Neuro Anesthesia Flashcards
1
Q
What are the signs/symptoms of ischemic optic neuropathy?
A
Painless visual loss within first 24-48 hours
Sluggish pupils
Visual field deficits
2
Q
What are the risk factors for ION?
A
Age over 50 Prone position Spine, cardiac, head/neck surgeries Hypotension Hemorrhage Anemia Hemo dilution (don't give over 2L crystalloid) HTN, diabetes, smoking Male sex Surgical time Obesity
3
Q
What is the pathophysiology of ION?
A
Ischemia to optic nerve leading to atonal destruction
4
Q
What are the types of ION?
A
Anterior and posterior
Arteritic and non-arthritic
5
Q
Which type of ION is more common after spine surgery?
A
Posterior
6
Q
Which type of ION is more common after cardiac surgery?
A
Anterior
7
Q
What are the treatment methods for ION.
A
Acetazolamide Diuretics Steroids Transfusion Position changes (avoid venous congestion) Maintenance of bp
8
Q
What does botulinum toxin do?
A
Inhibits release of Ach at NMJ causing flaccid paralysis by cleaving SNARE proteins
9
Q
How does tetanus toxin travel?
A
Retrograde entering presynaptic neurons in the spinal cord
10
Q
What is not associated with POVL?
A
Deliberate hypotension
11
Q
What is the treatment for pneumocephalus?
A
Head of bed up, 100% FiO2, avoid maneuvers that increase ICP
12
Q
How do you diagnose pneumocephalus?
A
CT scan
13
Q
What are the hallmarks of autonomic hyperreflexia?
A
Hypertension and reflexive bradycardia
Other symptoms: sweating, piloerection, facial erythema, headache, nasal congestion, feeling of doom
14
Q
What causes autonomic hyperreflexia?
A
Distention of a viscous in a patient with spinal cord lesion T7 or above.
- any noxious stimulation can trigger
15
Q
What is the mechanism behind autonomic hyperreflexia?
A
The negative feedback from the CNS cannot mitigate the sympathetic stimulation below the lesion.
16
Q
Why doesn’t autonomic hyperreflexia occur with lesions lower than T6?
A
Greater splanchnic ganglion receives innervation from T5-9 can buffer the response
17
Q
What happens above the lesion in autonomic hyperreflexia?
A
Vasodilation –> flushing, nasal congestion, headaceh
18
Q
How do you treat autonomic hyperreflexia?
A
Remove the stimulus
Deepen the anesthesia
Administer vasodilators: nifedipine, nitroglycerin, nitroprusside
19
Q
What class of med should be avoided in autonomic hyperreflexia?
A
Beta blockers due to unopposed alpha stimulation
20
Q
When does autonomic hyperreflexia syndrome occur in relation to the initial lesion?
A
3-4 weeks after when the spinal reflexes have returned.
21
Q
Why should the patient with autonomic hyperreflexia by monitored for 7-10 days after the initial episode?
A
Because they are at a high rate of recurrence.
22
Q
What are the predictors of postoperative mechanical ventilation in a MG patient?
A
- Pyridostigmine > 750 mg/day
- Vital capacity <2.9L
- NIF less than 20 cm H2O
- inability to clear secretion or produce a strong cough.
- Disease for more than 6 years
23
Q
What is the leading predictor of postoperative mechanical ventilation in a MG patient?
A
Inability to clear secretions or produce a strong cough
24
Q
What is the gold standard for estimating brain parenchyma temperature?
A
Jugular bulb temperature because of the proximity of the bulb to the brain
25
What must you do to ensure adequate cooling of brain in deep hypothermic circulatory arrest?
Run CPB for 20-30 minutes once goal blood temp is reached
26
What will be seen on intraventricular drain monitor when there is an acute increase in ICP?
A plateau wave (Lundberg's A wave)
27
What is normal ICP?
5-13 mm Hg
28
What does P1 represent on ICP monitoring?
P1 = percussion wave, arterial pulsation
29
What does P2 represent on ICP monitoring?
Tidal wave and it represents incranial compliance
30
What does P3 represent?
The dicrotic wave and it represents aortic valve closure
31
What is a normal ICP waveform?
P1 > P2 > P3
32
What does it mean if P2 becomes higher than P1?
Reduced intracranial compliance
33
What are B and C waves?
correspond to changes in ICP with respiration and arterial blood pressure
***no clinical significance
34
What strategies can be employed to prevent a hyperkalemic periodic paralysis episode?
