustained ICP > 20 mmHg
|
|
T/F It is the ambient pressure within the skull that that causes symptomatic increases in ICP
|
False
It is the interaction with other pathology that causes the increase |
|
Which of the following area will recover from ischemia no matter how long the ischemia is for
a) penlucida b) penumbra |
penlucida
|
|
The reflex response to intracranial HTN (IC HTN) is
a) increased cerebrovascular resistance b) decreased cerebrovascular resistance c) increase in CBV d) increased ICP |
decreased cerebrovascular resistance (when this decreases there will be more volume of blood & CSF)
increase in CBV increased ICP |
|
T/F With systemic HTN, the baroreceptor mediated bradycardia leads to "cushings reflex" which eventually worsens IC HTN
|
True
|
|
Describe Cushings Reflex
|
MAP < ICP (loss of perfusion)
HYPOTHALAMUS ↑ SNS stimulation Vasoconstriction = ↑ contractility, and CO ↑ BP detected by baroreceptors in carotids Triggers PSNS → Bradycardia Irregular Resp. pattern (eventually depressed) d/t ↑ pressure on brainstem |
|
T/F Cushings Reflex often precedes herniation
|
True
|
|
T/F During autoregulatory failure CBF & vessel size are dependent upon CPP
|
True
|
|
AutoRegulation is impaired by
a) Traumatic Brain injury b) Tumor tissue c) high dose inhalation agents d) vasodilators |
Traumatic Brain injury
Tumor tissue high dose inhalation agents vasodilators |
|
T/F Vasogenic edema is a result of
impairment of BBB function & translocation of fluid |
True
|
|
Auto Regulation
a) determines cerebral blood flow b) occurs at MAP 50 -150 mmHg c) requires a normal ICP d) accomplished via compensatory changes in cerebral vascular resistance |
Determines cerebral blood flow
occurs at MAP 50 -150 mmHg requires a normal ICP accomplished via compensatory changes in cerebral vascular resistance |
|
Decreasing PaCO2
a) vasoconstriction b) decreased CBV c) increased CBV d) vasodilation |
vasoconstriction
decreased CBV |
|
When treating IC HTN
a) need to reduce cerebral blood flow b) promote venous outflow c) promote vasoconstriction d) Position with head above heart |
need to reduce cerebral blood flow
promote venous outflow (no inc. in CVP) promote vasoconstriction ( maintain CPP) Position with head above heart |
|
T/F Prolonged hyperventilation > 48 hrs causes a loss in CSF buffering capacity
|
True
|
|
Hypoxia
a) potent vasodilator b) potent vasoconstrictor c) has no effect on vessels |
potent vasodilator
|
|
Mannitol + Lasix
a) decrease CSF production b) decrease brain H2O content c) decrease blood viscosity d) promotes diuresis |
decrease CSF production
decrease brain H2O content decrease blood viscosity promotes diuresis |
|
Minimum CPP for tissue perfusion
a) 20 mmHg b) 50 mmHg c) 90 mmHg d) 100 mmHg |
50 mmHg
|
|
Formula for CPP
|
MAP - ICP = CPP
or MAP - CVP = CPP |
|
If CPP is too high what could result?
