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ABA basic > Central and Peripheral Nervous System > Flashcards

Central and Peripheral Nervous System Flashcards

1
Q

The preganglionic fibers of the SNS originate from what spinal cord levels?

A

T1-L3

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2
Q

What two tissues/organs only receive innervation from SNS and not PNS?

A

Spleen and Sweat glands

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3
Q

Where does the preganglionic fibers of the PNS orginate?

A

The brainstem and sacral segments of the spinal cord. (cranial nerves III, VII, IX, X)

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4
Q

What nerve accounts for 75% of PNS activity?

A

Vagus nerve

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5
Q

What is the preganglionic and postganglionic SNS neurotransmitter?

A

Preganglionic: Ach
Postganglionic: NE (exception is sweat glands which have Ach for postganglionic as well)

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6
Q

What is the primary neurotransmitter for the PNS?

A

Ach

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7
Q

Are skeletal muscle and autonomic nervous system nicotinic receptors the same?

A

No. Skeletal muscle nicotinic receptors are not identical to ANS ganglia nicotinic receptors.

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8
Q

Influx of what ion releases preganglionic neurotransmitters?

A

Calcium

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9
Q

How much oxygen does the brain consume and 60% of that oxygen consumption is used for what task?

A

The brain consumes 20% of the total body oxygen. 60% of that consumed oxygen is used to generate ATP.

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10
Q

What is the average CMRO2 for adults?

A

3-3.8 mL/100g/min (50mL/min)

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11
Q

If cerebral blood flow is interrupted how long does it take to become unconscious?

A

10 seconds. If blood flow is not reestablished withing 3-8 min ATP stores are depleted and irreversible cellular injury occurs.

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12
Q

What is the brain glucose consumption rate?

A

5mg/ 100g/ min

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13
Q

What is the average total CBF?

A

50mL/ 100g/ min; flow in gray matter is 80mL/100g/min and white matter is 20mL/ 100g/ min. In an adult total CBF is ~750mL/min (15-20% of cardiac output).

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14
Q

What happens when CBF is between 20-25mL / 100g /min? Between 15-20mL/ 100g/ min? Below 10mL /100g/min?

A

20-25mL/ 100g/ min: cerebral impairment with slowing EEG
15-20mL/ 100g/ min: flat (isoelectric) EEG
<10: irreversible brain damage

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15
Q

What is normal brain tissue oxygen tension?

A

20-50mmHg (less than 10 is indicative of brain ischemia)

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16
Q

Equation for Cerebral Perfusion Pressure

A

CPP= MAP -ICP (or CVP if it is greater than ICP): normally 80-100mmHg. CPP is the net pressure gradient causing cerebral blood flow.

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17
Q

Relationship between CPP and CBF

A

CBF= CPP/CVR (CVR is cerebrovascular resistance)

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18
Q

What is the range of autoregulation for CBF?

A

CF remains nearly constant between MAPs of 60-160mmHg. Beyond these limits blood flow is pressure dependent.

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19
Q

What is the most important extrinsic influence of CBF?

A

Respiratory gas tensions (PaCO2). CBF is directly proportionate to PaCO2 between tensions of 20-80mmHg.

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20
Q

How much does blood flow change per mmHg change in PaCo2?

A

1-2mL/ 100g/ min per mmHg change in PaCo2 or 2%. Effect may last up to 24-36 hrs.

21
Q

Does PaO2 alter CBF?

A

Severe hypoxemia PaO2 < 50mmHg increases CBF

22
Q

How does CBF change with temperature?

A

CBF changes 5-7% per 1 degree celsius change in temp. Hypothermia decreases CMR and CBF.

23
Q

What governs the movement of a substance across the blood brain barrier?

A

Size, charge, lipid solubility, degree of protein binding in the blood. CO2, O2 and lipid soluble molecules freely enter. Ions, proteins, and large substance do not.

24
Q

What disrupts the blood brain barrier?

A

Severe hypertension, tumors, stroke, trauma, infection, marked hypercapnia, hypoxia, sustained seizure activity.

25
Q

What is normal total CSF production in an adult?

A

21mL/hr (500mL/day) yet CSF volume is only ~150mL.

26
Q

Is CSF isotonic, hypertonic or hypotonic with plasma?

