*Apex- Brain Flashcards
Match each glial cell with its physiologic function:
Oligodendrocytes
Microglia
ependymal cells
Astrocytes
Phagocytosis
CSF production
Metabolic support to neurons
Increase neuronal conduction velocity
Oligodendrocytes
>increase neuronal conduction velocity
Microglia: Phagocytosis
ependymal cells: CSF production
Astrocytes: Metabolic support to neurons
What type of glial cells form the myelin sheath in the CNS?
Which cells form the myelin sheath in peripheral nerves?
Oligodendrocytes -CNS
*Schwann cells -PNS
What is a neuron and what is its primary role?
It’s the functional unit of the nervous system and it’s primary role is to receive and send information
What’s a collection of nerve cell bodies in the CNS called?
a nucleus
What kind of cells act like nerve glue to support neuronal function?
Glial cells: astrocytes, ependymal cells, oligodendrocytes, and microglia
Most brain tumors arise from what kind of cells?
glial cells
What part of the neuron forms the grey matter vs white matter
Cell bodies - gray
Axons - white (myelinated)
What type of neurons make up most of the CNS neurons?
Multipolar
Where are pseudounipolar nerves found? (2)
dorsal root ganglion
cranial ganglion
Where are bipolar neurons found (2)?
Retina & Ear
(crazy people see shit and hear shit, eyes and ears)
Match each brain lobe with its function:
Parietal
Temporal
Occipital
Frontal
Motor cortex
Vision
Sensation
Audition
Parietal - sensation
Temporal - auditory
Occipital- vision
Frontal - motor cortex
The brain can be divided into what 4 areas?
- Cerebral hemispheres
- Diencephalon
- Brainstem
- Cerebellum
The cerebral hemispheres contain (4)
Diencephalon (2)
Brainstem (4)
CH: cerebral cortex, hippocampus, amygdala, basal ganglia (cerebral cortex + limbic system)
D: thalamus and hypothalamus
BS: midbrain, pons, medulla, RAS
What does the corpus callosum do?
connects the 2 cerebral hemispheres
What lobe contains the motor cortex?
Frontal
What lobe contains the somatic sensory cortex
Parietal
(PARIETAL = SENSORY)
Which lobe contains the speech centers?
Temporal
Wernicke’s vs Broca’s area functions
Wernicke’s = understanding speech (Receptive aphasia)
Broca’s = motor control of speech (Expressive aphasia)
Wernicke’s vs Broca’s location?
Wernicke’s = temporal lobe
Broca’s = frontal (think motor control) - but it’s connected to Wernicke’s area via neural pathways.
What is responsible for fine motor control?
The basal ganglia
What is responsible for memory and learning?
Hippocampus
What is responsible for emotions, appetite, responses to pain and stressors?
Amygdala
What is the primary neurohumoral organ?
I have no idea what that means but the hypothalamus
What part of the brainstem has auditory and visual tracts?
Midbrain
Which part of the brainstem is responsible for autonomic integration
PONS & Medulla
What controls consciousness, arousal, and sleep?
(defective in your brain)
RAS
Match each part of the cerebellum with the function:
Archicerebellum
Paleocerebellum
Neocerebellum
- Regulates muscle tone
- maintains equilibrium
- coordinates voluntary muscle movement
Archicerebellum
>Regulates muscle tone
“need muscle tone to build architecture”
Paleocerebellum
>maintains equilibrium
“Dinosaurs maintain equilibrium”
Neocerebellum
>coordinates voluntary muscle movement
“new muscle movement”
Which cranial nerve is MOST likely to be compressed by a pituitary tumor?
CN2 - optic nerve
What cranial nerve is associated with Tic doulourex and what does it do?
trigeminal nerve (CN5) -generates excruciating neuropathic pain in the face
Bells palsy results from injury to which facial nerve? What does it result in?
CN 7 (Facial)
-ipsilateral facial paralysis
Parasympathetic output is carried by which cranial nerves?
3, 7, 9, 10
(think not 2 bc 2 is CNS but next one)
Mnemonic for cranial nerve names
On Occasion, Our Trusty Truck Acts Funny, Very Good Vehicle Any How
Mnemonic for cranial nerve functions
Some Say Marry Money But My Brother Says Bad Business to Marry Money
CN for somatic sensation and taste to posterior 1/3 of the tongue
Glossopharyngeal (9)
(think 1/3rd bc it’s such a small part all the way in the back)
CN for swallowing
Vagus
CN for pupil constriction
CN3 - occulomotor
CN for sensation to the face
Trigeminal (5)
V1- ophthalmic
CN for sensation to the anterior 2/3 of the tongue
what about taste to the anterior 2/3 of the tongue
CN 5- trigeminal
V2 - Maxillary
(think tongue in cheek, 2 structures, V2) - i SENSE that my tongue is in my cheek
(taste on anterior 2/3 is facial nerve-7)
>think Monica and her 7 orgasms, tasting things
CN for facial movement except mastication (what is the one for mastication)
facial movement = CN 7- facial
mastication = Trigeminal - CN 5, V3 (mandibular) - 3 M’s:
Mandibular, Muscles, Mastication
CN for hearing and balance
8- Vestibulocochlear
Which cranial nerve is responsible for eye:
adduction
abduction
adduction: CN3 (medial rectus)
abduction: CN 6 (lateral rectus)
Which cranial nerve is responsible for eye:
intorsion (depression)
extorsion (elevation)
intorsion (staying IN bc your Depressed) - CN 4 (superior oblique)
extorsion (extroverts are always elevated) - CN 3 (inferior oblique)
-introverts are superior and extroverts are inferior ; introverts let the extroverts go first so CN 3 = elevation followed by CN 4- depression
Which CN is responsible for infraduction of the eye and what is that
looking down and out - CN3 (inferior rectus)
Which cranial nerve?
