U7 APEX: NEURO CNS1 and Review Exam Flashcards
(412 cards)
1
Q
What are the cells that provide metabolic support to neurons?
A
Astrocytes
2
Q
Role of Ependymal cells in the brain?
A
CSF production
3
Q
Role of Microglia cells in the brain?
A
Phagocytosis
4
Q
Role of Oligodendrocytes
A
Increase neuronal conduction velocity
5
Q
Cells in the brain that acts as macrophages and phagocytize neuronal debris
A
Microglia
6
Q
What cells form the myelin sheath in peripheral nerves.?
A
Schwann cells
7
Q
What is the most abundant type of glial cells
A
Astrocytes
8
Q
Cells that form the choroid plexus?
A
Ependymal cells
9
Q
Repair neuron after neuronal injury?
A
Astrocytes
10
Q
The functional unit of the nervous system and primary role?
A
The neuron; Primary role is to receive and send information
11
Q
The cell bodies form the
A
grey matter.
12
Q
The axons form the
A
white matter.
13
Q
Most tumors arise from the
A
glia.
14
Q
Controlling reuptake of neurotransmitters is function of the
A
Glial cells
15
Q
Nerve cell with the role of modulating nerve conduction.
A
Glial cells
16
Q
Also known as nerve glue?
A
Glial cells
17
Q
Most of the CNS neurons are (pseudounipolar, bipolar vs multipolar)
A
Multipolar
18
Q
Examples of Pseudounipolar
A
Dorsal root ganglion
Cranial ganglion
19
Q
3 types of neurons in the brain , name them
A
Multipolar
Pseudobipolar
Bipolar
20
Q
2 places in the body with bipolar neurons
A
Retina and ear
21
Q
The cerebral cortex is divided into four lobes.
A
Frontal
Occipital
Parietal
Temporal
22
Q
Frontal lobe function
A
Motor cortex
23
Q
Occipital lobe function
A
Vision
24
Q
Parietal lobe function
A
Sensation
25
Temporal lobe function
Audition
26
The brain can be divided into four areas: C-CBD
Cerebral hemispheres
Cerebellum
Brainstem
Diencephalon
27
What connects the hemispheres ?
The corpus callosum
28
It is located deep in the longitudinal fissure.
corpus callosum
29
Wernicke’s area: (W is double U)
U - Understanding speech
30
Broca's area = (BMW motors)
motor control of speech
31
Part of the 4 lobes that Contains auditory cortex and speech centers
Temporal
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Part of the 4 lobes that Contains vision cortex
Occipital
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Part of the 4 lobes that Contains somatic sensory cortex
Parietal
34
Part of the 4 lobes that Contains the motor cortex
Frontal
35
The cerebral hemispheres contain the following structures: cognition, sensation, and movement
Cerebral cortex –
36
The cerebral hemispheres contain the following structures:
Cerebral cortex – cognition, sensation, and movement
37
Fine control of movement accomplished by which cerebral hemisphere structure?
Basal ganglia
38
Memory and learning accomplished by which cerebral hemisphere structure?
Hippocampus
39
Which cerebral hemisphere structure controls emotion, appetite, responds to pain and stressors
Amygdala
40
Diencephalon: 2 parts are
Thalamus
Hypothalamus
41
Role of the Hypothalamus
primary neurohumoral organ
42
Role of the Thalamus
acts as a relay station that directs information to various cortical structures
43
Midbrain – tracts involved
auditory and visual tracts
44
2 organs autonomic integration
Pons – autonomic integration
Medulla – autonomic integration
45
Controls consciousness, arousal, and sleep
Reticular activating system
46
Cerebellum : 3 parts
Paleocerebellum
Archeocerebellum
Neocerebellum
47
Archeocerebellum - role
maintains equilibrium
48
Paleocerebellum - role
regulates muscle tone
49
Neocerebellum - role
coordinates voluntary muscle movement
50
What is the nerve most likely to be compressed with a pituitary tumor?
Optic nerve.
51
In contrast to spinal nerves that arise from the spine, the cranial nerves arise from the brain and brainstem. There are ____ cranial nerve pairs.
12
52
All of the cranial nerves are part of the________exception is _______
Mnemonic for five branches of the facial n. (CN 7): Two Zebras Bit My Carrot.
peripheral nervous system.With the exception of the optic n. (CN 2),
53
The Parasympathetic output is carried by CN
3, 7, 9, and 10.
54
The only cranial nerve that is surrounded by the dura
Optic nerve
55
Eye movement is controlled by CN
3, 4, and 6.
56
Eye movement is controlled by cranial nerve (s)
3, 4, and 6.
57
Bell's palsy results from injury to the
Facial N. (CN 7).
58
This causes unilateral facial nerve paralysis
Facial nerve (CN 7)
59
Generates excruciating neuropathic pain in the face.
Tic douloureux (trigeminal neuralgia CN 5)
60
Mnemonic for five branches of the facial n. (CN 7):
Two Zebras Bit My Carrot.
Temporal
Zygomatic
Buccal
Mandibular
Cervical
61
Bedside test of swallowing is what branch
vagus
62
Shoulder shrug assess the
Spinal Accessory nerve (CN XI)
63
Hearing assess the
Vestibulocochlear nerve
64
Site of CSF production is the
Choroid plexus
65
What is the Foramen of Monro?
Pathway between lateral and third ventricle
66
What is the Aqueduct of Sylvius?
Pathway between third and fourth ventricle
67
What is the Site of CSF reabsorption ?
Arachnoid villi
68
The cerebrospinal fluid function
CSF Production
CSF volume is ~ 150 mL.
Specific gravity = 1.002 – 1.009.
It is produced by the ependymal cells of the choroid plexus at a rate of 30 mL/hr.
The choroid plexus is located in all 4 cerebral ventricles.
CSF pressure is 5 – 15 mmHg.
CSF Circulation
cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function. It is located in the:
69
Name the Ventricles?
(left lateral, right lateral, third, and fourth)
70
CSF location
Cisterns around the brain
Subarachnoid space in brain and spinal cord
71
Blood Brain Barrier role
The blood brain barrier separates the CSF from the plasma.
72
BBB in the neonates
Is poorly developed in the neonate.
73
BBB and ions and molecules regulation
Has tight junctions that restrict passage of large molecules and ions.
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BBB dysfunction
Becomes dysfunctional at sites of tumor, injury, infection, or ischemia.
75
Where is the BBB not present?
Is not present at the chemoreceptor trigger zone, posterior pituitary gland, pineal gland, choroid plexus, and parts of the hypothalamus.
