Week 2 Neuroanesthesia Pathophysiology Flashcards
1
Q
Circle of Willis Anatomy
A
2-23-2
-2 Internal Carotid Arteries = 70% of blood flow to COW
-2 Vertebral Arteries = 30% of blood flow to COW
-3 Cerebral arteries = A/M/P
-2 Communicating arteries= A/P
2
Q
Monroe-Kellie Doctorine
A
3 components in fixed skull.
-Brain tissue, CSF, Blood
-When one increases & occupies space the others need to decrease to compensate the increase in pressure
- Once autoregulatory mechanisms that keep ICP within normal are exhausted –> decompensation and brain herniation
3
Q
Cushing’s triad
A
Caused from elevated ICP
-HTN crisis with wide PP
-Bradycardia
-Irregular respirations
-
4
Q
How much cardiac output does the brain receive
A
15%
5
Q
How much total CSF volume is present at any given time
A
150 mL
6
Q
How much CSF is secreted hourly
A
~30 mL/hr
7
Q
How much CSF is secreted per day
A
~500 mL
8
Q
Cerebral Perfusion Pressure (CPP) or Transmural Pressure
A
MAP-ICP or CVP (whichever is higher)
-Optimal range 50-70 mmHg = want >60 mmHg
9
Q
Cerebral Blood Flow (CBF)
A
50 mL/100g whole brain tissue/min
10
Q
CBF Ischemia #
A
20 mL /100g of whole brain tissue/ min
11
Q
PaCO2 & CBF relationship
A
Linear. As PaCO2 increases, CBF increases
12
Q
Goal PaCO2 range
A
PaCO2 30-35 mmHg
13
Q
Hypercarbia causes what in cerebral vessels
A
Vasodilation = increased blood flow to brain = possible increase ICP
14
Q
Hypocarbia causes what in cerebral vessels
A
Vasoconstriction = blood flows out of brain = can decrease ICP temporarily
15
Q
CMRO2 & value
A
Rate of O2 consumption by brain
-3-3.8mL /100g brain tissue/min
16
Q
Cerebral autoregulation range
A
MAP 50-150 mmHg
-Maintained by ability of cerebral vessels to change diameter in response to physiologic changes
17
Q
Low PaO2 <50mmHg & cerebral pathophysiology
A
Arterial hypoxemia causes cerebral vasodilation & increased CBF that if there is disruption in BBB will promote vasogenic edema
-Important to avoid hypoxemia in TBI. If autoregulation is impaired then changes in BP & ICP have direct effect on CBF
18
Q
Chronic HTN & autoregulation
A
Curve shifts RIGHT
19
Q
Inhalation Volatile Anesthetics
A
Decrease CMRO2 but INCREASE CBF d/t vasodilation
20
Q
Ketamine & N2O
A
Increase CMRO2 & Increase CBF
21
Q
IV induction agents
A
Decrease CMRO2 & Decrease CBF
22
Q
Hypothermia
A
Decreases CMRO2 & Decreases CBF
-5-8% / 1 C
23
Q
Nidus
A
Vascular mass that directly shunts blood between arterial & venous beds with NO true capillary bed
24
Q
Cerebral AVM
A
-Lack of capillary bed
-Arterial hypotension
-Venous hypertension
-Spontaneous intracranial hemorrhage occurs in ~50% of AVM = often from Subarachnoid hemorrhage
-More commonly bleed into ventricle or parenchyma
-Can cause metabolic suppression, seizure activity, but Intracerebral Hemorrhage (ICH) is most common
25
3 AVM treatments
1. Endovascular Embolization = prep for surgery, less bleeding, allows for surrounding structures to adapt to blood flow changes
2. Radiosurgery = cannot reach leasions with surgery, NOT for lesions >3cm diameter
3. Microsurgical excision = low grade AVMs (1-3)
26
Spetzer Martin Grading Scale (AVM)
3-6 cm = #2
6 cm + = #3
Eloquent or noneloquent site
Superficial or deep
27
Arterial hypotension & autoregulation
Shifts curve to the LEFT
-Generally preserved responsiveness to CO2 before & after surgery
28
Cerebral Steal & AVMs
-Paradoxical response to CO2 & hypercapnia
Local hypotension & hypoperfusion = focal neuro defects w/ AVMs
-Should be thought of after interventions for malignant brain swelling or bleeding
29
Inverse Steal & AVMs
