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Advanced Anesthesia II > Neurosurgery I > Flashcards

Neurosurgery I Flashcards

1
Q

These two arteries supply the anterior circulation of the brain

A

ICAs

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2
Q

These arteries supply the posterior portion of the brain

A

Vertebral arteries

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3
Q

Basic jist of the circle of willis that you may want to know for orals

A

The two vertebrals combine to form the basilar artery, which forms a loop with extensions from the internal carotid artery. This loop provides collateral circulation between posterior and anterior, and L and R circulation.

There is some variability in the loop between individuals and all may not have the same degree of collateral flow.

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4
Q

These are the three paired arteries of the circle of willis

A

anterior, middle, and posterior cerebral arteries

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5
Q

What are radicular arteries and where do they originate from?

A

These are vessels that originate from the vertebral, deep cervical, intercostal, and lumbar arteries, and anastamose with the anterior and posterior spinal arteries.

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6
Q

Difference between collateralization of the cervical vs. lower spinal cord

A

There is rich collateralization in the cervical cord, but not so much in the lower cord.

The Artery of Adamkiewicz is the major supplier of the lower cord. So if you lose this (d/t clamping during vascular surgery, etc) there is high risk of cord ischemia due to poor collateralization.

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7
Q

Anterior spinal artery

A

There is one anterior spinal artery. It supplies the anterior 2/3 of the cord and the most lateral aspects of the cord. It perfuses about all spinal tracts except the dorsal column.

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8
Q

The two posterior spinal arteries originate from

A

the posterior inferior cerebellar arteries

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9
Q

Describe the functionality of the posterior spinal arteries

A

Each supplies the poster 1/3 of the cord on their respective side. They supply the dorsal columns, and having two arteries to supply the dorsal cord provides a better buffer against flow interruption.

Remember that the posterior cord is responsible for sensory transmission. Occlusion of one posterior spinal artery will result in ipsilateral loss of touch and temperature sensation.

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10
Q

SSEP monitors this part of the cord, while MEP monitors this part

A 
SSEP = posterior
MEP = anterior
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11
Q

What is the formula for normal cerebral blood volume?

A

CBV = 0.5mL/100g of brain tissue

Put another way, it is 5mL per kg

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12
Q

How are CVB and CBF related?

A

They have a direct relationship to one another, but it is not 1:1.

Remember that other factors have to be considered. Not just arterial flow and tone, but also venous drainage and tone. Things like positioning, PPV with high PIPs can decreased venous outflow.

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13
Q

Does ICP represent supratentorial or infratentorial pressure?

A

Supratentorial

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14
Q

In the lateral position, this can also be used to estimate supratentorial pressure

A

Lumbar CSF pressure

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15
Q

Components within the cranial vault

A

Brain (cellular and ICF) = 80%
This portion is under the surgeon’s control. The only things we can do to reduce this volume are steroids and diuretics.

Blood (arterial and venous) = 12%
This is what WE are most able to control to reduce ICP. This compartment is the most amenable to rapid alteration.

CSF = 8%
We can’t really do anything about this compartment unless a lumbar drain or ventriculostomy (IVC) is in place

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16
Q

What are the two major problems that result from high ICP?

A

1) Reduction in CPP (Remember that CPP = MAP - ICP). CPP can be reduced to the point where the brain becomes ischemic.
2) Herniation. Either across the meninges, down into the spinal column, or through an opening in the skull. These things happen along the right/upward portion of the curve.

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17
Q

Initial compensation that occurs in response to an expanding intracranial lesion to prevent IICP

A

Displacement of CSF and venous blood to the extra cranial spaces.

Once these measures are exhausted, small increases in intracranial volume result in exponentially higher ICPs. This can result in herniation of decreased CPP and ischemia.

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18
Q

What is intracranial elastance?

A

The change in ICP that occurs after a change in intracranial volume. Also can be viewed as (change in pressure/change in volume)

Low change = high elastane
Large change = low elastance

Compliance is another term often used interchangeably with elastance, although compliance is technically (change in volume/change in pressure)

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19
Q

4 modes of compensation that result in high intracranial elastance (ability to prevent increases in ICP)

A

1) Displacement of CSF from cranial to spinal compartment
2) Increased CSF absorption
3) Decreased CSF production
4) Decreased CBV (mainly venous)

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20
Q

Relation between PaCO2 and CBV

A

CBV increases 0.05mL/100g of brain tissue for every 1mmHg increase in PaCO2

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21
Q

How can the compliance of the brain be tested?

A

Inject 1cc of saline into an IVC. An ICP increase of 4mmHg or more indicates poor compliance and high risk of herniation at one of four sites:

1) Cingulate gyrus under the fall cerebri
2) Uncinate gyrus through the tentorium cerebelli
3) Cerebellar tonsils through the foramen magnum
4) Any area beneath a defect in the skull

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22
Q

How does auto regulation in the brain work

A

In hypotension, you get vasodilation and an increase in CBV

In HTN, you get vasoconstriction and a decrease in CBV

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23
Q

Formula for CPP

A

CPP = MAP - ICP (or CVP, whichever is greater)

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24
Q

Normal values for CPP

A

80-100mmHg

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25
Q

Formulas for CBF and CBV

A

CBF = 50mL/100g brain tissue/min = 750mL/min

CBV = 0.5mL/100g brain tissue

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26
Q

Cerebral blood flow is closely related to

A

Metabolism (grey > white)

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27
Q

These are important factors that impact CBF during anesthesia

A

1) Anesthetic agents used
2) Level of arousal
3) Metabolic byproducts (K+, H+, lactate)
4) Blood viscosity
5) Temperature
6) Concentration of CO2 and H+ ions
7) O2 levels

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28
Q

Is the coupling of metabolism and CBF global or regional?

