Neuro I Flashcards
1
Q
anterior spinal artery, # of posterior spinal artery
A
1, 2
2
Q
SSEPs look at ___ spinal bf, MEPs look at ___ spinal bf
A
Posterior, anterior
3
Q
What two things can obstruct venous outflow from brain
A
Positioning and PP vent w high PIP
4
Q
Components of brain vol and %: brain (___ and __, %, ml), blood (%, ml), csf (%, ml)
A
Cellular and icf 80%/1400 ml, 12%/150 ml, 8%/150 ml
5
Q
What is intracranial elastance
A
Change in ICP after a change in intracranial volume
6
Q
What 4 things are compensatory mechanisms for intracranial elastance
A
- Displacement CSF from cranial to spinal compartment 2. Inc CSF absorption 3. Dec csf production 4. Dec CBV (primarily venous)
7
Q
A waves= ___ waves. ICP= ___. What they signify
A
Plateau. >50. Compensation exhausted, intense vasodilation and severe ischemia
8
Q
B waves: __-__. What they show
A
30-40 ICP. CCP at lower limit of autoregulation
9
Q
C waves: ICP ___. What they mean
A
Normal. Nothing.
10
Q
CPP= how to calculate, normal value
A
MAP - ICP (or CVP if greater). 80-100
11
Q
Normal adult cerebral blood flow
A
50 ml/100g/min= 750 ml/min
12
Q
What gray and white matter each contribute to cerebral blood flow
A
Gray: 80ml/100g/min. White: 20. 50= an avg of the two
13
Q
What 7 things impact CBF during anesthesia
A
Anesthetic agents (all dilate except for ketamine), level of arousal, metabolic byproducts, blood viscosity, temp, concentration of co2 and h ions, 02
14
Q
H ions cause a ___ of cerebral vessels.
A
Vasodilation
15
Q
Acidic metabolic substances that increase CBF (2)
A
Lactic acid, pyruvic acid
16
Q
Each 1 mmhg change in paco2 between __-__ mmHG changes CBF by how much __-__ml/100g/min
A
20-80. 1-2.
17
Q
Below __mmhg paco2 what happens to cerebral blood vessels
A
Reflexive dilation in response to tissue hypoxia
18
Q
CBF response to paco2 lasts __-__ __ then will return tp normal despite altered co2 levels. Why.
A
6-8 hours. Bicarb transport.
19
Q
Brain: ___% total body mass, __% of body metabolism and cardiac output
A
- 15.
20
Q
CMRO2: ___ml/100g/min= ____ml/min 02
A
3.5= 50
21
Q
Pediatric patients have ___ cmro2: ___ ml/100g/min mean age __ years
A
Higher, 5.2, 6 years old
22
Q
What % cerebral metabolic rate is at in suppression. What is the only thing that can decrease the eeg below suppression into the basal homeostasis range
A
60%. Temperature (59-40%)
23
Q
Brain not capable of much ___ metabolism. Brain = ___% of total body glucose consumption. ___mg/100g/min= brain glucose consump
A
Anaerobic. 25%. 5
24
Q
02 utilization of brain remains within ___ ___. = ____ml02/100g brain tissue
A
Narrow range. 3.5
25
CBF increases dramatically if either of which 2 things drop.
If po2 of brain tissue drops below 30 mmhg or if pa02 drops below 50-60 mmhg
26
Brain response to increased 02 >___mmhg, why important
350= slight vasoconstriction, what we dont want to run 02 levels too high
27
CBF auto regulation between map: __-__
70-150 mmhg
28
Cerebral vasculature adjusts to changes in CPP/map after how long
1-3 minutes
29
Htn will shift auto regulatory range to __ minimum values and maximums of __-__
Higher, 180-200
30
What happens above the upper limit of auto regulation (3), what happens below the upper limit (1)
Above: bbb disruption, cerebral edema, cerebral hemorrhage. Below: ischemia
31
Cerebral circ has ___ sns innervention. Nerve transaction or mild-mod stim causes what kind of change and why
Strong sns. Neither causes much change due to auto regulation
32
SNS: may shift auto reg curve to ___. Sns minor role unless which two things occur
Right. Extreme bp rise (to prevent stroke) or hemorrhagic shock
33
CBF changes __-__% per 1 degree c change
6-7
34
Effect of hypothermia and hyperthermia on CBF and cmro2
Hypothermia decreases both, hyperthermia increases both
35
Decrease in hct will increase ___ but decrease __ __ __ of blood
CBF, 02 carrying capacity
36
Severe polycythemia can reduce ___. May intervene when hct __%. Hct __-__ probably no significant change in __
CBF. 55%. 33-45% in CBF
37
Cerebral ischemia secondary injury: __ and __. Elevated ICP secondary injury: __, __, and ___.