|
Cerebral Edema
|
|
Treatment of a herniation includes
a) hyperventilate b) mannitol (after dura open) c) 3% Na d) all of the above |
hyperventilate
mannitol (after dura open) 3% Na all of the above |
|
The brain compensates for increased ICP 1st by
a) CSF displacement b) Compression of intracranial blood volume |
CSF displacement
2nd is Compression of intracranial blood volume |
|
Changes in volume of one of the following parenchyma, blood, CSF will require compensatory changes in the volume in one or more of the other components to keep ICP constant
a) Mickey O'Rourke Hypothesis b) Monte Python Hypothesis c) Monro - Kellie Hypothesis d) Michael Landon Hypothesis |
Monro - Kellie Hypothesis
|
|
Vasogenic Edema caused by
a) trauma/ infection b) disruption in BBB c) Hydrocephalus d) abscess/tumor |
disruption in BBB
abscess/tumor there will be an inc. in ECF (IV & interstitial fluid) |
|
Cytotoxic Edema
a) trauma/ infection b) disruption in BBB c) Hydrocephalus d) abscess/tumor |
trauma/ infection
increased intracellular volume |
|
Which type of tumor is more dangerous
a) slow growing large tumor b) fast growing small tumor |
fast growing small tumor
b/c brain doesn't have time to adjust to the changes in pressure |
|
Cerebral Capacitance
a) stiffness of brain tissue b) rate that brain accommodates changes in intracranial volume c) brain can get only so big before it herniates |
rate that brain accommodates changes in intracranial volume
brain can get only so big before it herniates |
|
Cerebral Compliance
a) stiffness of brain tissue b) rate that brain accommodates changes in intracranial volume c) brain can get only so big before it herniates |
stiffness of brain tissue
How well brain responds to changes caused by tumor etc |
|
Treatment of a herniation includes
a) hyperventilate b) mannitol (after dura open) c) 3% Na d) all of the above |
hyperventilate
mannitol (after dura open) 3% Na all of the above |
|
The brain compensates for increased ICP 1st by
a) CSF displacement b) Compression of intracranial blood volume |
CSF displacement
2nd is Compression of intracranial blood volume |
|
Cytotoxic Edema
a) trauma/ infection b) disruption in BBB c) Hydrocephalus d) abscess/tumor |
trauma/ infection
increased intracellular volume |
|
Uncal herniation
a) upward pressure thru tentorium b) downward pressure thru tentorium c) displacement thru the foramen magnum d) brain protruding thru open skull |
downward pressure thru tentorium
|
|
Transcalvarial herniation
a) upward pressure thru tentorium b) downward pressure thru tentorium c) displacement thru the foramen magnum d) brain protruding thru open skull |
brain protruding thru open skull
|
|
Sublacine herniation
a) upward pressure thru tentorium b) downward pressure thru tentorium c) brain is pushed into other hemisphere d) brain protruding thru open skull |
brain is pushed into other hemisphere
|
|
The two infratentorial herniations are
a) Uncal b) "upward" c) tonsillar d) central |
upward
tonsillar |
|
Where is the Ventriculostomy places in the brain?
___________________ |
Frontal Horn in lateral ventricles near Foramen of Monro
|
|
T/F Lumbar Subarachnoid monitoring should not be done on pt with increased ICP
|
True, there is a risk of downward herniation
|
|
Movement of plasma components between peripheral IVF & ECF is based on
a) oncotic gradient b) osmolar gradient c) passively |
oncotic gradient
|
|
In the BBB movement of plasma components between IVF & ECF is based on
a) oncotic gradient b) osmolar gradient c) passively |
osmolar gradient
|
|
T/F Large amounts of iso-osmolar crystalloids will cause peripheral edema d/t dilution but not cause cerebral edema or inc. ICP
|
True
|
|
Examples of hyperosmolar fluids
a) Mannitol b) LR c) 3% Na d) 0.9% NS e) D5LR |
Mannitol
3% Na D5LR |
|
Examples of hypo-osmolar fluids include
a) Mannitol b) LR c) 3% Na d) 0.9% NS e) 0.45% NS |
LR
0.45% NS |
|
Example(s) of iso-osmolar fluids a) Mannitol
b) LR c) 3% Na d) 0.9% NS e) 0.45% NS |
0.9% NS
|
|
Hyperosmolar fluids
a) improve CO, dec periph vasc. resist b) osmotic shift of H2O from interstitial and intracellular spaces to intravasc. c) allow for rapid resuscitation with smaller volumes d) do not cause a fluid shift |
improve CO, dec periph vasc. resist
osmotic shift of H2O from interstitial and intracellular spaces to intravasc. allow for rapid resuscitation with smaller volumes |
|
T/F Na levels < 120 or > 170 can cause seizures & decreased LOC
|
True
with infusion of 3% Na or Mannitol need to look at serum Na levels before giving! |
|
Mannitol
a) hyperosmolar b) given just before dura open c) transient increase in ICP d) dec. brain volume for surgical exposure |
a) hyperosmolar
b) given just before dura open c) transient increase in ICP d) dec. brain volume for surgical exposure |
|
Hypercapnia, vasodilators, obstruction of venous outflow all _____________
|
cause Brain Swelling
|
|
Does Albumin contain clotting factors?