A

Regional.

Regional CBF parallels metabolic activity and can vary from 10-300mL/100g/min

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29
Q

Difference in metabolism between white and gray matter

A

In the brain:
Gray matter = 80mL/100g/min
White matter = 20mL/100g/min
Gray matter is cortical and controls most of our higher functioning. White matter is subcortical and has a much lower metabolic rate.

In the spinal cord:
Gray matter = 60mL/100g/min
White matter = 20mL/100g/min

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30
Q

Normal CBF rates for infants, children, and adults

A 
Infants = 40mL/100g/min
Children = 95mL/100g/min***
Adults = 50mL/100g/min

Children have nearly twice the CBF as adults!

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31
Q

Energy consumption by the brain goes towards…

A

60% of energy goes towards generating ATP to maintain electrophysiologic function (maintaining and restoring electron gradients; transport, synthesis, and reuptake of NTs)

40% goes towards cellular homeostatic activities

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32
Q

Relationship between CO2, H+, and CBF

A

CO2 + H2O = carbonic acid
Carbonic acid then dissociates and releases H+
Release of H+ ions causes a nearly proportional vasodilation of cerebral vessels.

High H+ concentrations actually depresses neuronal activity. The increased CBF serves to carry away the increased H+ ions that resulted from CO2 formation, thus maintaining a constant level of neuronal activity.

Other metabolic substances such as lactic acid and pyretic acid increase CBF as well.

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33
Q

A 1mmHg increase in PaCO2 will result in this increase in CBF and CBV

A

CBF will increase 1-2mL/100g/min
CBV will increase by 0.05mL/100g/min
Thus, a 15mmHg increase in PaCO2 will increase CBV by 10mL! This is why it’s important to maintain a low normal CO2 for these patients. Increasing your CO2 by 15 points is akin to injecting 10mL of fluid into your patient’s brain!

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34
Q

How long can hyperventilation be used to reduce ICP?

A

About 6 hours. Bicarb transport across the BBB occurs over 6-8 hours corrects pH, which returns CBF and CBV to normal. Hyperventilation for periods of time longer than this is not useful in ICP control and is perhaps harmful.

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35
Q

Why is excessive hyperventilation for a long time bad?

A

1) Alkalosis from hyperventilation shifts the dissociation curve to the left, making it difficult to offload O2 to the brain.
2) CBF becomes markedly decreased due to low PaCO2.

This combo is very bad! We really shouldn’t decrease PaCO2 below 30 or EtCO2 < 25. We should aim for an EtCO2 of about 25-30mmHg.

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36
Q

What should you not do in the patient who has been hyperventilated for a long time?

A

Quickly restore normocapnea. This could result in a dramatic increase in CBF and ICP.

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37
Q

Why is high CO2 bad in focal ischemia?

A

It causes global dilation and stealing of blood flow from theareas of the brain with the highest metabolic demand.

The same situation is bad in the event of a blocked artery. Collaterals are maximally dilated in this case, and blood is at risk of being shunted away in the case of high CO2.

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38
Q

What is the CMRO2 of the brain for adults and pediatrics?

A

Adult: 3.5mL/100g/min
Child: 5.2mL/100g/min

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39
Q

What you see clinically with reductions in CBF

A

50mL/100g/min = Normal
20-25mL/100g/min = Cerebral impairment with EEG slowing
15-20mL/100g/min = Flat EEG
< 10mL/100g/min = Irreversible brain damage

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40
Q

How far can we drive down CMRO2 with our anesthetics?

A

We can drive down O2 demand to the point that the EEG has flatlined. At this point, we have maximally decreased O2 consumption and energy needed for electrophysiologic activity. However, we can’t decrease the O2 needed for cell homeostasis! That remains a constant (see graph).

We are able to offer cerebral production by decreasing metabolism. However, we can’t change the amount required for general cellular upkeep, so we are only able to protect in this manner up to a certain point.

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41
Q

Brain’s capability of anaerobic metabolism

A

The brain is NOT capable of much anaerobic metabolism. It also has a high metabolism, coupled with low glycogen and oxygen stores. It needs a constant supply from blood flow! Thus, LOC occurs within only 5-10 seconds of loss of blood flow.

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42
Q

Brain glucose consumption and how much glucose is stored in the brain

A

Brain Glucose Consumption = 5.5mg/100g/min

Only a 2 minute supply of glucose is stored in the brain!

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43
Q

Does the brain need insulin to take up glucose?

A

Fuck no! It does that shit by itself!

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44
Q

__% of the brain’s metabolism is aerobic

A

90%

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45
Q

During starvation, what becomes a major source of energy for the brain?

A

Ketone bodies like acetoacetate and B-hydroxubutyrate

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46
Q

How does hyperglycemia exacerbate global hypoxic brain injury?

A

It accelerates cerebral acidosis and cellular injury.

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47
Q

How does the brain produce energy during a lack of O2?