-Hypocapnia produces increased blood flow to ischemic regions of brain
-Vasoconstriction occurs in adjacent normal arterioles which increase perfusion pressure & collateral flow to ischemic maximally dilated areas
30
Normal Perfusion Pressure Breakthrough (NPPB)
-D/t repressurization of previously hypotensive regions
-Global cerebral hyperemia (increase CBF) = problematic
-Autoregulation intact but shifted LEFT
-CO2 reactivity preserved
-Should be thought of after interventions for malignant brain swelling or bleeding
31
Neuroanesthesia goals for AVMs
-Maintain adequate CPP
-Prevent increases in ICP
32
Most common perioperative complication of AVM
Intracerebral Hemorrhage
Intracranial bleeding
Normal Perfusion Pressure Breakthrough (NPPB)
33
AVM Preop Key Points
-Normally present w/ ICH, seizures, neuro deficit
-Antiepileptics preop must be given (Keppra or Dilatin)
-Where is it located & how big is it
-Intraop neuromonitoring
34
AVM Intraoperative management
-A-line, CVC, SSEPs, MEPs, EEG, direct CBF monitoring, Jugular venous saturation monitoring, Hgb noninvasive monitoring
35
3 SEPs = recorded from peripheral nerve
-SSEP = somatsensory (touch, pressure, vibration)
-BAEP = auditory (CN8)
-VEP = visual (CN1)
36
MEPs
Motor evoked potentials can be recorded from spinal cord, peripheral nerve, or muscle
-Popliteal nerve
37
AVM anesthetic techniques
-AVOID cerebral vasodilating agents = NO inhalational agents
-TIVA = propofol + remifentanyl
-Paralyzed
-Adequate CPP
-Fast postoperative neuro exam
-Plans to treat bleeding or brain swelling
-Some places Barbiturate load for burst suppression on EEG but then have longer emergence & even postop intubation
38
Anesthetic damages of AVM
-Systemic hypo or HTN, decreased O2 content, HYPO-osmolarity, hyperglycemia
39
Nonpharmacologic brain protection in AVM
1.Relaxed Brain
Good head position, CSF drainage, Diuretics/Osmotherapy, avoidance of excessive cerebral vasodilators, modest hypocapnia @ 30-35 mm Hg
2. Controlled Systemic and Cerebral Hemodynamics
3. Euvolemia and Optimal CPP
4. Fluid and Electrolyte Management
Isotonicity and Euglycemia
5. Temperature Management
Modest hypothermia intra-op and post-op prevention of hyperthermia
6.Controlled Emergence
Tailored awakening and autonomic control
40
AVM management goals
-Maintain CPP & adequate cardiac preload
-Avoid hypertonicity, hyperthermia, hyperglycemia
-Timely emergence from anesthesia without coughing, HTN, or tachycardia
41
AVM brain relaxation
-Avoid cerebral vasodilators.... if need to use volatile agent, make sure <1 MAC. Preferebly 0.5 MAC.
-PaCO2 30-35. Only <30 if indicated
42
AVM fluid management
-Fluid should never be withheld at expense of CV status
-Isotonic replacement = NS, blood, Hestarch
-Hestarch coagulopathies debate??
-Avoid solutions w/ sugar
-Avoid perioperative hypoosmolarity
43
Rewarming process complications
shivering, increased O2 consumption & increased CMRO2, vasoconstriction
44
AVM hypothermia recommendations
34-35 C until closure is imminent = conservative
45
AVM quick acting hemodynamic downers
Clevidipine (cleveprex), nicardipine, SNP
46
AVM quick acting hemodynamic uppers
Phenylephrine
47
Pseudoseizure
Motor activity that mimics a seizure but no evidence of epileptic activity on EEG
48
Partial epilepsy
Focal onset in brain
Simple= localized
Complex= spreads to other regions
49
Generalized epilepsy
No focal onset. Either inhibitory or excitatory
50
Induction agents that can induce myoclonic activity
Propofol, etomidate, thiopental
51
Drugs known to induce seizures in presence of epileptic history
Methohexitol, Etomidate, Ketamine.