3- Occulomotor
Inferior oblique
Superior rectus
Medial rectus
Inferior rectus
Which CN?
4- Trochlear (superior oblique)
(What you would be doing with your eyes to look at trochars in your stomach/superior obliques)
Which CN?
CN 6 - Abducens
Lateral rectus
(looking out the corner of your eyes for the devil - 6)
Match the corresponding items:
Site of CSF resorption
Pathway between 3rd and 4th ventricle
Site of CSF production
Pathway between lateral and 3rd ventricle
Choroid Plexus
Arachnoid villi
Foramen of Monro
Aqueduct of Sylvius
Site of CSF production - Choroid plexus
Pathway between lateral and 3rd ventricle - Foramen of Monro
Pathway between 3rd and 4th ventricle - Aqueduct of Sylvius (So Sly, it just sneaks between 3 and 4)
Site of CSF resorption- Arachnoid villi
Total CSF volume
150mls
Rate of CSF production and what is it produced by?
30mls/hr
produced by the choroid plexus
What separates the CSF from the plasma?
The BBB
T/F - the BBB is present at the chemoreceptor trigger zone
False - it’s not - which explains how some drugs that can’t pass through the BBB can elicit N/V
Specific Gravity of CSF
1.002 - 1.009
CSF presure
5-15mmHg
Mnemonic for CSF flow in the brain
Love My 3 Sums 4 Life, Man!
Lateral ventricles
Monro (Foramen)
3rd ventricle
Sylvius (aqueduct)
4th ventricle
Luschka
Magendie
Where is the arachnoid villi and what is it the site for?
CSF absorption / Superior sagittal sinus
What is hydrocephalus?
the excessive amount of CSF accumulation in the brain that can increase ICP
2 types of hydrocephalus. Which is more common?
- Obstructive - an obstruction to CSF flow in the ventricular system (most common)
- Communicating hydrocephalus (decreased absorption by the arachnoid villi - ie. ICH; or overproduction of CSF (very rare)
Treatment options for hydrocephalus (3)
- Placing a catheter in the cerebral ventricles to drain CSF (ventric drain)
- Placing a ventriculoatrial shunt (brain to heart)
- Placing a ventriculoperitoneal shunt (brain to belly)
Normal ICP
5-15 mmHg
(AKA: CSF Pressure)
What 5 Places is the BBB NOT Present?
CCPPH
Chemoreceptor trigger zone (why you get nauseous centrally)
Choroid plexus
Posterior Pitutiary (puts shit directly into blood)
Pineal gland
Hypothalamus
Identify areas on the cerebral blood flow graph:
PaCO2
Cerebral Perfusion Pressure
Intracranial Pressure
PaO2
A- ICP
B- PaCO2
C- CPP
D- PaO2
Cerebral blood flow is coupled to CMRO2 - what does that mean?
It means the greater the need for oxygen, the more blood flow there will be to satisfy that need
5 Things CMRO2 is decreased by
4 Things CMRO2 is increased by
Decreased by:
Hypothermia
Halogenated anesthetics
Propofol
Etomidate
Barbituates
Increased by:
Hyperthermia
Seizures
Ketamine
Nitrous oxide
Cerebral blood flow autoregulates between a CPP of what or MAP of what?
CPP of 50-150mmHg
MAP of 60-160
(remember CPP = MAP - ICP or CVP)
Whats the risk when CPP is < 50 or above >150
<50 - risk of hypoperfusion
>150 - risk of cerebral edema and hemorrhage
What does it mean when it’s said there is a linear relationship between PaCO2 and CBF?
For every 1mmHg increase in PaCO2, CBF will increase by 1-2ml/100g brain tissue/min
& Vice versa
(increase PaCO2 = increase CBF (to get rid of the toxic byproducts)
For every 1mmHg decrease in PaCO2, CBF will (increase/decrease) by _____ml/100g/brain tissue/min
decrease by 1-2ml
Max cerebral vasoconstriction occurs at what PaCO2?
CO2 -25mmHg
Maximum cerebral vasodilation occurs at an PaCO2 of what?
CO2 of 80-100mmHg
A PaO2 below what level causes cerebral vasodilation and increases CBF?
PaO2 below 50-60mmHg
CPP =
MAP - ICP
-a high venous pressure (going into the IVC >RA reduces the amount of venous drainage that can drain into the SVC>RA which results in increased cerebral volume, creating back pressure on the brain that reduces arterial/venous pressure gradient [not as much arterial blood can drop of nutrients with the venous pressure being high])
CBF =
CPP/CVR
CMRO2 =
3.8ml/O2/100g brain tissue/min
oxygen usage in the brain is 60% for _______ and 40% for _______
60% for electrical activity
40% for cellular integrity
*even if the brain is electrically silenced, it still has to consume oxygen to support cellular integrity
CMRO2 decreased ___% for every 1 degree C decrease in temp
7%
EEG suppression occurs between what temps?
18-20 degrees C
Hyperthermia beyond ____degrees C denatures proteins and destroys neurons and CBF decreases
> 42 degrees C
at temps > 42 degees C, does CBF increase or decrease
decrease, gives up. no hope .
How do Resp Acidosis/Alkalosis and Metabolic Acidosis/Alkalosis affect CBF?