A

In the absence of O2, the brain undergoes anaerobic metabolism. The problem with this, is that it lowers intracellular pH and only creates 2ATP (compared to aerobic, which creates 38). This rate of ATP production is not high enough for the brain. It compensates for this in 3 ways:

1) Continuing anaerobic glycolysis
2) Utilizing phosphocreatine stores
3) Shutting down electrophysiologic activity

If ATP production does not keep up, neurons will first become unexcitable, and then become irreversibly damaged.

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48
Q

What is the normal concentration of O2 in the brain?

A

3.5mLO2/100g of brain tissue

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49
Q

If the PO2 of brain tissue drops below ___mmHg or if PaO2 drops below ___-___mmHg, CBF will increase dramatically.

A

PO2 < 30 (normal is 35-45)
PaO2 < 50-60

CBF increases as a final “Haily Mary” effort to deliver O2 to the brain!

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50
Q

After __-__ minutes, ATP stores are depleted and irreversible injury begins to occur

A

3-8 minutes

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51
Q

These two parts of the brain are the most sensitive to hypoxic injury

A

Hippocampus and the cerebellum

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52
Q

What controls the hypoxic driven increase in CBF?

A

Several things.

1) Rostral ventrolateral medulla (O2 sensory within the brain)
2) NO release
3) Increased K+ through ATP/K channels

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53
Q

Can high O2 decrease CBF?

A

Yes, but not enough to be clinically relevant.

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54
Q

CBF is auto regulated very well between these MAPs

A

70-150mmHg (above or below this, flow is pressure passive)

If pressure is too low = ischemia
If pressure is too high = ICH, stroke, and cerebral edema

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55
Q

Cerebral vasculature will adjust to a change in CPP/MAP within __-__ minutes

A

1-3 minutes

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56
Q

The effect of persistent HTN on autoregulation

A

Shifts the auto regulatory range up to higher minimum values and maximums as high as 180-200mmHg

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57
Q

Mechanisms of cerebral autoregulation

A

The mechanisms are still unclear, but probably a combo of 2 mechanisms

1) Myogenic (smooth muscle intrinsic response causes the vessel to contract when it is stretched)
2) Metabolic (H+ ions, NO, adenosine, prostaglandins, etc build up when CBF is slow, causes the vessel to dilate to increase flow and facilitate their removal)

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58
Q

What can happen if BP rises above what the brain is able to autoregulate?

A

CBF increases rapidly overstitching or rupture of blood vessels resulting in cerebral edema or hemorrhage.

With a MAP of 120-160, you can see a disruption of the BBB and development of cerebral edema d/t extreme hydrostatic pressure.

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59
Q

In a patient with long-standing HTN, is the auto regulatory curve every able to return to normal pressures rather than being shifted to the right?

A

Yes, with long-term antihypertensive therapy.

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60
Q

What causes the shift to the right of the auto regulation curve with HTN?

A

Hypertrophy of the blood vessels. This process takes about 1-2 months to occur. The vessels hypertrophy in order to remain constricted at all times to prevent transmission of high pressures to the capillaries.

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61
Q

What factors can abolish the brain’s ability to autoregulate?

A

Trauma, hypoxia, and certain anesthetics and anesthetic adjuvants.

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62
Q

Describe the SNS innervation in the brain.

A

The cerebral vessels (especially the LARGE vessels) have significant SNS innervation. This controls flow to large areas of the brain, as opposed to local regulation. SNS signals arise from the superior cervical sympathetic ganglia.

Also there is a lot of innervation, and it may shift the auto regulation curve to the right, it doesn’t have ALL that much influence over auto regulation. Normal auto regulation measures (myogenic and chemical) still trump its influence.
The SNS may have a minor role in cases of sudden severe HTN (think about extreme stress during running from a bear, don’t want to stroke out while running away. That would be bad, mmmkay?)

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63
Q

Does the PSNS have a presence in the brain?

A

Yes, but its role is unknown. NTs used include Ach, 5HT, and VIP)

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64
Q

Effect of temperature change on CBF

A

CBF will increase by 6-7% for each 1 degree C change
This is a huge influence!

Hyperthermia will increase CBF and CRMO2, while hypothermia will do the opposite.

65
Q

Effect of hypothermia on the brain

A

It will decrease CBF and CRMO2. It decreased both basal metabolic AND electric metabolic requirements (this is different than our anesthetics which only decrease the electric metabolic requirements).

66
Q

Does clinical evidence support the use of hypothermia in neurosurgical patients?

A

No, hypothermia < 35C is not recommended in the neurosurgical population without CP bypass. Not great because it also causes coagulopathies and increases infection risk.

The only times it may be appropriate are following cardiac arrest and POSSIBLY in right risk patients after temporary focal ischemia.

67
Q

EEG becomes isoelectric at this temperature

A

20C

68
Q

This is the most effective method of protecting the brain during focal and global ischemia

A

Hypothermia. It’s great for protecting against ischemia, just not great for neurosurgery (d/t coagulopathy and infection).

69
Q

CBF and blood viscosity

A

A decrease in Hct will increase CBF, but also decrease the O2 carrying capacity of the blood.
An increase in Hct will decrease CBF.

There is little change in CBF between Hct of 33-45%, however, you may want to intervene by the time Hct reaches 55%.

In theory, it is most useful to have decreased viscosity in cases like focal ischemia where max dilation has already occurred, so the only way to increase CBF is by reducing viscosity.

70
Q

Describe the pathophysiology of how hypoxia leads to neuronal death.

