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Advanced Principles of Anesthesia > Neurophysiology - CBF & Metabolism > Flashcards

Neurophysiology - CBF & Metabolism Flashcards

1
Q

At rest, the brain consumes oxygen at an average rate of ______ ml oxygen per 100 g of brain tissue (…or ____ml/min)?

A

3.5 ; 50 ml/min

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2
Q

The brain weighs approx. _____ g?

A

1350

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3
Q

The brain utilizes _____% of total body glucose?

A

25%

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4
Q

What percentage of of the brain’s energy consumption is used to support electrophysiologic function (EEG)?

A

60%

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5
Q

What percentage of the brain’s energy consumption is used to maintain cellular homeostasis?

A

40%

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6
Q

The brain requires _____ and _____ for sustained function?

A

oxygen and glucose

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7
Q

In the complete absence of glucose, glycolysis could only be maintained for _____ min.?

A

5 min

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8
Q

How is the brain’s high demand for oxygen and glucose met?

A

By adequate blood flow

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9
Q

CBF is almost completely supplied by ______ and _________?

A

Internal carotid and vertebral arteries, which provide input to the circle of willis

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10
Q

What is the purpose of the circle of willis?

A

permits collateral blood flow in the event that a major vessel becomes occluded.

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11
Q

What contains most of the cerebral blood volume?

A

The veins and dural sinuses

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12
Q

What is the CMRO2 for the brain?

A

3.0-3.8 ml/100g/min

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13
Q

At normocarbia, global CBF is stable between _____?

A

45-65 ml/100g/min

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14
Q

Describe CBF-CMRO2 Coupling?

A

Cerebral blood flow is coupled to CMRO2 - meaning that the higher CMRO2, the higher the CBF

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15
Q

Identify 2 factors that decrease CMRO2 and 2 factors that increase CMRO2?

A

DECREASE (sleep, coma, general anesthesia)

INCREASE (sensory stimulation, mental tasks, epileptic activity)

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16
Q

Between ___ and ___ degrees C - CBF and CMRO2 increase.

A

37 and 42 degrees C

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17
Q

Above ____ degrees C, a dramatic reduction in CMRO2 occurs.

A

42 degrees C - hyperthermia beyond 42 denatures proteins and destroys neurons. At this point, CBF decreases

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18
Q

The brain receives what percentage of the cardiac output?

A

12-15%

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19
Q

CMRO2 decreases by ___ for each 1 degree C reduction in temperature.

A

6-7%

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20
Q

EEG suppression occurs at what temperature?

A

18-20 degrees C

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21
Q

In general anesthetics decrease CMRO2 except…?

A

Ketamine and N2O

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22
Q

Increasing plasma concentrations of anesthetics beyond the level of initial EEG suppression…?

A

Does not further decrease CMRO2; (The CMRO2 required to maintain cellular integrity i snot altered by anesthetics, only the electrophysiological aspects of CMRO2)

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23
Q

What is Cerebral Perfusion Pressure (CPP)?

A

CPP= MAP - ICP (or CVP, which ever is higher)

24
Q

What are the primary factors that control CBF in the normal brain?

A
  1. Carbon dioxide

2. Oxygen

25
Q

What law relates to CPP?

A

Ohm’s Law (Flow=P/R or P=FxR)

26
Q

What is the most potent physiologic determinant of CBF?

A

Carbon dioxide-

  • 1 mmHg increase in PaCO2 = CBF increases by 1-2 ml/100g brain tissue/min
  • 1 mmHg decrease in PaCO2 = CBF decreases by 1-2 ml/100g brain tissue/min
27
Q

Doubling the normal PaCO2 to 80 mmHg will….

A

Double the CBF, above 80 mmHg there is a plateau which reflects maximum vasodilation - also a reduction in CMRO2 occurs reflecting the anesthetic effect of extreme hypercarbia

28
Q

Reducing normal PaCO2 to one-half (20mmHg) will…

A

Approx half the CBF - decreasing PaCO2 below 20 mmHg has no effect d/t maximal vasoconstriction

29
Q

Evidence suggests that the normal brain will tolerate a ____% decrease in CBF without ischemic changes.

A

50%

30
Q

What abolishes the normal effect of PaCO2 on the vasculature system?