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BBB and carrier proteins
Does not have carrier proteins.
77
CSF volume is.
~ 150 mL.
78
Specific gravity =
1.002 – 1.009.
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CSF is produced where (cells) and at what rate?
It is produced by the ependymal cells of the choroid plexus at a rate of 30 mL/hr.
80
The choroid plexus is located in all
4 cerebral ventricles
81
CSF pressure is
5 – 15 mmHg.
82
Flow of CSF
Love My 3 Silly 4 Lorn Magpies
Lateral ventricles
Monro (foramen)
3rd ventricle
Sylvius (aqueduct)
4th ventricle
Luschka
Magendie
83
CSF Reabsorption: CSF is reabsorbed into the
venous circulation via the arachnoid villi in the superior sagittal sinus.
84
CSF Reabsorption is dependent on the
pressure gradient between the CSF and venous circulation.
85
CSF Composition: has its own
Chemical composition that provides optimal conditions for the brain.
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Glucose CSF vs plasma
CSF 60
Glucose 90
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Protein CSF vs plasma
CSF 35
Plasma 7000
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More acidic pH is is CSF vs plasma
CSF more acidic with a pH of 7.3 and plasma 7.40
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Autoregulation GRAPH
Review apex pic
PaCO2 - black line
Cerebral perfusion pressure - green line
PaO2 - purple line
Intracranial pressure - red line
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Cerebral Blood Flow: Define
We can define cerebral autoregulation as the brain’s ability to maintain a constant cerebral blood flow over a wide range of mean arterial blood pressures.
91
What is the benefit of CBF autoregulation?
The benefit of this process is that it ensures that the brain has a steady supply of oxygen and substrates in the face of blood pressure fluctuations that accompany everyday life.
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Cerebral Blood flow formula =
Cerebral Perfusion Pressure / Cerebral vascular resistance
93
Brain receives what % of CO
15%
94
Global brain blood flow? ml/g/min
45-55 ml/100g tissue/min
95
Cortical brain blood flow/
75-80 ml/100g tissue/min
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Subcortical brain blood flow (ml/100g tissue/min)
20 ml/100g tissue/min
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Critical Thresholds
CBF ~ 20 mL/100g tissue/min →
evidence of ischemia
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Critical Thresholds
CBF ~ 15 mL/100g tissue/min →
complete cortical suppression
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Critical Thresholds
CBF < 15 mL/100g tissue/min →
membrane failure & cell death
100
What are the 5 determinants of CBF:
1. Cerebral metabolic rate for oxygen
2. Cerebral perfusion pressure
3. Venous pressure
4. PaCO2
5. PaO2
101
Cerebral Metabolic Rate for Oxygen (CMRO2) = Normal range
CMRO2 = 3.0 – 3.8 mL/O2/100g brain tissue/min.
102
Cerebral blood flow is coupled to_______ –
CMRO2
103
CBF is coupled with CMRO2, what is the meaning?
the higher the need for oxygen, the more blood flow there will be to satisfy this need.
104
CMRO2 is increased by what 2 anesthetic agents?
ketamine, and nitrous oxide.
105
Hyperthermia, seizures on CMRO2
Increase CMRO2
106
At what point does Hyperthermia decrease CBF ? and why?
beyond 42 degrees C denatures proteins and destroys neurons. At this point, cerebral blood flow decreases.
107
Breakdown of oxygen utilization in the brain
Electrical vs cellular integrity.
60% is used for electrical activity
40% is used for cellular integrity
108
Even if the brain is electrically silenced, what occurs in the brain for cellular integrity?
it still has to consume oxygen to support cellular integrity.
109
Decreasing CMRO2:
7% for every 1 degree C decrease in temperature.
110
CMRO2 is decreased by what 3 anesthetics
halogenated anesthetics, propofol, Etomidate
111
Barbiturates on CMRO2?
Decrease CMRO2
112
EEG suppression occurs at what Celsius degrees?
18 – 20 degrees C.
113
We can improve outcomes in the patient who suffers anoxic brain injury by
reducing CMRO2.
114
Patients have an improved neurologic outcome following resuscitation from out-of-hospital ventricular fibrillation when they are treated with
mild hypothermia (32-34 degrees C) for 12 - 24 hours after hospital admission.
115
Classic doctrine suggests that the brain auto-regulates cerebral blood flow between a cerebral perfusion
pressure of 50 - 150 mmHg or MAP of 60 – 160 mmHg (the plateau on the curve represents this).
116
Below the lower limit of autoregulation (left of the plateau),.
the cerebral vessels are maximally dilated.
117
Cerebral perfusion becomes dependent on mean arterial pressure, and the brain is at risk of
hypoperfusion and ischemia.
118
Above the upper limit of autoregulation (right of the plateau), the cerebral vessels are
maximally constricted. Again, cerebral perfusion becomes dependent on mean arterial pressure, but this time the brain is at risk for cerebral edema and hemorrhage.
119
Cerebral autoregulation is mediated by products of 3 things
local metabolism, myogenic mechanisms, and autonomic innervation.
120
To ensure a CPP of 50 mmHg, MAP must be ______mmHG and ICP in the normal range ____________ mmHg
55 – 65 mmHg if ICP is in the normal range of 5 – 15 mmHg.
121
Chronic hypertension shifts the entire curve to the
right – the brain becomes more tolerant of hypertension, but it also becomes less tolerant of hypotension. In reality, the plateau of the curve narrows and CBF becomes more closely dependent on CPP. Furthermore, you can expect a high degree of patient-to-patient variability
122
When autoregulation is impaired, CPP becomes dependent on blood pressure. Autoregulation is abolished by:
Intracranial tumor
Head trauma
Volatile anesthetics
123
If ICP is elevated, cerebral perfusion requires a
higher mean arterial pressure.
124
In reality, there is a good degree of patient-to-patient variability, so we must not blindly assume that a minimum threshold for CPP (or MAP) ensures an
adequate CPP in all patients.
125
Venous Pressure: A high venous pressure on
decreases cerebral venous drainage and increases cerebral volume. This creates a backpressure to the brain that reduces the arterial/venous pressure gradient (MAP – CVP).
126
Conditions that impair venous drainage include:
-Jugular compression secondary to improper head positioning
-Increased intrathoracic pressure secondary to coughing or PEEP
-Vena cava thrombosis
-Vena cava syndrome
127
Respiratory disturbances and effect of CBF
Respiratory acidosis increases CBF.
Respiratory alkalosis decreases CBF.
128
Does Metabolic acidosis affect CBF?
