Neuro Flashcards
(113 cards)
1
Q
Glutamate neurotransmitter target are?
A
AMPA, kainate, NMDA
It is an excitatory neurotransmitter leads to membrane depolarization
2
Q
Which brain processes has the greatest amount of energy consumption thus more O2 consumption
A
Neuronal electrical activity
So drugs that decrease neuronal activity will decrease O2 delivery (blood flow) e.g barbiturates, propofol, etomidate
3
Q
The arterial BP in relation to CBF in a chronic hypertensive patients, the plot will shift to …. and the clinical relevance of this is to avoid …
A
Right
Global ischemic stroke following GA (with low MAPs)
So in chronic HTN, their baseline MAPs are higher than normal ptn
4
Q
Volatile effect on CBF
A
It increases it (iso> des > sevo) by direct cerebral arterial vasodilation, the relationship btw MAP and CBF become linear
Because it increases CBF it will increase ICP (des > iso > sevo)
5
Q
Methods to decrease CBF?
A
- IV anesthetic
- Decrease CMRO2 (prop, thiopental)
- Hyperventilating
- Avoid cerebral vasodilation and extreme HTN
6
Q
Methods to decrease CBF by increasing venous outflow
A
Elevate head
Avoid construction of the neck
Avoid PEEP and excessive airway pressure
7
Q
Methods to decrease CBF by reduction in CSF
A
- External ventricular drain.
- Lumber drain.
- Head elevation
- Acetazolamide
8
Q
Methods to decrease CBF by reduction of cerebral edema?
A
- Osmotic therapy (mannitol, hypertonic saline).
- Furosemide.
- Dexamethasone (vasogenic edema)
9
Q
Methods to decrease ICP?
A
1) decreasing Cerebral blood volume (decreasing CBF, increasing venous outflow)
2) Decreasing CSF
3) Reducing cerebral edema
4) Resection of space-occupying lesions
5) Decompression craiectomy.
10
Q
Whats the normal CBF?
A
50 mL/ 100g/min = 12-15% of CO
11
Q
Factors regulates CBF?
A
- CMRO2 via nerovascular coupling
- CPP via autoregulation
- PaCO2 & PaO2 via cerebrovascular reactivity.
- SNS
- CO
- Some anesthetics.
12
Q
What is neurovascular coupling?
A
defined a proportional change in CBF to change in CMRO2 (increase/decrease in CMRO2 results in increase/decrease in CBF).
13
Q
2 common causes decreasing CMRO2 and therefore decrease CBF?
A
Hypothermia (7% CBF for every 1 C below 37C)
IV anesthestics.
14
Q
CMRO2 increased by …
A
seizure activity
15
Q
CPP = … - …
A
MAP - ICP
16
Q
What is the cerebral auto regulation?
A
is the CPP range btw upper and lower limits where CBF remains stable (~ 50mL/100g/min)
17
Q
Conditions impairs cerebral autoregulation, and therefore resulting in a liner change between CPP and CBF
A
TBI, intracranial surgery, sever hypercapnia, inhaled anesthetics. ( so any changes in CPP will change the CBF due to the loss of autoregulation).
18
Q
relation between PaCO2 & CBF
A
directional change (increase/decrease in PaCO2 will increase/decrease CBF)
a change of 1 mmHg of PaCO2 from 40 mmHg will change 1 mL/100g/min in CBF
19
Q
How long the PaCO2-related changes in CBF lasts?
A
until the compensatory change in HCO3 concentration occur ~ 6-8 hours
20
Q
Relation between PaO2 & CBF
A
inversely related (decrease in PaO2 less than threshold ~50 mmHg, result in increase CBF).
21
Q
Effect of propofol and thiopental on CBF? and ICP?
A
decreases CMRO2 -> CBF via coupling effect.
decreases ICP
22
Q
Why ketamine is avoided in patients with known intracranial disease?
A
because of its controversial effect (it increases PaCO2, CBF, & ICP if used solely, but it has no effect if used with other sedatives).
23
Q
Effect of opoids and BZDs on CBF? ICP?
A
it decreases CMRO2 and CBF therefore decrease ICP. however the depression in respiration drive leads to increase in PaCO2 which may produce the opposite effect.