-Can be used to activate ictal foci during intraop ECoG
52
Etomidate
-Dichotomous actions on seizure activity
-EEG confirmed epileptic activity with induction doses in history of epilepsy
-Burst suppression & breaking status epilepticus at higher doses
53
Ketamine & seizures
Dose dependent
-Case reports say >4mg/kg
54
Barbs & Benzos for seizures
-Recommended to break epileptic activity in refractory status epilepticus
-Increases seizure threshold so harder to produce seizure
55
Propofol & seizures
-Safe w/ low epileptogenic properties
-Anticonvulsants properties well known
-D/C 20-30min prior to ECoG because it can increase Beta activity on EEG
-
56
SEVO & seizures
Reports that SEVO can generate convulsions + electrical spikes in history or no history
57
N2O and another agent
associated w/ seizure generation
58
Enflurane
Most common offender of inducing seizures +/- N2O
59
Synthetic opioids & seizures
Alfenta, sufenta, remifenta have proconvulsant properties
-Alfentanil 30 mcg/kg more effective than remi @ 1 mcg/kg
60
Dilaudid & morphine & seizures
at clinically relevant doses, does NOT appear to have proconvulsant properties
61
Muscle relaxants & antiepileptics
Long term anticonvulsant therapy with phenytoin (dilantin) or carbamazepine or both have been associated w/ resistant effects to neuromuscular blockers = consider using larger doses for effects
62
Anesthesia goals of Epilepsy surgery
CBF, systemic blood pressure, FAST emergence
63
Anesthesia preop evaluation for Epilepsy surgery
-Make sure anticonvulsants are given preop
-Avoid N2O w/ intracranial electrode placement
-Neurofibromatosis
-Keto diet w/ anticonvulsants = metabolic acidosis
-Possible intraoperative awareness & seizures
64
Diagnostic surgical procedures for Intractable epilepsy
-GETA generally used
-Hyperventilation may precipitate seizure activity (use briefly) = patients have lower CO2 reactivity of CBF than normal patients
65
Resection of Epileptic Brain Regions
-No Benzos w/ brain mapping but otherwise can be used
-Avoid antihistamines = can activate seizure foci in epileptics
-Little to no neuromuscular blockade
-Methohexital 25-50mg, Alfentanil 20mcg/kg, Etomidate 0.2 mg/kg for intraoperative epileptic discharges
-Severe bradycardia w/ amygdala-hippocampectomy = have atropine/glyco
66
Lateral hemispherectomy
-Lowest blood loss, shortest stay, less complications
67
Cerebral hemispherectomy
-Common in children
-Severe M/M = air emboli, cerebral hemorrhages, seizures, coagulopathies, electrolytes
-Continuous hemodynamic monitoring & vasopressor available
-ICU postop
68
Vagal nerve stimulator placement
-Usually placed on LEFT side to reduce risk of severe bradycardia because right branch of Vagus nerve innervates SA node. Left innervates AV node.
-Midcervical neck to avoid cardiac vagal branches
-Hoarseness & coughing common = unilateral vocal cord paralysis
-Optimize preop anticonvulsant therapy
69
Emergence from Epilepsy Surgery
-PONV up to 50%
-Respiratory issues & neuro deterioration ~10% = want to protect airway
-Cardiac issues up to 25%
-Postoperative seizures = prevent ventilation & oxygenation
-Avoid coughing & hyperextension of neck
70
Deep Brain Stimulators for Parkinsons
Awake craniotomy
-Patient does not take Parkinson's meds DOS so their tremors are exaggerated
71
Awake craniotomy
-Typically when tissue resection requires mapping
-Less complications
-Not technically awake (variable depths of anesthesia, where some use LMAs/ETTs)
-Scalp block works well
-Important discussion of expectations and realistic descriptions
-Want Fast on & Fast off meds
72
SUX SCI
Can within first 24h of injury but avoided for 9mo after
73
Hypoglycemia under GA detection
Difficult to detect AMS changes & other S/S of hypoglycemia under GA.
-Consider tachycardia as a sign
74
Can glucose cross the BBB?
No, it requires a transporter
75
What is the main source of energy in the brain?
Glucose
76
How does glucose provide energy to the brain?
Oxidative phosphorylation
-Glycolysis = glucose metabolized to pyruvate and forms ATP from ADP. Also produces NADH
-Pyruvates enters Citric Acid Cycle to produce more NADH
-Mitochondria use O2 to couple NADH back to NAD
-More ATP from ADP in mitochondria
-3 ATP from each NADH from EACH glucose molecule = max of 38 ATP molecules. Cannot yield more than 38 but some ATP is burned for this process.
-True yield = 30-35 ATP per molecule
77
What is anaerobic glycolysis?
Does not use O2 and only yields small amount of energy produced.
-Pyruvate converts to lactate = can cause acidosis
-Only 2 ATP are produced = insufficient for brain function
78
Why does the brain need energy?