Ischemia: hypoxia and hypotension. Elev ICP: cerebral edema, hemorrhage, herniation
38
Ischemia cascade: what inc intracellular and extracellular from atp dependent pump failure. Neurons do what. ___ released, more __ enters. ___ feedback cascade.
Intracellular: ca + na increase, extracellular: k decreases. Neurons depolarize excessively. Glutamate —> more ca enter. Positive.
39
Ischemia damage: high ca levels inc damage via __ and __ leading to what 2 things. __ and __ build up, ph __.
Proteases and phospholipases —->> free fatty acids and free radicals. Lactate and hydrogen. Drops.
40
Ischemia patho: __ acid is produced and converted to __ (intense __), ___, and ___ (___)
Arachidonic. Thromboxane (vasoconstriction), prostaglandins, leukotrienes (edema)
41
3 regions of focal ischemia
No blood flow/global ischemia, penumbra (collateral bf/partial ischemia), normal perfusion
42
Penumbra- marginal bf roughly
<15 ml/100g/min
43
What happens in: transtentorial herniation
Medial temporal lobe compressed against tentorium cerebelli. Posterior cerebral artery- visual changes
44
What happens in: subfalcine herniation
Asymmetric expansion of cerebral hemisphere, displaces cingulate gyrus under the falx cerebri (midline shift where ant cerebral artery is)
45
What happens in: tonsillar herniation
Cerebrallar tonsils through foramen magnum (can be life threatening, where cardiac and resp centers are)
46
What happens in: transcalvarial hernation
Through a skull defect
47
Subarachnoid space enclosing brain and SC capacity ___ ml
1650
48
Csf formed by what at what rate
Choroid plexuses, 0.3 ml/min, 21 ml/hr, turnover 3-4x/day
49
Csf reabsorbed by what. Act like __ way valves. Fluid flows when csf pressure ___ > than __ pressure
Arachnoid villi. One. 1.5 mmhg > venous
50
Csf flow: 1st: from __ ventricles passes through what. 2nd: to __ ventricle and down what. 3rd: to __ ventricle to what openings. Ends with what area, continuous with what
1st: lateral, intraventricular foramina/of Munro. 2nd: third, aqueduct of Sylvius. 3rd: fourth. 2 lateral foramina of luschka and a midline foramen of magendie. Last: cisterna magna, continuous w subarachnoid space
51
Csf production decreased by which drugs: 5, which clinically relevant (*)
Carbonic anhydrase inhib (acetazolamide)*, lasix*, corticosteroids, spironolactone, vasoconstrictors
52
Anesthetic agent impact on csf secretion: inc by 2, dec by 2, no change w 2
Inc: des and enflurane (bad). Dec: halothane, etomidate (good). Same: iso, fentanyl
53
Anesthetic agent impact on csf absorption: dec by 2, no change w 1, inc by 3
Dec: halothane and enflurane (bad). Same: des. Inc: isoflurane, fentanyl, etomidate
54
Composition of what can cross bbb (3)
Small, lipid soluble, nonpolar
55
BBB in all of brain parenchyma except for 3 areas
Hypothalamus, pituitary, area postrema
56
Movement across bbb depends on 4
Size, charge, lipid solubility, and protein binding in blood
57
Permeable in bbb: 6
H20, c20, 02, lipid sol subs. Anesthetics and etoh
58
Semi permeable in bbb: 5
Na, cl, k, ca, mg
59
Impermeable across bbb: 4
Polar molecule, plasma proteins, glucose (only facilitated diffusion), non lipid sol large organic molec (mannitol)
60
How anesthetics may be impacted by bbb
Anesthetics may produce conditions that lead to a breech in bbb or they may have diff effect on a brain with a disrupted bbb
61
Disruptions that lead to a breach in bbb: 10
Severe htn, tumors, CHI, stroke, infection, marked hypercapnia, hypoxia, prolonged seizures, osmotic shock, irradiation
62
Bbb disruption: movement dependent on __ rather than __ pressure
Hydrostatic > osmotic
63
Cerebral edema, when each occur: cytotoxic, vasogenic, interstitial
Cyt (ionic pumps failure in ischemia), vaso (reduced bbb integrity), interst (hydrocephalus or acute hyponatremia)
64
Volatile anesthetics lead to dose dependent impairment of what. Which impairs it the least.