|
NO
|
|
T/F When given PRBC's it is important to only give them to keep Hct at a "safe" level
|
True keep about 30 promotes max O2 delivery to tissue
|
|
A Hct > 30
a) viscous blood b) decreased O2 delivery to tissue c) both of the above |
viscous blood
decreased O2 delivery to tissue a Hct < 25 will also dec. O2 delivery to tissue but because of dec. carrying ability |
|
Cerebral Aneurism
a) 60 - 80 % of all pts have vasospasm b) incidence of vasospasm occurs 4 - 10 days after rupture c) vasospasm can cause ischemia & infarction |
60 - 80 % of all pts have vasospasm
incidence of vasospasm occurs 4 - 10 days after rupture vasospasm can cause ischemia & infarction |
|
Diabetes Insipidus
a) Lack of ADH release b) increase ADH release c) hypernatremia d) hyponatremia |
Lack of ADH release
hypernatremia |
|
Diabetes Insipidus
a) treat with 0.9% NS b) treat with 0.45% NS c) treat with Vasopressin or DDAVP d) causes hypovolemia, HOTN e) causes increased plasma osmolarity |
treat with 0.45% NS
treat with Vasopressin or DDAVP causes hypovolemia, HOTN causes increased plasma osmolarity |
|
Ideal fluid to treat Trauma pt with head injury
a) Whole Blood b) Iso-tonic crystalloids c) hypertonic crystalloids |
Whole Blood (requires less volume)
BUT usually not available So next best choice is isotonic (9%NS) |
|
Glascow Coma Scale
a) easy b) reliable c) helps with diagnosis & therapy choices d) has prognostic value |
easy
reliable helps with diagnosis & therapy choices has prognostic value |
|
Your pt opens their eyes to speech, is inappropriate, localizes pain
Glascow coma score |
11
|
|
T/F Lateral cervical spine films detect 80% of cervical spine fx in adults
|
True
|
|
T/F 5% of all spinal cord injuries are Children, who are more prone to high cervical injuries, which will unfortunately be undetected on X-ray
|
True
|
|
When treating a pt with an acute head injury and HTN what drugs would be the best choice
a) Nipride b) Esmolol c) Labetolol d) all of the above |
Esmolol
Labetolol these drugs don't increase ICP like Nipride |
|
Treatment for elevated ICP d/t an acute head injury includes
a) increasing venous outflow b) hyperventilation c) hyperosmolar fluids d) iso-osmolar fluids e) Hypothermia |
increasing venous outflow (HOB 30 degrees, no neck flexion)
hyperventilation (brief periods) hyperosmolar fluids Hypothermia |
|
Airway management in acute head injury
a) sedation b) assume c-spine fx c) avoiding nasal intubation d) all of the above |
sedation (but only if intubated)
assume c-spine fx avoiding nasal intubation (Fiberoptic intubation is gold standard) |
|
Induction of acute head injury pt with HTN
a) RSI/with cricoid pressure b) defasiculate/Sux c) STP d) Etomidate e) Lidocaine |
RSI/with cricoid pressure
defasiculate/Sux STP Lidocaine (dec ICP, blunts DL) NO ETOMIDATE it decreases seizure threshold |
|
Induction of acute head injury pt with HOTN
a) RSI/with cricoid pressure b) defasiculate/Sux c) STP d) Etomidate e) Lidocaine |
RSI/with cricoid pressure
defasiculate/Sux STP Lidocaine (dec ICP, blunts DL) AVOID HYPNOTICS!! |
|
T/F with acute head injury the ANS is activated which will elev. BP, HR, CO and also cause ST changes in EKG which mimic cardiac ischemia
|
True
|
|
Preventing Hypoxemia in acute head injury pt
a) keep PaO2 > 60 b) Treat pulmonary conditions c) Consider PEEP 10 cm or less d) all of the above |
keep PaO2 > 60 (or SaO2 > 90)