Does not affect cerebral blood flow. This is because H+ does not pass through the blood brain barrier.
129
Maximal vasoconstriction occurs at a PaCO2 of
25 mmHg.
130
Maximal vasodilation occurs at a PaCO2 of
80 – 100 mmHg.
131
For every 1 mmHg decrease in PaCO2, CBF will
decrease by 1 – 2 mL/100g brain tissue/min.
132
For every 1 mmHg increase in PaCO2, CBF will
increase by 1 – 2 mL/100g brain tissue/min.
133
The pH of the CSF around the arterioles controls
cerebral vascular resistance.
134
At a PaCO2 of 40 mmHg, What is CBF?
50 mL/100 g brain tissue/min.
135
Steal Phenomena:
Situations that cause cerebral vasodilation (hypercapnia, hypoventilation, administration of a vasodilator) vasodilate the vessels that supply healthy brain tissue. As a result, this can “steal” flow from ischemic areas. This phenomenon is called “cerebral steal.”
The cerebral vessels that supply healthy brain tissue have tone (they alter their diameter based on the PaCO2). Conversely, vessels that supply ischemic or atherosclerotic regions are maximally dilated.
136
“Inverse steal” or the “Robinhood effect” is the concept of using
hyperventilation to constrict the cerebral vessels that supply healthy brain tissue.
137
The idea is that flow will be redistributed to ischemic regions (remember they’re maximally dilated). Although nice in theory, hypocapnia has not been shown to produce a clinical benefit. Furthermore, it may cause harm by reducing
cerebral blood flow and shifting the oxyhemoglobin dissociation curve to the left (less O2 released to tissues). Therefore, best practice is to maintain normocapnia or very mild hypocapnia (PaCO2 = 30 – 35 mmHg).
138
Situations that cause cerebral vasodilation
Hypercapnia, hypoventilation, administration of a vasodilator) vasodilate the vessels that supply healthy brain tissue. As a result, this can “steal” flow from ischemic areas. This phenomenon is called “cerebral steal.”
139
Situations that cause cerebral vasodilation
(hypercapnia, hypoventilation, administration of a vasodilator) vasodilate the vessels that supply healthy brain tissue.
140
When PaO2 is
above 60 mmHg, it does not affect cerebral blood flow.
141
A fixed and dilated pupil suggests herniation of the:
temporal uncus.
142
The Monro-Kellie doctrine states that the
Since the oculomotor nerve (CN III) originates from the midbrain and crosses near the tentorium, herniation of this region puts pressure on and causes ischemia to CN III. Clinically this manifests as a fixed and dilated pupil.
brain, blood, and CSF are relegated to the confines of the cranium. If there is an increase in any one of these constituents, there must be a reduction in one or both of the others. If not, the pressure inside the cranium will rise.
143
The risk of elevated ICP is and the most common site of transtentorial herniation is at the temporal uncus. As ICP rises, the temporal uncus is forced from the supratentorial space into the infratentorial space. This increases pressure on the midbrain.
cerebral herniation,
144
The Monro-Kellie doctrine states that the
brain, blood, and CSF are relegated to the confines of the cranium. If there is an increase in any one of these constituents, there must be a reduction in one or both of the others. If not, the pressure inside the cranium will rise.
145
The risk of elevated ICP is
cerebral herniation
146
As ICP rises, the temporal uncus is forced from the
supratentorial space into the infratentorial space. This increases pressure on the midbrain.
147
Since the oculomotor nerve (CN III) originates from the
midbrain and crosses near the tentorium, herniation of this region puts pressure on and causes ischemia to CN III. Clinically this manifests as a fixed and dilated pupil.
148
Intracranial pressure is the
supratentorial CSF pressure.
149
Intracranial pressure is the
supratentorial CSF pressure.
150
States that an increase in one of the components must be countered with a decrease in one or both of the others. If not, then pressure inside the cranium will rise.
Monro-Kellie hypothesis
151
The brain lives in a rigid, bony box. Within this box, there are three components:
brain, blood, and cerebrospinal fluid.
152
Normal ICP (opening pressure) is
5 - 15 mmHg.
153
Cerebral hypertension occurs if
ICP > 20 mmHg.
154
The gold standard of ICP measurement is an
intraventricular catheter.
155
ICP measurement is indicated with a Glasgow Coma Scale score
< 7.
156
ICP can also be measured with a subdural bolt or a
catheter placed over the convexity of the cerebral cortex.
157
Signs and symptoms Intracranial HTN
Headache
Nausea and vomiting
Papilledema
Focal neurologic deficit
Decreased LOC
Seizure
COMA
158
At lower intracranial pressures, CSF is
shunted into the spinal canal. This is represented by the horizontal portion of the ICP curve. As intracranial volume rises beyond the inflection point on the graph, cerebral perfusion pressure begins to suffer (CPP = MAP - ICP).
159
At lower intracranial pressures, CSF is
shunted into the spinal canal. This is represented by the horizontal portion of the ICP curve.
160
Cushing's triad is a sign of intracranial hypertension.
Hypertension
Bradycardia
Irregular respirations
161
Intracranial hypertension reduces oxygen delivery to the brain. This sets off a vicious circle of
cerebral ischemia → cerebral swelling → decreased CPP → more ischemia
162
As intracranial volume rises beyond the inflection point on the graph, cerebral perfusion pressure
begins to suffer (CPP = MAP - ICP)
163
Increased ICP reduces
CPP. In an effort to preserve cerebral perfusion, blood pressure increases.
164
Hypertension activates what reflex?
baroreceptor reflex, leading to bradycardia.
165
Brain herniation tends to occur at four different locations:
Herniation of the cingulate gyrus under the falx.
Herniation of contents over the tentorium cerebelli (transtentorial herniation).
Herniation of the cerebellar tonsils through the foramen magnum.
Herniation of contents through a site of surgery or trauma.
166
The oculomotor nerve (CN III) originates from the
midbrain and crosses near the tentorium
167
Herniation applies pressure to the nerve, making it ischemic. Clinically this manifests as what kind of pupil?
fixed and dilated pupil.
168
What is transtentorial herniation?
Herniation of contents over the tentorium cerebelli
169
Compression of the medulla causes
irregular respirations.
170
Anesthetic management for the patient with an ICP of 25 mmHg undergoing craniotomy for tumor resection includes: (Select 3.
phenylephrine
dexamethasone.
PaCO2 30 mmHg.
171
This patient has an elevated ICP and is at risk for cerebral ischemia. Anesthetic management is tailored to
reduce ICP while preserving CPP.