Auto regulation. Sevo
65
Effect on CBF: vascular smooth muscle dilation, decreased cmr
Increase, decrease
66
Luxury perfusion changes: 0.5 mac, 1 mac, >1 mac
1/2: reduction predominate/dec CBF. 1: cmr and vasodilation in balance, no CBF change. >1: vasodilation, inc CBF
67
Cmr reduction least to most of volatile anesthetics
Halothane < enflurane < des < iso < sevo
68
Sevo iso and des max eeg reduction at __-__ mac= max __ reduction too
1.5-2 mac. Cmr
69
Vasodilation potency of volatiles
Halothane >> enflurane > iso = des > sevo
70
How much iso and halothane inc CBF in %
Iso 20% halothane 200%
71
__ and __ (volatiles) may decrease CBF in some areas of brain
Des and sevo
72
Left shift on autoregulation curve leads to what
Less protection with hypertension
73
Hyperventilation can blunt inc CBF/ICP with __ and __ (both volatiles) if initiated prior to start of VA
Enflurane, halothane
74
Hyperventilation can blunt the inc CBF/ICP with __ or __ (volatiles) even if initiated after the va is started. However this effect is abolished when what
Sevo, iso. >1.5 Mac
75
At __-__ mac ___ can precipitate seizure pattern on eeg. Enhanced by __ and __ stim
1.5-2. Enflurane. Hypocapnia and auditory stim
76
__ has been rarely assoc w seizures. But may avoid in pts with __
Sevo, epilepsy
77
___ can promote spike activity, does not progress to __. Has been used in what situation
Iso. Seizure. Status epilepticus
78
Nitrous oxide alone: greatest effect on ___. Cerebral ___ occurs. __ and __ increase.
CBF. Dilation. CMR and ICP increase
79
Nitrous oxide + VA: __ effect is intermediate. Nitrous + IV agent leads to what effects
CBF. IV: min effect on CBF/cmr/ICP
80
Nitrous oxide: risk with __ or __
VAE, pneumocephalus
81
Barbiturate effects (6)
Hypnosis, depress cmr (30% induc dose), reduce CBF (30% induc dose but inc cerebral vasc res?), anticonvulsant activity, reverse steal, help csf absorption
82
The only barb that increases seizure activity
Methohexital
83
Opioids: ___ in CBF, cmr, and ICP unless pt is __ then __
Decrease. Awake. Larger effect
84
Opioids indirectly may inc ICP how (5)
Resp Dep, histamine release, activate sz in temp lobe in epilepsy pts, chest wall rigidity, reflex cerebral vasodilation after sudden bp drop
85
Specific opioid/effect: histamine rel (__), activate sz in epilepsy pt (__), reflex cerebral vasodilation from sudden bp drop (__ and __)
Histamine- morphine. Sz- alfentanil. BP drop: sufentanil and alfentanil
86
Small doses remi can cause mild inc in __, large doses cause what
CBF, decrease CBF
87
Etomidate effects: 5
Dec: CBF, cmr, ICP. Dec csf production/enhances absorption. Maintained c02 responsiveness
88
Etomidate: when its bad. Caution in which pts/why
Inc tissue hypoxia/acidosis—- bad in ischemic events. Caution in epileptic pts, can look like sz or activate sz
89
Propofol: dec in 3. Beneficial effects 3. ___ is a concern with cardio depression.