Treat pulmonary conditions (r/t neurogenic pulm edema caused by SNS activation which increases pulm capillary permeability) Consider PEEP 10 cm or less |
|
Your pt has (1) dilated pupil it is probably caused by
a) contralateral Uncal herniation b) ipsilateral Uncal herniation |
ipsilateral Uncal herniation
|
|
HOTN in acute head injury
a) SBP < 90 mmHg b) long duration assoc. with poor outcome c) tx with vasopressors only d) tx with fluids/blood |
SBP < 90 mmHg
long duration assoc. with poor outcome tx with fluids/blood (vasopressors will not be used alone! treat with fluids 1st) |
|
T/F A decrease in SBP > 10mmHg with + pressure ventilation = 10% in blood volume
|
True This is a better indicator than CVP
|
|
T/F HTN in acute head injury impairs autoregulation
|
True
|
|
The best way to treat HTN in the acute head injury pt
a) Nipride b) Hydralazine c) Metoprolol d) Esmolol e) Labetolol |
Metoprolol
Esmolol Labetolol These drugs are NOT vasodilators so won't increase ICP like the others |
|
Do blood glucose levels match brain glucose levels in ischemia?
|
NO
|
|
Hyperventilation can cause
a) cerebral vasoconstriction b) cerebral vasodilation c) ischemia d) decreased CBF e) extracellular alkalosis |
cerebral vasoconstriction
ischemia decreased CBF extracellular alkalosis Hyperventilation should be avoided the first 24hrs |
|
The temperature that decreases CMRO2?
|
32- 33 degrees Celcius
|
|
T/F If you raise the HOB in a pt with acute head injury too high the MAP & CPP will decrease and cause ischemia
|
True
|
|
Hyperventilation can
a) lower systemic BP b) increase systemic BP c) leftward shift of oxyheme dissoc. curve d) inhibit hypoxic pulmonary vasoconstriction |
lowers systemic BP
leftward shift of oxyheme dissoc. curve inhibit hypoxic pulmonary vasoconstriction leading to bronchoconstriction |
|
Jugular desaturation is common after head injury, when would you be concerned
a) SJO2 < 90% b) SJO2 < 50% c) SJO2 < 80% d) SJO2 < 75% |
SJO2 < 50% PROFOUND DECREASE IN CBF LEADING TO ISCHEMIA
|
|
MOA of Mannitol
a) decrease brain H2O by increasing plasma osmolarity b) decreases ICP c) thru osmotic gradient created with INTACT BBB d) all of the above |
decrease brain H2O by increasing plasma osmolarity
decreases ICP thru osmotic gradient created with INTACT BBB The KEY is the INTACT BBB |
|
Barbiturates
a) decrease CMRO2 b) decrease CBF c) decrease CB Volume d) decrease ICP |
decrease CMRO2
decrease CBF decrease CB Volume decrease ICP |
|
T/F Barbiturates are the gold standard for sedating pts with refractory IC HTN
|
True
|
|
Describe the "triphasic hemodynamic response" to Mannitol
|
Transient HOTN (1-2 minutes after rapid infusion)
Increase in blood volume, CI, PCWP Transient increase in ICP 30 minutes later blood volume returns to normal AND PCWP & CI DROP BELOW NORMAL |
|
Burst suppression dose of Propofol
a) 50 mcg/kg/min b) 100 mcg/kg/min c) 150 mch/kg/min d) 200 mcg/kg/min |
200 mcg/kg/min
|
|
Propofol Infusion Syndrome signs
a) Acidosis b) Rhabdomylysis c) Renal faliure d) Fatty liver e) Cardiac Failure |
Acidosis
Rhabdomylysis Renal faliure Fatty liver Cardiac Failure |
|
Versed
a) decreases CMRO2 b) decreases CBF c) decreases CB Volume d) all of the above |
decreases CMRO2
decreases CBF decreases CB Volume |
|
You have given your acute head injury pt just a little too much Versed, why do you need to be cautious about giving Flumazenil?