172
Hyperventilation (PaCO2 30-35 mmHg) constricts
the cerebral vessels, decreases cerebral blood volume, and reduces ICP.
173
Dexamethasone on tumor
reduces swelling around the tumor (it does not shrink the actual tumor). Phenylephrine is used to support CPP.
174
PEEP on CBF
increases intrathoracic pressure and reduces venous outflow away from the brain
175
Does nitroprusside increase or reduce ICP?
Although nitroprusside reduces systemic blood pressure, it dilates the cerebral vasculature and increases CBF and ICP.
176
When and Why you SHOULD NEVER GIVE DEXTROSE?
D5LR contains glucose and in the setting of cerebral ischemia, excess glucose in the brain is converted to lactic acid, thereby worsening outcome.
177
Methods to reduce ICP can be divided into four areas:
CBV reduction
CSF reduction
Cerebral edema reduction
Cerebral mass reduction
178
Decrease Cerebral Blood Flow: HYPO vs HYPERVENTILATION
Hyperventilation → CO2 dilates the cerebral vessels → ↓ cerebral vascular resistance → ↑ CBF → ↑ ICP.
179
Hyperventilation (PaCO2 30-35 mmHg) on cerebral vessels, CVR, CBF
cerebral vessels → ↑ cerebral vascular resistance → ↓ CBF → ↓ ICP.
180
Lowering PaCO2 < 30 mmHg increases the risk of ______why>
risk of cerebral ischemia due to vasoconstriction and shifting the oxyhemoglobin dissociation curve to the left (this reduces oxygen offloading).
181
The effect of hyperventilation last for how long? and why?
only lasts 6 - 20 hours, because the pH of CSF equilibrates with the PaCO2.
182
Even in the traumatized brain,What is preserved?
CO2 reactivity is usually preserved.
183
Hypoxemia effect on the CBF and ICP?
Avoid Hypoxemia
PaO2 < 50 - 60 mmHg greatly increases CBF and ICP.
184
Drugs to avoid when attempting to decrease CBF.
Avoid cerebral vasodilators (nitroglycerine and nitroprusside)
185
Drugs that reduce CMRO2 are thought of as cerebral vasoconstrictors
(thiopental, propofol).
186
Hemodynamics Avoid extreme hypertension with brain surgery patients - why?
BP beyond the upper limit of autoregulation contributes to cerebral edema.
187
2 main ways to Increase Venous Outflow
Change of Position
Reduce Intrathoracic Pressure
188
2 main ways to Reduce Cerebral blood volume
Decrease Cerebral Blood Flow
Increase venous outflow
189
Change of position that can increase venous outflow : head elevation
Head elevation > 30 degrees facilitates venous drainage from the brain.
190
Neck position and how it affects CBV, ICP
Neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP.
191
Head down effect of CBV and ICP
increases CBV and ICP.
192
Cerebrospinal Fluid Reduction: 2 main ways
CSF Drainage and Drugs
193
Draining CSF is most useful when
There is an obstruction to CSF flow such as hydrocephalus.
194
Acute treatment of increase CSF
A drain placed in the lateral ventricles or intrathecal space improves ICP by reducing CSF volume.
195
Chronic treatment of increase CSF
A shunt drains CSF to the peritoneal cavity (ventriculoperitoneal shunt) or the right atrium (ventriculoatrial shunt).
196
2 main drugs that decrease CSF
Acetazolamide and furosemide reduce CSF production.
197
Cerebral Edema Reduction
2 medications
Diuretics and Corticosteroids
198
Loop diuretics and cerebral edema and mechanism of action
Reduce cerebral edema by inducing diuresis and decreasing the rate of CSF production
199
Osmotic diuretics and cerebral edema , dose
(mannitol 0.25 - 1.0 g/kg) increases serum osmolarity and "pull" water across the blood brain barrier.
200
If the blood brain barrier is disrupted, mannitol
Enters the brain and increases cerebral edema!
201
Mannitol transiently
increases blood volume, which can increase ICP and stress the failing heart.
202
While not a diuretic, how does 3% saline reduces cerebral edema?
the high tonicity of three percent sodium chloride also reduces ICP by "pulling" water across the blood brain barrier.
203
Corticosteroids Dexamethasone and methylprednisolone reduce
cerebral edema caused by mass lesions.
204
Corticosteroids cause hyperglycemia. Remember that hyperglycemia in the setting of
cerebral ischemia is associated with worse outcomes.
205
Steroids are also used for
spinal cord injury.
206
Should NOT be used for traumatic brain injury.
Steroids
207
Cerebral Mass Reduction
2 ways
a) Tumor debulking or evacuation of hematoma.
b) By reducing cerebral edema, diuretics (such as mannitol) reduce intracerebral mass (water mass - not cellular mass).
208
There is only one basilar artery. It is the main blood supply to the
brain's posterior circulation.
209
Gives rise to the paired posterior communicating arteries.
The basilar artery
210
Give rise to the paired vertebral arteries.
The subclavian arteries
211
Give rise the paired middle cerebral arteries.
The internal carotid arteries
212
The arterial cerebral circulation can be divided into two separate circulations:
anterior and posterior. They converge at the circle of Willis.
213
Anterior Circulation → The internal carotid arteries supply the anterior circulation. They enter the skull through the
foramen lacerum.
214
Supply the anterior circulaton is the _____arteries
internal carotid arteries
215
Anterior Circulation route Aorta →
Carotid a. → Internal carotid a. → Circle of Willis → Cerebral hemispheres
216
Posterior Circulation: What arteries supply the posterior circulation? Where do they enter the skull?
The vertebral arteries supply the posterior circulation. They enter the skull through the foraman magnum.
217
Posterior Circulation route : Aorta →
Subclavian a. → Vertebral a.→ Basilar a. → Posterior fossa structures and cervical spinal cord
218
Circle of Willis
The anterior and posterior circulations converge where?
at the circle of Willis
219
The primary function of the circle of Willis is to provide
redundancy of blood flow in the brain.
220
If one side of the circle becomes occluded, then the other side should
theoretically be able to perfuse the affected areas of the brain.
221
While this only holds true in.
42 – 52 percent of the population, there are usually additional collateral networks that provide circulatory redundancy
222
Venous Circulation: The venous cerebral circulation can also be divided into two separate circulations.
Venous blood from the cerebral cortex
Venous blood from the basal brain structures
223
Venous blood from the cerebral cortex and cerebellum drain via the
Superior sagittal sinus and the dural sinuses.
