Neuroanesthesia Flashcards

1
Q

What is the normal cerebral blood flow?

A

50 ml/100 g/min
<20 ml/100 g/min - ischemic changes
<10 ml/100 g/min - neuronal death

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2
Q

How is cerebral blood flow regulated?

A

Cerebral autoregulation:
(1) blood pressure
(2) PaCO2

(1) ensures constant blood flow over a wide range of blood pressure ~60-160 mmHg: above or below, autoregulation is lost and CBF becomes solely dependent on MAP
(2) cerebral vasculature reacts from 20-80 mmHg: vasoconstriction - hypocarbia
vasodilation - hypercarbia

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3
Q

How does hypertension affect cerebral autoregulation?

A

Shifts to the right - requires higher pressure to maintain adequate perfusion
e.g. 100-180 mmHg

Over time, treated hypertension may revert back to the usual range

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4
Q

Describe CBF/CMRO2 relationship

A

Under normal conditions, the CMRO2 is directly related to CBF

Cerebral vasculature dilate or constrict to supply for the demand aka coupling

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5
Q

How does PaCO2 affect cerebral perfusion in normal and ischemic regions?

A

(1) hypercarbia - vasodilation
(2) hypocarbia - vasoconstriction

(1) normal tissues vasodilate more –> more blood shunted to non-ischemic area aka Steal Phenomenon
(2) normal tissues vasoconstrict more –> more blood shunted away from non-ischemic aka Reverse Steal or Robin Hood Phenomenon

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6
Q

Describe the use of hyperventilation in neuroanesthesia

A

(A) aims to rapidly decrease ICP and ‘relax’ the brain
ETCO2 25-30 mmHg ~PaCO2 30-35 mmHg
Short-term effect of 6-10hrs only, afterwards bicarbonate ions start to compensate

Prolonged hyperventilation –> respiratory alkalosis –> oxyhemoglobin curve shifts to the left –> decreased unloading of O2 –> further ischemia

(B) lowers seizure threshold

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7
Q

How to manage increased ICP?

A

– hyperventilation (most rapid)
– diuresis: mannitol, furosemide, hypertonic saline
– head elevation: at least 15 deg to facilitate drainage
– control BP: nicardipine
– if ventilated: use lower PEEP - higher intrathoracic pressure may block venous drain

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8
Q

What are the expected nociceptive stimuli in cranial surgery?

A
  • laryngoscopy, intubation
  • placement of pins
  • scalp incision
  • opening of skull up to dura
  • High-dose opioid: e.g. fentanyl 5-10 ug/kg
  • lidocaine 1.5 mg/kg to help blunt response to laryngoscopy/intubation
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9
Q

Basic principles in providing anesthesia during neurosurgery

A
  • maintain cerebral perfusion
  • manage ICP (keeping the brain relaxed during surgery)
  • burst suppression if needed (propofol, thiopental): usually during temporary clipping
  • monitor serum glucose, acid-base balance, temperature
  • use short-acting agents (to facilitate early neurologic assessment)
  • blunt response to nociceptive stimuli
  • smooth emergence
  • upright/sitting position: at-risk for VAE
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10
Q

Options for preinduction anxiolysis

A
  • individualized
  • dexmedetomidine > BZD

Dexmedetomidine - respiratory function is preserved, reduced interference with EP monitoring; can be continued as infusion intra-op
BZD - disinhibition, can delay awakening and interfere with postoperative assessment

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11
Q

Sudden drop in ETCO2, sudden hypotension in a craniotomy patient positioned upright

A

T/C VAE - air entrainment whenever operating field is higher than the right atrium

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12
Q

What is the most sensitive modality in detecting VAE?

A
  1. TEE - <0.25ml
  2. Doppler
  3. PA catheter, ETCO2
  4. Cardiac output, CVP, BP
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13
Q

What are the steps to do if VAE is suspected?

A
  1. alert surgeon
  2. stop further air entrainment: flood the field with saline, press neck veins to increase JVP
    *Durant maneuver - left lateral decubitus
  3. prevent expansion of entrained air - D/C N2O
  4. support CV function: inotropes, vasopressors, fluid
  5. aspirate air (if with RA catheter)
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14
Q

Complications associated with VAE

A

a) stroke or MI - especially if with patent foramen ovale
b) pulmonary hypertension - secondary to INC pulmonary vascular resistance
c) CV collapse
d) bronchoconstriction

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15
Q

Most common causes of nontraumatic SAH

A

Cerebral aneurysm, AVM

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16
Q

Complications associated with aneurysmal SAH

A

1) Rebleeding
- leading cause; will rebleed if untreated
- highest during 1st 24hr post-ictus

2) Vasospasm
- r/t breakdown of RBC byproducts released into the subarachnoid space
- highest 5-7days post-ictus

17
Q

Optimal time for aneurysmal clipping

A
  • within 72hr

Temporary clipping - tolerated for ~10-14mins
>30mins lead to ischemia
> use burst suppression

18
Q

What agents are used to induce burst suppression?

A

barbiturate (thiopental), propofol, etomidate, isoflurane (2 MAC)

19
Q

Perioperative management in aneurysmal SAH

A

Triple H: hypertension (~20-30 mmHg above baseline), hypervolemia (CVP ~8-10 mmHg), hemodilution (Hct ~27-30%)

  • strict control of BP: nitroprusside/nitroglycerin, labetalol, nicardipine
  • control of intravascular volume
  • intra-op IABP and CVP monitoring
  • burst suppression
  • duration of temporary clipping
20
Q

What Hunt-Hess grading do you expect changes in sensorium?

