Principles Ii, Exam Final

Front 1

Brain weighs approximately

Back 1

3 lbs

Front 2

The # of neuron cells in our brain is more than

Back 2

100 billion!!

Front 3

The brain is approximately_____% of our total body weight

Back 3

2%

Front 4

Neurons multiply at a rate of 250,000/minute during

Back 4

early pregnancy

Front 5

PERIPHERAL NS
Somatic (Sensory)
_____, _______, ______
Autonomic
_____,_____,_____

Back 5

Skin
Muscles
Joints

Sympathetic
Parasympathetic
Enteric

Front 6

The neuron consist of what parts on the axon
and cell body

Back 6

axon- axon terminal, myelin sheath- schwann cells+ node of rangier,
cell body-nucleus, dendrites

Front 7

Controls involuntary visceral functions

Back 7

Autonomic Nervous System

Sympathetic
Parasympathetic
Enteric

Front 8

SNS has _______ “outflow” or neurons begin at the _______ portions of the spinal cord.

Consists of cell bodies in the________ of the spinal cord.

Preganglionic axons secrete .
Postganglionic fibers secrete

Back 8

thoracolumbar, thoracic and lumbar (T1-L2)

lateral horn
acetylcholine, norepi

Front 9

PSNS has _______ “outflow” or neurons begin at the brain stem________ and ________spinal cord.
________ is secreted at preganglionic and ______postganglionic fibers.

Back 9

craniosacral, (cranial nerves 3,7,9,10), sacral (S2-S4)

Acetylcholine

Front 10

ANS- Usually divided into these 2 pathways


Within these 2 systems, there are _______ and _______synapses between neurons.

Back 10

SENSORY (AFFERENT)
MOTOR (EFFERENT)
inhibitory, excitatory

Front 11

Sensory or AFFERENT pathways transmit ______.
Also include senses of vision, taste, hearing, smell, & equilibrium.

Back 11

pain, temperature, pressure, touch, vibratory sense, and proprioception

Front 12

Primary afferents ascend to the medulla and synapse on the _______ side!
Secondary afferents cross

Back 12

IPSILATERAL
in the medulla to the other side!

Front 13

Motor or EFFERENT pathways transmit from brain to

Back 13

voluntary muscles of the body, smooth and cardiac muscles, and some glands.

Front 14

The carotids lead into the ________. (no IJ lines if elevated ICP! …..decrease drainage from brain)

Back 14

circle of Willis

Front 15

is the primary blood flow to the brain.
It creates redundancies in the vessels so that if one becomes occluded it can compensate from another area.

Back 15

Circle of Willis

Front 16

The primary substrate used for energy production in the brain is ________.
Cerebral function is dependent on_________.

Back 16

glucose

Front 17

Glucose is used by the brain at a rate of______mg/100g/min.
Cerebral Metabolic Rate (CMR) is______ml/100g/min.
Typically CMR is described in terms of ________. (CMRO2)

Back 17

5,
3-4,
oxygen consumption

Front 18

Most cerebral oxygen consumption is used to make_______ to support the electrical activity of the neurons.
Increases or decreases in CMRO2 result in_____ increases or decreases in CBF.

Back 18

make ATP, proportional

Front 19

Hypothermia decreases CMRO2 and CBF______% for every ____ Celsius decrease below normal.

Back 19

7%, 1 degree

Front 20

______ of cardiac output or_____ ml/min
Normal CBF = ______ml/100g/min

Back 20

15-20%, 750, 40-50

Front 21

CBF is determines by many things: some of which are

Back 21

CMRO2, PaCO2, CPP & Autoregulation, PaO2, and anesthesia drugs

Front 22

PaCO2: THIS IS A CRITICALLY IMPORTANT CONCEPT TO NEUROANESTHESIA!!
Change in PaCO2 produces directional change in CBF between a PaCO2 of______.

Back 22

20-80

Front 23

CBF increases or decreases____ml/100g/min for every __mmhg increase or decrease in PaCO2 from___.
If you hyperventilate your patient to a PaCO2 of 30 you would have decreased CBF by approx. _____ml/100g/min.


If you lower to a PaCO2 of 20, CBF is approximately ___% decreased.

Back 23

1-2, 1, 40
10-20
50

Front 24

_______easily crosses the BBB, but ____ does not because of H ions.

This is why acute changes in_____, but not _____ affect CBF. This alteration in pH of the CSF surrounding arterioles leads to dilation or constriction of cerebral arterioles.