224
Venous blood from the basal brain structures drain via the
inferior sagittal sinus, vein of Galen and the straight sinuses.
225
Both venous pathways converge where?
Both venous pathways converge at the confluence of sinuses.
226
All venous blood exits the brain via the
paired jugular veins.
227
Within how many hours can IV recombinant tissue plasminogen activator be given after a patient exhibits symptoms of an acute ischemic stroke?
3 hours
228
A person who exhibits a sudden change in neurologic function or a progressive change in neurologic status is most likely experiencing a
cerebrovascular accident (CVA).
229
We can classify the type of CVA as either.
ischemic or hemorrhagic
230
Ischemic strokes are more common and most likely stem from a
cardio-embolic event, such as atrial fibrillation.
231
A transient ischemic attack (TIA) or "mini stroke" is a
focal neurologic deficit that spontaneously resolves within 24 hours.
232
It's a warning sign of
cerebrovascular disease and impending stroke.
233
Most Important of Risk Factors of Ischemic Stroke
Hypertension (most important)
234
Other Risk Factors for ischemic Stroke
Smoking
Diabetes mellitus
Hyperlipidemia
Excessive alcohol intake
Elevated homocysteine level
235
Since the etiology of CVA cannot be determined by clinical criteria alone, the patient should receive an
emergent non-contrast CT.
236
In the first few hours after the precipitating event, CT will reliably detect
intracerebral hemorrhage. If bleeding is ruled out, the patient most likely suffers an ischemic stroke.
237
If treatment can begin < 3 hours after the onset of symptoms, the patient with an ischemic CVA should r
eceive an intravenous thrombolytic such as recombinant tissue plasminogen activator (tPA).
238
An alternative if tPA cannot be administered.
Aspirin
239
What is indicated after an acute CVA,
During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue and is associated with worse outcomes. Monitor serum glucose and treat hyperglycemia with insulin.
Hyperthermia increases CMRO2 and cerebral oxygen consumption. Controlled hypothermia reduces CMRO2.
Immediate assessment of airway reflexes and ventilatory drive. however the majority of patients can protect their airways and only require supplemental oxygen.
240
Common after ischemic CVA.
Hypertension
241
An elevated BP supports
CPP and cerebral oxygenation.
242
Hypotension reduces CPP, which worsens ischemia.
The target pressure should be maintained under
185/110.
243
During cerebral hypoxia, what happens to glucose?
glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue and is associated with worse outcomes..
244
Monitor serum glucose and treat hyperglycemia with
insulin
245
2 Roles of Fluid replacement
supports blood pressure, cardiac output, and CPP. It also improves CBF by decreasing viscosity.
246
Hyperthermia increases
CMRO2 and cerebral oxygen consumption.
247
Controlled hypothermia and CMRO2
reduces CMRO2.
248
Prevention and treatment of cerebral vasospasm following subarachnoid hemorrhage includes: (Select 3.)
nimodipine.
hematocrit 30%
daily transcranial Doppler exams.
249
What is the leading cause of morbidity and mortality after subarachnoid hemorrhage?
Vasospasm
250
Prevention consists of vasospasm include 2
nimodipine and triple H therapy (hemodilution, hypervolemia, and hypertension).
251
The patient at risk for VASOPASM the patient should receive
frequent neurologic evaluation as well as daily transcranial Doppler examinations.
252
Since nimodipine is the
only calcium channel blocker that reduces morbidity and mortality associated with vasospasm
253
Go against triple H therapy.
Controlled hypotension and mannitol
254
The most common cause of subarachnoid bleeding is
aneurysm rupture.
255
Most aneurysms arise in the
circle of Willis
256
Arterial bleeding usually occurs in the
subarachnoid space (between the arachnoid and pia).
257
Venous bleeding usually occurs in the
subdural space (between the dura and arachnoid).
258
Aneurysm Rupture: what predisposes rupture?
An increased transmural pressure predisposes the aneurysm to rupture. As the vessel bursts, blood flows into the subarachnoid space
259
We like to think of MAP as the.
pressure pushing outwards against the aneurysmal sac and ICP as the counter pressure that pushes against it. In essence, ICP creates a tamponade effect.Using this model, it's easy to see that the risk of rupture is increased by hypertension and/or an acute reduction in ICP.
260
Morbidity is usually the result of
Obstructive hydrocephalus
Rebleeding
Vasospasm
261
The most common sign of SAH is an
intense headache that is often described as the "worst one in my life."
262
Consciousness is lost about.
50 percent of the time, and other s/sx include focal neurologic deficits, N/V, photophobia, and fever
263
Meningismus (signs of meningitis) occurs as
blood spreads throughout and irritates the subarachnoid space. Furthermore, blood can block CSF flow, causing obstructive hydrocephalus and increasing ICP.
264
What is cerebral vasospasm?
delayed contraction of the cerebral arteries.
265
Vasospasm can lead to
It can lead to cerebral infarction and is the most significant source of morbidity and mortality in the patient with SAH.
266
Increases the risk of vasospasm.
Free hemoglobin that is in contact with the outer surface of the cerebral arteries i
267
There is a positive correlation between the
amount of blood observed on CT and the incidence of vasospasm.
268
Vasopasm occurs in _____patients and most likely when following SAH
It occurs in about 1:4 patients and is most likely 4 - 9 days following SAH.
269
Treatment of vasospasm is aimed at
maintaining cerebral perfusion pressure (CPP = MAP - ICP or CVP whichever is higher).The idea is that ischemic areas of the brain are already maximally vasodilated, so perfusion to these regions is pressure dependent.
270
Monitor for the development vasospasm.
Frequent neurologic checks and transcranial Doppler exams
271
If vasospasm occurs, triple H therapy (hypervolemia, hypertension, and hemodilution to Hct 27 - 32 percent) is
the standard of care. It should be noted that there is little evidence for this.
272
During vasospasm these 2 Together these improve cerebral blood flow.
Liberal hydration supports blood pressure and CPP. It also creates a state of hemodilution, which reduces blood viscosity and cerebrovascular resistance.
273
Nimodipine real action
Interestingly, it does not actually relieve the spasm, but instead it increases collateral blood flow.
274
Surgical Options of aneurysm
Surgical options include
aneurysm clipping or endovascular coiling. The goals of anesthetic management are similar for both types of procedures.
275
To reduce the risk of rebleeding, surgical repair should take place _______
24 - 48 hours following the initial bleed. Intervention at this time makes triple H therapy safer (hypertension can cause rebleeding if the aneurysm isn't clipped).