Resp Acidosis > decreased pH (increased CO2) > decreases CVR (cerebral vasodilation) > increased CBF
Resp alkalosis > increased pH (decreased CO2) > increased CVR (cerebral vasoconstriction) > decreased CBF
*Metabolic acidosis does not directly affect CBF This is because H+ ions in the blood do not pass through the BBB
…..mmmk.
To ensure a normal CPP of 50mmHg, Map must be between what, assuming an ICP in the normal range of 5-15mmHg.
What if someone has elevated ICP? do you need MAPs lower or higher to maintain CPP
MAP 55-65mmHg to ensure CPP of 50
*If ICP is elevated, a higher MAP is required to maintain CPP
(think extra pressure in the cranial vault is going to compress the vasculature in the brain and you will need a higher MAP to maintain perfusion to the vessels in the brain)
What is cerebral steal?
When there are ischemic or atherosclerotic regions in the brain, the vessels that supply those regions maximally dilate to try and increase o2 to those areas.
Situations that cause cerebral vasodilation (hypercapnia, hypoventilation, vasodilators) - vasodilate the vessels that supply the healthy brain tissue and “steal” flow from ischemic areas.
Cerebral vasodilation or constriction:
hypercapnia
vasodilation
Cerebral vasodilation or constriction:
hypoventilation
vasodilation (hypoventilation = increased PaCO2)
What is “inverse steal” or the “Robinhood effect” the concept of?
The concept of using hyperventilation (decreasing CO2) to constrict the cerebral vessels that supply healthy brain tissue.
- Thought process being that the flow will redistribute to the ischemic regions - but the vessels supplying those regions are already maximally dilated and hypocapnia as not been shown to provide clinical benefit.
- It can actually cause harm from cerebral ischemia (not enough CBF) - oxyhemoglobin dissociation curve shifts to the left - left/love - less O2 released to the tissues (body thinks low co2, low metabolic state, don’t need as much o2 to go to cells that aren’t working hard)
Cerebral vasodilation or constriction:
Hyperventillation
cerebral vasoconstriction (decreased CO2)
CBF is unaffected by PaO2 when the PaO2 level is above what?
>60 PaO2 - CBF unaffected
<50-60 - vasodilation, increased CBF
4 conditions that impair venous drainage from the head (increasing CBV and requiring a higher map to maintain CPP)
- Jugular compression from improper head positioning (head flexion in the sitting position)
- Increased intrathoracic pressure second to coughing or PEEP
- Vena cava thrombosis
- Vena cava syndrome
What are the 5 determinants of cerebral blood flow
- CMRO2 (3.8)
- CPP ( MAP - ICP, 50-150)
- PaCO2 (<25, 80-100)
- PaO2 (<50-60, >60)
- Venous pressure
A fixed and dilated pupil suggests herniation of the:
A. cingulate gyrus
B. Choroid plexus
C. Temporal uncus
D. Cerebellar Tonsils
C. Temporal uncus
Intracranial HTN is defined as
ICP > 20mmHg
What does the Monro-Kellie hypothesis (or doctrine) have to deal with?
The pressure-volume equilibrium between the brain, blood, and CSF within constraints of the cranium.
-Increase in one of these components must be contracted with a decrease in one or both of the others
If not, then ICP within the cranium will rise .
What is Cushing’s triad and what is it a sign of?
It’s a sign of intracranial hypertension and it consists of:
Hypertension
Bradycardia
& Irregular respirations
What’s the most common site of transtentorial herniation? What does it lead to?
At the temporal uncus
-herniation applies pressure to the oculomotor nerve (3), making it ischemic. Manifests as fixed and dilated
What’s the gold standard for ICP measurement?
What are 2 other ways to measure it?
Gold standard = intraventricular catheter
- subdural bolt
- catheter placed over the convexity of the cerebral cortex (mmmk)
ICP measurement is indicated with a GCS of what
= 7
s/s intracranial HTN (other than cushing’s triad) - 7
- Headache
- N/V
- Papilledema (swelling of optic nerve- CN2)
- Pupil dilation and non-reactivity to light (CN3, temporal uncal)
- Focal neurologic deficit
- Seizure
- Coma
What is the condition where ICP increases for no apparent reason (2 names)
Pseudotumor cerebri
Idiopathic intracranial HTN
What’s the deal with hyperventilating a patient with increased ICP?
Mild hyperventilation (PaCO2 30-35) constricts cerebral vessels > decreased CBV > decreased ICP
T/F Decadron shrinks brain tumors
False, it reduces swelling around the tumor
Phenylephrine …. good or bad for increased ICP patients
Good- increased ICP leads to decreased CPP, need to increase MAP to maintain CPP
Why do you want to avoid D5LR in neuro patients?
D5LR contains glucose and when there is cerebral ischemia, excess glucose in the brain is converted to lactic acid and worsens outcomes
5 ways to reduce cerebral blood volume in the patient with intracranial HTN
- mild hyperventilation (PaCO2 30-35) - [vasocx > decrease cbv]
- Avoid hypoxia [PaO2 < 50-60 = vasodilate > increase cbv]
- Avoid vasodilators/Give pressors
- elevate HOB > 30 degrees and avoid neck flexion
- Decrease intrathoracic pressure (avoid peep)
2 ways to decrease cerebral edema in the intracranial HTN pt
- Diuretics (mannitol)
- Steroids (dexamethasone, methylprednisone)
2 ways to decrease CSF in someone with ICHTN
- Ventric drain or VP shunt
- Acetazolamide (Diamox) or Furosemide
Why does lowering the PaCO2 < 30mmHg increase the risk of cerebral ischemia?