A

Abnormal or pathologic states

31
Q

The PaCO2 effects on CBF are not sustained. CBF will return to normal ….

A

Over a period of 6-8 hours (CSF pH gradually returns to normal d/t retention of bicarbonate - metabolic compensation)

32
Q

What happens when PaO2 below 60 mmHg?

A

CBF increases rapidly (the vasodilation is mediated by acidic metabolic products like lactic acid)

33
Q

What is cerebral autoregulation?

A

CBF is constant between a CPP of 50-150 mmHg

34
Q

What are the 3 components of the cranium and their volumes?

A
  1. Brain - 80%
  2. Blood - 12%
  3. CSF - 8%
35
Q

CPP above 150 results in?

A

Hypertensive encephalopathy d/t BBB disruption, edema, and ischemia

36
Q

CPP below 50 mmHg results in?

A

maximal vasodilation and CBF becomes pressure dependent

37
Q

Chronic HTN shifts curve to the _____?

A

Right, the brain becomes more tolerant of HTN, but it also becomes less tolerant of hypotension

38
Q

What abolishes cerebral auto-regulation? Why is this significant?

A

CVAs, tumors, SAH, AVMs, trauma, volatile anesthetics

When autoregulation is impaired, CPP becomes dependent on blood pressure.

39
Q

What is the effect of volatile anesthetics?

A

All cause a dose related increase in CBF and a decrease in CMRO2.

Beyond 1 MAC - direct cerebrovasodilation which increases CBF and cerebral blood volume.

40
Q

Sevoflurane effects?

A

Like isoflurane, it causes little or no increase in ICP at concentrations up to 1.5 MAC

41
Q

N2O effects?

A

When used alone with oxygen N2O is a potent vasodilator and may increase ICP

Clinically, it may be prudent to discontinue N2O in the case of a “tight brain”

42
Q

Intravenous Anesthetics?

A

Most produce a reduction in both CMR and CBF, and autoregulation and CO2 responsiveness are preserved in during IV anesthetic drug use.

*Ketamine causes increased CBF and CMR

43
Q

Barbiturates?

A

Decrease both CBF and CMRO2

Have a direct vasoconstrictive effect

44
Q

Incremental doses of pentothal and may decrease CBF and CMRO2 by _____%?

A

55-60%

45
Q

Propofol?

A

Reduces CMRO2 and secondarily decreases CBF, CBV, and ICP

46
Q

Etomidate?

A

Reduces ICP without causing a decrease in CPP

47
Q

Benzodiazepines?

A

Reduce CBF d/t a decrease in CVR and CMRO2

48
Q

Flumazenil?

A

Flumazenil reverses the benzo effects and may increase CBF and CMRO2 above pre-midazolam levels. –> Should be used with caution in patients with impaired intracranial compliance.

49
Q

Ketamine?

A

Increases CMR and CBF (increased CMR will lead to vasodilation)

Sub-anesthetic doses (0.2-0.3mg/kg) can increase CMR by 25%

Should be avoided as a single anesthetic agent in patients at risk of high ICP

50
Q

Narcotics?

A

Minimal to modest depressive effects on CBF and CMRO2.

51
Q

Local Anesthetics?

A
  • Rapidly cross the BBB d/t lipid solubility
  • In subtoxic doses, LAs cause a modest decrease in CMRO2 and CBF
  • Toxic doses that induce seizure activity will increase CMRO2 and CBF
52
Q

Muscle Relaxants?

A

Muscle relaxation in general can reduce ICP by preventing coughing and straining, which results in lowered CVP

*SUX may cause an increase in ICP d/t increased cerebral input d/t fasiculations - can give a defasiculating dose

53
Q

Atracurium?

A

Causes histamine release

Metabolite laudanosine readily crosses the BBB (may cause seizures in large doses)

54
Q

Pancuronium?

A

In pts with intracranial pathology and defective auto-regulation, can increase CBF and ICP d/t tachycardia and HTN

55
Q

Vecuronium?

A

No cerebral effects - was the most common muscle relaxant used in neurosurgical patients.

56
Q

Rocuronium?

A

Similar to Vecuronium

Advanced Principles of Anesthesia (3 decks)

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