Neuroanesthesia Umb

Front 1

What percent of total body O2 consumption is the brain responsible for?

Back 1

20%

Front 2

What is the cerebral metabolic rate?

Back 2

3-4ml/100g/min

Front 3

HOw long of a disruption in O2 will result in loss of conciousness?

Back 3

<10 seconds

Front 4

What is the cerebral glucose utilization?

Back 4

5mg/100g/min

Front 5

What is the average cerebral blood flow?

Back 5

750ml/min

Front 6

what cerebral blood flow will produce a flat
EEG? (isoelectric activity)

Back 6

15-20 ml/100g/min

Front 7

What factors are responsible for regulation of cerebral blood flow?

Back 7

CPP
Autoregulation
Extrinsic mechanisms

Front 8

What is the formula for Cerebral perfusion pressure (CPP)?

Back 8

MAP-ICP or
MAP-CVP

Front 9

What is the normal CPP?

Back 9

80-100mmHg

Front 10

What maintains CPP in the normal range (80-100mmHg)?

Back 10

Autoregulation

Front 11

Cerebral blood flow remains fairly constant with MAPS between_____ and _____.

Back 11

60-160mmHg

Front 12

When Maps are outside 60-160mmHg, CPP is dependent on _____________.

Back 12

pressure

Front 13

Decreases in CPP result in______.

Back 13

cerebral vasodilation

Front 14

Increases in CPP result in _______.

Back 14

cerebral vasoconstriction

Front 15

Pressures above _____________can disrrupt the blood brain barrier, resulting in ___________.

Back 15

150-160mmHg
cerebral edema and hemorrhage

Front 16

Pts with chronic hypertension tend to have a ____________shift on their cerebral autoregulation curve.

Back 16

Right

Front 17

The autoregulation of curve of a pt with controlled hypertension appears:
A.normal
B.right shifted
C. left shifted

Back 17

Normal

Front 18

What are the most important extrinsic factors on cerebral blood flow?

Back 18

Respiratory gas tensions, esp PaCO2

Front 19

Cerebral blood flow is directly proportionate to PaCO2 between tensions of _____________.

Back 19

20-80mmHg

Front 20

Cerebral blood flow changes 1-2 ml/100g/min for every __________.

Back 20

mmHg change in Pa CO2

Front 21

How long will hyperventilation cause a decrease in cerebral blood flow?

Back 21

24-48 hrs, then the body compensates.

Front 22

What are 3 other extrinsic mechanisms of cerebral blood flow regulation?

Back 22

1) Temperature -hypothermia decreases CBF by decreasing CMRO2
2) Viscosity-decreased hct can decrease viscosity and improve blood flow
3) Autonomic influences-variable input

Front 23

What characteristic of the blood brain barrier allows passage of lipid soluble substances but restricts movemtnet of those that are ionized or have large molecular wieghts?

Back 23

The junctions between cerebral vascular endothelial cells are nearly fused. It is a lipid barrier that allows lipids to pass.

Front 24

the blood brain barrier governs passage of substances based on_______, ____________,_______________ and _______________.

Back 24

size, charge, lipid solubility and protein binding in blood

Front 25

What can feely enter the brain thru the BBB?

Back 25

CO2, O2 and lipid soluble substances (such as most anesthetics)

Front 26

What penetrates the BBB poorly?

Back 26

most ions, proteins, and large substances (mannitol)

Front 27

Since water moveds in "bulk flow across the BBB, rapid electrolyte chaanges can create an osmotic gradient across the BBB. What is the effect on the brain?

Back 27

acvute hypertonicity of plasma results in net movement of water out of the brain;
acute hypotonicity causes movement of water into the brain

Front 28

What is the major role of CSF?

Back 28

protect the CNS from trauma

Front 29

Most CSF is formed by the _________ in the _________.

Back 29

choroid plexus
lateral ventricles

Front 30

What is the total CSF volume in the "normal" adult?

