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Basic Science II > Neurophysiology (Ding) > Flashcards

Neurophysiology (Ding) Flashcards

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1
Q

What arteries supply the blood flow to the normal brain?

A

Two carotid arteries (L/R) and two vertebral arteries (More posterior L/R)

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2
Q

What provides collateral circulation in the brain?

A

Circle of Willis

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3
Q

At what level of the spine do the carotid arteries bifurcate into the external and internal carotid arteries?

A

C3

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4
Q

Describe the bifurcations of the internal carotid artery into the cerebral circulation.

A

Internal carotid artery give rise to 7 branches

It ultimately bifurcates into the anterior and middle cerebral arteries

Together, the anterior+middle cerebral arteries define the anterior cerebral circulation.

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5
Q

Which arteries supply the spinal cord and what parts of the spinal cord do they perfuse?

A

Anterior spinal arteries (2): anterior 2/3 of spinal cord

Artery of Adamkiewicz: thracolumbar cord (joins the anterior spinal artery in the lower thoracic)

Posterior spinal arteries (2): posterior 1/3 of spinal cord

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6
Q

Describe the flow of CSF.

A

Lateral ventricles –> interventricular foramina (of Monro) –> third ventricles –> cerebral aqueduct of Slyvius –> fourth ventricle –> spinal cord –> arachnoid granulations –> absorption via dural venous sinuses

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7
Q

How much CSF volume exists at anyone time? How much is produced in a 24 hour period?

A

150 mL at any one time

> 450 mL / day

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8
Q

What is the function of the CSF?

A

Cushions the brain

Maintains brain function by regulating pH and electrolytes

Carries away waste products and delivers nutrients

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9
Q

How does cerebral blood flow respond to changes in PaCO2?

A

As arterial CO2 increases from 25 mm Hg to 65 mm Hg, cerebral blood low increases in a linear fashion.

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10
Q

How can hyperventilation be used as a therapy in the context of a patient’s neurology?

A

It can be used for short periods of time to relax the brain or decrease ICP.

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11
Q

How long does hyperventilation therapy last in decreasing ICP and why?

A

Hyperventilation will only decrease ICP for 4-6 hours.

After this time period, the body’s compensates for it (metabolic compensation to hyperventilation) and ICP goes back up.

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12
Q

Early hyperventilation in traumatic brain injury is associated with poor/good outcomes. (Choose one)

A

Poor

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13
Q

Describe CBF relationship with changes in PaO2.

A

CBF response to changes in PaO2 is flat until PaO2 falls < 50 mm Hg (then it rises quickly)

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14
Q

CBF is maintained between CPP of __ to __ mm Hg.

A

60-160

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15
Q

What is the difference between communicating and obstructive hydrocephalus?

A

Communicating hydrocephalus: failure to absorb CSF (typically due to dysfunctional arachnoid granulations); evolves over years and characterized by barely perceptional changes

Acute hydrocephalus: direct obstruction or compression of a CSF passageway; rapid progression that may require external ventricular drainage

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16
Q

What are the effects of inhalational anesthetics on CBF and metabolism?

A

(Dose dependent effects)

  1. 5 MAC: CMR suppression > vasodilation (decreased CBF)
  2. 0 MAP: CMR suppression = vasodilation (CBF unchanged)

>1.0 MAC: vasodilation > CMR suppression (significantly increased CBF)

17
Q

What is the effect of N2O on ICP and CBF?

A

it increases both.

18
Q

What is the effect of most of our IV anesthetic agents on CBF amd CMR?

A

Mostly decreases or does nothing to either EXCEPT for ketamine which increases CMR significantly.

19
Q

What information does EEG give us?

A

Ischemia

Seizures

Burt-suppression pattern

Functional assessment

Depth of anesthesia

20
Q

Indications for EEG include..

A

Carotid endarterectomy

Bypass

Cerebrovascular surgeries

Burst suppression necessary for cerebral protection

ICU

Suspected seizures

21
Q

EEG frequencies + names and their meanings.

A

Delta 0-3 Hz (deep anesthesia or coma)

Theta 4-7 Hz (transition to deep anesthesia)

Alpha 8-12 Hz (light anesthesia/relaxation)

Beta >12 Hz (awake)

22
Q

What is burst suppression and what are the indications for it?

A

Burst supression: periods of normal brain activity interrupted by stretches of greatly reduced activity >10 seconds

Indications:

Refractory high ICP

Refractory epilepsy

Intra-op neuroprotection

Cerebral vascular surgeries

23
Q

What can we do to induce burst suppression?

A

Deep anesthesia with anesthetic agents (esp. propofol, barbs, benzos, isoflurane)

Deep hypothermia

24
Q

In BIS monitors what is the proposed optimal range to prevent intra op awareness?

A

40-60

25
Q

In SSEP monitoring, what changes are considered clinically significant?

A

50% decrease in signal amplitude

10% increase in signal latency

26
Q

What anestheic agents can depress SSEPs?

Which ones can enhance it?

A

Volatiles including N2O

Opioids (large boluses)

BUT can be enhanced by ketamine and Precedex

27
Q

Which cranial nerve is monitored through BAEPs?

A

CNVIII

(brainstem auditory evoked potential)

28
Q

What anesthetics effect MEPs?

A

Volatiles (more sensitive than SSEPs)

NMBs

29
Q

What is the Transcranial Doppler? What are its indications?

A

Noninvasive monitor that evalutes relative flow changes through the large basal arteries of the brain.

Indications:

Suspected emboli (esp in TBI/traumatic brain injury)

Bypass

Vasospasm evaluation

Need for noninvasive ICP measurement

30
Q

Indications for ICP monitoring…

A

All severe TBI/traumatic brain injuries (GCS < 9) with abnormal CT scans

Severe TBI in which pt is > 40 y/o, is posturing, or has SBP < 90

31
Q

Ways to decrease ICP

A

30 degrees of head up (positioning)

Decrease CMR (anesthetics)

CSF drainage

Lasix

Hyperventilation

32
Q

How can we provide cerebral protection?

A

Hypothermia (35-36C for mild ischemic risk; 33-35C for planned period of focal ischemia; <20C for prolonged cardiac arrest)

Volatiles (esp isoflurane)

Propofol

Barbiturates (esp thiopental)

Euglycemia (controversial)

Basic Science II (9 decks)

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