Anesthesia For Neurosurgery Barash 37 Flashcards
1
Q
Basal Ganglia is made of
A
1-Caudate Nucleus 2-Substantia Nigeria 3-Red Nucleus 4-Globus Pallidus 5- Putamen
2
Q
Dysfunction if Extrapyramidal System lead to
A
Parkinson’s
Essential Tremors
Ataxia
3
Q
Supratentorium contains
A
1) Paired Cerebral Hemispheres
2) Diencephalon : Thalamus and Hypothalamus
4
Q
What makes the extrapyramidal system
A
Basal Ganglia
Cerebellum
Auditory and Vestibular system
5
Q
Where the diencephalon located
A
Cephalad to the midbrain
6
Q
Thalamus role
A
Sensory and motor Relay station
Connect the cortex and the rest of the nervous system functionally and physically
7
Q
Hypothalamus located where? It’s function ? It is connected to ?
A
Below the thalamus
Autonomic and Endocrine function
Connected to the pituitary glad via the Infundibulum
8
Q
Limbic play a role in (3)
A
1) Cognitve
2) Memory
3) Emotional
9
Q
The limbic system components are :
A
Amygdala
Hippocampus
Some regions of the Cortex : Insular region example
Part of the hypothalamus
10
Q
Brain stem has nuclei for CN 3 and 12 . true or False ?
A
True
11
Q
Brain receives 70 % blood from and 30 % from
A
70% from Two internal carotid arteries .
30% from vertebral arteries posteriorly forming the basilar artery , subsequently converge to for circle of willin
12
Q
Common carotid emerges from the
A
Aortic arch and divides at the level of the thyroid cartilage in the internal and the external carotid arteries
13
Q
The internal carotid artery traverse the ____through the ____and subsequently travels through the _____and into the _____
A
The skull though foreman lace rum
The cavernous sinus and into the carotid groove .
14
Q
Bil vertebral arteries originate from the_____and converge to form the ____at the _____junction
A
From the Subclavian arteries
Form the basilar artery
At the pontmedullary junction
15
Q
Basilar reached midbrain and divides into the
A
Posterior cerebral arteries and anastomoses with the PCOMs = completes the circle of Willis .
16
Q
Less than ___% of people demonstrate a complete circle of Willis
A
50 %
17
Q
All the sinus Darin into the
A
Sigmoid sinus and thereafter the internal jugular veins
18
Q
CSF is produced mostly by choroid Plexus of lateral and third ventricle. True or False ?
A
True
19
Q
Average volume of CSF in an adult is
A
150 ml ( approx)
20
Q
CSF is created at a rate of ___ and moves from
A
15- 20 ml .hr
Moves from the ventricles via the aqueduct of sylvius to the fourth ventricle .
21
Q
CSF flow
A
Choroid plexus of third and lateral ventricle(aqueduct of Sylvius )»_space;4th ventricle» ( Foramen of Magendie and lateral foramina of Lushka)»_space;Subarachnoid space of the cranium .
22
Q
Primary sinus where CSF gets reabsorbed
A
Superior Sagittal Sinus via arachnoid villi and granulations
23
Q
Some CSF traverses the Foramen Magnum , enters the subarachnoid space of the spinal column . This movement is important how?
A
Acute and chronic compensation in elevated ICP
24
Q
How vertebraes
A
33 vertebrae 7 C 12 T 5L 9 fused sacral (5) And coccygeal (4)
25
Dorsal Columns containing tracts responsible for :
Proprioception, light touch
| Central gray Matter *
26
Lateral Spinothalamic Tract responsible for
Pain and temperature
| Central gray matter *
27
The outer white mater contains the ______Tract
lateral Corticospinal
28
Lateral gray column contain the cell bodies of the ______neurons that enter the _____chain , running on either side of the vertebral bodies , arising from
Preganglionic
Sympathetic chain
Arsing from T1 to L2/L3
29
Spinal cord ends
L1 or L2 in adults
| Conus medullaris and film terminale
30
Spinal cord receives blood from :
1 anterior spinal
| 2 posterior spinal arteries
31
The anterior spinal artery originates from
6 - 8 major radicular arteries derived from the aorta.
32
The largest of the radicular arteries in the anterior spinal artery is the
Artery of Adamkiewicz
| Occurs at T11/T12 but supplies T8 to conus medullaris terminus
33
Artery of Adamkiewicz is responsible for supplying blood to the _______of the spinal cord
Anterior 2/3 of the spinal cord
34
The posterior Spinal arteries supply the ______and ______and feeds ______of the spinal cord
Dorsal horn and the white matter
| Posterior 1/3 of the spinal cord.
35
Brain is ___% of total body weight and ___% of O2 consumption and ____% of total body glucose consumption
2% Total Body weight
20% O2 consumption
25% total glucose consumption
36
brain glucose consumption
5mg/100g/min
37
CMRO2 normal is
3 - 3.8 ml/100g/min
38
Normal CBF
50ml/100g/min or 750 ml/min .therefore the brain receives 15% of the cardiac output
39
Irreversible Brain injury will occur how long after lack of O2 supply ?
4 to 5 minutes of global ischemia
40
CBF is regulated by ...