|
Because Flumazenil increases ICP
|
|
An Extention Spinal Cord injury
a) Posterior column b) Anterior column c) r/t whiplash d) r/t diving accident |
Posterior column C5 - C7
r/t whiplash |
|
A Flexion Spinal Cord injury
a) Posterior column b) Anterior column c) r/t whiplash d) r/t diving accident |
Anterior column
r/t diving accident |
|
Anterior Column injury will have effect on which
a) motor b) sensory |
motor
|
|
Posterior Column injury will have effect on which
a) motor b) sensory |
sensory
|
|
Posterior Column injury will have effect on which
a) motor b) sensory |
sensory
|
|
Spinal Cord injury in CENTRAL cord
a) Ipsilateral paralysis, proprioception, touch, vibration & contralateral loss of pain & temperature b) Motor loss (arms>legs) bladder dysfunction c) Bilateral motor , pain & temperature loss d) Loss of touch & temperature |
Motor loss (arms>legs) bladder dysfunction
|
|
Brown-Sequard Spinal Cord injury
a) Ipsilateral paralysis, proprioception, touch, vibration & contralateral loss of pain & temperature b) Motor loss (arms>legs) bladder dysfunction c) Bilateral motor , pain & temperature loss d) Loss of touch & temperature |
Ipsilateral paralysis, proprioception, touch, vibration & contralateral loss of pain & temperature
|
|
ANTERIOR CORD SYNDROME
a) Ipsilateral paralysis, proprioception, touch, vibration and contralateral loss of pain and temperature b) Motor loss (arms>legs) bladder dysfunction c) Bilateral motor , pain and temperature loss d) Loss of touch and temperature |
Bilateral motor , pain and temperature loss
|
|
POSTERIOR CORD SYNDROME
a) Ipsilateral paralysis, proprioception, touch, vibration & contralateral loss of pain & temperature b) Motor loss (arms>legs) bladder dysfunction c) Bilateral motor, pain & temperature loss d) Loss of touch & temperature |
Loss of touch & temperature
|
|
Soft cervical collar / Philly cervical collar
decreases flexion, extension and rotation |
Philly cervical collar
|
|
In spinal cord injury Respiratory complications are the most common if injury is above C5 which muscles are effected
a) intercostal b) abdominal c) diaphragm |
diaphragm
|
|
In spinal cord injury Respiratory complications are the most common if injury is below C6 which muscles are effected
a) intercostal b) abdominal c) diaphragm |
intercostal
abdominal |
|
Spinal Shock happens in 4 phases, Phase I is
a) Lasts about 1 week, with some return of initial reflexes b) Flaccid paralysis, hyporeflexia c) Takes about 1 month, recurrence of initial hypereflexia d) Final hypereflexia |
Flaccid paralysis, hyporeflexia
HAPPENS IN 1ST 24 HRS |
|
Spinal Shock happens in 4 phases, Phase II is
a) Lasts about 1 week, with some return of initial reflexes b) Flaccid paralysis, hyporeflexia c) Takes about 1 month, recurrence of initial hypereflexia d) Final hypereflexia |
Lasts about 1 week, with some return of initial reflexes
|
|
Spinal Shock happens in 4 phases, Phase III is
a) Lasts about 1 week, with some return of initial reflexes b) Flaccid paralysis, hyporeflexia c) Takes about 1 month, recurrence of initial hypereflexia d) Final hypereflexia |
Takes about 1 month, recurrence of initial hypereflexia
|
|
Spinal Shock happens in 4 phases, Phase IV is
a) Lasts about 1 week, with some return of initial reflexes b) Flaccid paralysis, hyporeflexia c) Takes about 1 month, recurrence of initial hypereflexia d) Final hypereflexia |
Final hypereflexia
|
|
Neurogenic Shock happens during which phase of Spinal shock
a) Phase I b) Phase II c) Phase III d) Phase IV |
Phase I
|
|
Neurogenic Shock
a) peripheral vasodilation, HOTN b) loss of SNS tone c) increased venous capacitance d) venous pooling |
peripheral vasodilation, HOTN
loss of SNS tone increased venous capacitance venous pooling |
|
At what level do you lose cardioaccelerator fibers?