Due to vasoconstriction and shifting of the oxyhemoglobin dissociation curve to the left (reduces oxygen offloading- holds on to O2)
T/F: Induction drugs that reduce CMRO2 are thought of as cerebral vasoconstrictor (thiopental, propofol)
True
Which diuretics can reduce CSF production (2)
Acetazolamide and furosemide
Goal of Mannitol vs goal of furosemide in the neuro patient
Mannitol reduces intracerebral mass (water mass)- pulls water out of brain tissue , decreasing ICP
Furosemide reduces CSF production, decreasing ICP
How do osmotic diuretics work in the ICHTN pt?
Dose?
they increase serum osmolarity and “pull” water across the BBB
0.25-1g/kg
Why would mannitol increase cerebral edema?
If the BBB is disrupted, mannitol enters the brain and increases cerebral edema
Caution with mannitol and the heart failure patient
It transiently increases blood volume which can stress the failing heart (and transiently increase ICP)
How does 3% NaCl reduce ICP?
high solute concentration (high tonicity) “pulls” water across the blood-brain barrier and into the vasculature
Caution with corticosteroids and aiming to reduce cerebral edema caused by mass lesions
they can cause hyperglycemia, which in the setting of cerebral ischemia is associated with worse outcomes.
T/F: steroids should be given for the TBI patient
FALSE
T/F- steroids should be given in a patient with a functional pituitary adenoma
False!
The following vascular structures exist as pairs except the:
A. Posterior communicating artery
B. Vertebral artery
C. Basilar Artery
D. Middle cerebral artery
C. Basilar Artery
What does the basilar artery give rise to?
The paired posterior communicating arteries
What do the subclavian arteries give rise to?
The paired vertebral arteries
What do the internal carotid arteries give rise to?
The paired middle cerebral arteries
Primary function of the cirle of Willis
To provide redundant blood flow to the brain
-if one side of the circle becomes occluded, then the other side should be able to perfuse the affected areas of the brain.
What % of the population has a complete and functional circle of willis?
40-50%
-but there are usually additional collateral networks that will do the trick
The cerebral ARTERIAL circulation can be divided into how many separate circulations?
2- Anterior and posterior
They converge and the circle of willis
What supply the anterior circulation to the circle of willis?
The internal carotid arteries
Where do the carotid arteries enter the skull through?
The foramen lacerum
Aorta > _________ > Internal carotid artery > circle of willis > _________
Aorta > Carotid artery >ICA > CW > Cerebral hemispheres
T/F: The common carotid artery comes off the the aorta and bifurcates to the internal and external carotid arteries
True
What supply the posterior circulation to the circle of willis?
Where do they enter the s kill through?
Vertebral arteries
Enter the skill through the Foramen magnum
Aorta > _________ > Vertebral Artery > Basilar artery > _______________ & ______________
Aorta > SUBCLAVIAN ARTERY > vertebral > basilar> POSTERIOR FOSSA STRUCTURES AND CERVICAL SPINAL CORD
What comes off the ascending aorta
Innominate > right subclavian and right CCA
Left CCA
Left Subclavian
The cerebral venous circulation can be divided into how many separate circulations?
2:
- venous blood from the cerebral cortex and cerebellum drain via the Superior sagittal sinus & the dural sinuses
- Venous blood from the basal brain structures drains via the inferior sagittal sinus, the vein of Galen, and the straight sinuses
*Both pathways converge at the joining of the sinuses
& All venous blood exits the brain via the paired jugular veins
What do your jugular veins do?
Drain venous blood from the brain
Within how many hours can IV recombinant tissue plasminogen activator be given after a patient exhibits symptoms of an acute ischemic stroke?
4.5 hours
A TIA is a focal neurologic deficit that spontaneously resolves within ______hours.
24
What is the first line therapy in patients with acute ischemic stroke?
PO Aspirin
CVA patients should receive IV thrombolytics within ____hrs of symptom onset given eligibility.
4.5 hours
HTN is common after ischemic CVA as it supports CPP and cerebral oxygenation. What should the BP be kept under?
185/110
Why is it important to blood glucose levels for stroke patients?
Bc during cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue and is associated with poor outcomes.
Most important risk factor for a stroke + 5 others
*HTN
Smoking
DM
HLD
Excessive ETOH
Elevated homocysteine level
Eligible patients with a large vessel occlusion should undergo embolectomy within _____ hours of symptom onset.
6
Why should you avoid hypotension post stroke?
Bc it decreases CPP (MAP - ICP) and worsens ischemia
What CCB is designated for management of cerebral vasopasm?
2 other measures
Nimodipine
Hct 30% & daily transcranial doppler exams
What is the leading cause of M&M after SAH?
What does treatment consist of?
cerebral vasospasm
Nimodipine + triple H therapy:
Hemodilution, hypervolemia, and hyper
Most common cause of SAH
aneurysm rupture (most arise in the circle of Willis)
2 Surgical options for cerebral aneurysms
how does the anesthetic management differ
Aneurysm clipping or Endovascular coiling
-anesthetic goals are similar for both
*METICULOUS BP CONTROL DURING INDUCTION AND INTUBATION
-focus on reducing ICP and utilizing methods of cerebral protection
T/F Nimodipine relieves cerebral vasospasm
False- it increases collateral blood flow
Difference between SAH and Subdural bleed?
SAH is usually from ARTERIAL bleeding into the subarachnoid space (between arachnoid and pia)
Subdural bleed is usually VENOUS bleeding into the subdural space (between the dura and arachnoid)
What is “the worst headache of their life” usually indicative of?
How often is consciousness lost?
What other symptoms might they present with (4)
SAH
50%
focal neuro deficits, N/V, photophobia, fever
T/F - with SAH- blood can block CSF flow
Ture - this leads to obstructive hydrocephalus and increased ICP
Endovascular coiling requires heparinzation. If the aneurysm ruptures during the procedure, what should you do?