Flow- metabolism coupling
41
CPP is the
≠ between MAP and ICO or CVP depends on which is bigger
42
CBF itself equal to
CPP/CVR
43
Cerebral auto regulation remain intact between MAP of ___ and it function by ___
*60 -1 60 mmHg ( approx)
Lower limit autoregulation is > 60 mmHg, changes throughout the day , differs per individual.
*Functions by altering CVR on the order of 5 to 60 seconds ( within a minute)
44
In health brains the LLA may be as high as MAP of
80 mmHg
45
Altering CVR is accompanied by ( 2 things )
Rapid phase aka dynamic autoregulation (: pulsatile changes link to SBP
Slow phase aka Static autoregulation ( phenomenon that accommodate to changes in MAP over longer time intervals
46
Above the Upper Limit and Lower to the LLA CBF is
Pressure dependant
47
Below the LLA what occurs?
Max cerebral vasodilation and Ischemia
48
Above the autoregulation upper limit , what occurs ?
Max vasoconstriction
| Increased perfusion pressure >> disrupted BBB>> Cerebral edema or cerebral hemorrhage.
49
Chronic HTN, autoregulatory curve is shifted
Right
50
Anesthetics do what to your autoregulation ?
Anesthetics, especially the potent ones have a dose dependent DECREASE in autoregulation
51
What physiologic parameters play important role in regulating CBF ? Which is most important ?
A)MAP
B)PaCO2 : most important **
CBF is linear to PaCO2 ( but the PaCO2 must be between 20 and 80 mmHg )
C) Temp
52
Hypoventilation does what to the CBF ?
```
Increase
Remember CO2 ( vasodilates you )
```
53
What does hyperventilation to your CBF ?
Decrease
| Remember low CO2= vasoconstriction
54
A change in PaCO2 of ___mmHG correlates with changes in ___of _____
PaCO2 change of 1 mmHg = same change in CBF of 1- 2 ml/100g/min
55
What happens is PaCO2 is lower than 20 mmHG
Max cerebral vasoconstriction >> Tissue hypoxia >>> reflex vasodilation.
That’s why you start hyperventilating when your ICP is acutely elevated. But that reflex vasodilation can cause ischemia.
56
The effects of hyperventilation on CBF and ICP only sustainable for how long ?
only 6 hours .
| BC Phof CSF will renormalize
57
When does PaO2 have effect on CBF ?
Marked hypoxia aka PaO2 < 50 mmHg
| CBF increases dramatically!
58
When can PaO2 cause vasoconstriction
```
When > 350 mmHg
Slight vasoconstriction ( to protect itself from O2 toxicity ( O2 free radical formation )
```
59
How does Temp affect CBF ?
6- 7% DECREASE in CBF per 1 º C DECREASE in core temp .
60
Regional CBF is governed by
Humoral and Neurogenic factors
61
Catecholamines and mediators involved in regional cerebral vasoconstriction are
A1 agonists
Ionic Ca+
Endothelium
Thromboxane A2
62
Catecholamines and mediators involved in regional cerebral vasodilation are
B2 agonist
Nitric Oxide
Adenosine
PGs
63
Neurogenic influence over local CBF regulation :
Ach
Dopamine
Serotonin
Substance P
64
What the effects of Anesthetics on CBF ? ( not autoregulation)
Profound effect !!!
65
IV anesthetic effects on CBF
Propofol, Etomidate, Benzodiazepines, Thiopental DECREASE CBF bc >> decrease in CRMO2 >> flow-metabolism coupling .
* Autoregulation and PaCO2 remain intact with those !
66
Ketamine effects on CBF, CMRO2 , Autoregulation, PaCO2 ( 2)
1) Increases CBF and CMRO2
| 2) Little effect in autoregulation and PaCO2
67
Volatile anesthesic effects on CBF and autoregulation .
1) Potent volatiles Sevo, ISO and Des = DIRECT cerebral vasodilators ! but >> decrease CRMO2 >> flow-metabolism coupling >> offset CBF = none to min. Increase in CBF at lower dose , but at high doses >>max suppression of CRMO2>> major vasodilation>> increased CBF Therefore we say they have **dose- dependent effects of CBF
2) Autoregulation is inhibited : but vessels can still response to PaCO2 changes .
68
N2O effects on CBF
Direct cerebral vasodilator +
Minimal effect on CRMO2 +
Variable effect on cerebral autoregulation capacity
Propofol + N2O = preserved autoregulation
Sevo+ N2)= impaired autoregulation
69
Spinal Cord Perfusion Pressure SCPP=
MAP- SSSP ( Spinal subarachnoid Space pressure )
70
Volume of brain
1400 ml
71
volume of CSF in cranium
150 ml
72
CBV ( cerebral volume )
150 ml
73
Monroe Kellie Doctrine
Increase in the volume of one will lead to a rise in ICP unless it is matched by an equal reduction in the volume of another compartment.
Brain can’t compress so CSF and CBV adjust to maintain ICP
74
CBV decrease how ?
Reflex arterial vasoconstriction + increase venous Efflux from brain and venous sinuses .
75
Care of elevated ICP patients
1) Avoid Hypoventilation
2) Maintain CPP
3) Reduce intracranial volume : Mannitol, CSF 4)diversion, Cerebral vasoconstricting anesthetics ????