Back 30

150ml

Front 31

What is the rate of production of CSF?

Back 31

21ml/hr (500ml/day)

Front 32

Is a malfunctioning shunt considered a surgical emergency?

Back 32

YES! Production is 500ml/day, volume at any given time is 150 ml. ICP will increase quickly.

Front 33

How would you describe the protein content of CSF?

Back 33

limited to the very small amts that leak into perivascular fluid

Front 34

Absorption of CSF is proportional to________.

Back 34

ICP

Front 35

What three components make up the cranial vault?

Back 35

Brain (80%), CSF (8%), Blood (12%)

Front 36

What is the normal ICP in the supratentorium?

Back 36

10mmHg
(resources will vary from 8-15mmHg)

Front 37

Name 4 mechanisms of compensation for increases in ICP

Back 37

1. CSF displacement into spinal compartment
2. Increased CSF absorption
3. Decrease in CSF production
4. Decrease in venous blood

Front 38

What is the effect of hypertension on cerebral blood flow?

Back 38

Autoregulation may induce vasoconstriction to reduce cerebral blood flow

Front 39

What is the effect of hypotension on cerebral blood flow?

Back 39

Autoregulation may induce vasodilation to increase cerebral blood flow

Front 40

What is Cushing's Triad?

Back 40

HTN
Bradycardia
Irregular ventilations or hypoventilation

Front 41

What is Cushing's Triad indicative of?

Back 41

herniation

Front 42

what effect do volatile agents have on CMRO2?

Back 42

They all decrease it

Front 43

Which agents have the greatest/least effect on CMRO2?

Back 43

Iso and ENf reduce CMRO2 the most. HALO reduces it the least.

Front 44

What is important to remeber about enflurane when working with pts with increased ICP?

Back 44

Enflurane can cause seizures

Front 45

What effect do vaolatile anesthetics have on cerebral blood flow and volume?

Back 45

All agents dilate vessels and increase cerebral blood flow.
All agents impair autoregulation in a dose dependent manner

Front 46

Which VA impairs cerebral autoregulation the most? what is its effect on cerebral blood flow?

Back 46

Halothane
CBF is increased

Front 47

What is meant by the term "luxury perfusion"?

Back 47

the reduction of CMRO2 and the increase in cerebral blood flow

Front 48

What is meant by the term "circulatory steal phenomenon"?

Back 48

In the setting of focal ischemia, VA can increase blood flow in normal areas of the brainbut not in ischemic areas, where arterioles are already maximally dilated, resulting is a redistribution of blood flow away from ischemic to normal areas.

Front 49

Does the cerebral vasculature retain its response to CO2 with VA? What is the implication for the anesthetist?

Back 49

Yes, therefore use hyperventilation to abolish or blunt the initial effects of these agents on CBF

Front 50

Does N2O increase ICP?

Back 50

Yes-officially , don't use. In real life, its used.

Front 51

What are the 4 major actions of barbiturates and propofol on the CNS?

Back 51

1. Hypnosis(potentiates GABA, hyperpolarizes neurons)
2. Decrease CMRO2
3. Decrease CBF (vasoconstriction)
4. Anticonvulsant

Front 52

What effects does Etomidate have on CMRO2, CBF, and ICP?

Back 52

decreases

Front 53

What is myoclonus? With which drug is it associated?

Back 53

brief involuntary twitching of muscle or muscle groups-may be mistaken for seizure activity. Seen with etomidate.

Front 54

What effect do benzodiazepines have on CMRO2 and CBF?

Back 54

decrease, but pts wake up slower than with propofol making post op neuro checks difficult.

Front 55

What is "Reverse Steal"?

Back 55

barbiturate induced vasoconstriction causes blood flow to ischemic areas. vasculature in ischemic areas remain maximally dilated while "healthy" areas constrict, redirecting flow.