A
  • Aerobic metabolism is blocked and ATP becomes depleted.
  • ATP pumps fail, leading to a rise in intracellular Na+ and decrease in K+, causing excessive depolarization.
  • This causes rapid entry of Ca++ into the cells
  • Ca++ release causes glutamate to be released, which leads to more Ca++ being released from the ER and mitochondria.
  • Excessive intracellular Ca++ results in activation of multiple enzymes (proteases and lipases)
  • –> Lipases damage membrane phospholipids and release arachidonic acid, which is them converted to free radicals and other things that cause cellular injury. It also converted to thromboxane which causes intense vasoconstriction.
  • –> Proteases break down the cytoskeleton of the cell
  • –> Nitric oxide syntheses eventually causes damage to DNA, making the cell susceptible to apoptosis
  • Lactate and H+ accumulate, dropping the pH
  • No ATP is available to repair the damaged DNA, proteins, or lipids
71
Q

Are barbiturates beneficial in focal or global ischemia?

A

Focal

72
Q

Describe focal ischemia

A

Usually due to a tumor, hemorrhage, trauma, or embolus affecting one area. There are three areas involved:

1) No blood flow (same as global ischemia)
2) Penumbra
- This area is only partially ischemic and receives collateral blood flow. Flow may be as low as < 15mL/100g/min. This area may recover completely is further damage is prevented and normal flow is rapidly restored. More neurons will survive if collateral flow is increased by mechanisms such as inverse steal from TPL. Preventing secondary brain injury is the key following focal brain injury.
3) Normal perfusion

73
Q

Describe global ischemia

A

The ENTIRE brain is affected, so you don’t want to have preferential blood flow to one area over another. This occurs in total cardiac or pulmonary arrest (cardiac arrest, drowning, asphyxia, etc.)

74
Q

CPP < 50 causes
CPP between 25-40 causes
CPP < 25 causes

A

CPP < 50 causes slowing of EEG
CPP between 25-40 causes flat EEG
CPP < 25 causes irreversible brain damage if sustained

75
Q

Describe transtentorial herniation

A

Blowing a pupil! The medial temporal lobe is compressed against the tantrum cerebelli, causing compression of CNIII and the PSNS fibers that run along it (results in pupillary and oculomotor paralysis on the side of the lesion.

The PCA is also compressed resulting in ischemia to the visual cortex causing temporary blindness.

76
Q

Describe subfalcine herniation

A

Expansion of one cerebral hemisphere causes the cingulate gyrus to be herniated under the fall cerebri.

This places the pt at high risk for compression of the ACA, resulting in ischemia of the primary motor or sensotry cortex. This manifests as weakness/numbness of the legs..

77
Q

Describe tonsillar herniation

A

Displacement of the cerebellar tonsils through the foramen magnum. This is also known as “brain stem” herniation, and causes the respiratory and CV centers in the medulla oblongata to be compressed.

This is LIFE THREATENING! Disruption of major vital centers in the brain. Can also cause kinking and hemorrhage of branches of the basilar artery.

78
Q

Describe transcalvarial herniation

A

Herniation through a skull defect, usually from trauma.

79
Q

The entirety of the subarachnoid space has a volume capacity of ____mL, but of this, only about ____mL is CSF

A

Total capacity of 1650mL (most is brain and cord tissue)

CSF volume is 100-150mL

80
Q

What produces CSF and at what rate?

A

CSF if made by the choroid plexus, found mostly in the lateral ventricles at a rate of 0.3mL/min.

About 500cc is made each day, meaning that the total volume of CSF is replaced 3-4x per day.

81
Q

How is CSF reabsorbed?

A

It is reabsorbed by the arachnoid villi. The villi are extensions of the arachnoid mater that extend into the saggital sinus. These function as one way valves that open once CSF pressure is > 1.5mmHg than venous pressure.

This means that high venous pressure will decrease the outflow of CSF.

82
Q

Communicating vs. noncommunicating hydrocephalus

A

Communication refers to the potency of the pathways of CSF.

In communicating, the pathways are open, but there is a problem with the function of the arachnoid villi (infections or large bleeds can clog up the arachnoid villi.

In non-communicating, there is a physical obstruction along the pathways such as a tumor that blocks flow from its point of exit at the villi.

83
Q

Describe the flow of CSF

A

Fluid from the lateral ventricles flows to the third ventricle via the intracentricular foramina (Foramen of monro). There is one channel from each lateral ventricle that empties into the third ventricle. From here it flows through the small Aqueduct of Sylvius into the fourth ventricle. More fluid is added here (because some is made in the 4th ventricle), and exits via one of three holes: There are two later foramina of Luschka which moves CSF into the subarachnoid space, and a midline Foramen of Magendie, which moves CSF into the cistern magna (which also empties into the subarachnoid space). CSF then moves around the brain, having a grand old time, before it is moved into the venous system via the arachnoid villi.

84
Q

How is CSF formed?

A

Via the choroid plexus by transport of Na, Cl, and bicarbonate with osmotic movement of water.