24
Q
why opiods should be carefully administered in patients with intracranial disease?
A
it depresses consciousness, causes miosis, and the depression effect on respiratory drive causes increase PaCO2 which leads to increase ICP.
25
Effect of alpha agonist on CBF?
decreases arterial pressure -> decrease CPP & CBF with minimal effect on ICP
26
Effect of volitle on CBF at > 0.5 MAC? and ICP?
potent cerebral vasodilation and increase CBF & ICP even though they decrease CMRO2 (except N2O, it increases CBF & CMRO2 but often attenuated by co-administration of other anesthetics).
27
What defines ICP? and effect?
a sustained increase of >15 mmHg in cerebral pressure leading to decrease in CPP and CBF therefore resulting in cerebral ischemia.
28
What IV anesthetic causes Increases EEG frequency and therefore it is avoided in patients with seizures?
Etomidate. to prevent increase in ICP.
29
Can NMBs increases ICP?
it has no effect, but if they induce histamine release and hypotention then cerebral vasodilation occur which increases CBF and ICP (Succinlycholine increases ICP through increasing CBF for unknown mechanism).
30
Where do you place the A-line transducer to reflect CPP?
Tragus level
31
At what volume of CBF ischemia is detectable by EEG?
15 mL/100g/min
32
DI vs SIADH vs cerebral salt wasting after brain injury in terms of plasma Na?
DI: High serum Na
SIADH: low
CSW: low
33
Parasympathetic effect ?
SLUDD
Salivation
Lacrimation
Urination
Digestion, Defecation
34
Only opioid increases CBF?
Sufentanil
35
BBB prevents passing off ....
Glucose, electrolytes, mannitol, dextrose, amino acids, protein.
Allows lipid soluble, volatiles, water, CO2 and O2
36
2 medications decreases CSF production
Acetozolmide and furosemide
37
Only opioid increases CBF?
Sufentanil
38
BBB prevents passing off ....
Glucose, electrolytes, mannitol, dextrose, amino acids, protein.
Allows lipid soluble, volatiles, water, CO2 and O2
39
2 medications decreases CSF production
Acetozolmide and furosemide
40
Contralateral upper limb paralysis or sensory loss
- /+ aphasia (if dominant hemisphere)
- /+ hemineglect (if non-dominant hemisphere)
MCA lesion
Contralateral sensory/motor upper limbs or face
Temporal lobe- wernicke’s
Frontal lobe-Brock
41
Contralateral lower limb sensory loss or paralysis
ACA
42
Contralateral hemianopia with macular sparing a symptom of which lesion ? And what vessel effected?
Occipital or visual cortex
Supplied by PCA
43
Symptoms of lesion in;
Lateral medulla-vestibular nuclei
Lateral SPinothelamic
spinal trigeminal nucleus
Nucleus ambiguous
Sympathetic fibers
Inf cerebellar peduncle
Vomiting vertigo nystagmus
Ipsilateral face pain and sensation loss
Contralateral body pain and sensation loss
Dysphagia and horeseness, decrease gag reflex
Ipsilateral horner’s
Ataxia, dysmetria
These are supplied by PICA
44
Decreased lacrimation, salivation, taste, corneal reflex, and hearing
Differentiates a lesion supplied by ... from PICA
AICA
45
Lesion supplied by .... will manifest as lock in syndrome, quadriplegic and loss of facial,mouth and tongue movements (with preservation of consciousness and blinking)
Basilar artery
46
Therapies that can be performed in the operating room to decrease ICP, and therefore improve CPP, include:
controlled mechanical ventilation to decrease the PCO2, diuretics, head up positioning, draining of CSF, administration of neuromuscular blockade under general anesthesia, IV anesthetics to reduce cerebral metabolic rate for O2, and maintenance of MAP.
47
Cerebral perfusion pressure (CPP) is dependent on ... and ....
mean arterial pressure (MAP) and ICP.
48
The theories behind postop cognitive dysfunction?
Anesthesia ass. Central cholinergic insufficiency vs beta-amyloid phosphorylation (like Alzheimer’s)
49
Process of Nor and Epi synthesis
Tyrosine-> dopa -> dopamine-> NorEpi-> Epi
50
What DOC for Parkinson’s patient if po levodopa cannot be given?