Maintaining normal body temperature
Dextrose containing K-free fluids
Decreasing serum potassium concentrations to low normal
regional
35
What are the potential triggers of hyperkalemic periodic paralysis?
```
Hyperkalemia (metabolic acidosis)
Potassium rich meals
Rest after exercise
Stress
Succinylcholine
```
36
What is hyperkalemic periodic paralysis?
Mutations in the voltage gated sodium channel in skeletal muscle that interfere with channel inactivation leading to prolonged depolarization and subsequent myotonia, membrane desensitization and paralysis.
37
What is the goal CPP in a patient with TBI?
50-70 mm Hg
38
What cerebral artery is being evaluated by TCD?
Middle cerebral
39
What does TCD detect intraoperatively during carotid endarterectomy?
Embolization in more than 90% of patients
40
What are isonation windows?
Areas of the skull where the bone is less dense and therefore more amenable to US penetration.
41
What does the mean flow velocity following clamping of the carotid artery correlate with in CEA?
the degree of cerebral ischemia
42
What percentage of mean flow velocity indicates ischemia?
<40% of the preclamped mean flow velocity
| Severe = <15%
43
What do volatile agents do to CMRO2 and CBF in a dose dependent manner?
Uncouple the CMRO2 and CBF - cause a decrease in CMRO2 while increase CBF the higher the MAC
44
What affects somatosensory evoked potentials?
Anemia
Hyper/hypothermia
Hypoxia
45
How much will dropping a patient's PaCO2 by 1 mm Hg effect the CBF?
It will decrease CBF by 1-2 ml/100g/min
46
At what PaCO2 does local ischemia start?
PaCO2 of 25 mm Hg
47
What arterey is SSEP a poor monitor of?
The ASA because it gives blood supply to the motor portions.
48
How does the somatosensory pathway get to the brain?
Through the dorsal columns to the thalamus and cortex
49
Where does the lateral funiculus lie?
In the anterior portion of the spine
50
What does the lateral funiculus supply?
Sensory portion to LE
51
What are the considerations in neurofibromatosis?
1. Altered responses to neuromuscular blocking agents
2. Neurofibromas in the airway that can cause obstruction
3. Cervical spine abnormalities, scoliosis
4. Intracranial tumors
5. Endocrine disorders: pheo, medullary thyroid CA, hyperparathyroidism
52
When is vasospasm suspected on TCD?
When flow velocity of the MCA is > 120cm/s
| or FVMCA: FVICA ratio is larger than 3
53
What is the mechanism behind neurogenic pulmonary edema within a few hours of TBI?
Massive sympathetic discharge
54
What are the clinical manifestations of neurogenic pulmonary edema?
Rapid onset
| Intraalveolar hemorrhage
55
What is unique about brainstem auditory evoked potentials?
They are most resistant to anesthetic technique
56
Contralateral or bilateral changes in the BAEP recordings indicates what?
Changes in global physiology and blood supply to the auditory pathway
57
What is the path of stimulus to terminal recording of a somatosensory evoked potential?
Peripheral nerve --> dorsal root ganglia --> posterior spinal cord --> (decussation at the cervicomedullary jxn) medial lemniscus --> thalamus --> cortex
58
What does a decrease in amplitude or increase in latency of SSEP indicate?
Cortex ischemia
59
What does jugular bulb venous monitoring measure?
Direct cerebral oxygenation and global cerebral oxygen metabolism by measuring jugular venous oxygen sat and arterial-jug venous oxygen content differences.
60
What does SSEP measure?
MCA so can detect subcortical sensory cortex response to peripheral sensory nerve stimulation
61
What does internal carotid stump pressures reflect?
Collateral flow back-pressure in the circle of Willis originating from the contralateral carotid artery.
Detect hypoperfusion at pressures <50 mm Hg
***cannot detect emboli
62
What is EEG used for in CEA?
Monitoring for cerebral ischemia and for selective shunting during CEA
63
What is the pathogenesis of tetanus?
Inhibition of neurotransmitter release from inhibitory neurons in the CNS. Happens by cleavage of a protein component of synaptic vesicles, synaptobrevin II which prevents release of inhibitory NTs
64
What is the pathogenesis of botulism?
Inhibition of NT release for NMJ at alpha motor neurons
65
What is the pathogenesis of polio?
Destruction of cells in the CNS, particulary the spinal cord
66
What can cause exacerbations of MS?