Immediately reverse heparin with 1mg of protamine for every 100units of heparin administered
+lower MAP into the low/normal range
(adenosine may be given to temporarily arrest the heart making it easier for the interventional radiologist to control the bleeding)
aneurysm repair….general rule, intraop BP should be between __________. If the patient undergoes an open repair, the clamp is commonly placed where?
Why that pressure?
What if they don’t use a clamp? – issue?
If BP is too high what can happen? What if too low?
120-150mmHg
- clamp placed on a proximal feeder vessel
- high/normal BP to perfuse collateral circulation
- no clamp = controlled hypotension (drawback: reduces CPP)
If BP too high, transmural pressure rises and increases likelihood of rebleeding
If too low, CPP may be inadequate as autoregulation is usually impared following SAH .
T/F: there is a positive correlation between the amount of blood observed on CT and the incidence of vasospasm
True - free hgb that contacts the outer service of the cerebral arteries increases risk for vasospasm
When is cerebral vasospasm most likely to occur
4-9 days following SAH
most common presentation of cerebral vasospasm
new neuro deficit or altered LOC
Gold standard for diagnosis of cerebral vasospasm
Cerebral angiography
Why is the treatment for cerebra vasospasm aimed at maintaining CPP?
Goal MAP?
Bc the ischemic areas of the brain are already maximally vasodilated, so perfusion to these regions is pressure dependent
-Goal: MAP 20-30 mmHg above baseline
Thought process behind triple H therapy for vasospasm
Liberal hydration supports BP and CPP,
creates a state of hemodilution which reduces blood viscosity and CVR
>together these improve cerebral blood flow
What can medically-refractory vasospasm be treated with?
What if medical tx fails?
Intra-arterial vasodilators:
CCBs (verapamil and nicardipine),
paverine, milrinone
If medical tx fails - balloon angioplasty to forcibly dilate the constricted vessel
Who is at risk for cerebral salt-wasting syndrome? (CSW)
pts who suffer aneurysmal SAH
T/F: hyponatremia is most commonly the result of Cerebral salt-wasting syndrome – not SIADH.
True
-The brain releases naturitic peptide (just like the overfilled heart)
>volume contraction, hyponatremia, and salt wasting by the kidney
(SIADH is associated with slight hypervolemia (or euvolemia) and is treated with fluid restriction)
How is CSW treated?
with isotonic crystalloids
Management for the patient with TBI on clopidogrel includes (select 2):
Hypertonic saline
Methylprednisolone
Platelet transfusion
FFP
Hypertonic saline (to treat TBI- supporting hemodynamics and has osmotic effect that reduces brain water)
&
Platelet transfusion (to reverse anticoagulant)
4 key thoughts surrounding the head trauma patient
- C-Spine stabilization
- Airway protection
- Optimization of hemodynamics
- Cerebral protection
GCS < ___ is consistent with TBI
<8
3 things that can reverse warfarin
- FFP
- Prothrombin complex concentrate
- Recombinant factor 7a
T/F: albumin should be readily available for TBI patients
false, it is associated with poor outcomes
Steorids with TBI- yes or no
No- linked to worse outcomes
GCS for your viewing pleasure + pupil reactivity score
(what 3 things are assessed)
Main reason you shouldn’t use nitrous in a TBI patient
bc other injuries, such as PTX, may only become evident after anesthetic induction and PPV
-can also cause pneumocephalus
Motor responses 1-6 on GCS
1- no movement
2- decerebrate (think decerebrate worse, CERE, cerebral)
3- decorticate
4- withdraws to pain
5- localizes to pain
6- follows commands
Verbal responses 1-5 on GCS
1- no response
2- incomprehensible sounds
3- inappropriate words
4- confused speech
5- normal
Eye opening response scores on GCS 1-4
1- no eye response
2- opens eyes to pain/pressure
3- opens eyes to sound/voice
4- opens eyes spontaneously
For TBI, what should CPP be maintained above?
70mmHg
Clopidogrel can be reversed by what 2 treatments?
- Platelet transfusion
- Recombinant factor 7a
What is the result of abnormal electrical discharges in the brain?
Seizures
What does it mean if someone had a partial/focal seizure
the seizure activity is localized to a particular cortical region
(generalized occurs when the seizure activity affects both hemispheres)
What is it called when a partial seizure can progress to a generalized seizure?
Jacksonian march
What is epilepsy characterized by?
Idiopathic seizures typically diagnosed in childhood
What are new-onset seizures in adults usually the result of (2)?
Structural brain leasion
or metabolic distrubance
How do inhalational agents affect EEG activity?
They reduce it in a dose-dependent fashion
T/f: local anesthetics reduce the seizure theshold
True!
-but a properly executed regional anesthetic does not increase risk of seizures
(does this mean I shouldn’t use IV lidocaine on induction for people with hx of seizures?)
High homocystine levels usually indicate a deficency in what?
Vitamin B-12 or folate
What is homocysteine
An amino acid produced when proteins are broken down, high levels can contribute to blood clots
Which is the tonic vs clonic phase of seizures
Tonic = whole body rigidity (you tense up if your gonna be offered tonic water)
Clonic = repetitive jerking movements
What defines status epilepticus?
Main concern?
Tx?
Seizure activity lasting > 30 mins
or
2 grand mal seizures without regaining consciousness in-between
Concern: resp arrest –> hypoxia (increased o2 consumption by brain and muscles)
Acute tx: phenobarbitol, thiopental, phenytoin, benzos, propofol, GA
What are 4 metabolic derangements that can lead to new onset seizures in adults?
