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Anesthesia > Neuro > Flashcards

Neuro Flashcards

1
Q

Why is the CNS so sensitive to ischemia and hypoxia?

A

Highly metabolically active with little oxygen reserve

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2
Q

Contents of the supratentorial compartment of the cranium

A

The cerebral hemispheres and the diencephalon (thalamus and hypothalamus)

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3
Q

Contents of the infratentorial compartment of the cranium

A

Brainstem and cerebellum

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4
Q

Anterior blood supply to the brain

A

Internal carotid arteries

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5
Q

Posterior blood supply to the brain

A

Vertebral arteries

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6
Q

What types of molecules cannot permeate the blood brain barrier?

A

Macromolecules and proteins

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7
Q

What types of molecules can penetrate the blood brain barrier?

A

Lipid-soluble substances including CO2, O2, and anesthetic drugs.

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8
Q

Normal cerebral blood flow rate

A

50 mL/100 g/min

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9
Q

What percent of cardiac output does the brain receive?

A

15%. It makes up 2% total body weight.

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10
Q

Describe the concept of neurovascular coupling (aka cerebral metabolism-flow coupling)

A

An increase or decrease in CMRO2 results in a proportional increase or decrease in CBF

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11
Q

By what percent does CBF decrease for every 1 degree Celsius drop in temperature below 37?

A

7%

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12
Q

How is CPP calculated?

A

MAP-ICP

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13
Q

What does the lower limit of the cerebral autoregulation curve signify?

A

The CPP level below which the CBF decreases linearly with decreasing CPP. Basically, the point where vasoconstriction can no longer compensate adequately to maintain CPP.

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14
Q

What does the upper limit of the cerebral autoregulation curve signify?

A

The CPP level above which the CBF increases linearly with increasing CPP. Basically, the point where vasodilation can no longer compensate adequately for increased CBF.

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15
Q

What are the lower and upper limits of cerebral autoregulation?

A

60 mmHg and 150 mmHg

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16
Q

What does the plateau phase of the autoregulation curve signify?

A

The CPP range at which CBF remains stable d/t compensatory changes in blood vessels.

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17
Q

What effect do volatile anesthetics have on cerebral autoregulation?

A

At high concentrations, volatiles cause a direct vasodilatory effect on cerebral blood vessels, thus impairing cerebral autoregulation.

18
Q

What effect do IV anesthetics have on cerebral autoregulation?

A

No effect. Autoregulation is preserved.

19
Q

How do changes in PaCO2 affect CBF?

A

Changes in PaCO2 produce corresponding and same-directional changes in CBF when PaCO2 is between 20 and 80 mmHg.

20
Q

How does a 1 mmHg increase or decrease in PaCO2 from 40 mmHg affect CBF?

A

Each 1 mmHg change in PaCO2 above 40 increases CBF by 1 mL/100 g/min. Each 1 mmHg decrease in PaCO2 below 40 produces a decrease in CBF by 1 mL/100 g/min. (About a 2% change in flow)

21
Q

What is the relationship between PaO2 and CBF?

A

Decreases in PaO2 less than a threshold of 50 mmHg result in an exponential increase in CBF.

22
Q

Formula for cerebral oxygen delivery

A

Arterial blood oxygen content x CBF

23
Q

IV anesthetic effect on CMRO2 and CBF

A

Decrease both

Exception: there is debate about ketamine and it is usually avoided in pts with known intracranial disease. (In ventilated pts there is no known effect. In spontaneously ventilating pts ketamine can cause hypercarbia which leads to increase in CBF and ICP)

24
Q

What drugs should be used cautiously in spontaneously ventilating patients with intracranial disease?

A

Opioids and benzos can lead to respiratory depression and hypercarbia resulting in increased CBF and ICP. Ketamine can also cause hypercarbia.

25
Q

Alpha-2 agonist effects on CBF and ICP

A

Decrease CBF with no effect on ICP.

26
Q

Nitrous oxide effect on CMRO2 and CBF

A

Increases both.

27
Q

Three components of the intracranial compartment

A

Blood
CSF
Brain matter

28
Q

Definition of elevated ICP

A

ICP > 15 mmHg

29
Q

Onset and time to peak mannitol

A

Onset 5-10m

TTP 20m

30
Q

Why is the use of PEEP discouraged during intracranial surgeries?

A

Excessive PEEP can impair cerebral venous drainage and increase ICP

31
Q

Why are dextrose-containing solutions avoided in intracranial surgeries?

A

Dextrose solutions are rapidly distributed throughout body water and if BG concentrations decrease more rapidly than brain glucose concentrations then water will cross the BBB and cause cerebral edema.

Also, hyperglycemia augments ischemic neuronal fell damage by promoting neuronal lactate production.

32
Q

Why is labetalol often the preferred beta blocker in the setting of intracranial surgeries?

A

It reduces MAP without causing cerebral vasodilation

33
Q

Tension pneumocephalus

A

A neurosurgical emergency that occurs when subdue always air causes mass effect over the underlying brain parenchyma, often from a ball-valve mechanism causing one-way entry of air into the subdural space

34
Q

Most common cause of intracranial hemorrhage

A

Intracranial aneurysm rupture

35
Q

What percent of pts with SAH will develop vasospasm?

A

35%

36
Q

Treatment of post-aneurysmal vasospasm

A

Triple H therapy
Hypertension, Hypervolemia, Hemodilution
+ CCB (nimodipine)

Fluids and inotropes targeted to goal CVP 10-12 and goal SBP 160-200 (if aneurysm clipped) or SBP 120-150 (if not clipped)

Angioplasty also an option

37
Q

Time course of cerebral vasospasm

A

3-5d after SAH

38
Q

What is the foremost cause of morbidity and mortality after SAH?

A

Vasospasm

39
Q

Gold standard treatment of symptomatic carotid artery atherosclerosis

A

Carotid endarterectomy

40
Q

Regional anesthetic option for CEA

A

Deep or superficial cervical plexus block

41
Q

BP goal during carotid clamping in CEA procedures

A

20% above pt baseline to ensure adequate collateral flow through the Circle of Willis

42
Q

What type of fluid should be avoided in TBI pts?

A

Albumin

Anesthesia (14 decks)

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