276
If an endovascular coil is placed, the patient will require
heparinization.
277
If the aneurysm ruptures during the procedure,
If the aneurysm ruptures during the procedure, you should immediately reverse heparin with 1 mg of protamine for every 100 U of heparin administered. MAP should be lowered into the low/normal range. While it wasn't cited in our references, adenosine can be given to temporarily arrest the heart, so the interventional radiologist can control the bleeding.
278
Intraoperative BP Control: Aneurysm repair?
As a general rule, intraoperative SBP should be between.
120 - 150 mmHg
279
If the patient undergoes an open repair, a clamp is commonly placed on a.
proximal feeder vessel. This reduces transmural pressure and the risk of intraoperative rupture, while also circumventing the need for controlled hypotension
280
A high/normal BP is required toon.
perfuse the collateral circulation.Some surgeons won't use a clamp and may request controlled hypotension. The most significant drawback of this technique is a reduction in CPP.
281
Meticulous BP control during induction and intubation is critical! If rupture occurs during this time, the focus of anesthetic management is on
reducing ICP and utilizing methods of cerebral protection.
282
If BP is too high, transmural pressure
rises and increases the likelihood of rebleeding.
283
If BP is too low, CPP may be
inadequate, as autoregulation is usually impaired following SAH.
284
Cerebral Salt-Wasting Syndrome: the most common result of cerebral salt wasting syndrome,
Hyponatremia is most commonly the result of cerebral salt-wasting syndrome (not SIADH).
285
Cerebral Salt-Wasting Syndrome: mechanism
The brain releases natriuretic peptide (just like the overfilled heart), and this leads to volume contraction, hyponatremia, and sodium wasting by the kidney. Cerebral salt-wasting syndrome is treated with isotonic crystalloids.
286
As a point of comparison, SIADH vs Cerebral salt wasting, SIADH causes
euvolemia or slight hypervolemia and is treated with fluid restriction.
287
Management for the patient with traumatic brain injury on clopidogrel includes:
hypertonic sodium chloride.
platelet transfusion.
288
Head trauma can be blunt or penetrating. Initial considerations include
stabilization of the cervical spine, airway protection, optimization of hemodynamics, and cerebral protection.
289
Head CT rapidly determines the presence of intracranial bleeding. If a patient with minor head trauma satisfies the following criteria, a head CT probably isn't required:
No physical evidence of trauma above the clavicles
No headache
No N/V
No neurologic deficit
No impairment of short term memory
No intoxication
No seizures
Age < 60 years
290
Warfarin can be reversed with.
FFP, prothrombin complex concentrate, and/or recombinant factor VIIa.
291
There is also evidence of reversal with
Recombinant factor VIIa
292
Anesthetic Management for traumatic Brain injury : CPP , ICP
Keep CPP > 70 mmHg
You'll want to reduce ICP with all of the techniques we described a few pages back, but there are two things you should specifically avoid in the patient with TBI.
293
Anesthetic Management for traumatic Brain injury : CPP, ICP
- Keep CPP > 70 mmHg
- You'll want to reduce ICP with all of the techniques we described a few pages back, but there are two things you should specifically avoid in the patient with TBI.
294
Prolonged hyperventilation can worsen
cerebral ischemia in patients with TBI. Hyperventilation is only indicated as a temporary measure to acutely reduce ICP.
295
Steroids and TBI
worsen neurologic outcomes
296
TBI Fluid Selection: Hypertonic saline restores
intravascular volume and decreases brain water.
297
TBI Fluid Selection: Hypotonic solutions are
avoided, as they increase cerebral edema.
298
Glucose containing solutions worsen
neurologic outcome in the setting of cerebral ischemia.
299
Glucose is only indicated in the
hypoglycemic patient.
300
Albumin and TBI
has been linked to a poorer outcome.
301
Nitrous Oxide and pneumothorax
Nitrous oxide can rapidly expand a pneumothorax or cause pneumocephalus. Do not use it in the patient with TBI.
302
Which agent should be avoided in the patient with epilepsy?
Ketamine
303
Seizures are the result of an..
abnormal electrical discharge in the brain
304
A partial (focal) seizure results when a seizure
activity is localized to a particular cortical region
305
A generalized seizure occurs when the
activity affects both hemispheres.
306
A partial seizure can progress to a
generalized seizure. This is called a Jacksonian march.
307
Epilepsy is characterized by
idiopathic seizures. It is diagnosed in childhood.
308
In the adult, new onset seizures are usually the result of a:
Structural brain lesion: tumor, head trauma, or cerebrovascular event.
309
Metabolic cause of seizure
hypoglycemia, drug toxicity, withdrawal, or infection.
310
Effects of Anesthetic Agents: Inhalational Agents
Although all of the inhalational agents have been implicated in producing seizure activity, these drugs tend to reduce EEG activity in a dose dependent fashion.
311
Seizures can occur under general anesthesia. Signs include
tachycardia, hypertension, and increased EtCO2 as a result of increased oxygen consumption.
312
Etomidate commonly causes
There are several case reports of propofol induced seizures and opisthotonos (rigid posture with arched back). Keep in mind that propofol is a first line agent for control of acute seizure activity.
myoclonus. This is not associated with increased EEG activity in patients that do not have epilepsy.
313
In patients with seizure disorders, DRUGS that increases EEG activity and can be used to help determine the location of seizure foci during cortical mapping.
methohexital, etomidate, and alfentanil
314
Normeperidine is a metabolite of
meperidine. It is capable of producing seizure activity.
315
Local anesthetics reduce the
seizure threshold, but a properly executed regional anesthetic does not increase the risk of seizures.
316
Cisatracurium also produces
laudanosine, but in a much smaller quantity.
317
Atracurium metabolism yields
laudanosine, a proconvulsant. This is only a potential issue with long-term infusions in the ICU.
318
There are several case reports of propofol induced
seizures and opisthotonos (rigid posture with arched back). Keep in mind that propofol is a first line agent for control of acute seizure activity.
319
What is status epilepticus?
Seizure activity that last 30 minutes OR 2 Grand mal seizures without consciousness in between
320
Which drug is excreted unchanged by the kidneys?
Gabapentin
321
Gabapentin is unique how?
among the anticonvulsants, because it is excreted unchanged by the kidneys
322
Valproic acid inhibits
hepatic enzymes.
323
Carbamazepine, and phenytoin and hepatic enzymes
induce hepatic enzymes.
324
Valproic acid, carbamazepine, and phenytoin are metabolized by the
liver.
325
What is the mechanism of phenytoin?
