Neuro

Question 1

What is minimal level of cerebral metabolic rate of O2 consumption (CMRO2)?

Answer 1

3mL/100g/min (adults)

Question 2

What is the average cerebral blood flow (CBF)?

What is the level for cerebral impairment?

Answer 2

50mL/100g/min

20-25mL/100g/min

Question 3

How do you calculate cerebral perfusion pressure (CPP)?

What is normal values?

Answer 3

MAP - ICP or MAP - CVP

80-100 mmHg

Question 4

Pressure auto regulation of cerebral vasculature keeps the CCP between what MAP values?

How does the vasculature respond to high or low MAP values?

What happens to these values during chronic HTN?

Answer 4

50-150 mmHg

High MAP = vasoconstriction (if too high, cerebral edema and hemorrhage can occur)
Low MAP = vasodilation (if too low, ischemia occurs)

They can reset

Question 5

How is CBF affected by CO2?

How long does this effect last?

Answer 5

*lOw CO2 = vasOconstriction (decreases CBF/CPP)
       Only CO2 (NOT HCO3) crosses the BBB

After 24-48 hours, CSF HCO3 compensates for PaCO2

Question 6

How does CO2 affect the Hgb dissociation curve?

Answer 6

Low CO2 shifts curve to L –> decreased O2 unloading at the tissues

Question 7

How does Hct effect CBF auto regulation?

Answer 7

Decreased Hct (hemorrhage) = decreased viscosity –> increased flow but decreased O2 carrying capacity

Question 8

How do volatile anesthetics affect the CMR and CBF coupling?

Answer 8

Uncoupling –> decreased metabolic demand of brain with INCREASED CBF

• Decrease CMR
• Vasodilation of cerebral vasculature

Question 9

Value for normal ICP?

Value for intracranial HTN?

Answer 9

10 mmHg

> 15 mmHg

Question 10

Describe circulatory steal phenomenon?

Answer 10

Ischemic areas of the brain are already maximally dilated –> no increase in blood flow

There is increased blood flow to “NORMAL” perfused areas via vasodilation and this redistributes blood away from the ischemic areas

Question 11

Effect of barbiturates on CNS?

Answer 11

Decreases CBF, ICP, CMRO2
INCREASES CPP (the decrease in ICP is greater than the decrease in MAP)

Question 12

What is the Robin Hood Phenomenon?

Answer 12

“Normal” vessel vasoconstriction from decreased metabolic rate redistributes blood to ischemic areas which are maximally dilated already

Question 13

Propofol effect on CNS?

Answer 13

Decreases CBF, ICP, CMRO2

Question 14

What side effect must you monitor for with use of etomidate on CNS?

Answer 14

Myoclonic movements (NOT seizures)

*Also causes decrease of CBF, ICP (like propofol)

Question 15

Ketamine effects on CNS?

When not to use ketamine?

Answer 15

INCREASES CBF, ICP, CMRO2

*Increased ICP (trauma, tumors)

Question 16

Signs of increased ICP?

Answer 16

Headache
Nausea/Vomiting
Papilledema
Focal neuro deficits
Altered consciousness

Question 17

What can occur if the ICP continues to rise (aside from herniation)?

Answer 17

Decreased CBF –> brain ischemia –> ischemia leads to cerebral edema/swelling –> further increases the ICP -> more ischemia and cycle repeats

Question 18

What is Cushing triad of increased ICP?

Answer 18

1) HTN
2) Bradycardia
3) Irregular respirations

*Denotes extremely high ICP (last ditch effort of body to decrease ICP)

Question 19

What are ways to decrease ICP?

Answer 19

1) Mannitol (osmotic diuretic –> hyperosmolar)
2) Hyperventilation (causes LOW CO2 = vasoconstriction of cerebral vasculature)
3) Corticosteroids (dexamethasone promotes repair of BBB and decreases inflammation and subsequent edema)
4) Loop diuretics
5) IV anesthetic agents (NOT inhaled gases)

Question 20

Methods the brain uses to protect against ischemia?

Answer 20

1) Optimize CPP (increase MAP or decrease CVP)
2) Normoglycemia (less anaerobic metabolism and lactic acid production)
3) **Normocarbia
**Low PaCO2 = vasoconstriction = aggravates ischemia
**High PaCO2 = vasodilation = steal phenomena w/ focal ischemia
4) Hypothermia (32C) - decreases CMRO2 and CBF
5) **Magnesium (blocks excitatory neurotransmitters after traumatic injury)
also crosses BBB to prevent edema
6) Anesthetic agents (barbs, etomidate, propofol all lower CMR)

Question 21

Why is TIVA a good choice for neuro cases?

Answer 21

Allows for intra-op NM monitoring if needed (can’t use long lasting paralytics)

Question 22

During cranial cases, what 2 renal complications can occur and what area is usually involved in the brain?

Answer 22

Proximity to Pituitary gland

1) Cerebral salt wasting –> kidney looses ability to reabsorb Na and end up peeing out tons of Na and fluid
2) Central DI –> peeing out lots of water but holding onto Na

Question 23

How do you differentiate b/w cerebral salt wasting syndrome and SIADH?

Answer 23

Urine studies

CSW: urine osmolarity is low + high flow rate
SIADH: very concentrated urine + low flow rate

Question 24

With Conn syndrome, what 2 factors must be addressed intraoperatively?

Answer 24

1) Hemodynamic changes
Manipulation of adrenal gland can cause release of catecholamines

2) Hypokalemia
Avoid respiratory alkalosis (PaCO2 reflection of H+ levels)
Avoid sevoflurane use (induces polyuria)
Can prolong the action of NMB agents

Question 25

With adrenal surgery, what anesthetic agent should be avoided and why?

Answer 25

Etomidate

Suppresses cortisol synthesis