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Anesthesiology > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
Q

3 main components within the cranial vault that can cause ICP?

A
  1. CSF (obstruction, overproduction, decreased clearance) 2. Blood volume (hypotension, high CVP) 3. Brain tissue (edema)
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2
Q

What does cerebral perfusion pressure equal?

A

CPP = MAP - ICP (or CVP whichever is higher)

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3
Q

What is a normal ICP?

A

< 10 mmHg

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4
Q

What MAP range is cerebral vascular resistance auto-regulated?

A

70 mmHg to 150 mmHg, above that, cerebral vascular resistance cannot increase anymore to restrict pressure dependent increase in flow

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5
Q

How does cerebral vascular resistance change with hypercarbia?

A

CVR and flow increases in a linear fashion until > 80 mmHg where the curve starts to flatten, and gets flat at 120 mmHg

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6
Q

How does cerebral vascular resistance change with hypoxia?

A

Little effect until PaO2 drops below ~50 mmHg and then rises exponentially; no effect between 60 mmHg and 300 mmHg

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7
Q

How do volatile anesthetics affect cerebral blood flow and cerebral metabolic rate?

A

VA’s “uncouple” flow from consumption in that O2 consumption decreases and CBF (and therefore oxygen delivery) increases

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8
Q

What is the normal cerebral metabolic rate (CMRO2)?

A

3.5 cc/ 100g/ min

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9
Q

What is the normal cerebral blood flow?

A

50 cc/ 100g/ min

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10
Q

How much CSF does an average adult have at any one time? How much CSF is produced per day?

A

~150 cc, 500cc produced per day

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11
Q

What happens in the brain when the ICP is 30?

A

CPP decreases -> decreased blood flow -> decreased O2 delivery -> ischemia -> cellular break down -> edema -> increased ICP -> decreases CPP more

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12
Q

What does dexamethasone do to CSF production and absorption?

A

Decreases production, decreases absorption in animal studies

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13
Q

How does mannitol work?

A

Increases serum osmolality -> fluid shift into intravascular space -> increased UOP

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14
Q

What do you worry about with mannitol and intracranial hematomas?

A

Decreased brain swelling can cause a hematoma that was being tamponaded by the swollen brain tissue to expand

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15
Q

What happens to cerebral blood flow with 1 MAC of sevoflurane?

A

Increases about 20%

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16
Q

How does propofol affect cerebral blood flow and cerebral consumption of oxygen?

A

Decreases both

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17
Q

What happens in reverse steal of the brain?

A

Normal brain vasculature vasocontricts to stimulus (i.e. propofol) while ischemic brain cannot response -> normal brain is underperfused

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18
Q

How does hypercarbia affect cerebral blood flow?

A

Changes the H+ concentration

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19
Q

Mechanisms of action for cerebral ischemia with a PaCO2 less than 20?

A
  1. Decrease in cerebral blood flow 2. Left shit in the oxyhemoglobin dissociation curve
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20
Q

Which anesthetic agents decrease cerebral metabolic rate of O2?

A

Most anesthetic agents except ketamine and N2O

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21
Q

Does hypothermia uncouple CMRO2 and CBF?

A

No, it just decreases both of them

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22
Q

Is autoregulation affected by high doses of propofol?

A

No, but propofol does decrease CBF, cerebral blood volume, and ICP

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23
Q

How does thiopental affect CMRO2 and CBF?

A

Decreases it in a dose dependent manner until 50%

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24
Q

What IV induction agent do you worry about in patients with seizures?

A

Etomidate (can be epileptogenic in patients with seizure disorders)

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25
Q

Which narcotic can provoke seizures in patients with epilepsy?

A

Alfentanil

26
Q

Do volatile anesthetics impair autoregulation and if so, which ones more than the others?

A

Yes in a dose-dependent manner Sevoflurane impairs less than iso or des, halothane impairs it the most

27
Q

How does nitrous affect CMRO2, CBF, and ICP?

A

Increases all three of them

28
Q

What level of consciousness do you see when an EEG shows delta waves? theta waves? alpha waves? beta waves?

A

Delta: deep sleep Theta: first stage of sleep/drowsiness Alpha: relaxed bu alert Beta: Highly alert

29
Q

Which volatile anesthetic has epileptiform discharge during induction and at 2 MAC?

A

Sevoflurane and Enflurane (not clinically significant)

30
Q

Blood flow to the brain comes what what two main arteries?

A

Internal carotid (80%) and vertebrobasilar system (20%)

31
Q

What are the main areas of aneurysms in the brain?

A

Anterior communicating artery (25%) MCA (25%) Internal carotid artery between posterior communicating and anterior choroidal arteries (22%) Basilar bifurcation (7%) Internal carotid bifurcation (4%)

32
Q

Put these in order of most to least sensitive for detecting VAE: TEE, PA pressures, ETN2, Precordial doppler

A

TEE > Doppler > PA pressure changes > ETN2

33
Q

What are the first steps needed after diagnosis of a VAE?