Postpartum period
Spinal anesthesia
Hyperthermia
67
How can you decrease the incidence of myalgia after succinylcholine administration?
Calcium gluconate pretreatment (stabilizes celular membranes)
Lidocaine pretreatment
Perioperative vit C (stabilizes endothelial cells)
68
AT what point in CBF does irreversible brain damage begin to occur?
6-12 ml/100g/min
69
At what point in CBF does ischemia of brain begin to occur?
20 ml/100g/min
70
What is average CBF in the normal brain?
50 ml/100g/min
71
What is the ischemic penumbra?
The time period in which membrane failure and neuronal death can be prevented.
May be hours!
72
How much does CBF changes with 1 degree Celsius change in temperature?
5-7%
73
What does an entropy monitor do?
Processes the EEG signal with a publicly known algorithm that primarily measures the degree of disorder or variability within the EEG signal.
74
What are the CNS differences in the elderly
1. BBB is more permeable
2. Loss of brain volume that is not uniform
3. Decrease in neuronal density that is not uniform
4. Regional reductions of NTs
5. Reduction of blood flow and oxygen consumption in gray matter
6. Decreased CSF volume
7. Decreased response to hypoxia/hypercarbia
8. Higher pain thresholds
75
What are the changes of neuraxial anesthesia in the elderly?
Larger spread due to more epidural permeability, lower CSF volume and space.
76
What is the desired endpoint for barbiturate infusion during an open aneurysmal clipping?
Burst suppression
77
What are delta waves on EEG indicative of?
deep coma, anesthesia or encephalopathy
78
What are theta waves on EEG indicative of?
Encephalopathy
79
What are alpha waves on EEG indicative of?
Awake, but eyes closed
80
What are beta waves on EEG indicative of?
Wakefulness
81
What should not be used as an anesthetic technique in a patient with T1?
Spinal anesthesia with opioid only because it will not prevent autonomic hyperreflexia
82
What is complication not commonly seen with a sitting craniotomy?
POVL
83
What is the most worrisome complication of sitting craniotomy?
VAE because noncollapsible venous channels such as venous sinuses can be violated during surgery and air is entrapped in them due to negative pressure gradient between the surgical site and the heart.
84
Who is at the highest risk for developing tension pneumocephalus?
Posterior fossa or cervical dural incisions in the seated position due to possible air trapping and tracking cephalad in the higher regions of the brain
85
What position can decrease the risk of pneumocephalus?
The "ski-jump" position where the patient is in some reverse T and the neck slightly flexed so the occiput is level with or slightly below the level of the neck.
86
How much total body oxygen does the brain consume?
20%
87
What is average CMRO2?
3-3.8 ml/100 g/min or 50 ml/min
88
Where is CMRO2 greatest in the brain?
The gray matter of the cerebral cortex
89
What is total CBF in adults?
750 ml/min (15-20% of CO)
90
What flow rate of CBF is associated with cerebral impairment?
20-25 ml/100g/min
91
What is the normal global CBF rate?
50 ml/100g/min
92
What flow rate of CBF is associated with isoelectric EEG?
15-20 ml/100 g/min
93
What CBF rate is associated with irreversible damage?
10 ml/100 g/min
94
What is normal velocity of the MCA?
55 cm/sec
95
What does the Lindegaard ratio tell you?
Distinguishes between vasospasm and hyperemic blood flow
MCA velocity 3X the velocity of the ICA = vasospasm
96
What are the indirect measures of adequate CBF and brain tissue oxygen delivery?
TCDs
Near Infrared spectroscopy (primarily reflects cerebral venous oxygen saturation)
Brain tissue oximetry (through Clark electrode in a bolt)
Microdialysis (analyzes cerebral lactate, NTs, glucose, inflammatory medidators)
97
What is normal brain tissue oxygen tension?
20-50 mm Hg
98
What is normal CPP?
80-100 mm Hg
99
What CPP is associated with an isoelectric EEG?
25-40 mm Hg
100
At what range of MAP is CPP unchanged?
60-160 mm Hg
101
At what MAP is the BBB disrupted?
150-160 mm Hg
102
At what temperature does brain injury begin to occur?
42 C
103
At what temperature is the EEG isoelectric?
20 C
104
How much does CBF change by degree in temperature?
5-7%
105
How much CSF is made per hour in adult?
21 ml/hr
106
How much total CSF is there in an adult?