A

3 - confusion/lethargy starts, mild focal deficits
5 - comatose, posturing

1 - mild headache, no deficits
2 - nuchal rigidity, moderate to severe headache

21
Q

Perioperative management in AVM

A

Strict BP control to avoid rupture - cautious use of deliberate hypotension
‘Autoregulation breakthrough’ - esp. with large AVM
- more blood flow to the previously poorly perfused area –> cerebral edema and/or hemorrhage

22
Q

Perioperative concerns in posterior fossa tumor

A
  • critical area because of proximity to the brainstem and cerebellum
  • WOF vagal reflexes during dissection/manipulation (inform surgeon, glycopyrrolate or BB)
  • be alert for Cushing reflex in sudden bradycardia
  • position: sitting, prone
  • post-resection ‘reperfusion’ –> swelling, increased ICP
23
Q

Important in the preoperative evaluation of a patient for transsphenoidal pituitary resection

A

Hormonal evaluation and imaging

24
Q

How to optimize the transsphenoidal surgical field?

A

Pushing the tumor inferiorly into the sella:
- controlled/permissive hypercapnia - PaCO2 40-45 mmHg
- lumbar drain (for larger tumors) - injecting isotonic saline or draining CSF
- injecting air into the subarachnoid
- elevating head

25
Q

Postoperative concerns for transsphenoidal surgery

A

Diabetes insipidus - monitor fluids, serum Na
Bleeding –> increased ICP

26
Q

Upon opening the dura, the surgeon complains of a tight brain. What to do next?

A
  • transiently hyperventilate to a PaCO2 25-30 mmHg
  • elevate head
  • diuresis:
    • mannitol (time with removal of bone)
    • furosemide
  • shift volatile to TIVA
  • drain CSF in 10-20ml aliquots
  • deliberate hypotension (last resort)
27
Q

Fluid choices for neurosurgery

A

NSS - commonly used; WOF hyperchloremic acidosis (assoc. w/ AKI)
BSS - to minimize hyperchloremic acidosis e.g. plasma-lyte
Colloids may be used

Avoid dextrose-containing: once glucose is metabolized, becomes slightly hypotonic –> cerebral swelling

28
Q

Type of traumatic brain injury that is a true neurosurgical emergency

A

Epidural hematoma - displaced temporal bone fracture –> middle meningeal artery –> rapidly expanding hematoma
- can experience lucid interval

Subdural hematoma - more insidious

29
Q

Important consideration in a patient with traumatic brain injury?

A

Assume cervical injury: in-line stabilization during intubation

30
Q

Perioperative management of TBI

A
  • glucose 100-160 mg/dl (hyperglycemia is associated w/ worse prognosis)
  • CPP: 60-70 mmHg (SBP > 100 mmHg)
  • coagulopathy: treat INR > 1.4 and PC < 75,000
  • fluids and electrolytes (esp. with diuresis, IVF resuscitation)
  • hyperventilation is avoided in the 1st 24h (reserved if herniation is imminent)
  • empiric steroid has no benefit
  • seizure: levetiracetam
  • postop ventilation: low TV, PaCO2 35-40 mmHg, PEEP <15 cm H2O, PaO2 >60 mmHg
  • avoid hyperthermia (infectious vs central fever)
  • neurogenic PE (secondary to SNS stimulation after injury)
31
Q

What % is considered severe stenosis?

A

> 70% - candidate for CEA or stenting

32
Q

What is the significance of stump pressure?

A

Stump pressure - taken after clamping CCA & ECA
- to assess adequacy of collateral flow and/or need for shunt
- >40-50 mmHg is adequate

33
Q

Anesthesia used in CEA:

A

a) GA - IV or IH
b) RA - deep or cervical plexus block (C2-C4 levels) - preferred for continuous neurologic assessment

34
Q

BP goals in CEA:

A
  • high-normal intra-op
    > permissive hypertension (~10-20% above) to increase collateral flow during clamping
    > deliberate hypertension (~30-40% above) until ischemic symptoms resolve
  • low-normal after clamping (relief of stenosis)
35
Q

Why is low-normal BP preferred post-CEA?

A
  • decreases stress on suture
  • decreases risk of reperfusion
  • decreases myocardial workload
36
Q

Postop concerns in CEA

A

Airway obstruction:
- secondary to expanding hematoma

Reperfusion Injury:
- usually 1-5 days postop
- associated with poorly controlled BP after unclamping

Loss of chemoreceptor function:
- up to 10 months postop
- do not respond well to hypoxia and increased resting PaCO2 ~6 mmHg

37
Q

Possible problems during preoperative embolization

A

Done within 48hr of open repair to minimize intra-op blood loss

1) hemorrhagic
- sudden increase in MAP
- protamine to reverse heparin (1mg per 100u)
- anti-hypertensive
- mannitol
2) thrombotic
- increase BP to increase collateral blood flow
- maintain normocarbia
- tissue plasminogen activator, GP IIb/IIIa inhibitor

38
Q

BP goal post-embolization

A

permissive hypotension (~15-20 mmHg above) for 24hr - to prevent cerebral edema & hemorrhage

~20-30% above MAP - to prevent vasospasm