Apomorphine SQ
51
Anesthetic consideration in Parkinson’s dis ptn?
- Patients meds should be administered on morning surgery.
- Avoid dopamine antagonist (phenothiazines, droperidol, metoclopramide)
- dystonic rxn can occur with rapid administration of fentanyl or alfentanil.
- dyskinesia May occur upon induction and emergence with propofol.
- they are at risk for NMS from dopamine agonists.
- autonomic dysfunctions is common( orthstatic hypotension May aggregated by vasodilation effect of anti-Parkinson’s meds and volatile)
- salivation & esophagus dysfunctions common -> aspiration risk.
52
Anesthetic considerations of Huntington dis ptn?
- dysfunctional of pharyngeal muscles common -> aspiration risk.
- anticipation of delayed emergence and postop respiratory complications.
- short NMB preferred although they might have decreased plasma cholinesterase activity which may prolong succ.
- consider spinal.
53
MUSCARINIC stimulations effect mnemonics?
SLUDGE-Mi
```
Salivation
Lacrimation
Urination
Defection
Gastrointestinal upset
Emesis
Miosis
```
54
Radioactive xenon and jugular venous O2 tension assess for?
Indirectly CBF, CMRO2 and O2 delivery to brain
55
SPinothelamic tract transmits ?
Pain and Temp
56
Dorsal column transmits ?
Touch and proprioception
57
Factors increases latency of SSEP?
- Hypooo carbia
- Volatiles
- Etomidate and ketamine (increases amplitude not latency)
- Hypotension (MAP <40)
- Anemia
- Extreme temp
58
```
SSEP somatosensory evoked potential
EEG
VEP visual evoked potential
AEP auditory evoked potential
MEP motor evoked potential
```
- assess ascending signals (dorsal SC and cerebral cortex)
- EEG and VEP asses cerebral cortex
- AEP and brainstorm SSEP assess brain stem
- MEP asses descending signals and ventral spinal cord
59
Sustained Increase in ICP above ... defines intracranial hypertension
15 mmHg
60
Triad of cerebral salt wasting?
Hypo Na
Volume contraction
High urine Na
It usually seen in ptn’s with SAH.
61
CPP calculation?
MAP-ICP (or CVP)
MAP = SBP+(double DBP)/3
62
The afferent input of SSEP is carried through ....
Dorsal columns in SC
It assess the integrity of the peripheral nerve (post tibial nerve, dorsal columns, brain stem, medial lemniscus, internal capsule, and contralateral somatosensory cortex)
63
What % change in CBF for each mmHg increase in PaCO2?
2%
64
Robin Hood phenomena is ...
Blood flow directed from normal region of the brain to an ischemic region (luxury perfusion)
65
What’s the PaCO2 range for induced hyperventilation ?
25-30 mmHg
Within this range, reduction of ICP is maximal and risk of cerebral ischemia is minimal.
Excessive hyperventilating can cause reap alkalosis which can cause hypoK- induced cardiac arrhythmia
66
Why D5W is CI in neurosurgery patients?
1) it causes brain edema (glucose can cross BBB and metabolized rapidly leaving only free water)
2) increases the severity of neurological damage in cerebral ischemia patients ( due increased lactate production during anaerobic glycolysis during ischemia period).
67
How much CBF change for PaCO2 of 35 to 45 mmHg?
10 mL/100g/min
For every 1 mmHg increase, a 1 mL/100g/min (2%) increases in CBF
68
The change in CBF due to change in CO2 wanes after 6-10 hours because...
The extra cellular fluid pH is gradually normalized by reabsotption of HCO3 and excretion of H by the kidney
69
In autonomic hyperreflexia, the afferent sympathetic activity below the cord transection initiates impulses that are transmitted to SC at the same level which elicits reflex sympathetic activity over the splanchnic nerves. (Because modulation of this reflex sympathetic from higher centers in CNS is lost, the baroreceptors will respond by ...
Bradycardia due to the Intense generalized vasoconstriction and hypertension
70
Thx oh autonomic hyperreflexia?