5) Consider decompression craniectomy
76
Normal ICP is
7 - 15 mmHg ( 5-15 mmHg PP)
77
Poor neurological outcome is from ICP above
20 - 25 mmHg
78
High ICP does what to CBF ?
Decrease
79
Intracranial elastance curve
Visualizing the ICP -Volume relationship
80
Cerebral elastance formula
E= dP/dV
| Lumbardrain, extraventricular drain.
81
“Flat of the curve “( intracranial elastance curve means :
Elastance is low
| In normal brain , changes in volume compensated for easily by CSF and CBV
82
Elbow of the curve ( intracranial elastance curve )means :
Elastance increases
| Small increase in volume = rapid rise in ICP
83
Most common cause of elevated ICP is
**Cerebral edema **
Cytotoxic : increase intracellular water i.e Post ischemia.
Vasogenic: loss of integrity of BBB. Happens in tissue around tumors, abcess, contusion. Dexamethasone*
Interstitial : increase extrecellular fluids + intact BBB i.e hydrocephalus
84
Why dexamethasion only can treat vasogenic edema ?
BC it upregulates the proteins responsible for the integrity of the tight junctions
85
How can increase CBV increase ICP ?
Increase arterial inflow plus decreased venous efflux = rise in ICP
86
What can increase arterial inflow ?
Vasodilators
Hypercapnia
Severe hypoxemia/ Acidosis
87
What can cause decreased Venous efflux ? Thus increasing ICP
Jugular vein obstruction
| Elevated pressure within the airways
88
Clinical symptoms of elevated Intracranial Hypertension.
Headache
N/V
Papilledema
89
As ICP continues to increase you will see what ?
Cushing Triad
1 HTN
2 Bradycardia
3 Irregular respiration
90
Signs of herniation
```
Depends on structures herniating
Pupillary Dilation
Oculomotor weakness
Absent light reflex
Cardiorespirations
```
91
CT results of elevated ICP
Effacement of Sulci
Compression of ventricles
Midline shift
Even possible ventriculomegaly
92
In acute phase of spinal cord injury , what are the s/s ?
Flaccid paralysis and hypotension
93
Flaccid paralysis and Hypotension are seen in which phase of spinal injury ?
Acute
94
Spastic , Pain and risk for autonomic hyperreflexia are seen in which phase spinal cord injury ?
Chronic
95
Both chronic and acute spinal injury may have what s/s ?
Loss of sensory, motor, autonomic function below the level of injury.
96
Most important monitor of CNS function is
Neuro exam of an an awake and responsive patient.
97
BAEP and VEPs are less commonly used. True or False ?
True
98
Amplitude is measured in ____ for SSEP and BAEP and measured in _____for MEPs
Microvolts
| Millivots
99
Latency is measured in ___ refers to the _____
Milliseconds
| Refers to The delay in peak signal following stimulation and reflects transit time along the neural pathway.
100
SSEP elicited from ____and is measured at the level of ______
A peripheral nerve
| Subcortex : upper cervical spine , inion and cortex : scalp.
101
SSEP stimuli travel through
Posterior Column/ Medial Lemnicus pathway in the CNS
102
SSEP is useful for monitoring integrity of
```
Peripheral Nerves
Dorsal Column
Brainstem
Subcortex ( upper cervical spine, inion)
Sensory cortex of the brain
```
103
SSEP stimuli are recorded in the contralateral side scalp because
Sensory tracts crosses at the brainstem before getting through the thalamus and up the sensory Cortex
104
SSEP are used during
Spine Surgery
| Neurovascular brain surgery : cerebral aneurysm clipping.
105
Significant changes in SSEP means
Decrease amplitude by 50%
| Increase Latency by 50%
106
MEPs are produced at the level of the
Cortex by direct stimulation of the cerebral cortex or by
| Indirect stimulation of the scalp
107
Lower extremity SSEP which artery ?
ACA
108
Upper extremity SSEP which artery ?
MCA
109
MEPs for assessing what ?
Motor cortex and anterolateral spinal cord ( containing the corticospinal tracts )
110
MEPs how is stimulation produced ?
Indirect electrical stimulation of motor cortex via scalp electrodes >>pulses travel caudad>> depolarization of upper motor neurons in spinal cord>> accumulating in the ventral horn >> alpha motor neurons >>motor endplates>> muscle movement
111
Muscles relaxant effects on SSEP vs MEPs
SSEP muscle relaxants helpful to remove artifacts by the EMG activity
MEP muscle relaxants inhibit measurement of muscle response
112
Change Latency of MEPs less worrisome change than in SSEPs
True
113
EMG sensitive to what type of injury ?
Mechanical and Thermal
| Does not monitor ischemia ,
114
Is EMG sensitive to muscle relaxant ?
Yes !
115
What are BAEPs used for ?
```
Integrity of
Auditory Canal
Tympanic membrane
Hair cells
Spiral ganglion
Vestibulocochlear nerve
Cochlear nuclei
Superior Oliver’s complex
Lateral lemniscus
Inferior Colliculus
Medial geniculate thalamic nuclei
```
116
VEPs and anesthetics ?
Exquisitely sensitive to almost any anesthetic regimen , diff to obtain and interpret the signals = they are not used often
117
Potent volatile and N2O causes what to SSEPs
Greatest inhibition >> Decreased amplitude , increase latency
118
IV anesthetics , limited effect on SSEPS unless?
| What about opioids ?