Pumps ions across membranes where the pumps function to maintain a continuous gradient
-**ATP direct ion pumps = Na/K ATPase pump
-Na gradient ion pump with calcium, hydrogen, glutamate
-Neuron RMP is -60 to -70 mV
79
Brain & anesthesia
Anesthesia reduces ATP used for functional activity (60%)
-40% to maintain cellular integrity = but anesthesia does not affect ATP used here
80
Brodmann's area of brain
-Area 4 = voluntary muscle activity
-Area 1 = Somatosensory cortex
81
Cerebral cortex (4 parts)
-Thalamus = receives input from cerebral cortex
-Hypothalamus = temp, hunger, thirst
-Limbic system = reward, punishment, learn, memory, emotions
-Basal Ganglia = motor function & movements
82
What part of the brain does Parkinson's effect?
Substantia nigra = dopaminergic area
Causes cascade of changes through Basal Ganglia
83
Cerebellum function
Postural control (why we check babinski reflex + other posturings)
84
Brainstem
-Continuous w/ SC = midbrain, pons, medulla
-Medulla = CN 3, 8?, 12
-Ascending & descending pathways transverse in the brainstem
-Controls BP, HR, breathing, swollowing & other bodily functions
-RAS & reticular formation = alertness & consciousness
-
85
Why do/can patients get sleepy after a spinal anesthetic?
Decreases sensory & sympathetic input which "suppresses RAS)
86
Loss of blood flow to brain tissue causes?
Cerebral ischemia where brain is most sensitive organ to ischemia.
87
What causes brain ischemia?
Loss O2 or blood flow to tissue = decrease phosphorylation (2 vs. 36 ATP), ion pumps become dysfunctional & "blocked", increased release of glutamate
-Decreased ATP is a TRIGGER
-Lactate production
88
Increased glutamate in brain causes?
NMDA receptor activation
-Increased N/K pump
-Calcium worsens ischemia
89
Ischemic brain cell death
-Can develop arachodinic acid
-Leads to thromboxane, PG, and leukotriene production = further vasoconstriction leading to worse ischemia
-Necrosis = mitochondrial function is lost
90
Nonperfused penumbra
Tissue dies without reperfusion
-Idea IP = 100%
91
Reperfused penumbra
Tissue survives
-Ideal IP = 0%
92
rTPA must be given within ______ hrs if ischemic?
Within 3 hours
93
Prompt reperfusion via 2 possible routes
Pharmacological +/- mechanical
94
Hypothermic treatment for ischemia
-Severe hypothermia (<27 degrees) = significant reduction in cerebral metabolism --> circulatory arrest or aneurysm treatment
-Typically want < 10 min
-Moderate hypothermia (32-34 degrees) = less side effects
95
Complications of Deep Hypothermia
-CV = myocardial depression, HoTN, dysrhythmias leading to V-fib, poor perfusion & ischemia
-Coags = PLT dysfunction, thrombocytopenia, fibrinolysis, increased bleeding
-Metabolism = prolonged metabolism of anesthetic agents, prolonged neuromuscular blockade, increased breakdown of proteins
-Shivering = increased O2 consumption, CO2 production, increased CO, Arterial O2 desaturation, hemodynamic stability
96
Lidocaine & brain protection
Na channel influx blocker
97
Nimodipine
Used for cerebral vasospasm prevention & treatment
(often seen in SAH)
98
Magnesium & brain protection
NMDA receptors
99
Thiopental
Barbiturates --> great drugs for cerebral ischemia but hard to come by these days
-Has a drastic decrease in CBF & CMRO2 with no vasodilation
-Free radical scavenger
-Blocks Na, K, Ca
-Blocks seizures
-Improves regional blood flow
-Decreases ICP
100
Seizure & brain dysfunction
-Excessive brain discharge from neurons
-Uses more ATP
-Tx w/ Benzo to cease firing
-Follow cease w/ Dilantin or Keppra (more often)
101
What are the 4 parts of the GCS Eye Exam
-Spontaneous eye opening
-To voice
-To pain
-No response
102
What are the 5 parts of GCS Verbal Exam
-Oriented x3
-Confused
-Inappropriate words
-Incomprehensible sounds
-No response
103
What are the 6 parts of the GCS Motor Exam
-Follows commands
-Localizes pain
-Withdraws from pain
-Abnormal flexion (decorticate)
-Abnormal extension (decerebrate)
-No response
104
Primary brain injury
-Disruption of brain & blood supply
-CANNOT be reversed
- DAI, blood vessel disruption, brain herniation
105
Secondary brain injury
-CAN be reversed
-Can lead to cerebral edema & increased ICP
-Excitotoxicity, inflammatory responses, secondary ischemia from vasospasm, focal microvascular occlusion & vascular injury, energy failure w/ apoptosis
106
Relationship between CBF & CMRO2
Coupled = working together
-TIVA maintains coupling better than volatiles
107
How does Dilantin (Phenytoin) effect the liver
CYP450/3A4 inducer
108
How does Nitric Oxide (NO) moderate/mediate vascular tone?
