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Anesthesia Principles IV > Intro to Neuro Anesthesia > Flashcards

Intro to Neuro Anesthesia Flashcards

1
Q

What is the weight of the adult brain?

A

1350gm or 2% of tbw

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2
Q

CBF is approximately _____ to _____ mL/100g/min.

A

45-55mL/100g/min; or 750mL per minute, unless you are going to chop the guys cap off and weigh their brain… this is a better number to be familiar with!

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3
Q

Is the metabolic activity of the brain high or low?

A

HIGH; receives approximately 15% of CO

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4
Q

The brain receives approximately 12-15% of the CO. What % is distributed to the gray matter vs the white matter?

A

gray matter 80%; white matter 20% of the blood flow

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5
Q

Explain cerebral blood flow regulation in regards to “local cerebral metabolism”.

A

When cerebral activity in a particular region of the brain increases, a corresponding increase in BF to that region will occur…. conversely, a decrease in brain activity to a certain region of the brain results in a decrease in BF to that area.

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6
Q

What is another name for when you have TOO MUCH blood flow to the brain, which can result in an increased ICP?

A

hyperemia

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7
Q

What is the condition called when you have TOO LITTLE blood flow to the brain or a certain brain region?

A

ischemia

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8
Q

What factors are involved in the determination of CBF?

A

CBF=CPP/CVR; viscosity of blood, how dilated blood vessels are, and net pressure of blood flow into the brain (CPP— which is determined by BP) are all determining factors of CBF

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9
Q

Explain cerebral autoregulation.

A

cerebral blood vessels are able to change the flow of blood through them by altering their diameters; this AUTOREGULATION is accomplished with a MAP of 70-150 (myogenic regulation) (some sources say 65-150); CBF becomes PASSIVE outside of this range

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10
Q

What is the role of CO2 in the chemical regulation of CBF? PaO2?

A

CBF varies directly with arterial CO2 tension in a PaCO2 range of 25-70mmHg; if PaO2 falls below 60mmHg, CBF increases dramatically

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11
Q

What effect does vasopressors have on CBF?

A

if MAP is below lower limit of cerebral autoregulation, vasopressors increase systemic pressure and thereby increase CBF; if systemic pressure is within the limits of autoregulation, vasopressor induced increases have little effect on CBF;

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12
Q

What effect do vasodilators have on CBF?

A

systemic vasodilators vasodilate the cerebral circulation and can, depending on MAP, increase CBF…. it is mostly a result of its effect on systemic BP

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13
Q

What is the normal CMRO2?

A

3.5mL/100g/min (20% of total O2 consumption)

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14
Q

What effect does volatile anesthetics have on cerebral metabolic rate (CMR)?

A

ALL suppress CMR, and ALL (except halothane) can cause burst suppression on EEG; when there is burst suppression…. CMR is reduced by about 60%

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15
Q

What effect does volatile anesthetics have on CBF?

A

VA’s have dose dependent effects on CBF; in doses < MAC, CBF is not significantly altered; but >1 MAC, direct cerebral vasodilation results in an increase in CBF and cerebral blood volume

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16
Q

Which drugs have been found to exhibit a neuroprotective efficacy and can reduce ischemic cerebral injury?

A

barbiturates, propofol, ketamine, VA’s, and xenon; anesthetic neuroprotection is sustained only when the severity of the ischemic insult is mild

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17
Q

What has been found to result from use of Etomidate, in regards to neuroprotection?

A

administration of etomidate is associated with regional reductions in BF, and this can exacerbate ischemic brain injury

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18
Q

What effect does barbiturates, etomidate, and propofol have on CMR?

A

decreases CMR and can cause burst suppression on EEG (CMR reduced by 60%)… flow and metabolism coupling is preserved and therefore CBF is preserved; once EEG silence is reached NO FURTHER reduction in CMR/CBF is achieved

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19
Q

What effect does opiates and benzodiazepines have on CBF and CMR?

A

minor decreases in BOTH

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20
Q

What effect does Ketamine have on CMR and CBF?

A

increases CMR, which corresponding increase in CBF

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21
Q

What is the formula to determine CPP?

A

CPP=MAP-ICP

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22
Q

Name some factors that have been found to influence CBF.