Stop the stimulation
Direct acting vasodilation (nitroprusside/nitroglycerin)
Alpha antagonist (phentolamine)
Ganglionic blocking (trimethaphan)
71
Autonomic hyperreflexia should not be treated with propranolol or Beta antagonist for 2 reasons
Bradycardia can be potentiated by beta1 blockade
Paradoxical HTN and possible CHF by blocking Beta2 which leaves alpha receptors unopposed
72
Normal CMRO2 per min
3-5 mL/100g of brain tissue/min
The delivery of O2 is ~50 mL blood/100g brain tissue/min
73
Definition of ICP?
Normal ICP is 5-15 mmHg and it reflects the relationship b/ether rigid cranial vault and its content (brain, blood, and CSF).
Intracranial HTN; sustained ICP of 15-20 mmHg
74
Definition of Cerebral compliance
When intracranial volume increases such as with space occupying lesion, one of the other brain components (either CSF, blood, or brain) is displaced with ICP remains relatively normal.
This compliance eventually disrupted if intracranial volume increased leading to increase ICP and result into brainstem herniation
75
Definition of cerebral auto regulation?
Maintenance of constant CBF over a wide range of MAP
76
Definition of CPP?
The net pressure gradient b/w the force facilitating CBF (MAP) and the force impeding flow (ICP)
Normally 70-90 mmHg
77
Mgmt of elevated ICP?
- reduction of CBF by ...
- reduction in brain tissue volume ...
- decrease CSF ....
- hyperventilating, head elevation, avoidance intrathoracic pressure
- diuretic, steroids, mannitol, furosemide (reduces both edema and CSF)
- drain placement
78
Mnemonic for CBF regulators factors
Mr. PC Only Seems To Care About Everything
```
MR: CMRO2
P: Pressure CPP
C: CO2
O: O2
S: SNS
T: Temp
C: CO
A: Anesthetic
E: epilepsy
```
79
Which crani done awake?
If the pathology involves an eloquent area (wernkies or Broca)
80
Carotid bruits are associated with underlying ..... disease.
Bilateral Carotid bruits characteristic of ....
The bruit dose or dose not always correlates with amount of stenosis.
CAD
Aortic stenosis
Dose not
81
Latex allergies occur most often in children with ...
```
Myelomeningocele
Spina binfida
GU disease
Indwelling tubes
Multiple surgeries as a child.
```
82
Spinal or Epidural is a choice in MS patients?
Epidural
Spinal more likely to exacerbate MS flares and disease.
83
Spinal/epidural contraindicated in GBS patients?
Both
84
4 big concerns in Myotonic dystrophy?
1) contractions
2) sensitivity to anesthetic
3) aspiration risk
4) increased risk of MH.
3 things to avoid in contractions; succinylcholine, reversal anticholinestrase as is cause a sustained contractures and avoid hypothermia as leads to shivering and then contractures
85
ASA syndrome, there’s loss of ...
Motor, Temp, and pain
Because ASA supplies anterior 2/3 of SC contains CS (motor) and SpT (pain and Temp). In addition bladder and sexual dysfunction occur depends on level of lesion
Proprioception and vibrations preserved
86
An absolute CI for ECT
Intracranial HTN, aneurysm, and mass
87
So cervical nerve roots passes (Above) their respective vertebral pedicle and thoracic, and lumber/sacral nerve roots passes (Below) their respective vertebrae.
There is one cervical nerve root that is the opposite (passes below )
C8 it passes below the c7 vertebral pedicle
88
ICP maintained within normal range <15 mm Hg during intracranial HTN due to 3 compensatory mechanisms? but when these compensatory mechanism exhausted, small increase in ICV result into large change in ICP
1) Translucation of CSF from intracranial -> spinal sunarachinoid space.
2) translucation of intracranial blood through venous mainly to systemic circulation.
3) reabsorption of CSF across arachnoid villi into dura venous sinus into systemic circulation.
89
Most sensitive neuromonitering to volatile
VEP (visual) > SSEP > BAEP (brainstem auditory)
90
Most resistant neuromonitering to volatile
BAEP (brainstem auditory)
91
What is the most sensative test to detect intracardiac air?
TEE. precordial doppler can detect up > 0.25 mL of air where TEE detect even smaller volume.
92
The most sensitive to PaCO2 responsiveness in terms of blood flow regulation?