-Diffuses in to vascular myocyte
-Activate guanylate cyclase
-Forms cGMP
-cGMP stimulates protein kinases
-Light chain myosin undergoes phosphorylation
-Yields vascular relaxation
109
How is nitric oxide synthesized ?
From L-Arginine by nitric oxide synthase (NOS)
110
What 2 volatiles do NO interact with and what happens?
-ISO & Halothane
-Vasodilation
-Vasospasm associated w/ SAH
-Inhibiting NO, can cause further vasoconstriction
111
What does cCGRP increase?
cAMP which causes moderate cerebral vasodilation
112
How do prostaglandin effect cerebral vessels
Can cause vasodilation
113
Collateral pathways are _________ during chronic cerebral ischemia. What might need to be done in acute ischemia?
Effective/intact
-Increase in bp to push blood through collaterals
114
Where is the Circle of Willis located?
Subarachnoid space
115
What 2 arteries converge to form the basilar artery?
Posterior vertebral arteries
116
What physical law applies to blood flow through the cerebral circulatory system
Ohms
117
Whos law applies to cerebral circulatory resistance?
Hagen-Poiseuille
-Radius to 4th power = why controlling diameter most beneficial for controlling resistance
118
When autoregulation curve is not in range (sloping lines <50 or >150 mmHg) it is viewed as being ________ dependent
Pressure dependent
119
Post crani BP goals are often in systolic why?
Because systolic blood flow is related to pulsatile flow
120
Fahraeus Effect
The decrease in apparent relative viscosity that occurs when blood is made to flow through a tube whose diameter is less than about 0.3 mm is a well-known and documented phenomenon in physiology, known as the Fåhræus-Lindqvist effect (Farina, Rosso, & Fasano, 2021).
121
Where is velocity fastest when moving from the wall of a vessel inward toward the center?
Faster in the center
122
What does CO2 do at the level of the brain vessels?
Vasodilates
123
By decreasing extracellular pH (more acidotic) what is the activation cascade?
-Activates NO synthase
-Increased NO & cGMP production
-Activation of potassium channels that hyperpolarize vascular smooth muscle
-Blocks Ca2+ channels which decreases intracellular Ca2+
-VASORELAXATION
124
At what range of CO2 does it remain a linear relationship with CBF?
CO2 20-80 mmHg
125
What percent does CBF change per 1mmHg of CO2 change
2-4%
126
Increasing PaCO2 from 40 to 80 mmH can _______ CBF
Double
127
Decreasing PaCO2 too low <25 mmHg can do what to the OxyHgb dissociation curve?
Shift LEFT & HOLD onto O2 molecule d/t increased affinity (aLkalosis)
128
PaCO2 <10 mmHg can lead to...
glucose anerobic metabolism (think like a code or low CO state)
-Caution w/ repositioning & assess ETT after bc if right mainstem, it could be shown with hypocarbia = hose follows nose
129
At what PaO2 does CBF increase? When does it double? Why?
PaO2 50 mmHg
PaO2 30 mmHg
-Hypoxemia causes vasodilation
130
For each 1 degree Celcius, what percent does CMRO2 change?
7%
131
Up to what MAC is the CO2 response blunted?
1.5
->1.5 causes a significant increase in CBF
132
How does dexmedetomidine affect CBF & CMRO2?
-DECREASES CBF
-No change in CMRO2
133
Autoregulation can be interrupted by?
***Prematurity, neonatal asphyxia, diabetes mellitus
-Trauma, inflammation, acute ischemia, mass lesions
134
What is left-sided autoregulation failure?
Hypoperfusion & cerebral ischemia
135
What is right-sided autoregulation failure & what can it cause?
Hyperperfusion w/ dilation of arteriolar beds leading to intravascular engorgement, vasogenic edema, intracerebral hemorrhage (ICH)
136
What is hyperemia?
A rush of blood to an area creating a large volume of blood at the area
137
What is Normal Perfusion Pressure Breakthrough and when is it MOST seen?