Blocks voltage gated Na+ channels , membrane stabilizer.
326
Phenytoin Kinetics
Zero order kinetics
327
Valproic Acid Mechanism of action
Blocks voltage gated Na+ channels , membrane stabilizer.
328
Carbamezipine mechanism of action
Blocks voltage gated Na+ channels , membrane stabilizer.
329
Gabapentin and Pregabalin MOA
Inhibition of the alpha 2 delta subunit of voltage gated calcium channel in the CNS --> Decrease excitatory neurotransmitter release.
330
3 other things GABAPENTIN used to treat
Diabetic neuropathy
Postherpetic neuralgia
Reflex sympathetic dystrophy
331
What medication is used to treat TRIGEMINAL NEURALGIA
Carbamezipine (Tegretol)
332
Associated with Aplastic anemia
Phenytoin
333
Associated with Steven Johnsons Syndrome
Phenytoin
334
The duration of action of which drug will be prolonged in the patient treated with donepezil for Alzheimer's disease?
Succinylcholine
335
Are the mainstay of medical therapy for Alzheimer's disease.
Cholinesterase inhibitors
336
Inhibition of pseudocholinesterase in the plasma does what to succinylcholine?
increases the duration of action for succinylcholine and mivacurium.
337
Alzheimer’s disease is a It is the most common cause of dementia in patients 65 years and older. There is no cure for Alzheimer's.
chronic degenerative condition of the CNS.
338
It is the most common cause of dementia in patients 65 years and older.
Alzheimer’s disease
339
Key findings in Alzheimer's include the development of
diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain.
340
Consequences of plaque formation in Alzheimer's include:
- Dysfunctional synaptic transmission (most common in Ach neurons)
Apoptosis (programmed cell death)
341
Alzheimer's S/sx include
memory loss, apraxia, aphasia, and agnosia.
342
Treatment of Alzheimer's
Treatment is palliative and aims to restore the concentration of Ach.This is accomplished with cholinesterase inhibitors such as tacrine, donepezil, rivastigmine, and galantamine.
343
Anesthetic Management: MAC or regional with sedation
Patients are often confused, scared, and uncooperative, thus making them poor candidates for MAC and/or regional anesthesia with or without sedation.When a general is planned, shorter acting drugs are best. In theory, this allows the patient to return to his or her baseline cognition as soon as possible.
344
Alzheimer's and preoperative sedation
Preoperative sedation can worsen confusion, so it should be avoided if possible.
345
Anticholinesterase drugs and PNS
These drugs increase PNS tone, so s/sx of parasympathetic excess can develop: bradycardia, syncope, and n/v.
346
If an anticholinergic is required for patients with alzheimer's disease
glycopyrrolate is the best option since it does not cross the blood brain barrier.
347
Investigations claim there is an increased risk of alzheimers if ____? why?
undergone multiple general anesthetics prior to age 50.s Some of the halogenated anesthetics (halothane and isoflurane) increase beta amyloid production - the protein that is implicated in the genesis of Alzheimer's disease.
348
Which factors contribute to the pathophysiology of Parkinson's disease? (Select 2.)
Increased GABA in the thalamus
Decreased dopamine in the basal ganglia
349
In a nutshell, the pathophysiology of Parkinson's disease can be characterized by an imbalance between ____-? What neurons are destroyed.
dopamine and acetylcholine in the basal ganglia.Destruction of dopaminergic neurons favors a state of cholinergic over activity.In turn, this increases GABA activity in the thalamus leading to thalamic suppression. The final result is an inhibition of the cortical motor system and an overactivity of the extrapyramidal system.
350
Parkinson’s disease is a chronic neurodegenerative disorder of the
basal ganglia.
351
"Normal" muscle coordination requires a complicated feedback loop. Explain
The motor cortex sends instructions to the basal ganglia and the cerebellum. Next, the basal ganglia and cerebellum send information back to the cortex by way of the thalamus. This feedback loop is dependent on the relative concentrations of dopamine and acetylcholine in the basal ganglia.
352
Parkinson's Disease, Diagnosis requires two of the four cardinal signs:
Resting “pill rolling” tremor
Skeletal muscle rigidity
Postural instability – loss of balance with altered gait
Bradykinesia – very slow movement and reflexes
353
Parkinson's Secondary signs include:
psychosis, depression, dementia, lack of facial expression, diaphragmatic spasm, and oculogyric crisis. Patients may be unable to handle oral secretions.
354
What is the greatest risk factors for Parkinson's?
The greatest risk factor is old age. Other risk factors include exposure to manganese in welders as well as herbicides, pesticides, and possibly genetics.
355
Manganese in welders associated with this disorder
Parkinson's
356
Treatment of Parkinson's disease seeks to
Increase dopamine or decrease acetylcholine in the basal ganglia.
357
Levodopa and Carbidopa : why are these drugs given together?
When given together, these drugs increase the concentration of dopamine in the basal ganglia.
358
Levodopa is a precursor to
dopamine.
359
In the circulation, levodopa is metabolized to
dopamine, and DA in the blood does not penetrate the CNS.
360
Carbidopa is a
decarboxylase inhibitor.
361
Carbidopa is a decarboxylase inhibitor, what does it do?
By preventing levodopa metabolism in the blood, more levodopa can enter the CNS.
362
Carbidopa levodopa Cardiovascular side effects include
increased inotropy, tachycardia, and orthostatic hypotension. Other side effects include dyskinesia, nausea, and vomiting.
363
Selegiline: What is Selegiline
MAO-B inhibitors restore dopamine concentration by reducing dopamine metabolism in the CNS
364
Selegiline: Unlike Nonselective MAOIs
Unlike non-selective MAOIs, selegiline does not increase the risk of tyramine induced hypertensive crisis.
365
Parkinson's Patients are at risk for
Diphenhydramine has anticholinergic properties and is useful for sedation and reduction of tremor.
There is no contraindication to succinylcholine or nondepolarizers.
autonomic instability, orthostatic hypotension, arrhythmia, and aspiration.
366
Ketamine and parkinson's
Ketamine is controversial due to its effects on the SNS.
367
Alfentanil and parkison's
may cause an acute dystonic reaction due to interruption of central dopaminergic neurotransmission.
368
Treating hypotension with patient
Hypotension should be treated with intravascular volume expansion and direct-acting agents, such as phenylephrine.
369
Levodopa has a half-life of
6 – 12 hours.
370
Parkinson's medication DOS?
It must be given the morning of surgery to prevent worsening of symptoms such as rigidity, which can impact ventilation. For longer procedures, levodopa may be administered via an orogastric tube.