Very high doses
| Opioids Salem unless a bolus = decrease amplitude.
119
N2O affects amplitude or latency more ?
Amplitude
120
Etomidate and Ketamine effects on SSEP
Increases amplitude!!! Even are used to enhance SSEP
121
Scalp MEPs are sensitive to
Anesthesia
Potent volatile greatly inhibitory
But can still use Mac of 0.5
122
TIVA for MEPs is the usual . True or False ?
True
123
BAEPS are ____ regardless of anesthetic regimen being used . Deep anesthesia may cause _____ but ______will cause some increase in interweave latencies
Robust !
Small increase in latency
Cold irrigation of fluid at the brainstem
124
Most sensitive neuromonitoring modality to anesthesia ?
Very
Inhalation w/ or w/o N2O > TIVA
Use opioids TIVA, muscle relaxant and BIS
125
TCD measures
Blood Flow Velocity
126
Decrease arterial diameter does what to blood flow velocity ?
Decrease
127
Normal ICP
7 to 15 mmHg
| Monitoring begins when ICP > 20 mmHg
128
What ICP values means severe life threatening Intracranial hypertension?
ICP > 40mmHg
129
The presence of characteristic Lindbergh waves provides
State of brain
130
How many Lindbergh waves ? What are they ?
(3 ) A, B, C waves
131
A waves are
(1) Plateau waves
(2) Happen when compensatory mechanism for elevated ICP are severely exhausted.
(3) Due to intense vasodilation in response to decreased CPP
* Are ALWAYS pathologic.
132
B waves are
(1) Elevated ICP 20 - 30 mmHg above baseline , occurring 1 or 2 times a minute.
(2) reflects changes in vascular tome when CPP is at the LLA ( lower limit autoregulation)
133
C waves are
Small oscillation , 4 to 8 times a minute ,
ICO is Normal
Reflects systemic changes in vasomotor tone, with LITTLE pathologic significance
134
Most commonly use ICP monitoring device
Ventriculostomy or
External Ventricular Drain aka EVD ( transducer is zeroed at the auditory meatus )
Connected to lateral ventricle
135
What is the gold standard ICP monitoring ?
Ventriculostomy or EVD placed int the lateral ventricle
136
A ventriculostomy can
Monitor ICP
Drain CSF
Deliver drugs ( i.e ABX, thrombolytic)
137
EVDs have great risk for
Infection,
| CSF sepsis
138
What is SjVO2 ? What tool measures it ?
Mixed cerebral O2 tension
Indicative of brain’s global O2 consumption/extraction.
Jugular bulb venous oximetry , most commonly used technique,
catheter place in internal jugular, in the jugular bulb , X-ray confirms it at level of mastoid process
139
SjVO2 less than 55%=
Cerebral ischemia in the setting of hypotension or marked elevated ICP
Useful during hyperventilation which may cause vasoconstriction, so goal to keep it above 55%
140
Other measures of cerebral metabolism are brain tissue oxygen monitor and microdialysis catheter ?
True
141
Brain tissue o2 monitor measure what ?
Partial pressure of O2 ( PbtO2) in a portion of brain interstitium , directly or indirectly , via Clark-type electrode
142
What is normal PbtO2 ?
25 to 48 mmHg
| Reflects balance between O2 supply vs demand in the region around the electrode
143
What affects PbtO2?
```
FIO2
PaO2
CO
Hemoglobin concentration
Local O2 extraction
CBF
```
144
In pathologic brain state , PbtO2 less than ... are considered significant
PbtO2< 20 mmHg
145
What does SjVO2 80 - 85 % mean?
Low O2 extraction or high O2 delivery
146
When do we monitor brain tissue Oxygen ?
TBI and SAH
147
Glutamate level means ____and glycerol level means____ measured by cerebral microdialysis
```
Glutamate = ischemic neuronal stress
Glycerol= cell membrane degradation
```
148
Cerebral Oximerty is
Transcutaneous measurement of REGIONAL cerebral blood oxygenation ( rSO2) over the frontal cortices bilaterally.
149
Cerebral oximetry reflect arterial or venous blood ?
Both
| Bc Oxygenation is given as a %tage of maximum hemoglobin saturation. Oxymoglobin and deoxymoglobin
150
Significant hypoxia in cerebral oximetry is when
A decreased of at least 20 % from baseline
151
Cerebral Oximetry relies on pulsatile flow , True or False ?
False ! Pulse oximetry relies on pulsatile flow not cerebral oximetry
152
When you have low cerebral oximetry what factors can prevent long term injury
Increasing the systemic BP
increasing the CO
Increasing the FIO2
increasing the PaCO2 : fix the vasoconstriction
RBC transfusion= increase O2 carrying capacity
153
Brain is susceptible to rapid ischemic injury because?
1) High rate O2 and Glucose consumption
2) can’t store substrates
3) cant dispose of toxic metabolites quick
4) intracellular Calcium builds up when ischemic = quick neuro damage + lactic acid accumulates
154
Focal ischemia vs global ischemia
Focal due to regional insult ( embolus, arterial disruption . Treat by restoring perfusion to the region>> restore O2 and substrate the ischemic penumbra . The penumbra around the necrotic core is salvageable!
