Applied Physiology: Lecture 1 - Neurophysiology Flashcards
(179 cards)
1
Q
How much of Total Body Oxygen does the Brain consume?
A
20%
This consumption is significant given the brain’s weight of 1500g.
2
Q
What is the Cerebral Metabolic Rate of Oxygen (CMRO2)?
A
3-4 ml/100g/min OR 50 ml of O2/min
PAO2 less than 30 mmHg can lead to irreversible damage.
3
Q
How much Glucose does the brain use?
A
5mg/100g/min
4
Q
What can Hypoglycemia result in?
A
Brain injury
5
Q
How does a patient act with low Blood Sugar?
A
Slow, loopy
6
Q
What can Hyperglycemia result in?
A
Accelerates cerebral acidosis
7
Q
What is the normal cerebral blood flow (CBF)?
A
750 mL/min (around 20% of Cardiac Output) OR 50 mL/100g brain tissue/min
8
Q
Where is CBF increased in the brain?
A
Gray matter
9
Q
Low CBF can result in what?
A
Cerebral impairment and isoelectric EEG
10
Q
How do you measure CBF indirectly?
A
NIRS, transcranial doppler, etc.
11
Q
What is a NIRS monitor?
A
Near-Infrared Spectroscopy: A non-invasive cerebral oximeter that uses infrared light to measure regional oxygen saturation (rSO₂)
12
Q
What is the CBF and MAP relationship?
A
MAP remains constant between 60 mmHg – 160 mmHg
13
Q
What is autoregulation?
A
Brain maintains homeostasis between 60-160 mmHg
14
Q
What happens to the autoregulation curve with chronic hypertension?
A
Shifts to the right
15
Q
Result of a MAP above 160 mmHg?
A
Cerebral Edema
16
Q
What are BP goals for vessel occlusion?
A
Want to lower
17
Q
What is the Myogenic Response of the Cerebral Arterioles?
A
Respond to changes in MAP
18
Q
What is the Metabolic Response of Cerebral Arterioles?
A
Increased demand for metabolites results in vasodilation
19
Q
What is the relationship between PACO2 and CBF?
A
Directly proportional between 20 mmHg – 80 mmHg
Mechanism:
CO₂ crosses the blood-brain barrier → combines with H₂O → forms carbonic acid → dissociates into H⁺ ions
↑ H⁺ concentration in the brain causes vasodilation
Result: increased cerebral blood flow
Clinical Applications:
Hyperventilation (↓ PaCO₂) is used acutely to reduce ICP by causing cerebral vasoconstriction
However, prolonged or excessive hypocapnia can cause ischemia
In anesthesia and neurocritical care, PaCO₂ is tightly controlled to modulate CBF and ICP
20
Q
How much CBF is needed to change PACO2?
A
1-2 mL of Blood/100g/min per 1 mmHg change in PACO2 (2-4 % increase)
21
Q
How long does the CBF and PACO2 relationship change last?
A
Immediate effect (seconds to minutes), fully active by ~1–2 minutes… will last duration of the change.
Acute: CBF responds to PaCO₂ changes within seconds to minutes.
Chronic: After 6-8 hours, CSF buffering mechanisms may reduce CBF sensitivity to PaCO₂.
22
Q
A PACO2 less than 20 mmHg causes what?
A
Impairment due to left shift of O2 dissociation curve
23
Q
What does intrathoracic pressure do to CBF?
A
Decreases it
24
Q
What is the relationship between CBF and PAO2?
A
Hypoxia increases CBF
25
What is the relationship between Hypothermia and CMR and CBF?
Decreases both CMR and CBF
26
What is the degree change between temperature and CBF?
CBF changes 5-7% per degree Celsius
27
Is temperature monitoring an ASA standard?
No
28
What structures can pass the Blood Brain Barrier?
Lipophilic, small, uncharged substances
29
What can pass freely through the BBB?
CO2, O2, Anesthetic Agents, Water
30
What can disrupt the integrity of the BBB?
Hypertension, strokes, seizures, tumor, infection, acidosis
31
How much CSF is produced daily?
500 mL/day
32
What is the tonicity of CSF?
Isotonic
33
What decreases CSF production?
Carbonic Anhydrase Inhibitors, Lasix, Isoflurane
34
What is the relationship between buoyancy and CSF?