Front 56

What effect do opioids have on CBF, CMRO2, and ICP?

Back 56

Minimal, unless hypoventilation and hypercapnea are induced

Front 57

What effect does opioid induced hypotension have?

Back 57

reduced CPP

Front 58

Why is morphine not considered optimal in neuroanesthesia?

Back 58

poor lipid solubility-slow CNS penetrationa and prolonged sedative effects

Front 59

What is the only IV anesthetic that dilates cerebral vasculature and increases CBF (>50%)

Back 59

Ketamine

Front 60

What are reasons to avoid ketamine in neuroanesthesia?

Back 60

dilates cerebral vasculature,
increases CBF
Increases ICP
possible pro epileptic
decreases CSF absorption

Front 61

If autoregulation is normal, vasopressors increase CBF at what parameters?

Back 61

MAP<50-60mmHg or MAP>150-160mmHg

Front 62

In the absence of autoregualtion, how do vasopressors increase CBF?

Back 62

By their effect on CPP

Front 63

What can disrupt the blood brain barrier?

Back 63

excessive hypertension

Front 64

What effect do muscle relaxants have on the brain?

Back 64

No direct actions but secondary effects -histamine mediated cerebral vasodilation increase ICP, while systemic hypotension lowers CPP

Front 65

What effect does succinylcholine have on ICP?

Back 65

transient increase in ICP

Front 66

How is ischemic brain injury classified?

Back 66

Focal (incomplete) or global (complete)

Front 67

Name two strategies for brain protection.

Back 67

1. Hypothermia (33-35C)reduces both electrical and basal metabolic requirements.
2. Anesthetic brain protection

Front 68

what is the goal of anesthetic brain protection?

Back 68

produce electrical silence on EEG to eliminate metabolic requirements caused by electrical burst activity

Front 69

What agents can be used for anesthetic brain protection?

Back 69

propofol or barbs-but remember, barbs can cause "robin hood " effect (inverse steal)

Front 70

How is intracranial hypertension defined?

Back 70

sustained increase in ICP >15mmHg

Front 71

What are S&S of increased ICP?

Back 71

H/A
N/V
Change in LOC
papilledema
neurologic deficits

Front 72

what is Cushing's Triad?

Back 72

HTN
paradoxical breathing
Bradycardia

Front 73

What are mechanisms of cerebral edema?

Back 73

1. Disrupted BBB
2. Vasogenic edema (trauma, HTN, CVA)
3. Osmotic changes (water intoxication)

Front 74

Name four ways for cerebral tissue to hernaite

Back 74

1.subfalcine
2. uncal (transtentorial)
3. cerebellar
4. transcalvarial

Front 75

what is the dose of Mannitol?
MUST KNOW FOR TEST!

Back 75

0.25-0.5G/kg

Front 76

Mannitol is an_____________.

Back 76

osmotic diuretic

Front 77

When is Mannitol NOT used?

Back 77

AVMS
intracranial hemmorhage(until open)
Geriatrics(?) Mannitol can cause subdural hematoma

Front 78

What are S&S of cranial mass lesions?

Back 78

H/A, Sz, Change LOC, neuro deficits

Front 79

Where is the A-line positioned for craniotomy in patient with cranial mass lesion?

Back 79

level @ head

Front 80

What is a particular complication of HOB elevated surgical positioning?

Back 80

venous air embolism

Front 81

How can obstruction of cerebral venous drainage be avoided?

Back 81

avoid rotation of neck
avoid IJ line placement

Front 82

what general consideratins should be considered in fluid management for craniotomy for intracranial mass?

Back 82

Keep pt "dry"
Glucose has been shown to have worse outcomes

Front 83

What type of emergence is desirable following craniotomy?

Back 83

rapid, to allow for assessment of neuro status

Front 84

What potential problem set is unique to craniotomy for mass in posterior fossa?

