Case 14 - intracranial mass, ICP, venous air embolism, autoregulation Flashcards

1
Q

what is cerebral autoregulation?

A

Cerebral autoregulation

  • cebral blood flow (CBF) is maintained constant over a wide range of CPP
    • CPP = MAP - ICP (or CVP)
  • normal CBF = 50 ml/100g of tissue/min
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2
Q

what are the major determinants of CBF, and what happens at the extremes of each determinant?

A

CBF components

1) cerebral autoregulation

  • CBF = CPP/cerebral vasc resistance
  • 50-150mm Hg
    • in extremes, CBF becomes CPP dependent
    • 50 mm Hg - max cerebral vasodilation
    • 150 mm Hg - max cerebral vasoconstriction

2) PaCo2

  • 20-80 mm Hg
  • low PaCo2 = cerebral vasoconstrict
    • lasts temporary; eventually CSF bicarb levels decrease to compensate for induced CSF alkalosis -> no more cerebral vasoconstrict
  • high PaCO2 = cerebral vasodilate

3) PaO2

  • PaO2 < 50 mmHg = cerebral vasodilation
  • CBF increases lineraly with decreasing PaO2

4) CMRO2
* increase CMRO2 = cerbral vasodilation (supply more blood to brain for nutrients and O2 supply)

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3
Q

what is normal ICP, what contributes to increase ICP, how does tumors increase ICP? What mechanism are there to prevent ICP increase?

A

Normal ICP = 5-13 mm Hg

Components = brain tissue, blood, CSF

Tumor

  • inc ICP 2 ways:
    • increase parenchymal tissue (increase brain tissue volume)
    • associated with surrounding edema (inc brain water content)

ICP increase

  • crainal vault = closed -> poor intracranial compliance
  • increase in one leads to a decrease in the others
  • mechanisms to prevent ICP =
    • shift CSF from cranial vault to spinal SA
    • increase absorption of venous blood into sinuses and then into systemic circ (dec blood volume),
    • increase absorption of CSF into systemic circ (dec CSF volume
  • once these mech are exhausted, see inc ICP
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4
Q

what is the effect of the following in terms of CMRO2 and CBF:

  • voltaile anes
  • N2O
  • bartiurates
  • propofol
  • Ketamine
  • Etomidate
A

Volatile anes

  • dose dependent
  • decrease CMRO2
  • increase CBF 2/2 cerebral vasodilation
    • decoupling of CRMO2 to CBF
  • **inhibit cerebral autoreg at > 1 MAC**

N2o

  • increase CBF
  • increase CMRo2

Barbiturates *

  • decrease CBF 2/2 cerebral vasoconstriction
  • decrease CMRO2
  • maintains coupling between CMRO2 and CBF

Propofol/Etomidate *

  • same as barbiturates

Ketamine

  • increase ICP
  • increase CBF
  • increase MAP
  • no change in CMRo2

* = recommended for pts with inc ICP

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5
Q

what is the effect of the following in terms of CMRO2 and CBF:

  • BZD
  • SNP/NTG
  • Labetolol/Nicardipine
  • fentanyl
A

BZD *

  • decrease CBF
  • decrease CMRo2

SNP/NTG

  • Decrease MAP
  • cerebral vasodilators
    • increase CBF
    • increase CBV

Labetolol* or Nicardipine *

  • decrease MAP
  • **NO EFFECT ON CBV**

fentanyl

  • no effect

* = recommended for pts with inc ICP

*

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6
Q

what are s/sx of increased ICP? Why are we seeing these symptoms/

A

symptoms of ICP

  • inc ICP will decrease CPP -> cerebral ischemia -> symp
  • inc ICP will shift brain contents, possible herniation through foramen magnum

s/sx of increased ICP

  • headache
  • n/v
  • mental status change (drowsy, coma)
  • Cushing triad
    • HTN, brady, abnormal respiratory pattern
  • absent brianstem reflexes
  • CN dysfunction
  • fixed and dilated pupils
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7
Q

How is ICP measured, what are the pros/cons of each?

A

1) ventriculostomy

  • most common tool
  • catheter placed through burr hole in ventricle
  • measure ICP, drain CSF

2) subdural bolt

  • device placed via twist drill hole in skull, into dural space
  • cannot drain CSF
  • only measures local ICP, does not provide global info

3) lumbar SA Drain

  • proper measurement involves patient lying supine (avoids gravitational effect on CSF pressure with spinal SA)
  • abrupt withdrawl of CSF -> brain herniation
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8
Q

How is increased ICP treated?