Helps protect brain
35
Why so many DVST (deep venous sinus thrombosis) in Denver?
Due to altitude, chronic dehydration, birth control pills
36
How does DVST impact flow of CSF?
Decrease
37
What are the three components of the cranial vault and their percentages?
* Brain Tissue – 80%
* Blood – 12%
* CSF – 8%
38
What is normal ICP?
10 mmHg
39
Where is ICP measured?
Left Ventricle
40
What is CPP?
CPP = MAP-ICP or CVP (whichever is greater)
41
Can the body compensate for an increased ICP?
Yes
42
How does position affect ICP?
Lower head: increases, Elevated head: decreases
43
Symptoms of Positioning Changes when a patient has increased ICP?
* Nausea and Vomiting
* Headache
* Vision Changes
* Photophobia
* AMS
44
What Opioids not to use for Neuro Cases?
Dilaudid (due to uncertainity in duration of action)
45
What Opioids use for Neuro Cases?
* Fentanyl
* Remifentanil
46
Is Versed (Benzos) typically given Pre-Op with Neuro Procedures?
No - so privoder can know baseline before and after brain surgery
47
Anesthesia and Neuro Cases?
Not a one size fits all
48
Types of surgeries in Neuro cases?
Burr holes
Tumor
Crani for bleeding
Stroke
Aneurysm clipping
Rupture
Meningioma
Glioma
Glioblastoma
Dvst
Chiari malformation
Positioning
Approach
Neuromonitoring
49
What are anesthetic goals in neuro cases?
Limit increases in ICP
Ensure patient monitoring
Proper positioning
Brain relaxation
Controlling: diuresis, PACO2 management, .5 MAC
50
How does positioning effect the patient when sitting?
Decrease blood flow to brain
51
What is a VAE Treatment?
Flood system with saline
Drop patient to Trendelenburg and even put on side
Increase PEEP to decrease blood return to heart pushing the Air Bubble back through the hole in Vein hopefully
52
Clinical signs of a VAE?
* Massive drop in ETCO2
* Hypertension
* Tachycardia
53
Concerns for prone positioning in Neuro Cases?
* Flexed
* Airway
* Hemodynamic
54
What are the goals of Mayfield pins?
Keep patient’s head stable
55
What are blood pressure goals during neuro surgeries?
* During - 140
* Post – Under 140
56
What are possible ways a person could end up in surgery for bleeding in the brain?
* Trauma
* Ruptured vessel
* Bleeding Tumor
57
With some type of bleeding in the brain what kind of shift should you be aware of?
Midline shift
58
Cushing’s Triad is what when considering a brain bleed?
* Hypertension
* Bradycardia
* Irregular Respirations
59
What are anesthesia goals for an aneurysm clipping?
* Adequate brain relaxation
* Avoid drastic increase in BP
60
Monitoring considerations with an aneurysm clipping?
* Neuromonitoring
* Full TIVA may be requested
61
What is burst suppression?
An EEG pattern characterized by alternating periods of high-voltage activity and low-voltage lines
62
Which aneurysms are clipped?
Wide necked aneurysms
63
Which aneurysms are coiled?
Small necked aneurysms
64
What do you always need in OR during aneurysm clipping?
Blood and adenosine
65
Are post op CT scans done after aneurysm clipping?
Yes
66
What can you expect to already be done following massive head trauma?
Likely already intubated in field or ICU
67
What drips might a patient come in from the field with on following a massive head trauma?
Something to control the pressures
68
What can you expect when you have an open head wound?
ICP is 0mmHg
69
What drips do you want to prepare for a massive head trauma?
* Epi
* Norepi
70
What kinds of Lines and Access do you want for a massive head trauma?
A-lines
Large bore IVs
Central lines
ICP monitor
Foley catheter
NG/OG tube
71
Why does unconsciousness occur within 10 seconds?
Rapid oxygen consumption and absence of O2 reserves
72
How long does blood flow need to be reestablished to minimize brain injury?
3-8 min
73
What parts are most sensitive to hypoxic injury?
More rostral, higher regions (cortex, hippocampus)
74
What is the relationship between CBF and viscosity?
Decrease hematocrit leads to improved CBF
75
At normocarbia, volatile anesthetics do what?