Causes hyperemia from pressure differences between arterial (HoTN) and venous (HTN) where the vasomotor effects of the vessels become paralyzed when AVM is resected = surrounding pressure in tissues normalize & cerebral vascular resistance is paralyzed (does not work)
-Hyperemia = can lead to edema & hemorrhage
-Most seen in AVM & carotid sx
138
What is cerebral reperfusion injury related to?
CBF & metabolic demand mismatch
139
What is Cerebral Steal?
Blood flow diverted from ischemia areas to non-ischemia areas.
-Usually under control of elevated CO2
140
When might "induced HTN" be seen in carotid artery surgery?
During cross clamp
141
How do Barbiturates affect cerebral blood flow?
Shunts blood from non-ischemic areas to ischemic areas
"Intracerebral steal phenomenon/Robinhood effect"
142
How is a proximal vasopasm best treated?
Mechanical Stent
143
How is distal vasospasm best treated?
Intra-arterial vasodilator therapy
-***Nimodipine
-Nicardipine
-Verapamil
144
What artery supplies blood to the spinal cord the most & what fraction? Dermatome level?
Anterior Spinal Artery (2/3)
T10
145
Critical supplemental artery of the Anterior Spinal Artery
Artery of Adamkiewicz
146
What levels of the spinal cord is the Artery of Adamkiewicz?
T10-T12
147
What can occur when there is an occlusion below the level of the Artery of Adamkiewicz
Paralysis
148
A spinal cord injury above this level can alter CBF
T6
149
What is the SCBF rate?
~46 mL / 100g / min
150
What region of the spine has the lowest SCBF rate & why?
Thoracic d/t less grey matter in this region & compression (smaller space)
151
How much more grey matter than white matter is in the spinal cord?
5x more grey matter
152
Isoflurane may be most ideal inhalational agent for spinal cord surgery?
Neuroprotective properties
153
Where is CSF formed & how much per day?
In Choroid Plexus
-500-600 mL/hr
-Has fenestrated junctions where protein-rich fluids filter out
154
What is the specific gravity of CSF?
1.007-1.009
155
Pathway of CSF
1. Produced & secreted by choroid plexus in each lateral ventricle
2. Through IV foramina into 3rd ventricle
3. Choroid plexus of 3rd ventricle adds more CSF
4. Down cerebral aqueduct into 4th ventricle
5. Choroid plexus of 4th ventricle adds more CSF
6. Flows out 2 lateral apertures & one median aperture
7. CSF fills subarachnoid space, bathing brain & SC
8. Arachnoid villi, CSF reabsorbed into venous blood of venous sinuses
156
What does Acetazolamide do to CSF?
-Decreases CSF FORMATION up to 50%
-Good use in hydrocephalus
157
How do steroids affects CSF?
Can decrease both absorption & formation of CSF
158
How does vasopressin effect CSF?
Decreases both absorption & formation of CSF
159
How does Theophylline effect CSF?
Increases CSF formation
160
What are 4 metabolic regulators that decrease CSF formation?
Hypothermia, hypocapnia, metabolic alkalosis, increased serum osmo
161
At what range ICP is the Volume of Formation for CSF constant?
ICP 2-22 cmH2O
162
If FOCAL cerebral ischemia and patient is hypercapnic (high PaCO2) what changes occur in the brain? What is this termed?
Blood vessels in the normal area of the brain vasodilate, causing blood to shunt away from the ischemia areas.
-Cerebral Steal or Reverse Robinhood Effect
163
If FOCAL cerebral ischemia & patient is hypocapnic, what changes occur in the brain? What is this termed?
Robinhood effect or Reverse Cerebral Steal
-No benefit found in animal studies
164
In lay person terms, what is the Robinhood effect?
Stealing from the rich and giving to the poor.
165
N2O use in brain lesions with air. Adverse effects?
Can occupy space & expand the air-filled location.