Gobal is due to severe hypotension, severe anemia. Treat by restoring Cerebral perfusion, O2 delivery i.e CPR , RBC transfusion ,
155
Saving the Penumbra
Increase CPP and reduce brain edema
156
Repercussion injury of the brain
Reperfusing ischemic brain tissue leads to worse neuro outcome bc of free radicals from O2, mediators of inflammation and repeat of Injury of microvasculature when the flow is restored
157
Hypothermia and cerebral protection
In theory should be protective to brain and spinal cord , it lowers CRMO2 . But also , even 1ºC decrease protects , so other pathway beside decrease CRMO2 may be involved
But works best for global ischemia not so much focal ischemia
158
27 ºC is
Profound hypothermia used in cold- cardiopulmonary bypass
159
12 to 18 ºC is
Deep hypothermia used in circulatory arrest
160
Cerebral hyperthermia is good or bad
Detrimental !
Ischemia tripled 1ºC in animals
Must be avoided in cerebral ischemia
161
Satins upregulate
Nitric oxide synthase.
162
How are volatiles cerebral protectors (5) ?
1) Reduce ischemia-induced glutamate release
2) Increase antiapoptotic mediators
3) Activate ATP- dependent K channel
4) Reduce excitotoxic stressors
5) Increase CBF
163
What is the only subtstrate that can be aerobically metabolized by the brain under normal conditions ?
Glucose
164
Is glucose stored in the CNS ?
No
When no sugar bc of limited cerebral circulation >> no ATP >> energy requirement not supplied >> cellular injury quickly ensues .
165
Cerebral glucose consumption normal value is _____and it parallels what ?
5mg/100g/min
| Cerebral Glucose Consumption parallels CRMO2
166
Hypoxemia or hypoglycemia , which is more detrimental to brain ?
Roughly EQUALLY detrimental
167
Define hyperglycemia ___ and what effect on neuro outcome .
BG> 180mg/dL
Worsen neuro outcome
By worsening cerebral acidosis in an anaerobic setting (bc the glucose converts to lactic acid !)
168
Temporary clipping of cerebral vessel what anesthetic you give ?
Propofol 1- 2 mg/kg followed by 150 mcg.kg.min to induce “Burst suppression” prior to the planned ischemia
169
Deep hypothermia in what cardiac and neuro sx to protect nervous system?
Aortic arch repair or giant basilar aneurysm clipping - 12ºC to 18 ºC
170
Prior to throracoabdominal aortic aneurysm repair what can be done for neuro protection?
Placement of a lumbar CSF drain >>to lower the CSF and maintain spinal cord perfusion when radicular arteries from the aorta are at surgical risk
171
Preop of patient with Intracranial mass lesions what is the most important thing to ascertain ?
Ascertain presence or extent of Intracranial Hypertension , this should be assumed until proven otherwise .
get this info from H&P, CT , MRI, ICP measurements.
172
What do patients with elevated ICP complain of ?
```
Headache
Dizziness
Visual or gait disturbances
N/V
Seizures
```
173
What do patients with elevated ICP show on physical exams?
```
Altered LOC
Confusion
Papilledema
Loss of strength or sensation
Cranial nerve dysfunction
```
174
Radiology studies quantify degree of ICP showing
Slit ventricles or
| Shift of midline brain > 5 mm = advanced pathology
175
What lab may accompany elevated ICP ?
Electrolyte disturbances due to pituitary pathology SIADH
| Or due to diuretics , steroids, anticonvulsants
176
Premedication with Benzo and opioids even in small doses can lead to what ?
Elevated ICP bc they depress respirations >> elevated PaCO2>> ICH
177
What meds to continue preop with these patients with elevated ICP?
Corticosteroids ( i.e Dexamethasone ) and anticonvulsants
178
Preop for Spine surgery , especially acute focus on
Airway exam
Hemodynamics
Level of injury
The degree of injury : complete vs non complete
179
Induction of GA and airway mngmt in elevated ICP , unsecured aneurysm , cervical spinal cord injury focus on
Hemodynamics
Slow and controlled induction for high ICP patients with constant blood pressure maintenance
Avoid HYPOTENSION
Opioid and Lidocaine to blunt the systemic response to DL
Avoid HHYPOVENTILATION and HYPOCAPNEA
Should give a muscle relaxant after induction but Sux be careful
Avoid HYPOTENSION and low CPP
Cervical spine sx: not only maintain MAP , but techniques to prevent further compromise
180
What does SUX do to ICP ?
Increased ICP but short acting
Use it with caution in patients with motor deficits bc upregulation of nicotinic receptors at the NMJ lead to increased risk Hyperkalemia
181
During intubation of pt with high ICP
Rapid rise in arterial BP will worsen ICP esp when autoregulation fails , or pt w. Unsecured aneurysm
182
Maintenance of GA in intracranial sx with high ICP what is paramount until the dura mater is opened?
ICP control
183
Once Mayfield fixation and head positioned safely give
Mannitol 0.5 1.5 mg/kg if you need to control the ICP
Give dexamethasone 10 mg
Sometimes give anticonvulsant prophylactic
184
High ICP, volatile MAC is limited to ___if used at all
0.5 MAC
| Instead give IV anesthetic i.e.propofol w/ or w/o opioids short acting i.e. remifentanil or Alfentanil
185
> 0.5 MAC may interfere with SSEP and MEPs true or false ?