Back 24

CO2 , HCO3

PaCO2, HCO3

Front 25

DECREASE CSF pH =
INCREASE CSF pH =

The CBF-lowering effect is not______ !!

Back 25

Cerebral Vasodilation
Cerebral Vasoconstriction

sustained

Front 26

THE ABILITY OF ______ TO ACUTELY DECREASE CBF, CBV, & ICP IS A FUNDAMENTAL CONCEPT IN ________!!!

Back 26

HYPOCAPNIA, NEUROANESTHESIA

Front 27

Hyperventilation causes the pH of both the CSF and the brain’s extracellular fluid space to increase which in turn decreases CBF abruptly.
HOWEVER, by alterations in function of the enzyme _______, the concentration of bicarb in the CSF and ECF is reduced and in a time course of______hours the pH of these compartments returns to ______. Hence, CBF returns to normal levels.

Back 27

carbonic anhydrase, 6-18
normal

Front 28

CPP = ____-_____or _____ (whichever is greater).
CPP is more dependent on _______ because_____ normally 10.

Back 28

MAP – ICP , CVP
map, ICP

Front 29

_________: maintains a constant CBF spite changes in CPP.
Maintains CBF between MAP of _______mmhg, beyond this CBF is pressure dependent.

Back 29

AUTOREGULATION, 50-150

Front 30

Cerebral vasculature adapts rapidly to any changes in CPP.
However, it takes _____mins. to develop so an abrupt increase in ______ is associated with a brief moment of hyperperfusion and vice versa.

Back 30

1-3 , MAP

Front 31

IMPORTANT POINT: pts with chronic HTN have a “______” shift on their cerebral autoregulation curve!!
In chronic hypertension, cerebral ischemia may occur despite pressure of >___.

Back 31

right, 50

Front 32

PaO2 as a determinant of CBF
Less than ______mmhg = exponential _______ in CBF!

Back 32

50, increase

Front 33

Total normal CSF production: ____ml/h or ____ml/day
Total normal CSF volume is ml

Back 33

21, 500
150

Front 34

CSF- Mission is to protect the brain and spinal cord from trauma.
Formed in the _______ of ventricles
Reabsorbed into the venous system of the brain via the

Back 34

Choroid Plexus
Arachnoid Villa.

Front 35

Path of CSF

Back 35

Choroid plexus – lateral ventricles –
foramen of Monro- 3rd ventricle -
aqueduct of Sylvius – 4th ventricle –
foramen of Megendie –
foramen of Luschka – subarachnoid space

Front 36

Lipid barrier that allows passage of lipid soluble substances freely but restricts the passage of those substances that are _______ or have large _______.
CO2, O2, (most anesthetics) do/do not pass freely .
Water _____moves freely, sodium/glucose ____moves freely.

Back 36

ionized, molecular weight
do
does, does not

Front 37

Acute hypertonicity = water (in/out)
Acute hypotonicity = water (in/out)

Back 37

in
out

Front 38

What are some causes of BBB disruption

Back 38

Acute systemic hypertension
Trauma
Infection
Arterial hypoxemia
Marked hypercapnia
Tumors
Sustained seizures

Front 39

Cranium is a fixed structure with 3 components:
Brain (__%)
Blood (__%)
CSF (__%)

Back 39

80, 12, 8

Front 40

Intercranial HTN
Defined as sustained ICP > 15mmhg
Examples of Initial compensation are

hyperventilation only works for about __ hours.

Back 40

Displacement of CSF from cranial to spinal compartments. (cord canal)
Decrease CSF production
Decrease CBF
6

Front 41

S&S if increased ICP

Back 41

Headache
Nausea
Papilledema
Unilateral pupillary dilatation
Oculomotor or abducens palsy
Depressed LOC
Irregular breathing

Front 42

Cushings triad

Together these signs are usually a clinical indicator of impending ______

Back 42

HTN
Bradycardia
Irregular breathing

herniation

Front 43

Methods to Decrease ICP

Back 43

Elevation of the head to improve venous outflow
Hyperventilation
CSF drainage
Osmotic and other diuretic drugs
Administration of drugs that reduce intracranial blood volume (barbs/propofol)
Avoidance of cerebral vasodilating drugs (volatiles)

Front 44

anesthesia and ICU management of neuro patients relies HEAVILY on the manipulation of____+______ !!