85
Q

These medications will decrease CSF production

A 
Carbonic anhydrase inhibitors (Acetazolamide)* 
Corticosteroids
Spironolactone
Furosemide* 
Vasoconstrictors
Halothane
Etomidate

Acetazolamide and furosemide are the 2 clinically useful ones that we can use

86
Q

These medications will increase CSF production

A

Enflurane and desflurane

87
Q

Effect of fentanyl and isofluane on CSF production

A

No change

88
Q

CSF absorption is increased by isoflurane, fentaand etomidate

A

isoflurane, fentanyl, and etomidate

89
Q

CSF absorption is decreased by

A

halothane and enflurane

90
Q

This anesthetic gas is pretty shitty when it comes to CSF production/absorption

A

Enflurane. It increases CSF production and decreases reabsorption

91
Q

These anesthetic gases are considered good agents in term of not increasing CSF volume

A

Iso and sevo

92
Q

The BBB is formed by

A

fenestrations between endothelial cells in the brain. These fenestrations are 1/8 the size of fenestrations in other areas of the body

93
Q

The BBB exists at all capillary membranes in the brain parenchyma EXCEPT

A

Hypothalamus, pituitary, and area postrema.

These areas need to be in direct communication with the blood because they are responsible for detecting levels of hormones, etc in the blood

94
Q

Movement across the BBB depends on

A

Size, charge, lipid solubility, and degree of protein binding (similar to the glomerulus)

95
Q

Difference between BBB and blood-CSF barrier

A

BBB involves tight junctions between epithelial cells as well as foot processes from astrocytes to add to the integrity.

Blood-CSF barrier of the choroid plexus involves tight junctions between epithelial cells only and has fenestrations and gaps that allow free movement of molecules

96
Q

These are substances that are permeable, slightly permeable, and impermeable to the BBB

A

Permeable:

  • H2O
  • CO2
  • Lipid soluble substances (ETOH, anesthetics, etc)
Slightly permeable (electrolytes):
- Na, Cl, K, Ca, Mg

Impermeable:

  • Polar molecules
  • Plasma proteins
  • Glucose (only gets through via facilitated diffusion)
  • Large organic molecules (Mannitol)
97
Q

These factors can cause disruptions in the BBB

A

Severe HTN, stroke, tumors, infection, marked hypercapnia, hypoxia, prolonged seizures, osmotic shock, and irradiation

98
Q

Effect of IAs on cerebral hemodynamics

A

Dose dependent ncrease in CBF, but decrease in CRMO2 and electric activity (more supply, but less demand).

Dose dependent impairment of autoregulation (at high MAC, you get less protection against HTN –> risk of edema and stroke!)

The effect on ICP depends on CSF dynamics, CBV, PaCO2, surgical stimulation, other drugs given (TPL), and baseline compliance

99
Q

These 2 factors can blunt the increased CBF from IAs

A

Hypocapnea and TPL

100
Q

This IA preserves autoregulation the most

A

Sevoflurane

101
Q

CMRO2/CBF balance at various MACs

A

0.5 MAC –> A reduction in CMRO2 is the major factor. Thus CBF is slightly decreased d/t less demand. This is good!

1 MAC –> CMRO2 and vasodilation are balanced, resulting in no change in CBF.

> 1 MAC –> Vasodilation is dominant, resulting in increased CBF.

New research suggests that CBF may actually be decreased with sevo and des at 1 MAC

102
Q

All IAs decrease CMRO2. This is the order from most to least in which they do it

A

SIDE-H
Sevo > iso > des > enflurane > halothane

With sero, iso, and des, max EEG/CMR reduction occurs at 1.5-2MAC.

103
Q

These are the two IAs of choice in neuro-anesthesia

A

Iso and Sevo

They are both good in terms of CSF absorption/secretion and are the most powerful at decreasing CMRO2. Plus, servo has demonstrated cerebral protection during ischemia in rats. Sevo also preserves autoregulation the most.

104
Q

Order of vasodilation potency of IAs from most to least

A

HEIDS
Halothane&raquo_space; enflurane > iso = des > sevo
Again reason why iso and sevo are good!

105
Q

What is the most important factor in determining ICP?

A

CBV

106
Q

With IAs, CBV usually increases by about

A

10-12%

107
Q

With halothane and enflurane, the increase in CBF/ICP can be blunted if

A

Hyperventilation is started PRIOR to start of the IA

108
Q

With isoflurane and sevoflurane, the increase in CBF/ICP can be blunted if

A

hyperventilation is started even AFTER the IA is started.

However, this effect is abolished > 1.5 MAC (thought you shouldn’t be going this high in neuroanesthesia anyway)

109
Q

Circulatory steal syndrome in focal ischemia

A

In ischemic areas, the vessels are already maximally dilated to try to perfuse the area. If a VA is added, the blood is redistributed away from the ischemic areas as the rest of the vasculature dilates.

110
Q

Why are seizures so dangerous under anesthesia?

A

Because they increase CMRO2 by 400%, greatly placing at risk for ischemia.

111
Q

Enflurane and seizure activity

A

Seizure patterns van occur at 1.5-2MAC especially when combined with hypocapnea and auditory stimulation

112
Q

Issues with N2O in neurosurgery

A

When used alone, it has the biggest increase in CBF. CMRO2 and ICP increase as well. This effect is blunted a little when used with an IA.
If used with an IV agent like TPL, there is minimal change on CBF, CMR, or ICP. However, use with ketamine can worsen the effect 5x.

Use is controversial in near patients. Risk with VAE or pneumocephalus, and may have direct neurotoxic effect! (exposure with folic acid deficiency can cause cord degeneration).