Dilate cerebral vessels and impair autoregulation in a concentration dependent manner.
76
What volatile anesthetic has the greatest impact on CBF?
Halothane
77
Is volatile anesthetics time dependent on CBF?
Yes, with continued administration (2-5 hrs), blood flow begins to return to normal
78
What is luxury perfusion?
Decrease in neuronal metabolic demand with an increase in CBF
79
Is coronary steal in the brain possible with volatile agents?
Yes
80
What is the ICP and volatile anesthetics relationship?
ICP is a result of changes in Cerebral Blood Volume, delayed alterations on CSF dynamics and arterial CO2 tension
81
Nitrous oxide and ICP relationship?
When given alone can cause cerebral vasodilation and potentially increase ICP
82
What effect do IV induction agents have on CMR and CBF?
Little to no effect, with the exception of Ketamine
83
What is preserved with IV induction agents?
Cerebral autoregulation and CO2 responsiveness
84
What happens with barbiturates in normal vs ischemic areas?
Vasoconstriction only occurs in normal areas, thus redistributing blood to ischemic areas
85
Why does the ischemic area remain maximally dilated in the brain?
Due to ischemic vasomotor paralysis
86
When has ICP reported increasing with opioid administration?
With intracranial tumors
87
Etomidate and its effects on CSF?
Decreases production, enhances absorption
88
What is Propofol known for in neuro anesthesia?
Significant anticonvulsant properties
89
Why has Droperidol fallen out of use in neurosurgery?
Creates a prolongation in the QT interval
90
Can reversal agents affect CBF and CMR?
Yes, reversing opioids and benzos reverses those effects
91
Vassopressors and CBF?
Only increase CBF when MAP is below 50-60 mmHg or above 150-160 mmHg, increase CBF by their effect on CPP
92
Vasodilators and CBF?
Decrease BP, but CBF usually maintained
93
NMBs and effects on brain?
Lack direct action on the brain but important secondary effects; hypertension and histamine-mediated cerebral vasodilation increases ICP; hypotension from histamine release or ganglionic blockade lowers CPP
94
Can succinylcholine increase ICP?
Can increase ICP (minimally and clinically unimportant extent), using a small defasciculating Non-depolarizer can blunt this
95
When should CBF be increased using vassopressors?
When MAP is below 50-60 mmHg or above 150-160 mmHg
## Footnote
Increase CBF by their effect on CPP
96
What effect do vasodilators have on CBF?
They decrease BP, but CBF is usually maintained
97
What are the secondary effects of neuromuscular blockers (NMBs) on the brain?
Hypertension and histamine-mediated cerebral vasodilation increases ICP; hypotension lowers CPP
98
What is the effect of succinylcholine on ICP?
Can increase ICP minimally and clinically unimportant extent
99
What typically causes increases in ICP related to NMBs?
Being too light, tracheal intubation, hypercapnia, or hypoxemia
100
What are the ultimate goals to protect the brain during ischemia?
Optimize CPP, decrease CMR, and block mediators of cellular injury
101
Is hypothermia ever used in protecting the brain?
Yes, for up to 1 hour during total circulatory arrest
102
What can produce burst suppression?
Barbiturates, etomidate, propofol, isoflurane, desflurane, sevoflurane
103
Which anesthetic agents are nonuniform in their effect on the brain?
Barbiturates
104
What can be a protective agent in children?
Dexmedetomidine
105
What is used to treat vasospasm associated with subarachnoid hemorrhage?
Nimodipine
106
What should be avoided in neuro cases?
Hypotension, increases in venous pressure, and increases in ICP
107
What is the hyperglycemia amount to stay under?
180 mg/dL
108
What are the EEG changes based on light vs heavy anesthesia?
Light anesthesia: high-frequency and low-voltage; Deep anesthesia: low-frequency and high voltage
109
What effect do inhalational anesthetics like ISO, DES, and SEVO have on EEG ay high doses?
Produce burst suppression patterns at high doses
110
What principle explains volume compensation within the cranial vault?
Kellie-Monroe Hypothesis
111
At what CBF does irreversible brain damage occur?
<10 mL/100g/min
112
What are the main factors that regulate CBF?
* CO2
* H+ ions
* O2
* Astrocyte-released substances
113
How does CO2 affect cerebral blood flow?