True
186
Why is N2O avoided in elevated ICP cases ?
Mild vasodilating effect
Potential intradural air
Or can interfere with monitoring
187
MEP and EMG you can give muscle relaxants , what can you use instead ?
Remifentanil infusion 0.2 mcg/kg/min
188
Have you vasopressor on board to maintain the
CPP
189
When autoregulation is inhibited either bc of the disease or the anesthetic , what does CBF depends on
MAP
| So that means avoid hypertension
190
Ventilation Management in neurosurgery , Intracranial sx , what is Tidal Volume and peak pressure goal ?
Maintain at 6- 8 mL/kg = minimize inflammatory lung injury
Peak pressure < 40 cmH2O
Esp patients with SAH and TBI
And esp patient w/ ALI , ARDS
191
Why do you avoid PEEP in elevated ICP pts
( unless you need it for better oxygenation )
| Bc : increase intrathoracic pressure >> impede cerebral venous drainage
192
What mode is used in neuro sx ?
PPV ( positive pressure ventilation) bc it allows direct control of PaCO2 !!!
Esp in sitting craniotomy where negative intrathoracic pressure >> VAE ( venous air embolism )
193
Primary goal of fluid management in neuro surgery is to
Maintain cerebral perfusion , not to dry them out !, keep euvolemic . Give isotonic solution if you have to give large amount
AVOID hypotonic such as LR ??? if need large amount = cerebral edema
194
Can we give fluids with dextrose to those neuro patients ? Why ?
No.
1) Bc hyperglycemia = detrimental to Cerebral metabolism ( parallel increase in CRMO2) + worsen neuro outcome by worsening lactic acidocis in an anaerobic ( ischemic tissue is anaerobic ) bc sugar becomes lactic acid in aneorobic environment.
2) Bc Glucose get quickly metabolized and is not osmotically active , leaving free water = worsen brain edema
195
Moderate to severe hyponatremic state give
3% saline at rate of
50 to 100 ml/hr
Check serum Na+ q 1 hr
196
Central Pontine myelinosis can happen when ...
Rapid rise in serum Na+ > 3-4 mEq/L/hr
| AVOID that !!
197
Mannitol can cause short lived electrolyte imbalance which are ?
How can Mannitol impair cerebral perfusion ?
Hyponatremia
Hyperkalemia
By causing dehydration = impair cerebral perfusion
198
What can large amount of 0.9%NS cause ?
Hyperchloremic acidosis >> AKI due to renal tubular acidosis
199
Preop Coags must be corrected. True or False
True
| Patients on anticoagulants = required to draw preop coag labs
200
Non urgent Neuro surgery patients should have platelet count of
100,00/mm3
| Craniotomy with low bleeding risk a Type and Screen ( T&S) with neg Antibody ( ABS ) is enough
201
Neuro surgery with high risk bleeding are ____ what should be available ?
Aneurysm clipping
AVM resection
Tumor craniotomies that invade the cranial sinuses
RBC that are T&C should be available for intro op
202
For coagulopathy that happens bc of brain releasing tissue thromboplastin you may need available
FFP, PLTs, Cryo
203
Which Neuro surgery usually associated with more profound blood loss, volume shifts and need for transfusion
Comple Spine sx especially planned osteostomies or tumor
Multiple blood products should immediately available for these cases
Repeat CBC and Coags should be performed
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Strict glycemic control in neuro sx is target of
90 to 180 mg/dL = improved outcome , it is no longer 80 to 100 mg/dL bc that target can lead to hypoglycemia.
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If hyperglycemia in neuro sx give
Insulin IV bolus + infusion
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If hypoglycemia give
50% Dextrose
20 to 50 mL
Keep monitoring sugar to titrate how much to give
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Emergence from GA in Neurosx what 2 things do you watch ?
Hemodynamics and ventilatory parameters while ensuring prompt neuro exam
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Postcraniotomy , what happens to BP often ?
HTN >> worse cerebral edema , increased surgical site bleed
Labetalol, Esmolol, nicardipine, clevidipine
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Posterior Fossa Surgery , those pts w/ pre brainstem dysfunction , emergence is
Slow
| Time to safe extubate prolonged
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What to avoid on emergence in elevated ICP patients ?
Coughing ..
| So give a low dose infusion of Remifentanil or/and intratracheal Lidocaine
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How to prevent PONV in ICP patients ?
Dexamethasone prophylactic
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What patients you do not give Dexamethasone to ?
1) dx of lymphoma = can cause tumor lysis of lymphoma >> can’t diagnosis ( at least delay giving it until after diagnosis .
2) avoid in pituitary sx because it suppresses the hypothalamic -pituitary- adrenal axis + can increase false positive post op hypopituitarism .
213
MC metastatic tumors to the brain
Melanoma
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Supratentorial lesions are MC tumors from support cells
Yes
215
After the mayfield pins are applied what response can you see ? How can you fix it ?
Same response as laryngoscopy . Give proprofol , opioids, or short acting BB such as Esmolol.