A

CMR (assuming flow-metabolism coupling is intact): anesthetics, temperature, arousal/seizures, PaCO2, PaO2; Vasoactive drugs: anesthetics, vasodilators, vasopressors; Myogenic: autoregulation/MAP; Rheologic: blood viscosity; Neurogenic: extracranial sympathetic and parasympathetic pathways, intra-axial pathays

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23
Q

A substrate is a molecule in which an enzyme acts upon. The brain’s substantial demand for substrate must be met by adequate delivery of ______ and _______.

A

oxygen and glucose

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24
Q

Explain what CMR and flow-metabolism coupling is.

A

increased neuronal activity= increased local brain metabolism (or CMR)= increased CBF to that area—> referred to as flow-metabolism coupling; precise mechanism of flow-metabolism coupling is unknown:
glutamate is released with increased neuronal activity—> synthesis and release of NO (a potent cerebral vasodilator);

recent data shows role of glia (glial cells are non-neuronal cells that fold neuronal cells in place, supply O2 and nutrients to neurons, insulate neurons, and participate in pathocytosis)–> uptake of glutamate released from neurons by glia triggers increased glial metabolism and lactate production–> since glial processes make contact with neurons and capillaries, glia may serve as a conduit for the coupling of increased neuronal activity with increased glucose consumption and regional blood flow

Nerves innervating cerebral vessels also release peptide neurotransmitters (vasoactive intestinal peptide, substance P, cholecystokinin, somatostatin, and calcitonin gene related peptide)…. they may be involved in neurovascular coupling

OVERALL: it is a complex process regulated by many factors or combinations of metabolic, glial, neural, and vascular factors.

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25
Q

Explain the changes in CMR that occur during varying functional states.

A

CMR decreases during sleep and increases during sensory stimulation, mental tasks, or arousal of any cause; during epileptic activity increases in CMR can be extreme…. whereas regionally after brain injury and globally with coma, CMR can be substantially reduced

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26
Q

In review, what is the simple conclusion for the effects of anesthetic drugs on CMR?

A

in general, anesthetic drugs suppress CMR, with ketamine and N20 being notable exceptions

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27
Q

What effect does temperature have on CMR?

A

CMR decreases by 7% for every 1C decrease in body temp below 37 degrees

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28
Q

At what point will hypothermia cause complete suppression of the EEG?

A

~ 18 to 20 degrees celsius

29
Q

What is the difference in reduction beyond the point at which initial EEG suppression first occurs in regards to anesthetic drugs vs temperature?

A

decreases in temperature DOES produce further DECREASE in CMR, however once the first suppression is achieved with anesthetic drugs further reduction in CMR is NOT achieved;

this occurs because although anesthetic drugs reduce only the component of CMR associated with neuronal function, hypothermia decreases the rate of energy utilization associated with both electrophysiologic function AND the basal component associate with maintenance of cellular integrity

30
Q

What effect does hyperthermia have on cerebral physiology?

A

OPPOSITE EFFECT: between 37 and 42 degrees celsius, CBF and CMR INCREASE…. however above 42 degrees celsius, a dramatic reduction in cerebral oxygen consumption occurs, an indication of a threshold for a toxic effect of hyperthermia that may occur as a result of protein (enzyme) denaturation (structural change)

31
Q

Label in order of greatest to least, in regards to ability to decrease CBF: etomidate, propofol, thiopental

A

thiopental>etomidate>propofol

32
Q

Label in order of greatest to least, in regards to ability to decrease CBF: etomidate, propofol, thiopental

A

thiopental>etomidate>propofol

33
Q

What is the myogenic hypothesis?

A

cerebral autoregulation probably occurs d\t direct changes in tone of vascular smooth muscle; myogenic means “originating in muscle tissue, as opposed to neurogenic”

34
Q

What is the MOST important determinant of viscosity?

A

hematocrit; Hct 33-45% probably only results if a significant change occurs; not a target of manipulation unless HCT is > 55%

35
Q

What are some components of neurogenic innervation for the regulation of CBF?

A

cholinergic, adrenergic, serotonin, vasoactive intestinal peptide

36
Q

What are some components of neurogenic innervation for the regulation of CBF?

A

cholinergic, adrenergic, serotonin, vasoactive intestinal peptide

37
Q

What is the change in CBF seen when manipulating PaCO2, and when is this response attenuated?