Back 84

1.obstructived hydrocephalus
2.injury/compression to brain stem (resp center, hypotension, arrhythmias)
3.unusual positioning (seated-potential hypotension)
4.Pneumocephalus
5.VAE (head abovee heart)

Front 85

What are the three categories of the GCS evaluation?

Back 85

1. eye opening
2. best motor response
3. best verbal response

Front 86

what are the highest and lowest possible scores on the GCS?

Back 86

3-15

Front 87

At what score on the GCS will you UNQUESTIONABLY intubate?

Back 87

8

Front 88

CSF leakage from nose and ears is associated with __________fx

Back 88

basilar skull fx

Front 89

Hypotension in neurotraumamay be due to_________ or __________.

Back 89

other injuries or neurogenic

Front 90

Where are cerebral aneurysms typically located?

Back 90

Bifurcation of major vessels or circle of Willis

Front 91

What causes most subarachnoid hemmorrhage

Back 91

aneurysm rupture

Front 92

What is the mortality after aneurysm rupture?

Back 92

10%

Front 93

What intervention is available for unruptured aneurysms? what is the anesthetic gaoal?

Back 93

To OR for clipping or "coil"
anesthetic goal is to prevent rupture (normal to decreased BP)

Front 94

What is the presenting sx of SAH? what is happening to ICP and CPP?

Back 94

sudden LOC ->increased ICP with reduction in CPP

Front 95

What are dlayed complications of ruptured SAH?

Back 95

vasospasm (up to 30%)
rerupture
hydrocephalus

Front 96

What are the goals of the anesthetist in management of SAH surgical pt?

Back 96

smooth, non stimulating intubation
judicious fluid management

Front 97

What hemodynamic effect might be seen if SAH pt is on Ca++ channel blockers

Back 97

hypotension

Front 98

What should be avoided to prevent vascular spasm in management of ruptured aneurysms?

Back 98

hyperventilation

Front 99

rapid brain relaxation after ruptured cerebral aneurysm might cause_______.

Back 99

further bleeding by reduction of tamponade.

Front 100

Controlled hypotension:

Back 100

reduces wall tension

Front 101

What is useful prior to clamping in repair of ruptured aneurysm?

Back 101

Pharmacologic "burst suppression"

Front 102

what kind of IV access is needed when repairing cerebral aneurysm

Back 102

Large Bore IVS!! May bleed!!

Front 103

How can vasospasm post surgical repair of aneurysm be prevented?

Back 103

Triple H Therapy:
Hypervolemia
Hypertension
Hemodilution

also, Ca++ channel blockers (Nimodipine a& Nicardipine)

Front 104

Can vasospasm be broken with Ca++ channel blockers post cerebral aneurysm repair?

Back 104

No, effective prophylactically only

Front 105

What factors contribute to venous air embolism?

Back 105

Pressure within vein<atmospheric pressure
Surgical site is above the heart

Front 106

What percent of the population has patent foramen ovale?

Back 106

10-20%

Front 107

Which surgical procedure has the highest rate of VAE? (venous air embolism)

Back 107

craniotomy (20-40%)

Front 108

What determines the consequences of a VAE?

Back 108

volume of air entry
rate of air entry
presence of PFO

Front 109

What are the S&S of VAE?

Back 109

decreased etCO2
hemodynamic collpse
paradoxical air embolism (VAE in circulatrion from PFO) -> stroke or coronary occlusion

Front 110

What tools can be used to monitor for VAE?

Back 110

TEE
Doppler

Front 111

How is VAE treated?
MUST KNOW FOR TEST!

Back 111

1. Notify surgeon
2. Flood the field with fluid and pack
3. D/C N2O
4. Aspirate CVP
5. Give fluids

6. Treat hypotension
7. Head down
8. Bilat Jugular venous compression
9. PEEP(?)
10. CPR

Front 112

AREN'T YOU GLAD WE'RE DONE???

Back 112

YES!!!!!