- hypoglycemia
- drug toxicity
- drug/etoh withdrawal
- infection
What are 3 structural brain lesions that can cause new onset seizure in the adult?
Tumor, head trauma, or cerebralvascular event
What would you see if someone was having a seizure under general anesthesia? (3)
- tachycardia
- HTN
- increased EtCO2 as a result of increased o2 consumption
What is laudanosine
The active metabolite of atracurium & cisatracurium (Atracurium produces much larger quanity)
In patients with seizure disorders, what 3 drugs can increase EEG activity and help determine the location of seizure foci during cortical mapping?
- methohexital
- etomidate
- alfentanil
Which drug is excreted unchanged by the kidneys:
Phenytoin
Gabapentin
Carbamazepine
Valproic acid
Gabapentin
(all the others are metabolized by the liver)
Which anticonvulsant is unique in that it is excreted unchanged by the kidneys?
Gabapentin
*elimination is dependent on renal function
Which 2 anticonvulsants induce hepatic enzymes?
Carbamazepine and phenytoin
Which anticonvulsant inhibits hepatic enzymes?
Valproic acid
Which 2 anticonvulsants contribute to a resistance of NON-depolarizing NMBs? Why?
Phenytoin and Carbamazepine
*hepatic enzyme inducers - need increased doses of NDMR
Which anticonvulsant can cause significant tissue injury if extravasation or arterial injection occurs?
Phenytoin
What are the 4 main anticonvulsants
- Phenytoin
- Valproic acid
- Carbamazepine
- Gabapentinoids (Gabapentin and pregabalin)
T/F: Gabapentinoids such as gabapentin and pregabalin are GABA agonists
FALSE
Which anticonvulsant can cause hepatotoxicity and thrombocytopenia (risk of surgical bleeding)
Valproic acid
Which anticonvulsant would concern you for postop resp depression when combined with opioids.
Gabapentinaoids (gabapentin and pregabalin)
Indications of gabapentinoids other than seizures (3)
Diabetic neuropathy, postherpetic neuralgia, complex regional pain syndrome
MOA of phenytoin, valproic acid, and carbamazepine
Blocks voltage-gated sodium channels & stabilizes membranes
MOA of gabapentinoids (gabapentin and pregabalin)
They inhibit the alpha-2 delta subunit of voltage gated CALCIUM CHANNELS in the CNS
>decreased excitatory neurotransmitter release
*they are chemical analogues of GABA, but they are not GABA agonists and not metabolized into GABA
Which anticonvulsant works via zero-order kinetics
Phenytoin
(WAP HAT)
Warfarin, Alcohol, Phenytoin, Heparin, Aspirin, Theophylline
Therapeutic level of phenytoin
10-20mcg/mL
Match the anticonvulsant with the side effect:
Extravasating (at what rates)
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
P (if IV rate > 50mg/min)
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G):
Gingival hyperplasia
P (put a pee-pee in your mouth and you’ll get gum issues)
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
Aplastic anemia
P & C
you’ll get PAC’s if your Anemic (A for anemia/aplastic)
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
Cerebral-vestibular dysfunction (nystagmus and ataxia)
P - take a big p-p in you and your eyes will shake and you wont be able to walk
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
Steven Johnson Syndrome
P
-Johnson = PP
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
Birth defects
P
-need a PP to make a baby
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
-Slows phenytoin metabolism
Valproic acid
-due to enzyme inhibition, less enzymes to metabolize phenytoin
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
-hepatotoxicity
V- toxicity
C = dysfunction
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
-thrombocytopenia and increased surgical bleeding
V*
and C
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
-Leukopenia
C
Match the anticonvulsant with the side effect:
Phenytoin (P), Valproic acid (V), or Carbamazepine (C), Gabapentioid (G)
-useful for trigeminal neuralgia
Carbamazepine
Why do gabapentinoids need to be tapered in the patient with hx seizures
bc it can produce seizures -taper over 1 week
What kind of drugs will result in resistance to NON-depolarizers?
Enzyme inducers
(Smokers [love] A Cold PBR
Smokers [love]
Alcohol
Carbamazepine
Barbituates
Rifampin
Why does is the DOA of Sux prolonged in the patient treated with donepezil for Alzheimer’s Disease?
What other 2 drugs would be prolonged?
Because Donepezil is a cholinesterase inhibitor (mainstay tx for alzheimers). Inhibition of pseudocholinesterase in the plasma (enzyme that breaks sux down is inhibited) - increases the DOA for sux,
mivacurium and ester-type local anesthetics.
Class of drug, What it’s used for, anesthetic concern:
Tacrine
Cholinesterase inhibitor (restore ACH)
tx Alzheimers
prolonged duration of sux, mivacurium, and ester-local anesthetics
Class of drug, What it’s used for, anesthetic concern:
Donepezil
Cholinesterase inhibitor (restore ACH)
tx Alzheimers
prolonged duration of sux, mivacurium, and ester-local anesthetics
Class of drug, what it’s used for, anesthetic concern:
Rivastigmine
Cholinesterase inhibitor (restore ACH)
tx Alzheimers
prolonged duration of sux, mivacurium, and ester-local anesthetics
Class of drug, what it’s used for, anesthetic concern:
Galantamine
Cholinesterase inhibitor (restore ACH)
tx Alzheimers
prolonged duration of sux, mivacurium, and ester-local anesthetics
What is the most common cause of dementia in patients 65 and older?
Alzheimer’s Disease (no cure)
What kind of anesthetic approach would you want to avoid in patients with alzheimers?