371
Drugs to avoid with parkinson's
Antidopaminergic drugs such as metoclopramide, butyrophenones (haloperidol & droperidol), and phenothiazines (promethazine) may exacerbate extrapyramidal s/sx.
372
What drugs may be used to treat acute exacerbation of Parkinsonian symptoms?
Anticholinergics may be
373
What drugs may be used to treat acute exacerbation of Parkinsonian symptoms?
Anticholinergics
374
Diphenhydramine and parkinson's?
has anticholinergic properties and is useful for sedation and reduction of tremor.
375
Muscle Relaxants and Parkinson's
There is no contraindication to succinylcholine or nondepolarizers.
376
What do you do with a patient with Parkinson's disease is having a deep brain stimulation ?
If deep brain stimulation is planned, it may be helpful to withhold levodopa. Holding levodopa causes symptoms to worsen, which facilitates optimal electrode placement.
377
Deep brain stimulation : What is done?
requires a burr hole to insert electrodes into the subthalamic nucleus, globus pallidus, and ventralis intermedius. This is done under stereotactic guidance.
378
Parkinsons , Pt head placement?
The patient’s head is placed in a rigid frame. This can complicate airway management. Avoid over sedation and respiratory depression. To determine optimal electrode placement, the patient must be awake, but can be lightly sedated with opioids and/or dexmedetomidine.
379
For parkinson's patient coming for a DEEP BRAIN STIMULATOR insertion, What is avoided?
Because of the crucial role of GABA in the thalamus, GABA agonists, such as propofol or benzodiazepines, are avoided as they can interfere with electrophysiologic brain monitoring.
380
The sitting position increases the risk of venous air embolism. A precordial Doppler aids in diagnosis. If VAE is detected, the patient
should not take a deep breath, as this entrains more air. Instead the surgeon must flood the field with saline. The patient may need to be re-positioned supine and hemodynamic support provided as needed.
381
During Deep Brain stimulator, what can be done to minimize intracranial hemorrhage?
To minimize the risk of intracranial hemorrhage, SBP should not exceed 140 mmHg.
Seizures can be treated with a small dose of propofol, barbiturate, or benzodiazepine.
382
Ischemic optic neuropathy (ION) MOST commonly occurs after
Spinal surgery
383
What is the most common cause of peri-operative vision loss. It occurs most often after surgery on the spine.
Ischemic optic neuropathy
384
In the perioperative period: What is the most common eye complication
Corneal abrasion
385
ION is a consequence of ischemia of the optic nerve. The most likely explanation is an
inadequacy of blood to the optic nerve due to venous congestion in the optic canal that reduces ocular perfusion pressure. Increased intraabdominal and/or intrathoracic pressure can also increase intraocular pressure.
386
Ocular Perfusion Pressure =
MAP - Intraocular Pressure
387
Vision loss typically occurs how long after surgery? Is it associated with pain?
24 - 48 hours after surgery. It is not associated with pain.
388
ION is most common after spinal surgery in the prone position. It has also occurred following
cardiopulmonary bypass and radical neck dissection. Prevention of ION targets modifying those risk factors that we can at least partially control in the operating room.
389
ION Patient risk factors>
Male sex
Obesity
Diabetes
Smoking
HTN
Old age
390
ION procedure risk factors
Prone
Wilson Frame
Long duration of anesthesia
Large blood loss
Low ratio of colloid to crystalloid resuscitation
Hypotension
391
The internal carotid artery gives rise to the______ artery which, in turn, gives rise to the______
ophthalmic ; central retinal artery.
392
Because the central retinal artery perfuses the entire retina, central retinal artery occlusion (CRAO) can lead to
blindness.
393
Central Retinal Artery Occlusion (CRAO) , affected patient typically presents with
The affected patient typically presents with sudden, painless, vision loss in one eye upon emergence of anesthesia.
394
Note that there are several branches of the central retinal artery. Occlusion of the vessels lead to
Occlusion of any of these vessels leads to branch retinal artery occlusion (BRAO). This complication can be thought of as a “milder” form of CRAO, where the patient presents with only a partial visual field defect.
395
Fundoscopic examination reveals a
reveals a “cherry red” macula while the surrounding retina appears pale.
396
Why might a patient experience CRAO? T
The most common cause is external compression on the globe from improper head positioning in the prone position. This reduces venous outflow, increases intraocular pressure, and impedes retinal perfusion.
397
We can prevent CRAO by avoiding the
horseshoe headrest.
398
What makes the horseshoe headrest particularly problematic?
The slightest degree of head rotation can compress the eye on the same side.
399
For CRAO, Better options include a
foam face pillow with large cutouts for the eyes or Mayfield pins. Regardless of the head positioning device used, performing frequent eye checks to verify the eyes are free from external pressure is essential.
400
Embolism is another cause of central retinal artery occlusion.We can prevent embolism in this context by
placing a filter on the cardiopulmonary bypass circuit. Avoiding areas of plaque in the aorta is another best practice.
401
CRAO The most common perioperative cause is
cardiac surgery with cardiopulmonary bypass.
402
Another population at risk for CRAO includes patients who receive
nitrous oxide following retinal detachment surgery with intraocular gas bubble placement. Nitrous oxide can cause gas bubble expansion, raising intraocular pressure, ultimately impairing retinal perfusion.
403
Which glial cell is responsible for neural repair?
Astrocytes
404
Arterial bleeding MOST commonly occurs between the:
arachnoid and pia mater.
405
All of the following are peripheral nerves EXCEPT:
CN II
406
Which of the following are types of neurons? (Select 2.)
Pseudounipolar
Bipolar
407
Select the true statements regarding cerebral blood flow. (Select 2.)
The pH of the CSF around the arterioles controls the cerebral vascular resistance.
Maximal cerebral vasoconstriction occurs when PaCO2 is 25 mmHg.
408
Cerebral perfusion pressure =
MAP - ICP (or CVP) whichever is HIGHER In this case CVP is higher
409
CSF is reabsorbed into the venous circulation via the:
Arachnoid villi
410
Order the flow of blood from the aorta to the circle of Willis.
1st vessel + Subclavian artery
2nd vessel + Vertebral artery
3rd vessel + Basilar artery
4th vessel + Posterior cerebral artery
411
A 1 mmHg increase in PaCO2 increases CBF by
1 - 2 mL/100g tissue/min.
412
Which of the following reduces cerebral blood flow while preserving CMRO2/cerebral blood flow coupling?
Hypothermia 34 degrees C