-N2O can also cause nausea within its properties which we want to avoid in neurosurgical patients
166
Isoflurane cerebral influences
1. Low cerebral vasodilation
2. Drastic/high decrease in CMR = cerebral protective
3. Can increase CSF absorption & CBV
167
Sevoflurane cerebral influences
*Inconclusive. May have similar effects as ISO
168
Desflurane cerebral influences
-Can increase ICP
-Can increase CSF production & decrease absorption
-Rapid on/off = nice for rapid neuro assessment but can cause coughing/bucking
169
Barbiturate cerebral influences
-Favorable d/t drastic decreased in ICP & possible neuroprotection
-Drastically decreases CMR (appears like the most)
170
Etomidate cerebral influences
-Risk for clonus & adrenalcortical suppression
-Decreases CMR
171
Propofol cerebral infleunces
Great drug for neuro
- AS LONG AS MAP IS MAINTAINED
-Decreases CBF the most
172
Succinylcholine cerebral influences
-Can raise ICP (but very short period)
-May be used in full stomachs & RSI
-Consider defasiculation
173
What anesthetic agents increase CBF & subsequently ICP?
ISO, DES, SEVO, N2O, Ketamine
174
Benzos & Lidocaine _________ CMR?
Benzos & Lido decrease CMR approximately the same
175
Does lidocaine increase or decrease CBF?
Decreases (double down arrow)
176
Does ketamine increase or decrease ICP?
Can significantly increase ICP
177
What physical law is associated with ALARA?
Inverse square law = doubling distance will reduce the dose rate to a quarter
178
What are the main focuses of Neuro IR anesthesia?
1. Keep patient immobile
2. Need quick on/off drugs for rapid recovery assessment
3. Anticoagulation = heparin
-Reversed w/ Protamine (any allergic rxns to protamine?)
4. Procedure specific concerns = vasospasm + hemorrhage
5. Pre-op CCBs?
6. Contrast allergy? Renal function?
7. A-line? Ask surgeon for BP goals
179
MAC for IR? Criteria.
-Cooperative patient (still/not move)
-"Little bumps of fentanyl works pretty good"
180
Consider general anesthesia if anticipate an intervention to be made during interventional radiology. Things to think of.
-Extension on IV tubing & anesthesia circuit
-Watch for drains & clamp prior to moving
-Gtts close to patient
*minimize dead space & onset of meds
181
Key point when moving patient with EVD?
CLAMP when moving
-If do not clamp, can rapidly drain ventricle = trouble
-Watch for other drains
182
1st step in initial resuscitation when emergency arises in Neuro IR
COMMUNICATE w/ team, call for help, secure airway & ventilate w/ 100% O2
183
2nd step in initial resuscitation when emergency arises in Neuro IR?
Determine if problem is hemorrhagic or occlusive
184
Hemorrhagic emergency in Neuro IR
After securing airway. Immediately reverse heparin!
*1 mg protamine/ 100u of heparin given
*Low normal MAP goals
185
Occlusive emergency in Neuro IR
*Deliberate HTN
-titrate BP to findings of neuro exam
-Angiography or physiologic imaging or to clinical context
186
After initial resuscitation in Neuro IR emergency, what further resuscitation techniques are important to use?
-PaCO2 manipulation consistent w/ clinical setting otherwise normocapnia
-Mannitol 0.5 g/kg rapid IV infusion
-Titrate IV agent to EEG burst suppression
-Consider ventriculostomy
-Consider anticonvulsant
187
What is the estimated IV heparin dose given for IR to achieve anticoagulation?
70 units/kg Heparin
-To a 2-3x normal vaseline PTT/ACT
188
What should be given if suspected Antithrombin II deficiency?
FFP
189
Protamine dose for heparin reversal
1 mg/100U
190
What medications can be given if Heparin Induced Thrombocytopenia (HITT)
-Bivalrudin = 25min t1/2
-Lepirudin = longer t1/2
191
When to induce deliberate HTN during Neuro IR?
-During vasospasm or occlusive emergency
-Increase BP 30-40% of baseline
192
When to induce deliberate HoTN during Neuro IR?