↑CO2 → ↓pH → vasodilation → ↑CBF
114
What is the change in CBF per 1mmHg change in PaCO2?
1–2 mL/100g/min
115
How does H+ affect CBF and neuronal activity?
↑H+ = ↑CBF but ↓neuronal activity
116
What is the brain’s oxygen consumption rate (CMRO2)?
3.5 mL O2/100g brain tissue/min
117
What happens when cerebral PO2 drops below 20mmHg?
Coma may result
118
What MAP range supports autoregulation of CBF?
60–160 mmHg
119
What is the daily CSF production rate?
500 mL/day
120
What is the total volume of CSF in the CNS?
About 150 mL
121
What is the flow of CSF?
Formed in lateral ventricles → foramen of monro → third ventricle → aqueduct of sylvius → fourth ventricle → foramen of magendie or foramina of luschka → cisterna magna → subarachnoid space → arachnoid villi → venous sinuses
122
Where is CSF absorbed into the venous system?
Arachnoid villi → venous sinuses
123
What position decreases venous return the most?
Prone
124
What vessels form the Circle of Willis?
Internal carotid and vertebral arteries
125
What artery supplies the medial frontal and parietal lobes?
Anterior cerebral artery (ACA)
126
What artery supplies the lateral frontal, parietal, and temporal cortex?
Middle cerebral artery (MCA)
127
What artery supplies the occipital and medial temporal lobes?
Posterior cerebral artery (PCA)
128
What are the two main types of stroke?
* Thromboembolic (>75%)
* Hemorrhagic
129
What are common deficits in MCA stroke?
* Motor
* Sensory
* Language
130
Does the brain have venous drainage?
Yes, via superficial and deep systems into the jugular veins
131
What type of molecules can cross the blood-brain barrier (BBB)?
Small, lipid-soluble molecules
132
What factors influence cerebral blood flow (CBF)?
* CMRO2
* CPP
* PaO2
* PaCO2
* Ischemia
133
What percentage of total body O2 does the brain use?
20%
134
What is normal brain tissue PO2?
20–50 mmHg
135
What is the formula for cerebral perfusion pressure (CPP)?
CPP = MAP – ICP
136
What is a dangerous CPP level?
<25 mmHg = possible irreversible damage
137
What is normal intracranial pressure (ICP)?
<10 mmHg
138
What PaO2 level causes vasodilation in cerebral vessels?
<50 mmHg
139
Which anesthetics increase CBF?
* Volatile agents
* Nitrous oxide
* Ketamine
140
Which anesthetics decrease both CMRO2 and CBF?
* Propofol
* Etomidate
* Benzodiazepines (Autoregulation and CO2 responses not affected)
141
Which anesthetic is typically avoided in neuro cases?
Ketamine
142
How do opioids affect cerebral dynamics?
Generally unchanged CMRO2, CBF, autoregulation, and ICP
143
What patient positions are used in neurosurgery?
* Supine
* Prone
* Flexed
* Lateral
* Turned
144
What drugs are commonly used for craniotomy induction?
* Propofol
* Etomidate
* Opioid
* Paralytic
145
What medications are used for brain relaxation during craniotomy?
* Mannitol
* Lasix
* CO2 control
146
What is the dosage of Mannitol?
0.5-1 g/kg
147
What is the dosage of Keppra?
500 mg – 1000mg (will increase muscle relaxant metabolism)
148
What is the role of Keppra in craniotomy?
Seizure prophylaxis; may affect neuromuscular blockade
149
What BP med is commonly used in neuro cases?
Nicardipine (5–15 mg/hr), great because do not develop tachyphylaxis
150
What are signs of inadequate CPP?
* EEG changes
* Potential irreversible brain damage
151
What’s the importance of understanding neurovascular anatomy in stroke?
It helps predict clinical deficits based on affected vessels
152
Where does the brain receive its blood supply from?
Internal carotids = 70%, Vertebral arteries = 30%, both sets converge to form Circle of Willis
153
Where does the spinal cord get its blood supply from?
One anterior spinal artery and two posterior spinal arteries
## Footnote
The anterior spinal artery originates from 6-8 major radicular arteries from the aorta, the largest being the artery of Adamkiewicz, which usually occurs at T11 or T12 and supplies T8 to the conus medullaris terminus.