Back 44

intracranial volume (ICV) and intracranial pressure (ICP)

Front 45

What is luxury perfusion
is this good or bad? Why?

Back 45

there is a decrease in the energy activity in the brain. (decrease CMRO2) and also there is an increase in CBF

This could potentially increase ICP in pts with decreased intracranial compliance.

Front 46

The impact of the increase in CBF could be negated by hyperventilation but preferable to use_____ such as ____ as anesthesia

Back 46

IV agent, propofol.

Front 47

What effects do VA and nitrous have on CBF and CMRO2

Back 47

All modern agents decrease CMRO2 (Isoflurane and Enflurane the most)
>.5 MAC produces rapid cerebral vasodilation and results in dose dependent increases in CBF!! (important: hyperventilation early works to stop this!)
All abolish autoregulation when > 1 MAC
Nitrous also increases CBF and is thought to increase CMRO2 which could increase ICP. Still widely used.

Front 48

When should you start hyperventilation? Why?

Back 48

The volatiles do not abolish the response of cerebral vasculature to CO2, therefore, hyperventilation can blunt the early effects these agents have on CBF.
*** THIS ONLY WORKS IF HYPERVENT. IS INITIATED BEFORE VOLATILES ARE GIVEN!

Front 49

Which agent has the greatest decrease in CMR? WHich has greatest?
Which increases CBF the most

So the best VA to use is?

Back 49

Iso, Halothane
Halothane

Isoflurane because the net effect of volatiles on ICP includes changes in CBV, delayed alterations of CSF dynamics, and arterial CO2 tension, the best volatile agent is ISOFLURANE.

Front 50

What is Circulatory Steal Phenomenon

Back 50

This occurs during focal ischemia.
Vessels will maximally dilate. Ischemic areas are already maximally dilated.
Flow is shunted from the ischemic area to healthy areas.
“the rich stealing from the poor”

Front 51

Which drug is best to give for the robin hood effect

what side effect can they have?

Back 51

Barb induced vasoconstriction occurs only in normal areas.
Vasculature in ischemic areas remain maximally dilated while “healthy” areas constrict redirecting flow.
“robbing the rich to feed the poor”

Barbs are great for Robin Hood but can cause hang over effect and slow wake up.

Front 52

All IV anesthetics except ______ either have little effect on or reduce ____+_____
Autoregulation and CO2 responsiveness are ____ with all agents.

Back 52

KETAMINE
CMRO2 and CBF.
preserved

Front 53

Decreases CMRO2, CBF, and ICP.

Which one also can cause myoclonus and has been shown to have increased peaks on EEG so suggestive of seizure activity. Also, causes dose dependent adrenal suppression.

Back 53

Benzos (to lesser extent), Barbs, Propofol +Etomidate

etomidate

Front 54

Significant anticonvulsant activity
Short elimination half life
CAUTION in the elderly……decreases MAP and therefore CPP!

Back 54

propofol

Front 55

Facilitates the absorption of CSF = decreased CSF volume. Combined with decreased CBF and CBV = IDEAL TO DECREASE ICP!!!!

Most common neuro induction agent.
Remember the ROBIN HOOD PHENOMENON!!

Back 55

Barbiturates

Front 56

Neuro cautions: depressant effects on consciousness, production of miosis, and depression of ventilation!

Minimal effect of CBF, CMRO2 and ICP unless hypoventilation and hypercapnia are induced.

Back 56

opioids

Morphine can cause prolonged sedation because it is long acting and poorly lipid soluble.

Front 57

Dilates cerebral vasculature hence increasing CBF by as much as 50% !
No change to CMRO2
Possible proepileptic
Decrease CSF absorption

Back 57

ketamine

AVOID

Front 58

Thoughts on NMB on ICP

Back 58

Do not usually effect ICP unless they induce the release of histamine which causes vasodilation / hypotension
Succs may increase ICP through stimulation of muscles spindles, which can directly or indirectly increase CMRO2, which in turn increases CBF and thus ICP.
This increase in ICP not been a consistent finding especially if an adequate dose of thiopental or propofol is given.

Front 59

An increase in ICP from NMB is most likely from

Back 59

Any increases in ICP associated with NMBA is usually from hypertension due to light anesthesia during DL.

Front 60

What agents release histamine??