-To test cerebral reserve PRIOR to carotid occlusion
-To slow artery that is feeding AVM, prior to glue application
-Nicardipine (most common)
- Cleviprex (Clevidipine)
- SNP
193
Intracranial AVM possible anesthetic considerations
-Deliberate HoTN
-Postprocedure NPPB
194
Dural AV fistula possible anesthetic considerations
-Existence of venous HTN
-Deliberate HYPERcapnia
195
Extracranial AVM possible anesthetic considerations
Deliberate HYPERcapnia
196
Carotid cavernous fistula possible anesthetic considerations
-Deliberate HYPERcapnia
-Postprocedural NPPB
197
Cerebral aneurysm possible anesthetic considerations
-Aneurysmal rupture
-BP control
198
Ethanol sclerotherapy of AV or venous malformation possible anesthetic considerations
-Brain & airway swelling
-Hypoxemia
-Low BG
-Intoxication from ethanol
-Cardiopulmonary arrest
199
Balloon angioplasty & stenting of occlusive CV disease possible anesthetic considerations
-Cerebral ischemia
-Deliberate HTN
-Concomitant CAD, bradycardia, HoTN
200
Balloon angioplasty of cerebral vasospasm secondary to aneurysmal SAH possible anesthetic considerations
-Cerebral ischemia
-BP control
201
Therapeutic carotid occlusion for giant aneurysms & skull base tumors possible anesthetic considerations
-Cerebral ischemia
-BP control
202
Thrombolysis of acute thromboembolic stroke possible anesthetic considerations
-Postprocedure ICH = NPPB
-Concomitant CAD
-BP control
203
Intra-arterial chemo of head & neck tumors possible anesthetic considerations
-Airway swelling
-Intracranial HTN
204
Embolization for epistaxis possible anesthetic considerations
-Airway control
205
Clues for bleed in Neuro IR (2)
1. Extravasation of contrast via scan
2. Cushing's response
206
What are 2 important complications to be prepared for during cerebral aneurysm ablation?
1. Rupture
- Have anticoagulation reversal!
2. Vasospasm (25% of time)
-Papaverine, Cardene, Verapamil
207
Postop considerations after thrombolysis/thrombectomy for thromboembolic stroke
-Watch for hyperemia
-Edema/hemorrhage from rapid reperfusion
-Normal Perfusion Pressure Breakthrough
208
What reduction in amplitude during neuromonitorning deems a potential risk & requires attention?
50% reduction in amplitude (gets shorter in height) = less strong
209
What increase in latency during neuromonitorning deems a potential risk & requires attention?
10% increase in latency = slowed
210
What can cause change in signaling during neuromonitorning?
-What did the surgeon just do
-Technical challenges
-Anesthesia technique
-Positioning alterations
-Physiological challenges
211
When are Brainstem Auditory Evoke Potentials (BAEP) typically used & what effect does anesthesia have on them?
Posterior fossa surgery
-Anesthesia does not significantly affect
212
How do inhalational agents affect neuromonitoring & what agent is most depressive?
SSEPS
-Reduces synaptic transmission
-Dramatic nonlinear, dose-dependent reduction in cortical responses
-Gate sensory info @ brainstem which is activated in the brainstem
MEPS = more depressed in spinal cord
213
How does Ketamine affect cortical SSEPs & MEPS
Increases amplitude (strength)
214
How does Precedex affect SSEPs & MEPS?
OK for SSEPs
**May alter MEPS
215
How do muscle relaxants affect neuromonitorning?
Ok for SSEPs & ABR
** NOT ok for MEPS & EMG
216
How many spinal vertebrae are there & which regions of the spine have lordosis or kyphosis?
33 Vertebrae
Lordosis = Cervical & Lumbar
Kyphosis = Thoracic & Sacral
217
At what level of the spine is the Conus Medularis?
L1-L2 because this is where the spinal cord starts to end
218
The Corticospinal tract are all primary _________ impulses
Motor
219
Myelopathy affects what part of the spine?
Centrally affects the CORD itself
-Caution airway
220
What is radiculopathy?
Affecting the spinal nerve, root, or both
221
What is significant about the C7 vertebra?
Last cervical lamina
*Does NOT have vertebral artery travel through
222
What are 2 main intraoperative complications to consider with ACDF?
1. Esophageal perforation
2. Damage to carotid artery or IJ
223
What are a couple main postoperative complications to consider with ACDF?
1. Dysphagia --> from plates & screws
2. Recurrent Laryngeal Nerve = Hoarseness
224
What is an important but easy preventative intervention for ACDF?
Bite blocks d/t motor neuromonitoring
-Chris puts 3
225
Where is disc herniation most commonly seen in spinal surgery?
Lumbar
226
Cauda Equina Syndrome
Medical Emergency = must have LEVEL 1
-Bowel & bladder dysfunction
-Sensorimotor deficits
227
What is Lumbar Spondylolisthesis
Slipped disc
228
Consideration regarding ventilation in thoracic spine procedure?
Sometimes do One-Lung Ventilation (OLV)
229
Main difference with Anterior Lumbar Interbody Fusion (ALIF) than posterior or lateral approach
General/vascular surgeon to access lumbar spine by dissecting anterior to posterior.
*Most require complete paralysis
*High stakes real estate = iliac veins/arteries etc.
230
A Cobb angle >40 indicates what degree of scoliosis?
Severe