113
Q

In general, IV anesthetics, analgesics, and sedatives are associated with parallel reductions in CBF and CMR, with no adverse effect on ICP. The exception is

A

Ketamine

114
Q

Effect of IV drugs auto-regulation and CO2 responsiveness

A

No change

115
Q

Reasons why barbiturates are good as induction agents

A

1) Provides hypnosis
2) 30% reduction of CMR and CBF (coupled evenly)
3) Acts as an anticonvulsant
- Can produce isoelectric EEG
- Sz protection is good b/c it prevents secondary injury to already ischemic areas
- Exception is methohexital (can activate sz foci in temporal lobe epilepsy)
4) Robin Hood/ Reverse Steal Phenomenon
- - Blood flow is redirected to FOCAL ischemic areas
5) Facilitates absorption of CSF

116
Q

Opioids in neurosurg

A

If the pt is asleep, there is a minimal decrease in CBF, CMR, and ICP. Effect may be larger if the pt is awake.

  • May cause increased ICP via respiratory depression, histamine release (morphine), activation of sz foci (alfentanil), chest wall rigidity (increased CVP), and reflex cerebral vasodilation that occurs with a sudden drop in BP with sufentanil and alfentanil (can occur with any opioid, but more common with these two).
  • Low doses of remi can increase CBF a little. Higher doses will decrease CBF.
117
Q

Etomidate in neurosurg

A
  • Causes decreased CMRO2, CBF, and ICP
  • NOT PROTECTIVE DURING ISCHEMIC EVENTS (not a first choice in neuroanesthesia)
  • Good for CSF (decreased production and increased absorption)
  • CO2 responsiveness is retained
  • May have adrenal suppression
  • May increase local tissue hypoxia, acidosis, and near deficits d/t formulation in propylene glycol (when compared to EEG equivalent dose of desflurane)***
  • Caution in epileptic pts (may activate sz foci)
  • Associated with longer seizures during ECT than methohexital or propofol
118
Q

Propofol in neurosurg

A
  • Causes a decrease in CMR, CBF, and ICP
    - -> Decrease in CBF > decrease in CMR (good at reducing ischemic cerebral injury)
  • Has anticonvulsant properties
  • Short E1/2t (allows for immediate post-op assessment)
  • Has replaced TPL in practice
  • Cause cardio-depression –> concern for adequate CPP!!
  • Prop has more ventilatory suppression than barbs

Also it is an anti-convulsant, it can increase glutamate excite-toxicity and increase neuronal damage. TPL is still the preferred agent.

119
Q

Benzos in neurosurg

A
  • Decrease in CMR, CBF, and ICP
  • Strong anticonvulsants
  • Maintains CO2 responsiveness
  • Midaz is the best choice d/t short 1/2 life
  • Flumazenil will reverse these beneficial side effects and potentially dramatically increase ICP!!! Avoid this drug if possible.
  • Caution in large doses –> can reduce CPP (d/t low BP) and may prolong emergence.

With benzos and barbs, the decrease in CMRO2 is greater than the decrease in CBF

120
Q

Ketamine in neurosurg

A
  • Unique in that it dilates cerebral vasculature and increases CBF by 50-60%
  • No change in CMRO2
  • Can increase sz activity
  • Will decrease CSF apsorption (no change in formation)
  • Overall increase in ICP (this is in theory, but in practice, may be ok if given with other agents like propofol).

Used to be avoided, but now more controversial. May be neuroprotective by maintaining MAP, and may not increase ICP as much as once thought, especially when co-administered with other agents.

121
Q

Lidocaine in neurosurg

A

Remember that lidocaine also has sedative effects

  • It will decrease CMR, CBF, and ICP, but not as much as other agents.
  • Good adjunct b/c it doesn’t reduce MAP as much as prop or TPL
  • Keep the dose at 1.5-2mg/kg to prevent toxicity and resultant seizures
122
Q

Droperidol in neurosurg

A

Strong antiemetic with blackbox warning for QT prolongation

- Can delay emergence, but has little effect on cerebral hemodynamics unless MAP is decreased

123
Q

Narcan

A

Will eliminate any benefit derived from opioids. Can cause severe HTN.

124
Q

Adrenergic agents in neurosurg

A
  • If auto regulation is intact, pressers will only increase CBF if the MAP falls outside auto regulatory range
  • If auto regulation is not intact, then CBF will vary with pressure
  • Recocnize that the majority of neurosurgical patients will have impaired auto-regulation, so don’t give massive boluses of pressers!
  • The effect will depend on the pt’s baseline BP, the integrity of the BBB and auto-regulation, and what the change in BP is.

Alpha 1 Agonist - Little effect on CBF beyond the increased CPP
Beta 1 Agonist- Increased CMR and CBF, especially if the BBB is disrupted
Beta Blockers - No effect on CMR or CBF
Alpha 2 Agonists - Decrease CBF an CMR in parallel
–> caution with Precedex –> caution with the BP drop! It decreases CBF by about 30%

125
Q

Vasodilators in neurosurg

A

Ex- SNP, NTG, hydralazine, adenosine, CCBs

Although BP drops, CPP and ICP often remain the same or increase

126
Q

NMBs in neurosurg

A
  • NMBs have no direct action on cerebral hemodynamics
  • However, their side effects might. For example, we want to avoid histamine releasing NMBs (d-tubocurarine, atracurium, mivacurium, and metocurine) b/c they cause cerebral vasodilation causing increased ICP and decreased BP, overall decreasing CPP
  • Pancuronium increases BP and HR, which can be a problem if auto regulation is lost

Succinylcholine:

  • Increases ICP by about 5mmHg. However, this can be offset by other drugs such as TPL, defasciculating dose of NDMR, or with pre-hyperventilation.
  • Although it increases ICP, it is not contraindicated in emergencies. Just avoid in elective cases.
127
Q

What is the best choice in NDMR for neurosurg?