Back 60

Tubocurarine, atracurium, metocurine, and mivacurium

Front 61

Mannitol dose? When should it be avoided?

Back 61

0.25-0.5 G/kg IV
Osmotic Diuretic that begins to work within 10-15 mins and lasts about 2 hours.

Avoid with:
AVMs (tearing)
Intracranial hemorrhage (until open)
Geriatrics….can cause SDH ?? Pulls on the frail arachnoid and stretches it (theory)

Front 62

What are some ill effects of Mannitol?

Back 62

Rapid administration can cause peripheral vasodilation and hypotension which could increase ICP!!!

Acute Mannitol toxicity- results in decreased sodium and increased measured serum osmolality.

transient increase in intravascular volume can precipitate pulmonary edema in patients with cardiac or renal in sufficiency!!!

Front 63

When autoregulation is intact, vasopressors can only increase CBF when MAP is

Careful….elevations that are too abrupt or excessive can disrupt the

Back 63

below 50-60mmhg or above 150-160mmhg.
BBB!

Front 64

What effects can vasodilators have on CBF and ICP

Back 64

When BP is WNL, these agents typical increase CBF.
CBF is maintained spite the decrease in BP that they cause.

Careful…..the increase in CBF could cause an elevation in ICP in patients with decreased intracranial compliance.

Front 65

The brain is vulnerable because of it’s high _______ and it’s dependence on_____ metabolism.
Loss of oxygen, CBF, and glucose causes a detrimental spiral of events starting with depletion of

Back 65

metabolic demand, glucose
ATP.

Front 66

Goals of cerebral protection- optimize______ lessen_____ prevent______ and avoid
HCT >

Back 66

optimal CPP,
lessen the basal and electrical metabolic requirements,
try to prevent further cell damage, avoid hyperglycemia
30%

Front 67

MOST EFFECTIVE MEANS OF PROTECTING THE BRAIN DURING ISCHEMIA!!!

Back 67

hypothermia

Front 68

What is best protection against focal ischemia?
global ischemia?

Back 68

Barbs
hypothermia

Front 69

anesthesia effets on evoked potentials

Back 69

Most anesthetics DECREASE amplitude and INCREASE latency.

used to measure electrical activity in certain areas of the brain and spinal cord. Electrical activity is produced by stimulation.

Front 70

useful for monitoring cerebral perfusion and anesthetic depth.

Back 70

EEG

Most anesthetics produce biphasic pattern

Front 71

used to measure electrical activity in certain areas of the brain and spinal cord. Electrical activity is produced by stimulation.

Back 71

Evoked Potentials

Front 72

Space Occupying Lesions can be

Back 72

vascular, infectious, tumors, or congenital
slow growing or acute/rapid

Front 73

Intraoperative monitors for neuro patients

Back 73

Standard Monitors
Aline
Central Access, not required
Foley

Front 74

In pre-op eval give special attention to patient's
Look for signs of

Back 74

LOC
Inc. ICP

Front 75

It is important to have a smooth______ +_______

Back 75

induction / intubation in order to keep from increasing ICP or CBF.
Smooth wake up without bucking or coughing is the goal.

Front 76

Deep anesthesia and_______ before DL/tracheal intubation to avoid increasing ICP while maintaining CPP

Back 76

skeletal muscle paralysis

Front 77

Maintenance Minimize____ and maintain adequate ____
Opioid plus propofol or a volatile with or without Nitrous Oxide
Mannitol (_______ g/kg IV)
Maintain euvolemia, _____ free crystalloid.

Back 77

ICP, CPP
0.25-0.5
glucose

Front 78

Iv meds useful for smooth emergence

Back 78

Lidocaine, propofol, or thiopental

Front 79

Anesthetic requirements will differ, depending on the _____ and _____

Back 79

location and type of tumor.

Front 80

A state of profound unconsciousness produced by drugs, disease, or injury.
Tx

Back 80

Coma

Treatment:
AIRWAY (of course!!)
Provision of adequate cerebral perfusion and oxygenation.
Tests to determine level of brain activity (painful stimuli, cold irrigation, pupillary response)
Reaction to stimuli (ie: posturing)
Surgery if necessary

Front 81

Sudden neurologic deficit due to ischemia or hemorrhage.

Back 81

stroke

Front 82

Important steps in treatment of stoke

Back 82

Supportive therapy (airway, oxygenation, ventilation)
Control of blood pressure, glucose, and body temperture.