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How do you decrease brain volume for optimal surgical exposure and minimize retractor-related edema ?
Mild hyperventilation
Mannitol 0.5 to 1.5 mg/kg ( or as bolus for full effect )
Or hypertonic 3% saline at 50 to 100 ml /hr w/ na+ surveillance
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Be careful with what type of patient when giving mannitol and why ?
CHF , Pulm edema, Renal Failure
| Bc the initial elevation in central volume can be detrimental to those patients prior to diuretic phase .
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Choice of anesthetics depends heavily on
1) Avoiding increase in ICP ( at least until the dura mater is open ) ,
2) maintain the CPP,
3) what neuromonitoring is being used
4) And ensuring RAPID emergence
Short acting , tritrable drugs preferred : propofol, remifentanil, Sevo, Des and maybe N2O ( unless contraindicated )
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Normal GCS is 13 to 15 is extubted when ?
At end of case
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Adequate analgesia while avoiding obtunded patient with what meds ?
Short acting opioids , remi/fentanyl, LA infiltration , IV Tylenol, Precedex
221
What is special about patient with infratentorial tumors and tumors of the posterior fossa ?
Bc of how close they are to the brainstem = more hemodynamic problems intra op and post + changes in respiratory control and arousal level
They often stay intimidated bc of altered LOC and delayed emergence
222
Posterior fossa tumor sx require what type of neuromonitoring ?
Specific CN monitoring i.e. BAERs or EMG of cranial nerves .
Because they are close to the brainstem and CN they can cause : altered respiratory patterns, Cardiac dysrhythmia , CN dysfunction
223
Acoustic neuroma, mestases , meningiomas and hemangioblastomas are tumors of the posterior fossa . True or False ?
True.
| These tumors are close to the brainstem and cranial nerves
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Sitting position = risk for ?
VAE
225
When VAE causes significant hemodynamic change it is because ...
Air is entrained into the heart and pulmonary circulation >> impaired gas exchange >> intrapulmonary shunt >> hypoxemia and concomitant DECREASE in ETCO2 .
If air entrainment is severe >> arrhythmia, decreases CO , severe pulmonary hypertension , circulatory collapse
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How do you monitor VAE ?
Precordial Doppler US , detects presence of air, qualitative aspect of air
TEE , more sensitive, can detect quantity of air but can’t use continuously bc the probe will stop working as it gets hotter
227
Prevent VAE by doing what ?( 3)
1) Decrease height difference between operative site and the heart as much as possible.
2) Euvolemia
3) And surgeon using bone wax to close visible open Dural venous sinuses or larger veins .
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Treatment of VAE
1)Notify the surgeon to flood the surgical files
2)Give 100% O2
3)Aspirate air through multi orifice CVC positioned at the junction of the SVC and the right atrium
4) Support hemodynamic : vasopressors, fluids, inotropes, adjust OR table so head is at level of the heart <> that’s for severe VAE bc it will disrupt the surgical field
PEEP does not actually help, only in theory
If you are using N2O stop it immediately, it will increase air bubble
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Sellar mass patient have
Visual defects . Know that preop to ≠ if anesthetic is the cause .
SIADH is common with them bc the post pit is compresses >>Excess circulation ADH >> volume overload and hyponatremia
230
Pituitary surgery : acromegaly , what airway ?
Smaller size ETT
| Awake fiberoptic or VL
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Acromegaly and cardiac effects
Cardiac rhythm issues and HCM so careful with the cardiac depressant meds
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ACTH tumors cause
Cushing syndrome ( high cortisol level)
233
TSH secreting adenomas please do what with them before surgery ?
Make sure they are euthyroid before sx unless vision is threatened
234
Hallmark of DI is
Polyuria w/ dilute urine output
| Desmopressin and fluid replacement
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Tx of SIADH
Restrict water
Treat underlying cause
Demeclocycline , a tetracycline abx that inhibits ADH in the renal tubules
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What accident can happen with pituitary sx ?
Entry into the cavernous sinus or internal carotid
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Cerebral aneurysm MC occur where ?
40% ACA
25% PCOM
25 MCA
Only 10% vertebrobasilar system
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Small aneurysm are les than ___mm diameter
Large are ___to ___ mm diameter
Giant aneurysm are more than ____mm diameter.
Rupture risk increase when aneurysm is > ____6 mm , generally requiring treatment
Small 10 mm
Large 10 to 24 mm
Giant > 24mm
Rupture risk at > 6 mm = treatment required
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Ruptured aneurysm patient may also have ...
```
Rebleeding
Vasospam of cerebral artery
Hydrocephalus
Cardiac dysfunction
Neurogenic pulm edema
Seizures
```
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Nimodipine is the only intervention that decreases risk of ...
vasospasm
Statins via pleotrophic effect “may” also decrease vasospasm
241
Aneurysm surgery , you need to monitor BP very closely with ___ and prevent movement with ___
A- line , also for blood sample to repeat Coags since they get heparin periodically
Muscle relaxant
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During Aneurysm surgery , extravasation of dye into the brain parenchyma means
Aneurysmal or feeding rupture : give protamine quick !