MAC and regional
Key findings in alzheimers patients (2)
- Diffuse beta-amyloid-rich plaques
- Neurofibrillary tangles in the brain
Consequences of plaque formation in the brain with alzheimers patients (2)
- Dysfunctional synaptic transmission (most common in cholinergic neurons) (DECREASED ACH)
- so they give cholinesterase inhibitors (blocking the enzyme to break down ACH so more is available) - Apoptosis (programmed cell death)
If an Alzheimers patient requires an anticholinergic, what is the best option and why?
okay so they are lacking acetylcholine, so you want to avoid giving them an anticholinergic which will block the effects of what little acetylcholine they have.
-Glyco is the best option bc it does not cross the BBB
Which inhalational would you want to avoid in alzheimers patients and why
Isoflurane- increases beta-amyloid production
4 side effects of rivastigmine
- increase sux DOA
- N/V
- Bradycardia
- Syncope
(increases PNS tone by increases concentration of acetylcholine)
Good anesthetic plan for an alzheimers patient
General anesthetic with short acting agents so they can return to baseline cognition ASAP (no versed)
Describe parkinson’s pathophys in 1 sentence.
an imbalance between dopamine and acetylcholine in the basal ganglia.
>leads to
Destruction of dopaminergic neurons favors a state of cholinergic overactivity
Parkinson’s Disease
Disease with cholinergic deficency vs overactivty
Alzheimers = cholinergic deficiency
PD = cholinergic overactivity (and dopamine deficiency)
What 2 factors contribute to the pathophys of PD:
Decreased dopamine in the basal ganglia
Increased glutamate in the substantial nigra
Decreased ACH in the basal ganglia
Increased GABA in the thalamus
Decreased dopamine in the basal ganglia
Increased GABA in the thalamus
What do levodopa and carbidopa do when given together?
Increase the concentration of dopamine in the basal ganglia
Patients with parkinsons at ar risk for what 4 things during the perioperative period?
- Autonomic instability (wide BP/HR swings)
- Orthostatic hypotension
- Dysrhythmias
- Aspiration
What drugs are contraindicated in PD patients? (3)
- Metoclopramide
- Butyrophenones (haloperidol & droperidol)
- Phenothiazines (promethazine)
*may exacerbate extrapyramidal sxs
Procedural concerns during deep brain stimulator placement for s/sx of PD
- Lack of airway access during procedure
- Venous air embolism
Effects of decreased dopamine in the basal ganglia
- relative increase in ACH
- causes increased GABA in the thalamus (thalamic suppression)
- suppression of corticospinal motor system & overactivity of extrapyramidal motor system
Diagnosis of PD requires 2 out of what 4 cardinal signs
- Resting “pill-rolling” tremor
- Skeletal muscle rigidity
- Postural instability (loss of balance with an altered gait)
- Bradykinesia (very slow movement and reflexes)
Discuss how levodopa and carbidopa work. What are they and what do they do?
Levodopa is a precursor to dopamine
(tyrosine > L-Dopa by tyrosine hydroxylase, L-Dopa to dopamine by dopa decarboxylase)
In circulation, levodopa is metabolized to dopamine (increased concentration of dopamine - but DA in the blood doesn’t penetrate the CNS)
__________________________________________________
Carbidopa = decarboxylase inhibitor
-carbidopa prevents levodopa from being metabolized in the blood to dopamine so that more levodopa can enter the CNS first and then get metabolized into dopamine there?
CV effects of levodopa and carbidopa (3)
2 others
Inotropy, tachycardia, orthostatic hypotension
N/V & dyskinesia
What is selegiline used for and how does it work?
Parkinson’s Disease
It’s an MAO-B inhibitor and restores dopamine concentration by decreasing dopamine metabolism in the CNS
Half life of levodopa and perioperative considerations
6-12 hours
*must me taken morning of surgery to prevent worsening of symptoms such as rigidity which can impact ventilation
*for longer procedures, it can be given via an orogastric tube
T/F: There is no contraindication to succinylcholine or nondepolarizing NMBs in a patient with Parkinson’s disease
True
In what circumstance would you want a PD patient to hold levodopa the morning of surgery
for deep brain stimulation
-holding it allows symptoms to worsen which facilitates optimal electrode placement
What drugs should be avoided with deep brain stimulation and why
Gaba agonists (propofol, benzos) - can interfere with EP brain monitoring
first step if VAE is detected
surgeon must flood the field with saline
Goal BP for deep brain stimulation and why
SBP < 140 - to decrease risk of ICH)
What MAO-B inhibitor restores dopamine concentration by reducing dopamine metabolism in the CNS?
Selegiline
What drug class can be used for acute exacerbation of parkinsonian symptoms?
Anticholinergics
What is the most common cause of postop vision loss and what kind of surgery does it most often occur after?
What 2 other procedures are considered high risk for POVL?
Ischemic optic neuropathy
-spinal surgery**
CBP and radical neck dissection
Treatment for corneal abrasion
Antibiotic drops and NSAIDS
(patching the eye is not recommended)
What can result from improper head positioning in the prone position and why it’s best to avoid the horseshoe headrest
central retinal artery occlusion (CRAO) - occurs from external compression of the globe
T/F: ION can occur in patients who receive nitrous oxide following retinal detachment surgery with intraocular gas bubble placement.
False- CRAO
-N20 can cause gas bubble expansion, increase IOP and reduce retinal perfusion
What does the cornea do?