A

Vecuronium, because it has no effect on BP, HR, or ICP.

Rocuronium has some vagolytic effects at doses higher than 0.9mg/kg. Again this is a problem in loss of auto regulation, and many neurosurg patients have impaired auto regulation.

128
Q

These classes of drugs provide cerebral protection

A 
CCBs
Steroids
Diuretics
Anticonvulsants
Statins and magnesium may provide benefit as well (Mg prevents Ca++ entry)
129
Q

CCBs for neuroprotection

A

Nimodipine reduces the frequency of vasospasm following SAH (works for SAH only, no other types of brain bleeds).

Although it decreases vasospasm, it’s unclear if there are any long-term improvements in outcome.

130
Q

Steroids for neuroprotection

A

Used for reducing edema associated with tumors.
Used for tumors only, not useful for other neurosurgical populations, and may in fact be harmful.

Steroids for 48 hours prior to crani can reduce edema and improve clinical condition. Steroids are maintained during and after surgery as well. Steroids improve the pressure-volume response as well.

131
Q

Diuretics for neuroprotection

A

Mannitol and lassie are used to reduce the volume of the brain’s ICF and ECF

Osmotic diuretics such as mannitol are preferred d/t speed and efficacy. However, can only be used if the BBB is intact (otherwise it can enter brain parenchyma and worsen swelling). If surgeons feel as though it improved surgical conditions, they may repeat the dose. If ineffective or if serum osmolality reaches 320, then a second dose is withheld.

132
Q

Anticonvulsants for neuroprotection

A

Any irritation of the cortical surface of the brain (head injury, SAH, cortical incisions, irritation from retractors, etc) has the potential to cause seizures.

Remember that seizures can increase CRMO2 by 400%. We want to avoid this!

133
Q

Our goals to protect brain tissue after an ischemic event

A
  • Give adequate anesthesia
  • Prevent seizures (we want to avoid the increase in CMRO2 associated with them)
  • Normocapnea and normoglycemia.
  • Keep CPP at least 60, MAP 70-80 (or within 30% of baseline). We want to keep perfusing the brain!
  • Mild hypothermia (to decrease CMR. Remember that hypothermia is the only way to decrease basal metabolic rate)
    • -> Following global ischemic injury from cardiac arrest, cool to 32-34 C for 24 hours. Rewarm slowly.
    • -> No benefit for trauma patients. Mostly just global ischemia. Although remember that regional hypothermia can be used during cross clamping to avoid spinal ischemia. Studies for use in stroke are on-going.
134
Q

What is an EEG?

A

The EEG signal represents summations of excitatory and inhibitory post-synaptic potentials in the dendrites of neurons in the cerebral cortex. If the summation is large enough, the voltage is detected on the scalp.

The EEG recording plots voltage against time.
Usually looks at 16 channels.

135
Q

EEG waves and what they represent

A 
D-TAB
Delta Waves (0-3 Hz)
  - Deep sleep, deep anesthesia, or pathology such as tumor, hypoxia, or metabolic encephalopathy 
Theta Waves (4-7 Hz) 
   - Sleep and anesthesia in adults, hyperventilation in awake patients
Alpha Waves (8-13 Hz)
  - Awake, but resting with eyes closed
Beta Waves (>13 Hz)
  - Mental activity or light anesthesia

On induction, alpha waves decrease and beta waves dominate. As anesthesia depends, the frequency continues to decrease until theta or delta waves dominate. Further deepening of anesthetic will result in burst suppression (near maximal suppression of cerebral metabolic activity).

136
Q

Intra-op uses of EEG

A
  • To detect cerebral ischemia during CEA, aneurysm repair, CPB, or deliberate hypotension
  • To detect intra-op seizures
  • To assess how well your anesthetics are working (ex- to get the pt into burst suppression, or preventing recall with BIS, etc.)
137
Q

Difference between EEG and evoked potentials

A

EEG looks at large, random signals (>50microvolts)

EPs look at smaller responses (0.1-20microvolts) that result from a specific stimulus. Looks at the way the stimulus travels through a set pathway. EPs must cancel out extraneous electoral noise from the OR (ECG, EEG, muscle activity, etc) is a process called signal averaging

138
Q

Three sensory evoked potentials that we use (SEPs)

A

Somatosensory (SSEP)
Brainstem auditory (BAEP)
Visual (VEP)

139
Q

Compromise or injury to a neurologic pathway will manifest in this way in evoked potentials

A

Increased latency or a decrease in waveform amplitude

140
Q

What are SSEPs and what nerves are commonly used for monitoring?

A

They evaluate the ability of the dorsal spinal column to conduct a signal from the periphery or a cranial nerve to the cerebral sensory cortex.

Nerves used: Median, ulnar, common perennial, posterior tibial, tongue, trigeminal, and pudendal!

141
Q

Use of SSEP in surgery

A

Used to prevent near damage during certain surgeries, such as spinal tumor resection, brachial plexus exploration, spinal instrumentation and fusion, CEA, and aortic surgery.

Significant mechanical or vascular compromise is occurring from the surgery if amplitude is reduced by 50% or latency increased by 10% from the patient’s baseline.

142
Q

Effect of our anesthetics on SSEP

A

IAs, TPL, and Nitrous
–> Increased latency, and decreased amplitude, so we want to minimize the amount used. The combo of IA and N2O causes a PROFOUND depression of SSEP and VEP.