Dec in ICP, CBF, cmr. Beneficial: anticonvulsant, short e 1/2 allows post op assessment, reduces ischemic cerebral activity. CPP
90
Benzos: dec __ and __, comparison to barbs/etomidate/prop/opioids
CBF and cmr. Less than barbs/benzos/prop. More than opioids
91
Benzos: __ __ maintained. __ is best choice. Risk of using flumazenil
CO2 responsiveness. Midaz. Dramatically inc ICP
92
Ketamine: how its unique compared to anesthetics. No effect on __. Can cause ___.
Dilates vasculature- inc CBF. No change cmr. Seizure activity
93
Ketamine: dec __ __, overall inc __ but might be ok if
Csf absorption. ICP, if used w other agents like prop
94
Adrenergic agents: if auto reg intact fx. If not intact fx.
If intact pressors inc CBF only when map outside of autoreg. If not intact CBF varies w pressure
95
Alpha 1 agent fx
Little influence on CBF beyond inc CPP
96
Beta agonist effects
Inc cmr and CBF w b1 stim, esp if bbb disruption
97
Beta antagonist effects
No effect on cmr/CBF
98
Alpha 2 agonist effects
Decrease CBF and cmr in parallel. Precedex dec CBF by 30%
99
Vasodilator effects: 4
Cerebral vasodilation and inc CBF. CPP same or inc, ICP same or inc
100
NMB: no __ __, only __ __ can be problematic
Direct actions. Side effects
101
NMB: histamine releasing ones (4) what they can lead to
Atra, miva, sux, d tubo. Vasodilation, inc ICP, dec CPP from hypotension
102
NMB: sux can do what, not contraindicated in
Inc ICP about 5 but can be offset by drugs or dec LOC. Emergency
103
Nmb: why avoid panc
Tachycardia and htn- sympathetic effect
104
CCB: which in particular helpful/in which situation for neuro pts
Nimodipine- reduces vasospasm incidence in SAH pts
105
When steroids are useful, when they arent
Reduce edema r/t tumors. Could be harmful in other neurosurg procedures, esp SAH
106
How diuretics are cerebral protective
Reduce vol of icf and ECF compartments
107
Protec after ischemic event: CPP > __, map __-__ or ___% of baseline, prevent ___. If global ischemia w cv arrest keep temp:
60. 70-80 or within 30%. 32-34 c for 24hrs
108
EEG signal represents the summations of __ and __ ___ potentials that create electrical potentials in ___ of neurons
Excitatory and inhibitory postsynaptic, dendrites
109
EEG intraop uses: detection of cerebral ___ or ____ assessment of brain. Detection of intraop ___. Assess pharmacological intervention __ ___ w tpl or ___ prevention w ___
Ischemia, functional. Seizures. Burst suppression, recall w/ BIS
110
How evoked potentials and eeg are different
EEG: spontaneous activity, nonspecific, large signal >50 Mv. Evoked pot: smaller amplitude 0.1-20 mv, specific stim and pathway
111
How peaks and troughs characterized in evoked potentials
Amplitude and latency (how long it takes signal to be detected)
112
Sensory evoked potentials: monitor integrity of __ sensory pathway in ___/___ ___ spinal cord.
Ascending, afferrent/posterior lateral
113
SEPS: somatosensory= ___. Auditory ___. Visual ____. * which affected by anesthetics
SSEP, BAEP, VEPs*
114
SSEPs: evaluate ability of ___ spinal column to conduct signal from __ or __ ___ to sensory cortex. Usually measured at which two places. ___ signal.
Dorsal. Periphery or CN. Subcortex (upper cervical spine) and contralateral cortex (scalp). Small.
115
SSEPs: which nerves stimulated (7)
Median, ulnar, common peroneal, post tib, tongue, trigeminal, pudendal
116
SSEP: ___% reduction in ____ or ___ > ____% from baseline in response to surgical maneuver considered significant
50% in amplitude, latency > 10%
117
SSEPs: what three things poorly affect them, how they effect them
VA, TPL, N20. Decrease amplitude and increase latency
118
SSEPs: which 3 agents only slightly effect them
Opioids, benzos, propofol.