Cerebrum > cerebellum > spinal cord
93
In placing multiorificed right atrial catheter (in siting position surgery to prevent air-embolism traveling), where would you want the tip to be? and how would you confirm its position?
Air has tendency to localize at the junction of the SVC and RA (this is the targeted spot)
by intravascular ECG (position confirmed when a large negative P complex is obtained). Also TEE can confirm it.
94
Critical CBF (below the level, EEG will show evidence of ischemia) for each gas:
Sevo, Iso, Des
Enflurane
Halothane
Sevo, Iso, Des 10 mL/100g/min
Enflurane 15 mL/100g/min
Halothane 20 mL/100g/min
95
What effect of cerebral ischemia on CBF autoregulation?
abolishes and become passively dependent on cerebral perfusion.
96
The most rapid maneuver for loweing ICP in interacranial mass?
Hyperventilation.
97
patient conditions contraindicated for sitting position?
Ventriculoarterial shunt
R-L intracardial shunt
platpnea-orthodeoxia
98
How long patient should wait for elective surgery after experience CVA to prevent a second vascular accident
Time needed for the changes occurred to loss of vasomotor responses to changes in PaCO2 and arterial BP in the area of ischemia to return back to normal or stabilized. Also the disrupted BBB takes at least 4 weeks preferably 6 weeks.
99
SSEP assess peripheral nerve (usually tibial/median), up to ..., ..., ..., ..., and ends to COntralateral sematosensory cortex.
dorsal column, brain stem, medial lemniscus, internal capsule and ends contralaterally somatosensory cortex
(No SpT or corticospinal)
100
How much decrease of CBF for each decrease in PaCO2
1 to 1 (30 mmHg of PaCO2 is a decrease of 10 from normal 40 mmHg, therefore CBF ~40mL/100g/min)
101
What effect of gas on SSEP? N2O?
Volatile and barbiturates decrease amplitude and increase latency.
N2O only decreases amplitude.
102
Dose Etomidate effect SSEP?
Yes, increases both amplitude and latency
103
Will the volatile and IV anesthetics effect MEPs?
yes they increase the latency of MEP response. (fentanyl is an exception).
104
What ketamine effect on CBF?
It increases it by vasodilation and increase CMRO2. no effect on CO2 response and autoregulation.
105
What effect of N2O, barbiturate, fentanyl on autoregulaiton?
None.
106
Effect of volatile on CMRO2?
Decreases it, however it increases CBF. uncoupling effect
107
Spinal cord injury above T4-T6 produces ...
- spinal shock acutely (decrease systemic aeteriolar and venois vasomotor tone and abolishes vaspressor reflexes causing hypotension)
- hypothermia as unable to vasoconstriction BV in cool environment and loss of thermoregulation (because hypothalamic center unable to communicate with peripheral sympethetic pathway).
- Neurogenic pulm edema.
after spinal shock resolve within 6 weeks, autonomic hyperreflexia develops.
108
What induction agents are good choice in carotid artery disease with TIA patient?
Thiopental, midazolam, propofol, or etomidate.
for maintenance; Iso/sevo/des in conjunction with N2O, opoids (theses gases reduced the critical CBF amount which may provide cerebral protection).
109
Would you induce hyperventilation to get the inverse steal phenomenon/robin hood effect in TIA patients?
so therotically yes (by decreasing PaCO2, the normal tissue CBF will constrict and the ischemic tissue keeps dilated as its already lost its autoregulation and therefore gets the most CBF), but not recommended as this effect is unpredictable. so best to keep normal atrial BP and PaCO2.
110
The triple H treatment for cerebral vasospasm?
Hypervolemia, Hypertension, and hemodilution.
111
```
the following medicaitons are treatment for;
Demeclocycline
Tolvaptan
DDAVp
chlorpropamide
```
Demeclocycline -> interfers with ADH at kidney level (SIADH)
Tolvaptan -> Vasopressin antagonist (SIADH)
DDAVP -> (DI)
chlorpropamide -> (incomplete DI)
112
When hypertonic is the treatment for SIADH?
sever hypoNa (<120)
500 mL 5% saline over several hours.
if not sever fluid restriction first
113
EEG waves
BAT Dead
Beta > Alpha > Theta > Delta (deep sleep)