|
T2 - T5 (according to Diane, other's have told us T1 - T4)
|
|
In spinal cord injury loss of temperature control happens
a) above injury b) below injury |
below injury
If injury is above T6 pt will become POIKILOTHERMIC (take on temp of environment) |
|
Evoked Potential
a) response of nervous system to external event b) response of nervous system to internal event |
response of nervous system to external event
Visual, Auditory, Somatosensory |
|
When doing Somatosensory evoked potential why would you place a lead on the unaffected side?
|
To act as a control
|
|
T/F The more synapses a stimulus must pass thru the more anesthetic drugs will effect the response
|
True
|
|
When using upper extremities for Somatosensory evoked potentials where do you place the leads?
|
Median nerve
Erbs point (clavicle) |
|
When using lower extremities for Somatosensory evoked potentials where do you place the leads?
|
Post tibial nerve
Popliteal Fossa |
|
If patient had a tumor at T1 where would you place the leads?
|
on both upper and lower extremities
The risk for injury however is below the injury/tumor |
|
What effects Latency of SEP
a) pt height b) pt weight c) temp of extremity or cortex d) drugs (barbs, propofol) e) conduction velocity/ # of synapses f) presence of CNS dz |
pt height
temp of extremity or cortex drugs (barbs, propofol) conduction velocity/ # of synapses presence of CNS dz |
|
Operative variables that effect Latency of SEP
a) physiologic (temp) b) drugs c) pressure/retraction d) changes in CBF & CSF e) stretching of spine |
physiologic (temp)
drugs pressure/retraction changes in CBF & CSF stretching of spine |
|
SEP's are being done during your spinal surgery case, your pts blood pressure has just sky rocketed would you choose Nipride or Inhalation agent to help decrease the BP
|
Nipride, the gas will interfere with the SEP monitoring
|
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Normal CBF
a) 20 ml/100g/min b) 50 ml/100g/min c) 15 ml/100g/min d) 25 ml/100g/min |
50 ml/100g/min
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When CBF is 20 - 25 ml/100g/min
a) EEG is Isoelectric b) Evoked potentials are suppressed c) EEG slowing is noted d) Irreversible damage occurs e) Cell death with massive efflux K |
EEG slowing is noted
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When CBF is 15 - 20 ml/100g/min
a) EEG is Isoelectric b) Evoked potentials are suppressed c) EEG slowing is noted d) Irreversible damage occurs e) Cell death with massive efflux K |
EEG is Isoelectric
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When CBF is <15 ml/100g/min
a) EEG is Isoelectric b) Evoked potentials are suppressed c) EEG slowing is noted d) Irreversible damage occurs e) Cell death with massive efflux K |
Evoked potentials are suppressed
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When CBF is <10 ml/100g/min
a) EEG is Isoelectric b) Evoked potentials are suppressed c) EEG slowing is noted d) Irreversible damage occurs e) Cell death with massive efflux K |
Irreversible damage occurs
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When CBF is <6 ml/100g/min
a) EEG is Isoelectric b) Evoked potentials are suppressed c) EEG slowing is noted d) Irreversible damage occurs e) Cell death with massive efflux K |
Cell death with massive efflux K
metabolic cascade |
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Which of the following areas is most susceptible to effects of anesthesia when doing evoked potentials
a) peripheral nerves b) subcortical area c) lumbar spine d) sensory cortex |
sensory cortex
the other areas are somewhat resistant |
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T/F Opioids cause major depression of all responses during evoked potentials
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False they cause only a mild depression and in fact are quite often used during recording of cortical sensory responses and motor evoked potentials
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