A

ICP: brain tissue, CSF, Blood

Goals: lower blood volume, lower brain water content, lower CSF volume

1) Lower blood volume

Venous

  • raise head - promote venous drainage
  • avoid venous outflow obstruction
    • patient head is neutral, check for improperly placed tape or devices around neck
  • prevent straining or coughing on ETT
    • increases CMRo2 and CBF (inc CVP 2/2 backflow of venous pressure into brain)
    • opioid, propofol, deep anesthesia, muscle relax

Arterial

  • hyperventilate to EtCO2 27-30 mm Hg (PaCO2 30-35 mmHg; gradient b/w etco2 and paco2
    2) reduce CSF Volume
  • drain CSF via ventric or lumbar SA catheter
    3) reduce brain water content
  • Mannitol (takes 30 min onset)
  • loop diuretics (lasix)
  • steroids (Decadron)
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9
Q

What is the mechanism for venous air embolism in a sitting patient?

A

VAE

  • higher association with sitting position
  • air enters venous system via noncollapsible venous channels (like dural sinuses)
  • head elevated above heart -> see pressure gradient (atm pressure exposed to low venous pressure) -> facilitates entrainment of air (high to low pressure)
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10
Q

how can you monitor for VAE?

A
  • TEE
    • Most sensitive (0.1 mL of air detected)
  • precordial doppler
    • second most sensntive (0.25 mL of air)
  • pulmonary artery pressure
    • increased 2/2 air embolism -> inc PVR
  • SaO2
    • dec 2/2 air embolism -> v/q mismatch (dead space ventilation)
  • ETCO2
    • decrease 2/2 decrease pulm blood flow
  • EtN2
    • due to air escaping from blood into lungs into alveoli (gas)
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11
Q

intra-op, you notice a patient in the sitting position undergoing posterior craniotomy for tumor resection all of a sudden has acute hypotension. You are suspecting VAE, what do you do?

A

Tx of VAE

1) notify surgeons to flood surgical field with saline, apply bone wax

2) Increase venous pressure in head

  • lower head relative to heart or T-berg
  • jugulary vein compression

3) discontinue N2O (avoid further air expansion)

4) left lateral decub or tilt tabel to left

  • moves air away from RVOT

5) Cardiovascular support

  • fluids
  • inotropes
  • pressors
  • FiO2 100%

6) aspirate from multiorfice catheter

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12
Q

resident suggests to use PEEP in an attempt to increase CVP during treatment of VAE, what are your thoughts?

A

PEEP in tx of VAE = controversial

  • decreases venous return -> decrease SV -> hypoten
  • paradoxical air embolism
    • PEEP causing decrease SV will result in low LA pressure.
    • right atrial pressure may be increased (RV strain + backflow of blood 2/2 acute pulm HTN from pulm air emboli),
    • and in the face of low LA/LV filling pressure, can see paradoxical emboli
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13
Q

are there contraindications to sitting position?

A

no absolute contraindications

relative contraindications

  • PFO
  • ventriculoatrium shunt
  • cervical pathology (sitting up results in dec spinal cord perfusion pressure)
  • hemodynamicaly unstable patient
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14
Q

what are your anesthetic goals for a patient coming for brain tumor resection, who is showing signs of increased ICP (n/v, headache, vision changes)?

A

Anesthetic Goals/considerations:

1) Avoid increase in ICP:

  • avoid inc blood volume, csf volume, brain water
  • deep anesthesia (avoid symp stimulation during intubation, incision)
  • hyperventilate
  • mannitol
  • maintain normal MAP (avoid cerebreal ischemia -> cebreal edema -> worsen ICP)

2) avoid hypotonic solutoins, avoid glucose containing solutoins
3) fast emergence -> post-op neurologic eval

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15
Q

how will you induce and maintain anesthesia? what additional IV access do you need?

A

Pre-op: assess mental status and s/sx of inc ICP

Induction

  • goal - avoid excessive symp stimulation, avoid hypotension
  • bzd, opioid, lido
    • blunt airway reflex (cough), avoid symp with intubation, lower iv anes induction dose (lessen hypotension)
  • IV anes induction (prop, etom) + muscle relax
  • ensure patient is deep prior to intubation

IV access

  • large bore IV and arterial line
    • potential for blood loss

maintenance anes

  • balance anesthesia
    • low dose volatile anes < 1 MAC + propofol infusion or opioid infusion (remi)
    • think about quick emergence
  • avoid inc in ICP
    • hyperventilate
    • mannitol
    • avoid hypotonic solutions
  • normovolemia
    • IVF + blood products as needed
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