A

Isotonic despite lower potassium, bicarbonate, and glucose concentrations.

27
Q

What drugs decrease CSF production?

A

carbonic anhydrase inhibitors, corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors.

28
Q

What are the volumes in the cranial vault?

A

80% brain (tissue water > solid material), 3-6% blood and 5-15% CSF. Arterial volume is the smallest 7-8mL of the 50mL total intracranial blood.

29
Q

Intracranial hypertension is a sustained increase in ICP above…

A

15mmHg

30
Q

Afferent input for SSEP is carried through which spinal cord tract?

A

Dorsal columns

31
Q

During acute focal cerebral ischemia what happens to CBF?

A

Regional vasoparalysis results in impaired coupling between CBF and CMR and CBF is passively associateed with systemic arterial blood pressure.

32
Q

3 compensatory mechanisms for intracranial HTN?

A
  1. shift CSF from intracranial to spinal subarachnoid space
  2. shift intracranial blood to systemic
  3. Reabsorb CSF across arachnoid villi
33
Q

Order from greatest to least the sensitivity of SSEP, VEP, BAEP to volatile anesthetics.

A

VEP>SSEP>BAEP; BAEP is the most resistant to volatile agents.

34
Q

What effect does cerebral ischemia have on CBF autoregulation?

A

Cerebral ischemia abolishes CBF autoregulation. CBF becomes passively dependent on CPP.

35
Q

Volatile anesthetics increase or decrease CMR? CBF?

A
  • Decrease CMR in dose dependent fashion (Iso the most).
  • Dilate cerebral vessels and impair autoregulation; increase CBF. (Sevo produces the least vasodilation). Hyperventilation with administration can prevent increase in CBF and ICP.
36
Q

Describe circulatory steal phenomenon.

A

With volatile anesthetics CMR decreases while CBF increses which causes luxury perfusion. Blood flow increases to normal areas of the brain but not areas of focal ischemia that are already maximally vasodilated.

37
Q

CSF and inhaled anesthetics.

A
  • Isoflurane facilitates absorption.
  • Desflurane increased CSF production.
  • Halothane decreases absorption and minimally decreases formation.
38
Q

What happens to CBF and ICP with nitrous oxide?

A

When given alone it causes mild cerebral vasodilation and can potentially increase ICP. With IV agents it has min effects on CBF, CMR, and ICP.

39
Q

IV induction agents on CMR and CBF.

A

With the exception of ketamine, all IV agents have little effect or reduce CMR and CBF. Cerebral autoregulation and CO2 responsiveness are preserved with all agents.

40
Q

Barbiturates effects on CNS.

A
  • Hypnosis, depression of CMR, reduction of CBF, anticonvulsant activity.
  • Facilitate CSF absorption
41
Q

Robin Hood or reverse steal phenomenon.

A

Barbiturates induce cerebral vasoconstriction in normal parts of the brain and redistribute blood flow to ischemic areas that are maximally vasodilated with vasomotor paralyis.

42
Q

Opioids effects on CNS.

A
  • Minimal effects on CBF, CMR and ICP.

- If PaCo2 rises 2/2 respiratory depression or if BP drops, can cause vasodilation.

43
Q

Etomidate effects on CNS.

A
  • Decreases CMR, CBP and ICP.
  • Decreases production and enhances absorption of CSF.
  • Small doses can activate seizure foci in epileptic patients.
44
Q

Propofol effects on CNS.

A
  • Reduces CBF and CMR.

- Capable of producing burst suppression.

45
Q

Benzodiazepine effects on CNS.

A
  • Lower CBF and CMR but to lesser extent than other IV agents.
  • Anticonvulsant properties.
46
Q

Ketamine effects on CNS.

A
  • Increases CBF (vasodilation)
  • Total CMR does not change (activates and depresses various brain regions)
  • Seizure activity in thalamic and limbic areas.
  • Decreases absorption of CSF.
47
Q

Lidocaine effects on CNS.

A

-Decreases CMR, CBF and ICP.

48
Q

Vasopressor effects on CNS.

A

-With normal autoregulation and intact BBB only increase CBF when BP 150-160. In absence of autoregulation increase CBF by their effect on CPP.

ABA basic (17 decks)

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