A

Flood the field, stop N2O, 100% O2, T-berg, positive pressure vent (pressure on SVC), compression of jugular vein, fluids/pressors, aspiration of central line

34
Q

If you have an unruptured aneurysm and surgeon asks for hyperventilation and mannitol, what do you do?

A

No! Since transmural pressure of the aneurysm is MAP - ICP, once the cranial vault is open, ICP is 0 and then you can do it to prevent rupture since transmural pressure = MAP

35
Q

What ECG changes do you see with subarachnoid hemorrhages?

A

Sympathetic stimulation can cause dysrythmias (i.e. PVCs, prolonged QT, ventricular tachyarrythmias)

36
Q

What is Cushing’s response?

A

From high ICP: bradycardia, HTN, irregular breathing (Cheyne Stokes)

37
Q

When is the peak time you would expect cerebral vasospasm after SAH?

A

1 week peak (rarely occurs after 2 weeks): thought to be from oxy-Hgb in subarachnoid space leading to free radical production = decreased NO = more vasoconstriction

38
Q

What is the treatment for cerebral vasospasms?

A

HHH: Hypertension (SBP ~160), hypervolemia (CVP >8), and hemodilution (Hct of ~30) Nimodipine (CCB)

39
Q

Lucid interval following head trauma, lenticular appearance on CT

A

Epidural hematoma

40
Q

Associated with old age, crescent shape on CT expanding past skull sutures

A

Subdural hematoma

41
Q

RBCs in CSF means what?

A

Subarachnoid hematoma

42
Q

Diffuse bleeding into an area of cerebral contusion is what kind of hemorrhage?

A

Intracerebral hematoma

43
Q

What is neurogenic pulmonary edema?

A

ARDS in the setting of TBI

44
Q

Patient after TBI has a sodium of 154 and nearly 200cc of urine in an hour. Diagnosis and treatment?

A

Diabetes insipidus Tx: DDAVP

45
Q

What is neurogenic diabetes insipidus?

A

Lack of ADH secretion

46
Q

What is syndrome of inappropriate ADH secretion?

A

Too much ADH leading to hyponatremia and fluid retention (patients normally euvolemic)

47
Q

What is cerebral salt wasting syndrome?

A

After brain injury, salt wasting (hyponatremia) poorly responsive to fluid restriction and are often hypovolemic from fluid losses (SIADH patients are euvolemic)

48
Q

Treatment for cerebral salt wasting syndrome?

A

Replacing fluid loss with NS and generally resolves over days to weeks

49
Q

Treatment for SIADH?

A

Fluid restriction + salt tablets (symptomatic) + “vaptan” drugs - vasopressin analogues

50
Q

What is the Monro-Kellie hypothesis?

A

Cranial compartment is incompressible and the volume inside is fixed made up of: blood, CSF, and brain tissues

51
Q

What does line A, B, and C represent?

A

A: O2

B: CO2

C: MAP

52
Q

Which actually slightly increases cerebral blood flow: sufentanil, alfentanil, fentanyl, remifentanil

A

Sufentanil (the rest slightly decreases CBF)

53
Q

The blood brain barrier prevents the passage of: glucose, water, CO2, lipid soluble compounds

A

Glucose

54
Q

What two drugs decrease CSF production?

A

Acetazolamide and furosemide

55
Q

Which decreases cerebral blood flow and cerebral metabolic rate: fentanyl, ketamine, isoflurane, lidocaine

A

Lidocaine (remember that isoflurane and other volatile anesthetics uncouple CMRO2 and CBF)

56
Q

Compared to serum, which is proportionately the lowest in CSF: protein, glucose, sodium, bicarbonate

A

Protein

57
Q

Class C nerves are used in what?

A

Nociception and post-ganglionic autonomic system

58
Q

Where are the cell bodies of the first order neurons for pain signaling? 2nd order neurons?

A

1st: Dorsal root ganglion
2nd: Dorsal horn of the spinal cord

59
Q

What tracts does pain and temperature go up in the spinal cord?

A

Spinothalamic tract (after crossing over to the contralateral side)

60
Q

What is the precentral gyrus responsible for? Postcentral gyrus?

A

Pre: motor cortex

Post: sensory cortex

61
Q

What does beta-1 activation do? Beta-2 activation?

A

1: increased chronotropy/inotropy/lusitropy, lipolysis, renin secretion
2: bronchodilation, smooth muscle relaxation, glycogenolysis

62
Q

How does the SNS affect GU organs? ADH secretion?

A

Relaxes GU organs (i.e. uterus, etc.) and increase ADH secretion (to increase BP)

Anesthesiology (21 decks)

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