150 ml
107
How does the CSF flow?
Lateral ventricles --> foramina of Monroe (intraventricular) --> third ventricle --> fourth ventricle --> cerebellomedullary cistern --> subarachnoid spaced
108
Where is the foramin of Monroe?
Between the lateral and third ventricles
109
Where is the cerebral aqueduct of Sylvius?
Between the third and fourth ventricle
110
Where is foramen of Magendie?
Fourth ventricle to cisterna magna?
111
Where is foramen of Luschka?
Fourth ventricle to cisterna magna
112
Where is the CSF absorbed?
Arachnoid granulations over the cerebral hemispheres to the cerebral venous sinuses
113
What is the tonicity of CSF?
Isotonic with lower potassium, bicarb and glucose than plasma
(Choroid plexus actively secrete Na)
114
How are perivascular and interstitial protein returned to the blood?
By absorption of CSF
| no lymphatics in CNS
115
What are the major compensatory mechanisms for rises in ICP?
1. Movement of CSF from brain to spinal cord compartment
2. Increase CSF absorption
3. Decrease CBV mainly via venous sinuses
4. Decrease CSF production
116
What drugs/medications decrease CSF production?
```
Acetazolamide
Isoflurane
Lasix
Steroids
Spironolactone
```
117
How much does CBV increase with each 1 mm Hg increase in PaCO2?
By 0.05 ml/100 g
118
What are the four herniation site?
1. Cingulate gyrus under falx cerebri
2. Uncinate gyrus under tentorium cerebelli
3. Cerebellar tonsils thru foramen magnum
4. Any area under a defect in the skull (transcalvarial)
119
What do all the volatile agents do to CBF?
Increase it, thereby increasing ICP
120
What do all volatile agents do to CMR?
Decrease it
121
Which anesthetics decrease CMRO2, CBF and ICP?
```
Propofol
Etomidate
Lidocaine
Barbiturates
BZDs
```
122
Which volatile agent has the greatest effect on CBF?
Halothane
| At concentrations > 1%, it abolishes autoregulation
123
Which volatile agent has the greatest effect on CMR?
Isoflurane (50%)
124
How can you blunt the response of CBF and CMR to volatiles?
With hyperventilation/hypocapnia as the response of the cerebral vasculature to CO2 is retained with volatile agents
125
What is luxury perfusion?
The combination of a decrease in neuronal metabolic demand with an increase in CBF
126
What may happen with volatile agents?
You can get circulatory steal phenomenon due to increase blood flow to normal areas but not in ischemic areas where the arterioles are already maximally dilated.
127
How does isoflurane affect CSF?
It increases it absorption
128
How does halothan affect CSF?
It impedes its absorption
129
Which volatile agent produces the least cerebral vasodilation?
Sevoflurane
130
How much do barbs decrease CMR and CBF?
They decrease it in a dose-dependent manner until isoelectricity on EEG. This is about 50% of CMR and CBF
131
What are the CNS effects of barbs?
1. Dose dependent decrease in CBF and CMR
2. More decrease in CMR than CBF so get more metabolic supply than demand
3. Uniform decrease in CMR
4. Absorption of CSF
5. Robin hood steal phenomenon - redistribute blood flow to ischemic areas
6. anticonvulsant
132
What are the CNS effects of opioids?
Little effect on CBF, CMR, and ICP
133
Which opioids increase seizures?
Alfentanil
| Meperidine
134
Why is morphine a poor choice for neuroanesthesia?
Low lipid solubility
| Prolonged sedative effects
135
What are the CNS effects of etomidate?
1. Nonuniform decreases in CMR (more in cortex, than brainstem which may explain its greater hemodynamic stability)
136
In what patients should etomidate be avoided?
History of epilepsy
137
How does ketamine offer neuroprotective effects?
During times of increased glutamate concentrations as during brain injury
138
What is the principal advantage of lidocaine in neuroanesthesia?
It decreases CBF without causing hemodynamic effects
139
Which adrenergic receptors have the greater effect on the brain when the bbb is disrupted?
Beta 1 --> increase CMR and CBF
140
What does alpha 2 agonist due in the brain?
Cause vasoconstriction
141
When do vasopressors increase CBF?
Only when MAP is outside of the cerebral autoregulation curve
142
How can NMBs affect CMR and CBF?
HTN and histamine-mediated cerebral vasodilation
143
What is the pathophysiology of cerebral ischemia?