119
SSEPs: which 2 agents may improve signals
Ketamine and etomidate
120
Factors other than drugs that can effect SSEPs
Temp (even local changes), systemic bp (esp hypotension below auto reg), alt in paco2 and pao2
121
What you can do about alt in SSEP in or
Turn down gas/go to tiva, check bp, check hgb/hct, correct hypovolemia, tell surgeon, avoid giving boluses/or if you have to make sure they arent about to clip something
122
When MEPs are useful: 4.
Intramedullary tumor resection, scoliosis sx (anterolateral sc), cerebral tumors/cerebrovascular procedures near motor cortex, aortic cross clamping
123
MEPs: when n20 effects them. Other inhibitors
60% abolishes them, little change if 50% n20. VAs, benzos, barbs, propofol. Muscle relaxants do: need 1-2 twitches
124
MEPs: which 3 agents best to use
Fentanyl, etomidate, ketamine
125
EMG: used to monitor ___ or ___ nerves at risk. Sensitive to __ __
Cranial or peripheral. Muscle relaxants
126
EMG: detects __ or __ __ __ in ___ measurement, signal warns surgeon
Irritation, impending nerve damage, passive
127
Supine: pressure change by __ mmhg for every __ cm a point varies above or below heart
2, 2.5
128
Lateral decubitus: allows access to __ __ and ___ lobes and __ __ fossa.
Posterior parietal and occipital, lateral posterior
129
Lateral decubitus: useful for tumors at the ___ __ and aneurysms of the __ and ___ arteries
Cerebellopontine angles, vertebral and basilar
130
Lateral decubitus: if __ maintained in __ axis of body, almost no pressure gradient exists head to foot
Legs, long
131
Prone: __ __ and __ __ procedures requires neck ___, __ __, and elevation of __
Cervical spine and posterior fossa. Flexion, reverse tberg, legs
132
Sitting position: access to __ __- midline structures (floor of __ __, the ___ __, and the __)
Posterior fossa. 4th ventricle, pontomedullary junction, vermis.
133
Sitting position: transducers at which level. NIBP: water __ cm high exerts a p of ___. Consider pa if what
Circle of Willis. 32 cm, 25 mmhg. Cad or valvular heart dis.
134
Sitting position: ___ filling pressures decrease (___ > ___). ___ tone inc, ___ tone dec
Atrial, left > right. SNS, pns
135
Sitting pos: ___ system activated and result. Which 3 hemodynamics decrease, which increases
RAA- dec renal bf. CO, Stroke vol, cerebral BF. HR INC
136
Sitting position: CPP minimum of ___ in healthy pts. Higher in 5 pts
60. Elderly, hypertensive, cerebrovascular dis, cervical spine stenosis, sustained retractor pressure to brain or spinal cord
137
Sitting pos complications: pneumocephalus, why __ needs to be used w caution. Paradoxical air embolism occurs in which 2 conditions
N20. PFO and R to L shunt
138
3 methods of detecting VAE, which most sensitive to least
TEE more sensitive, identify r to l shunting of air. Precordial Doppler. Expired n2 (least sensitive- small unless large vae)
139
VAE sensitivity most to least/physio changes: ___ and ___, no physio changes. __ and __= modest changes.
Tee and Doppler none. Pap and end tidal modest
140
VAE detection: __ and ___ clinically apparent changes. __, ___, and ___ cardiovascular collapse
Co and cvp. Bp, ecg, and stethoscope
141
Mgmt of acute VAE: 3 that prevent further air entry. 4 that treat the intravascular air
Prevent further air: notify surgeon to flood or pack field, jugular compression, lower head. Treat air: aspirate via right heart cath, d/c n20, fio2 100%, pressors/inotropes/cpr
142
Right heart cath should be given to pts w which procedures
Sitting posterior fossa procedures
143
Right heart cath: where multiorifice Caths should be, where single orifice caths should be
Multi: tip 2 cm below SVC-atrial junction. Single: tip 3 cm above SVC-atrial junction