It contributes to the eye’s ability to focus by controlling the entry of light into the eye. It also shields the eye from microbes and debris
Ocular Perfusion Pressure =
MAP - intraocular pressure
(try to correlate it with CPP)
CPP = MAP - ICP
OPP = MAP - IOP
Procedural risk factors for ION (6)
- Prone position
- Long duration of anesthesia
- Large blood loss
- Low ratio of colloid to crystalloid resuscitation
- Hypotension
- Wilson Frame
Patient risk factors for ION (7)
- Male
- Old
- Obese
- Diabetic
- HTN
- Smoking
- Atherosclerosis
What supplies the central retinal artery?
Internal carotid > opthalmic artery > central retinal artery
What eye condition perioperatively can lead to blindness?
What’s the most common cause?
Central retinal artery occlusion (perfuses entire retina)
-from decreased venous outflow due to improper head positioning
What does a fundoscopic exam revealing a cherry red macula while the surrounding retina appears pale indicate?
CRAO
Which is a nerve problem vs vessel problem:
ION, CRAO
ION- nerve problem
CRAO- vessel probelm
Which POVL occurs 24-48 hours after surgery vs upon emergence
ION- 24-48hrs after surgery
CRAO - upon emergence /cherry red macula + pale surrounding
both painless
Most common cause of CRAO vs ION
ION - spine surgery in the prone position
CRAO - horseshoe headrest in the prone position
>improper head position reduces venous outflow, increases IOP and impedes retinal perfusion
What kind of vision loss is associated with CBP
CRAO from embolism
What kind of vision loss is associated with nitrous oxide following retinal detachment surgery with intraocular gas bubble placement?
CRAO (n20 can cause gas bubble expansion, raise IOP, and impair retinal perfusion
Which drug uncouples cerebral blood flow from the cerebral metabolic rate?
A. Propofol
B. Midazolam
- Fentanyl
- Isoflurane
- Isoflurane
- under normal conditions, a rise in CMRO2 is met with increased CBF to satisfy the increased o2 demand. Some drugs uncouple this response where CBF exceeds the metabolic requirements of the brain; decreased CMRO2 and increase in CBF (this can increase ICP which is problematic in patients with intracranial HTN)
Place the cerebral structures in order as CSSF flows from the site of production towards the site of reabsorption:
Foramen of Monro
Lateral Ventricles
Foramen of Magendie
Aquaduct of Sylvius
- Lateral ventricles
- Foramen of Monro
- Aqueduct of Sylvius
- Foramen of Magendie
During a craniotomy for tumor resection, the surgeon says the brain is “tight.” Which interventions will improve the conditions in the surgical field (select 2)
- D/C PEEP
- increase volatile agent
- administer nitroprusside infusion
- hyperventilate to a PaCO2 of 30-35
-
- D/C PEEP (peep increases ITP which may reduce venous drainage from the brain)
- hyperventilate to a PaCO2 of 30-35 (will reduce CBF and consequently IVP)
(volatile anesthetics increase CBF and will make it worse, vasodilators also increase CBF)
What is the MOST common cause of perioperative vision loss:
A. Corneal abrasion
B. CRAO
C. ION
D. Cortical blindness
C. ION
(corneal abrasion is the most common eye complication)
Which intervention is indicated in the primary treatment of cerebral vasospasm in a patient who underwent a cerebral aneurysmal clipping for a SAH?
- Erythrocyte transfusion
- Furosemide
- Dexamethasone
- Phenylephrine infusion
- Phenylephrine infusion (increase BP to augment cerebral blood flow) (triple H therapy - hypervolemia, hypertension, hemodilution)
+nimodipine
+/- ballon angioplasty
Which glial cell is responsible for neural repair?
Oligodendrocyte
Ependymal
Astrocyte
Microglia
Astrocyte
Arterial bleeding MOST commonly occurs between the:
Pia matter & Brain
Arachnoid and pia matter
Dura and arachnoid matter
periosteum and dura mater
Arachnoid and pia (subarachnoid space)
T/F - there is no epidural space in the brain
*where does it begin?
True
begins at the foramen magnum
Maximal cerebral vasoconstriction occurs with PaCO2 is what?
25mmHg
What does the pH of the CSF around the arterioles control?
cerebral vascular resistance
Order of blood flow from the aorta to the circle of willis: 1st, 2nd, 3rd, and 4th vessels
- basilar artery
- vertebral artery
- posterior cerebral artery
- subclavian artery
1- subclavian
2- vertebral
3- basilar
4- PCA
Which arterial blood gas is associated with higher cerebral blood flow:
pH 7.15/ PaO2 250/ PaCO2 75
PH 6.95/PaO2 60/ PaCO2 65
pH 7.15/ PaO2 250/ PaCO2 75
Which of the following reduces cerebral blood flow while preserving CMRO2/cerebral blood flow coupling
- Ketamine 2mg/kg IV
- Nitrous oxide 70%
- Hypothermia 34 degrees C
- Isoflurane 1 MAC
Hypothermia 34 degrees C
- The brain’s demand for o2 (CMRO2) determines how much blood goes to the brain. That is to say CBF and CMRO2 are coupled to eachother.
- Uncoupling occurs when CBF is disproportionate to CMRO2.
- The questioon is asking 2 things: what reduces CBF and what preserves the coupling response
- Hypothermia proportionally reduces CBF and CMRO2. It reduces CMRO2 7% for every 1 degree decrease in core body temp.
- Volatile anesthetics UNCOUPLE CBF from CMRO2 bc they dilate the cerebral vasculature indepedent of CMRO2 - they increase blood flow well beyond what the brain requires
The peripheral nervous system is made up of what 2 types of nerves
Spinal and cranial nerves
Central Nervous syttem: Nuclei :: Peripheral nervous system: ?
GangliA