Intracellular K decreases while intracellular Na and Ca increase.
Increased intracellular Ca results in activation of lipases, proteases which results in FFA and COX and Lipoxygenase activities --> prostaglandins and leukotrienes --> cell injury
144
What happens in reperfusion?
Tissue damage due to formation of oxygen-derived free radicals
145
Which volatiles do not cause electrical silence?
Sevo
Des
Nitrous
146
What does nitrous cause on EEG?
High amplitude activation
147
Which IV anesthetics produce isoelectricity?
Propofol, barbs, etomidate
148
What does ketamine produce on EEG?
High amp theta followed by high amp gamma and low amp beta
149
What do somatosensory evoked potentials test the integrity of?
The spinal dorsal columns and sensory cortex
150
What are short latency evoked potentials from?
The nerve stimulated or the brain stem
151
What are long latency evoked potentials from?
The cortex
152
What are motor evoked potentials good for assessing?
The anterior spinal cord perfusion (aortic surgery)
153
What is vasogenic edema?
Most common
| Follows disruption of bbb
154
What is cytotoxic edema?
From metabolic insults such as hypoxia
| Results from failure of brain cells to actively extrude sodium causing progressive cellular swelling
155
What is interstitial edema?
Results from obstructive hydrocephalus and entry of CSF into the brain interstitium.
156
What does vasogenic edema often respond to?
Corticosteroids
157
How does furosemide lower the ICP?
By removing intracellular water from normal brain tissue
| Decreasing formation of CSF
158
How does mannitol lower ICP?
By increasing serum osmolality (300-315 mOsm/L = goal)
159
What are the detrimental effects of mannitol?
Pulmonary edema due to transiet increase in intravascular volume
Vasodilation
Expand hematomas by osmotic diuresis of the normal brain tissue around it
160
Who should mannitol be avoided in?
Elderly patients
Intracranial aneurysms
AVMs
ICH/IVH
161
What position are frontal, temporal and parieto-occipital craniotomies performed in?
Supine
162
What are posterior fossa tumors associated with?
Obstructive hydrocephalus through the fourth ventricle or cerebral aqueduct of Sylvius
163
What should you think of first if you have an abrupt circulatory change during a posterior fossa surgery?
Brain stem injury to respiratory center
164
What are the risks of sitting position?
1. Excessive neck flexion - swelling of upper airway due to decreased venous drainage
2. Pneumocephalus (delayed awakening, neurologic dysfunction)
3. VAE -
165
Where does a precordial doppler sit?
Right of the sternum between 3rd and 6th ribs
166
What are the signs of VAE?
1. Decreased ETCO2 due to increased dead space and decreased CO
2. Reappearance or increase of NO2 in expired gases
3. Mill wheel murmur
4. Hypotension
167
What are the steps of treating a VAE?
1. Notify surgeon to flood surgical field with saline, bone wax or wet gauze
2. Turn off nitrous oxide and turn up O2 to 100%
3. Open fluids to increase intravascular volume and CVP
4. Bilateral jugular vein compression
5. Head down position
168
What does anesthetic management of a patient with head trauma entail?
PaCO2 30-35
CPP 110-160 mm Hg
Avoid vasodilators until cranium is opened
Use volume and alpha agonism for hypotension
169
What is DIC due to head trauma usually due to?
The release of large amounts of brain thromboplastin
170
What is the pathophys of autonomic hyperreflexia?
No inhibitory signals can reach below the level of the lesion so you get unopposed vasoconstriction (HTN, MI, arrythmias) and SNS effects below the lesion and exaggerated PSNS effects above the lesion
171
What are the best anesthetic techniques to limit autonomic hyperreflexia?
Spinal or epidural
| Deep
172
What is contraindicated in elevated ICP in patients with head trauma?
High dose glucocorticoids because they increase mortality
173
What is triple H therapy?
HTN, hypervolemia, hemodilution
174
How quickly should acute hypernatremia be fixed?
At a rate of 1-3 mmol/hr with max of 12 meQ per day
175
How quickly should chronic hypernatremia be fixed?
0.5 mmol/hr
176
What is clofibrate?
Hypolipidemic agent that causes release of ADH used as outpatient for central DI.
177
What is chlorpropamide?
An oral hypoglycemic agent which stimulates ADH release used for as outpatient med for central DI.
178
What is the treatment for central DI?
Free water replacement
| DDAVP
179
What is better nasal or IV DDAVP?