A

CBF changes 1-2mL/100g/min for each 1 mmHg change in PaCO2; response attenuated below a value of 25mmHg

38
Q

What can occur after acute normalization of PaCO2 after prolonged hypo or hyper ventilation?

A

significant CSF acidosis (after hypocapnia), and significant alkalosis (after hypercapnia); changes in CBF in response to alterations in PaCO2 occur rapidly, but are NOT sustained—> CBF returns to normal within a period of 6-8 hours; following long periods of hypocapnia…. an increase in CBF with concomittant increase in ICP can be noted once hypocapnia is discontinued.

39
Q

What effect does PaO2 have on CBF?

A

PaO2 between 60 and 300mmHg have little influence; BELOW 60….. CBF will increase rapidly

40
Q

Explain the factors that most likely play at role when CBF is 1: decreased….. 2: increased

A

Reduction in CBF–> stimulate release of vasoactive substances causing arterial dilation (H+, K+, O2, adenosine, and others); acute hypoxia is a potent vasodilator for the brain (NEEDS MORE BLOOD)

High CBF–> autoregulation most likely controlled by myogenic factors (cerebral smooth muscle constrict in response to elevated pressure and dilate in response to decreased pressure.

41
Q

What is the importance of the ventrolateral medulla?

A

within this part of the brain are the cells that control the heart, blood vessels, swallowing, breathing and many other functions that are not noticed at a conscious level (AUTONOMIC)

42
Q

What is the rostral ventrolateral medulla?

A

the part of the medulla known as the “PRESSOR AREA”; receives GABAergic input from caudal ventrolateral medulla (CVLM); the RVLM is primary regulator of SNS, sending excitatory fibers (catecholaminergic) to the sympathetic preganglionic neurons in the spinal cord, via the reticulospinal tract; RVLM is notably involved in the baroreceptor reflex

43
Q

A _______ in oxygen causes stimulation of the rostral ventrolateral medulla (RVLM), resulting in an ________ in CBF, but not in CMR.

A

decrease; increase

44
Q

What are some neuroglial cells and their function?

A

astrocytes (support, metabolic, nutritive functions; most abundant in cortex; may be predominant building block in the BBB), ependymal cells (line cavities in the CNS and make up walls of ventricles; secrete CSF and their cilia circulate it and make up the blood-CSF barrier), microglia (phagocytosis), oligodendrocytes (insulation for axons in the CNS–myelin sheath in brain and spinal cord), Schwann cells (insulation–myelin sheath in PNS; phagocytoic activity; they clear cellular debris and allow regeneration of peripheral neurons)

45
Q

What is the blood brain barrier?

A

effective isolation of brain and spinal cord—> separation of circulating blood from the brain extracellular fluid in the CNS; occurs along the capillaries and consists of tight junctions around the capillaries that do not exist in normal circulation (formed by endothelial cells); endothelial cells restrict the diffusion of microscopic objects (bacteria) and large or hydrophilic molecules into the CSF, while allowing the diffusion of small hydrophobic molecules (O2, CO2, hormones); cells of the barrier actively transport metabolic products such as glucose across the barrier with specific proteins; the junctions formed by endothelial cells PREVENT intracellular transport; midline brain structures receive neurosecretory products from blood and exist outside the barrier (area postrema, pituitary glad, pineal gland, choroid plexus, portions of the hypothalamus)

46
Q

What is the blood brain barrier?

A

effective isolation of brain and spinal cord—> separation of circulating blood from the brain extracellular fluid in the CNS; occurs along the capillaries and consists of tight junctions around the capillaries that do not exist in normal circulation (formed by endothelial cells); endothelial cells restrict the diffusion of microscopic objects (bacteria) and large or hydrophilic molecules into the CSF, while allowing the diffusion of small hydrophobic molecules (O2, CO2, hormones); cells of the barrier actively transport metabolic products such as glucose across the barrier with specific proteins; the junctions formed by endothelial cells PREVENT intracellular transport; midline brain structures receive neurosecretory products from blood and exist outside the barrier (area postrema, pituitary glad, pineal gland, choroid plexus, portions of the hypothalamus)

47
Q

List in order of greatest to least increase in CBF as a result of VA’s.

A

halothane»enflurane>desflurane=isoflurane>sevoflurane

48
Q

What overall effects do VA’s have on cerebral physiology?