Propofol
–> Good choice, minimal change in latency, slight decrease in amplitude

Ketamine and Etomidate
–> Good choices, may actually improve signals

Precedex
–> Minor depressant effect. This is an ok choice.

Opioids
–> Fine. No changes even in high doses.

143
Q

If your SSEP readings change, what can you do about it?

A

Decrease your IA, switch to IV meds, and do things to improve your perfusion (increase BP, correct anemia, improve PaO2).

Also ask the surgeon to reduce retractor pressure, stop dissection in the field, and to reduce harrington rod distraction.

144
Q

What are MEPs?

A

These test the function of descending motor pathways (anterior cord).
Stimulation can be direct (epidural) or indirect (transcranial via scalp electrodes). The signal descends through the dorsolateral and anterior spinal cord (through the pyramidal tracts primarily).
The EMG signal can be recorded from the spinal cord, or contralateral peripheral nerve/muscle.

145
Q

When are MEPs useful?

A

When the motor system is at risk:

  • Intramedullary tumor resection
  • Scoliosis surgery
  • Brain tumors near the motor cortex
  • Aortic cross-clamping
146
Q

This should always be placed when MEPs are being done

A

Bite block! To avoid tongue injury

147
Q

MEPs and anesthetic agents

A

MEPs are VERY sensitive to our agents!

  • 60% N2O will abolish MEPs
  • They are exquisitely sensitive to IAs
  • Benzos, barbs, and proposal also produce marked depression
  • MRs block transmission. Need 1-2 twitches. In reality, you’ll be asked to paralyze with sux and give no further MR.
  • Fentanyl, etomidate, and ketamine are the best agents to use b/c they cause little or no change***

Similar to SSEPs, MEPs can also become depressed in hypotension, hypothermia, hypoxia, etc.

148
Q

Basics of positioning in neurosurgery

A

Really pretty standard stuff

  • Surgeries can be very long! Make sure all pressure points are padded!
  • Avoid traction on nerves
  • TEDs and SCDs in place

HOB up 15-20degrees ensures optimal venous drainage

149
Q

Often for cranial surgery you want the HOB up 15-20 degrees to ensure optimal venous outflow. When would you NOT want the HOB elevated?

A

Chronic SDH patients (being flat helps prevent reaccumulation)

After CSF shunting procedures (helps prevent rapid collapse of the ventricles)

150
Q

Pressure decreased by __mmHg for ever __cm a given point is above the heart

A

Decreased 2mmHg for every 2.5cm

151
Q

This position helps improve venous drainage and decrease back strain

A

Lawn chair position. Slight flexion, pillows under the knees, slight reverse T

152
Q

These factors increase your risk of ischemic optic neuropathy in the prone position

A

Low BP, impaired venous drainage, low Hct, lengthy surgical time, HTN, DM, HLD, and smoking.

153
Q

Complications involved with the sitting position

A
  • Risk for decreased CPP. Make sure to level the transducer at the circle of willis.
  • Altered hemodynamics
  • Macroglossia (limit neck flexion by placing 2FB between mandible and sternum. Paraplegia could result as well from sustained extreme flexion by stretching of the cord and its vessels)
  • Pneumocephalus
  • VAE
  • Paradoxical air embolism (in the case of PFO)
154
Q

Hemodynamic changes in the sitting position

A
  • Atrial filling pressures decrease (left more so than the right)
  • PSNS tone decreases
  • SNS tone increases (resulting in an increased SVR by 30-60% and PVR by 50-100%)
  • RAAS is activated, and RBF decreases by 30-75%
  • SV decreases by 50%, CO drops by 20-40%, and HR increases by 30% in attempt to compensate
  • CBF decreases by 20%

Before surgery, ponder the patient’s ability to handle the reduced CO and increased SVR they will experience.
Hypotension can be prevented with aggressive pre-positioning hydration, TEDs and SCDs, slow positioning, and us of pressers.
We try to keep CPP at least 60mmHg in healthy patients. Keep it higher in the elderly, those with HTN, cervical spinal stenosis, cerebral vascular disease, or when there will be sustained retractor pressure on the brain or cord.

155
Q

You have higher risk of VAE during these procedures

A

Posterior fossa, upper c-spine, and supratentorial procedures (craniosynostosis, or procedures near the sinuses)

156
Q

Vessels that are often sources of VAE

A

Emissary and cervical epidural veins

Major cerebral venous sinuses (transverse, sigmoid, and the posterior had of the saggital sinus)

157
Q

Monitoring for VAE

A
  • Precordial doppler and ETCO2 are the current standard of care
  • TEE is the most sensitive however, and is able to identify right to left air shunting
158
Q

Management of acute VAE

A

Prevent further air entry

  • Notify the surgeon (flood or pack the surgical field)
  • Jugular compression to prevent more air from reaching the heart
  • Lower the HOB

Treat the air that has already entered

  • Aspirate via central line
  • Discontinue N2O
  • Give 100% O2
  • Support any hemodynamic changes that develop
159
Q

Central lines in neurosurgery (right heart catheter)

A
  • All patients undergoing posterior fossa surgery in the sitting position should have one (high VAE risk)
  • A multi-orifice catheter should be 2cm below the SVC-atrial junction (we want it INSIDE the RA)
  • If the catheter is single-orifice, the tip should be 3cm above the SVC atrial junction

Advanced Anesthesia II (6 decks)

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