Nasal because it lasts longer and has fewer pressor side effects
180
What does etomidate do to seizure duration?
Increases it
181
What does caffeine do to seizure duration?
Increases it
182
What is grade I on Hunt Hess?
Asymptomatic or mild headache
183
What is grade II on Hunt Hess?
Severe headache
| Nuchal rigidity
184
What is grade III on Hunt hess?
Drowsiness, confusion, or focal deficit
185
What is grade IV on Hunt Hess?
Stupid
| Hemiparesis
186
What is grade V on Hunt hess?
Coma
| Decerebrate posture
187
What is mild TBI defined by?
GCS of 13 or higher
188
What is moderate TBI defined by?
GCS of 9-12
189
What are the triggers for hypokalemic periodic paralysis?
Dextrose fluids, high sodium foods, ingestion of carbs, exercise, insulin, stress, hyperthermia
190
What are the hallmarks of hypokalemia periodic paralysis?
10-20 years of age, gets proximal muscle weakness with age,
Autosomal dominant alteration in cation channels
191
What is adenosine used for in aneurysmal clipping?
Circulatory arrest for 30-45 seconds
| During acute hemorrhage
192
What are the goals laid out by the American Association of Neurosurgeons for patient with head trauma?
ICP < 20-25 mm Hg
MAP > 80
PaO2 > 95
CPP > 60
193
What drug is used to prevent paralysis episode in both hypo and hyperkalemic periodic paralysis?
Acetazolamide
194
What are the treatments for hyperkalemia periodic paralysis?
Beta blockers
Acetazolamide
K-wasting diuretics
195
What are the treatments for hypokalemic periodic paralysis?
Acetazolamide
| K-sparing diuretics
196
What metabolic derangement can cause exacerbation of MS?
Hyperthermia because increased temperature blocks conduction of demyelinated nerves
197
Where should PaCO2 and CPP be kept in a TBI patient?
35-40 mm HG and 50-70 mm Hg respectively
198
What are the ST changes on ECG in SAH associated with?
Catecholamine release causing subendocardial ischemia
199
What is the path of stimulus to terminal of a motor evoked potential?
Lower limb cortex --> internal capsule--> brainstem --> corticospinal tract --> peripheral nerve
200
What is the path of stimulus of an auditory evoked potential?
Cochlea --> CN VIII --> cochlear nucleus --> inferior colliculus --> auditory cortex
201
What is the path of stimulus of visual evoked potential?
retina --> optic nerve --> optic chiasm --> optic trat --> superior colliculus --> visual cortex
202
What anti-epileptic can be used in central DI?
Carbamazepine because it sensitizes the collecting tubule to ADH
203
What does demeclocycline do?
Antagonizes ADH at tubule inducing DI. Used in SIADH
204
What is the correct pathway for eccrine swear gland innervation?
SNS preganglionic --> (via Ach) nicotinic --> SNS post ganglionic --> (Ach) muscarinic receptors
205
What organ has no postganglionic fibers?
Adrenal glands
206
How much does CMRO2 decrease for every 1 degree in temperature?
6 % with proportional changes in CBF
207
At what PaO2 does CBF become affected?
50 mm Hg
208
Where are the eccrine glands?
All over the body
209
What do eccrine glands do.
Provide cooling via sweating
210
Where are the apocrine glands?
Arm pits and perianal region
211
What are the clinical manifestations of neurogenic shock?
Unopposed vagal tone : Bradycardia, hypo tension from loss of cardiac accelerator fibers
Paradoxical shallow breaths indicate a lesion between C4-C7
212
What is the Bainbridge reflex?
When the heart rate increases due to stretch receptors in the atrial wall
213
What causes inhibition of acetylcholine at the NMJ?
Botulinum toxin
214
What areas do not contain the bbb?
Circumventricular areas and areas that regulate the ANS (area postrema, pineal gland, lamina terminals, median eminence, neurohypophysis)
215
What are the risk factors for intraoperative awareness?
TIVA with NMB
< MAC 0.7
Use of nitrous
Use of NMBs
216
Which gas is associated with the least amount of intraoperative awareness?
Isoflurane
217
Which gas is associated with the most intraoperative awareness?
Nitrous oxide
218
Why should you not push the CPP above 70?
Risk of ARDS
219
What is the response to stimulation in a paralyzed nerve compared to a normal nerve?
It is exaggerated due to extrajunctional Ach receptors