A

during normocapnia at >0.5MAC: dose related suppression of cerebral metabolism, vasodilation d\t direct effects on vascular smooth muscle, CBF/CMR ration is altered, result is increases in CBF

49
Q

What overall effects do VA’s have on cerebral physiology?

A

during normocapnia at >0.5MAC: dose related suppression of cerebral metabolism, vasodilation d\t direct effects on vascular smooth muscle, CBF/CMR ration is altered, result is increases in CBF

50
Q

T/F? Benzo’s, Barbs, and most probably propofol, reduce CMRO2 and CBF in a dose dependent fashion.

A

TRUE

51
Q

T/F? Benzo’s, Barbs, and most probably propofol, reduce CMRO2 and CBF in a dose dependent fashion.

A

TRUE

52
Q

What effects do narcotics have on CBF and CMR?

A

likely to have little to no effect

53
Q

What considerations with muscle relaxants should be made in regards to effects on CBF?

A

NDMB: only effect is from histamine release (d-Tubocurarine), so atracurium and mivacurium should only be used in doses not associated with hypotension

DMB (succinylcholine): increased ICP with lightly anesthetized patients, increased CBF d\t cerebral activation from muscle spindle apparatus, not contraindicated when rapid tracheal intubation is required–> defasiculate

54
Q

What are the 4 primary determinants of ICP?

A

brain (12%), intracellular water (78%), CSF (~75mL), and blood (~50mL); total 1200-1500mL

55
Q

What is the normal ICP range?

A

5-15mmHg; Miller says 8-12

56
Q

What is considered an elevated ICP?

A

> 15mmHg; can result from an increase in any of the 4 determinants

57
Q

When is it considered to be intracranial HTN?

A

a sustained increase in ICP above 15-20

58
Q

What is a reserve mechanism for the CSF?

A

CSF reserve can translocate to spinal canal; when there is an increased ICP, in most cases the CSF volume will decrease (absorbed or shunted to spinal compartment)

59
Q

What is a reserve mechanism for the CSF?

A

CSF reserve can translocate to spinal canal; when there is an increased ICP, in most cases the CSF volume will decrease (absorbed or shunted to spinal compartment)

60
Q

What are some signs and symptoms of increased ICP?

A

n/v, HTN, bradycardia, personality changes, altered LOC, altered patterns of breathing, papilledema

61
Q

What is the controversy surrounding hyperventilation as a method of reduction for ICP?

A

only last a few hours (~6); efficacy and duration of effect are unclear; concern that decreasing CBF will increase likelihood of ischemia and more edema

62
Q

Corticosteroids may be good or bad in the presence of increased ICP…. WHY?

A

may be used to decrease edema associated with mass lesions (therefore relieve pressure)…. but in the absence of a mass lesion, they may cause increased ICP and papilledema (swelling of optic disc)

63
Q

Corticosteroids may be good or bad in the presence of increased ICP…. WHY?

A

may be used to decrease edema associated with mass lesions (therefore relieve pressure)…. but in the absence of a mass lesion, they may cause increased ICP and papilledema (swelling of optic disc)

64
Q

What are some general anesthetic management goals for cases involving intracranial mass lesions?

A

avoid sedatives if suspect increased ICP, prevent undesirable changes in CBF and ICP, deep and rapid intubation to limit increase of ICP, timely wakeup to allow for neuro assessment, positioning of patient for maximal exposure and minimal blood pooling, minimize ICP and maintain adequate CPP, opioid PLUS propofol OR volatile agent

65
Q

Why is the use of N20 controversial for anesthesia involving intracranial mass lesions?

A

d\t role in increasing CBF (but used for years without notable difference in patient outcomes)

66
Q

What is the dosing for Mannitol?

A

0.25 to 1 gm/kg IV ; Have it ready to go!

mannitol is the most widely used osmotic diuretic for control of IC HTN. rapid administration can cause vasodilation, increased CBF, transient increase in ICP, and transient increase in circulating blood volume; CAUTION in patients with underlying cardiac dysfunction

67
Q

T/F? MOST CRNA’s run their craniotomy patients “dry”.

A

TRUE; maintain euvolemia (no fluid boluses)

68
Q

What is a concern or consideration for emergence with craniotomy patients?

A

AVOID coughing, bucking, systemic HTN during emergence and tracheal extubation

Anesthesia Principles IV (1 decks)

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