Hyperventilation
Mannitol
Burst suppression
Place EVD
Possibly get ready for an emergency craniotomy
243
AVMs are
Plexus of arteries and areterialized veins that form a nidus which may lead to cerebral hemorrhage, headache , seizures, or signs of ischemia due to “steal effect “
70 % are supatentorial
244
7% of cerebral AVMs include a flow-related cerebral aneurysm as well, make sure to look for this information and account for it in your
Anesthetic plan
245
AVM sx , what kind of access is rec ?
CVC bc the greates risk is rebleeding
246
Why do we avoid hypotension in AVMs ?
Bc they get seizures or focal neuro deficits from the ischemic steal that hypotension causes
247
Are AVMs shunts ?
Yes, high flow -low resistance shunts . Bc of that , rapid rise in BP during DL will less likely rupture the AVMs
248
AVMs emergence , make sure what is available
Antihypertensive meds
| Bc of NPPB Normal perfusion pressure breakthrough
249
NPPB is caused by
Autoregulation inhibited in normal brain vessels as they are maximally dilated as a result of long standing steal by the AVM. After the AVM is resected, those vasoparalyzed vessels don’t know how to constrict =>> cerebral hyperemia, cerebral edema, headache, risk for post op bleeding
250
Prophylactic anticonvulsant is given to AVM patients bc
50% experience seizures post op
251
Carotid surgery.
Remove carotid plaque causing
| symptomatic cerebral ischemia , indicated when plaque > 70 % in the ipsilateral ICA
252
Carotid endarterectomy better than carotid stenosis because _____but disadvantage is
Less post op stroke, and restenosis but disadvantage: need GA or regional , cardiac event , CN injury
carotid stenosis : very minimum sedation , less CN injury but higher stroke and restenosis post op
253
What block is done for carotid endarterectomy?
Superficial and sometimes Deep cervical plexus block to provide anesthesia to dermatomes C2- C4
Low remi or propofol may be given bc it’s important the patient to responds to commands on the contralateral side
254
Awake carotid endarterectomy requires laying flat for long time , who is not a candidate ?
COPD and CHF patients ?
255
If patient becomes confused during carotid endarterectomy what must CRNA do ?
Increase the systemic BP > 20% of preop values to assure adequate perfusion and oxygenation since ischemia has ensued.
256
Asleep carotid sx with
GA and monitoring of cerebral ischemia via EEG ( MC)
EEG shows ipsilateral slowing of oscillations as ischemia
SSEP and MEP may also be used
257
What is carotid Stump pressure ?
Pressure in the internal carotid artery distal to the cross-clamp
Reflects adequate collateral blood flow via circle of Willis
258
What is a desirable stump pressure?
> 50 mmHg
259
Hypoventilation and hypocapnia lead to steal phenomenon from watershed areas of cerebral perfusion.
Yes it does :)
| What the heck is water shed
260
BP control in carotid sx , why?
While morbidly of this surgery is caused by neuro complications, mortality is caused by cardiac complications.
They have chronic HTN pre op & other CV diseases & other comorbidities ,so keep their BP at baseline prior to cross clamping .
261
Where is cross-clamping done in carotid sx ?
Above and below the plaque , usually at the level of carotid artery below the plaque and the ICA above the plaque
262
Once cross- clamping happens what do you do with the BP ?
Increase it to improve collateral flow on the contralateral, use a vasopressor .
263
Why is bradycardia and even hypotension possible during carotid sx ?
Bc the surgeon manipulates the carotid baroceptors, he can infiltrate the carotid sinus with lidocaine to prevent that response .
264
Why does HTN remain peristaltic even after restoring the carotid flow?
Bc the surgery denervated the carotid baroreceptors + cerebral vessels distal to the stenotic carotid have been maximally dilated >> autoregulation is impaired . So now you have HTN + cerebral vasomotor paralysis = great recipe for cerebral edema and cerebral hemorrhage!
265
POST op carotid sx neuro compromise is because of
Cerebral emboli or ICA thrombosis
266
Are you worried about airway post carotid sx ? And why or why not ?
Yes
| Neck hematoma >>compromise airway >>may be hard to reintubate >> may first need to surgically explore the hematoma
267
Very common procedure for treatment of epilepsy is
Lobectomy with amygdalohippocampectomy
268
Antiepiletics can increase metabolism of
Muscle relaxants
Opioids
Dexmedetomidine
** need higher dosages
269
What meds can enhance epileptiform activity
Methohexital
Etomidate
Alfentanil (50mcg/kg)
270
What meds to avoid when electrocorticography ECoG planned ?
Benzo
271
Tp prevent awareness with very little effect adverse effect on ECoG, what meds ?
Scopolamine, N2O, high dose opioids
Or simply dexmetomidine .
Counsel the pt that awareness may happen
272
Hold propofol and potent volatiles to 0.5 MAC ____minutes prior to ECoG
30
273
Asleep-awake-asleep technique
Asleep with SGA or nasopharyngeal tube with propofol, remifentanil and dexmedetomidine
Awake : airway device removed so patient can tallk
274
Awake craniotomy .Airway is critical bc apnea may require intubation, but your patient is in the mayfield head holder fixed . So how do you put the drape?
In a way that allow Acces to face constantly .
| Padding and position before sedation *
275
How to treat seizures during craniotomy ?
Cold saline applied to brain surface by surgeon and small bolus of propofol 20 mg IV .