Front 83

positioning thoughts for neuro anesthesia

Back 83

Can be prone, supine, or lateral
Regardless, head is ALWAYS above the heart.
All pressure points padded!

Front 84

ADVANTAGES and
Disadvantages of sitting position

Back 84

DISADVANTAGES:
Decreased systemic blood pressure
Decreased CO
VAE!!!
ADVANTAGES:
Excellent surgical exposure
Enhanced venous/CSF drainage

Front 85

Vasospasm

Back 85

Variable causes!!
Calcium Channel Blockers most useful in preventing: Nimodipine and Nicardipine, but they are ineffective in “breaking” spasms.
Triple “H” Therapy
Hypervolemia
Hypertension (after aneurysm repair)
Hemodilution (↓ viscocity)

Front 86

Potential problems include obstruction of the 4th ventricles leading to tension pneumocephalus, injury to vital brain stem centers (such as apnea caused by hematoma), difficult positioning, cranial nerve injuries, and venous air embolism.

Back 86

Posterior Fossa space occupying lesions

Front 87

S&S of VAE

Back 87

Decrease in etCO2 (min change in PaCO2)
Hemodynamic collapse
Paradoxical Air Embolism (VAE in the circulation from PFO)
VAE monitoring
TEE
Doppler (mill wheel murmur)

Front 88

What happens with VAE

Back 88

Air enters the Right Atrium & Ventricle
Leads to interference with Right sided CO and BF into Pulmonary Artery
Air gets in the Pulmonary Artery causing pulm. Edema, reflex bronchoconstriction.
Death usually secondary to “vapor lock” causing RIGHT SIDED CO to plummet, acute RIGHT heart failure and ultimately arterial hypoxemia from the combination of cardiac and pulmonary insult!

Front 89

Venous Air Embolism (VAE)
Pressure within the vein is < or > atmospheric pressure
May occur in any position where surgical site is _____

Highest during !!! (20-40%)
Consequences are dependent on the volume and rate of air entry and PFO (10-20%)

Back 89

<
above the heart
craniotomies

Front 90

Tx of VAE

Back 90

Notify surgeon
Flood the field with fluid, then pack
d/c Nitrous
Aspirate CVP
Give fluids
Treat Hypotension
Head down
Bilateral jugular vein compression
PEEP (?)
CPR

Front 91

All TBI are considered to have a ______ pre-op

Back 91

full stomach

Front 92

Control of _____ +______ is most important with TBI's

Back 92

bleeding and hypotension

Front 93

Poor Outcome Factors with TBI

Back 93

Increased ICP
Systemic blood pressure < 70

Front 94

TBI
_______ are common combinations for anesthesia.
Treat ______aggressively

_____may be seen in patients with severe head injury.

Back 94

Barb-opioid-Nitrous-NMBA
hypotension
DIC

Front 95

Anesthesia for Aneurysms and AVMs

Back 95

GOAL is prevention of rupture!!!
Same as before with emphasis on NO SEDATION pre op to avoid hypercapnia.
Aline/Central Line
Elective hypotension???
Most patients should be extubated at the end.

Front 96

Anesthesia for Spine Surgery have a Potential for

Avoid these fluids
Keep _____

Back 96

large blood loss

dextrose containing solutions. If blood glucose decreases before brain glucose it pulls water in.
euvolemic

Front 97

Spinal shock

Back 97

all phenomenon surrounding physiologic or anatomic transection of spinal cord that results in temperature loss and depression of all or most spinal reflex activity below the level of injury
The end of spinal shock is signaled by the return of muscle spindle reflex arcs.

Front 98

What is found resting on the posterior fossa

Back 98

brainstem and cerebellum

Front 99

anterior cranial fossa rest on the
middle cranial fossa rest on

Back 99

frontal lobe
temporal lobe

Front 100

CSF is Formed in the _______ of ventricles
Reabsorbed into the venous system of the brain via the _______

Back 100

Choroid Plexus
Arachnoid Villa.

Front 101

The major arteries suppling the circle of willis are-

Back 101

Basilar and internal carotid

Front 102

The patient with a sudden increase in ICP >30 will exhibit- Hypo or hypertension with tachy or bradycardia

Back 102

HTN and Bradycardia- cushings triad

Front 103

What could cause the robin hood effect

Back 103

hyperventilation