154
How is CBF regulated?
Flow-metabolism coupling. Increase in regional activity = increases in CBF.
155
What is the relationship between MAP and CBF?
MAP (or CPP) yields a consistent CBF of 50 ml/100g/min due to autoregulation, intact from 60-160 mmHg by altering CVR.
156
What are the two phases of CVR?
Rapid Phase (dynamic autoregulation) and Slow Phase (static autoregulation)
157
What is the association between CBF and PaCO2?
Linearly associated between 20-80 mmHg. Changes of 1 mmHg PaCO2 correlate to 1-2 mL/100g/min.
158
What happens to the brain when PaCO2 is below its lower limit of 20 mmHg?
Maximal cerebral vasoconstriction leads to tissue hypoxia and a reflex vasodilation.
159
What is the effect of Propofol, etomidate, benzos, and barbiturates on CBF and CMRO2?
Decrease CBF due to decreasing CMRO2 requirements.
160
What are the low dosage effects of ISO, SEVO, and DES on the brain?
Direct vasodilators, offset by drug-induced decrease in CMRO2, resulting in minimal effect on CBF at lower dosages.
161
What are the high dosage effects of ISO, SEVO, and DES on the brain?
Maximal suppression of CMRO2, leading to dose-dependent increase in CBF.
162
What does the Monro-Kelli doctrine state?
Increase in volume in one intracranial compartment results in increased ICP unless matched reduction occurs in another compartment.
163
What are the most common means of evoked potential monitoring?
Somatosensory evoked potentials, motor evoked potentials, and electromyography.
164
What are the least common means of evoked potential monitoring?
Brainstem auditory evoked potentials and visual evoked potentials.
165
Do anesthetic drugs play a role in the success of intraoperative evoked potential monitoring?
Yes.
166
Are reliable pharmacologic and nonpharmacologic therapies to prevent neuronal ischemic injury available?
No, can only hope to prevent injury by ensuring adequate oxygen and substrate delivery.
167
What is an anesthetic consideration with intracranial mass lesions?
Intracranial hypertension; choice of drugs depends on extent of ICP and if neuromonitoring is being used.
168
What are the major goals when providing anesthesia care for neurological surgery?
Maintain adequate cerebral O2 delivery, optimize operative conditions, facilitate rapid, smooth emergence.
169
What factors affect CBF in the perioperative period?
PaO2, PaCO2, systemic BP, ICP, cerebral auto-regulation, various drugs.
170
What are major techniques to decrease ICP?
Head elevation, hyperventilation, CSF drainage, administration of hyperosmotic drugs, diuretics, corticosteroids, cerebral vasoconstrictors.
171
When does a VAE most commonly occur?
Sitting or head up position.
172
How to monitor for a VAE?
Precordial doppler ultrasonography, transesophageal echocardiography, end-expired CO2 measurement.
173
What is the treatment for a VAE?
Discontinue N2O, flood surgical plain with fluid, aspirate air via a central venous catheter, hemodynamic support.
174
Why should succinylcholine be used with caution in those with neurological disease?
Potential for transient increase in ICP and risk of hyperkalemia.
175
What is CBF per minute?
750 mL/min.
*** Highlighted Recap
176
What is CBF Autoregulation?
MAP between 60-160.
*** Highlighted Recap
177
What is the fastest way to control CBF?
PACO2, carbon dioxide is a vasodilator in the brain, meaning it causes blood vessels to widen and increase blood flow. When PaCO2 is low, the vessels constrict, leading to less blood flow
Effects last 6-8 hours
*** Highlighted Recap
178
What is in a Neuro Anesthesia Box?
PACO2 (huh?)
Mannitol: osmotic diuretic, .5-1g/kg, onset 20-30 mins
Nicardipine: L type dihydophyridine Ca channel blocker, 5-15 g/hr, bolus = 100-300 mcg
Hypertonic Solution 3% NS 300-500 mL over 10-30 minutes then 50 mL/hr, 4-6 mL/kg
Albumin
Remifentanil (neuromonitoring)
Propofol
*** Highlighted Recap
179
What is good for Neuro?
Volatile anesthetics (can be bad, but usually good)
Oxygen
IV anesthetics
Position is important
Choice of fluid
YOUR actions make a difference in Neuro
*** Highlighted Recap
