Obj. 12-17 Flashcards

0
Q

What is the preferred method of anesthesia with Evoked Potentials?

A

Narcotics-they cause little change

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1
Q

In what order are Evoked Potentials adversely affected by anesthetic agents? (greatest to least)

A

VEP > SSEP/MEP > BAEP

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2
Q

What are Visual Evoked Responses used for?

A

Visual Evoked Responses:

  • evaluate the optic nerve
  • used for tumor surgery that may effect the optic chiasm, pituitary or anterior cerebral vasculature
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3
Q

What are Brainstem Auditory Evoked Responses used for?

A

Brainstem Auditory Evoked Responses:

  • monitor the function of the auditory pathway between CN VIII and the brainstem and cortex
  • Used in pts with increased risk for brain injury during intracranial surgery
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4
Q

What are Motor Evoked Potentials used for?

A

Motor Evoked Potentials:

-monitor ischemia in the anterior (ventral) columns by stimulating the motor cortex to elicit movement

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5
Q

How do IV and inhalational agents effect Motor Evoked Potentials?

A

Motor Evoked Potentials:

  • are very sensitive to anesthetics (particularly VAs. N2O is < depressing than equivalent MACs of other VAs)
  • TIVA works well: narcotics, propofol. Propofol causes MEP suppression, but < than VAs
  • NDMR weaken MEPs! (Avoid during critical parts of surgery)
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6
Q

What are Somatosensory Evoked Potentials (SSEPs) used for?

A

SSEPs:

  • monitor sensory pathways (DORSAL COLUMN, brainstem, subcortex, and sensory cortex). Used during spine surgery& intracranial vascular surgery
  • the response of peripheral nerve stimulation to CONTRALATERAL somatosensory cortex
  • SSEPs are derived from EEG waves, just significantly less.
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7
Q

How do IV and inhalational agents effect SSEPs?

A
  • All VAs:dose-dependent increase in SSEP latency/decrease in amplitude
  • Adding N2O potentiates these responses of VAs & IV AGENTS (fentanyl) when used with GA, but N2O alone effects SSEPs LESS than equivalent MAC levels of gases
  • NDMRs do not hinder SSEPs & may improve waveform quality
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8
Q

Which two IV agents dramatically increase ampitude?

A

Etomidate & Ketamine

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9
Q

What is the suggestion for titration of VAs with any mode of Evoked Potentials?

A

Use < .5 MAC (.5-1) & avoid rapid changes in anesthetic depth (Find a good plane & keep them there!)

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10
Q

What is Electromyography (EMG) used for?

A

EMG:

  • assesses cranial and peripheral motor nerves with electrodes placed into or near specific muscles
  • used during spine surgery or to look at specific cranial nerves
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11
Q

How do IV and inhalational agents effect EMGs?

A
  • VAs do not affect EMGs

- AVOID MUSCLE RELAXANTS

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12
Q

What are the indications for cerebral oximetry monitoring?

A
  • mostly used in CEAs
  • intracranial surgery where a change in the patient’s neuro status may occur
  • shoulder surgeries and other sitting cases
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13
Q

How is cerebral oximetry used to monitor the neurosurgical patient?

A
  • Obtain baseline cerebral oximetry reading pre-induction
  • Monitor and keep it within 20% of baseline (more than that correlates with a change in neuro status)
  • Notify surgeon of sudden, drastic changes. Benefits are controversial.
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14
Q

How should fluids be managed in neurosurgery?

A
  • AVOID glucose-containing solutions
  • Keep the pt ISOvolemic, ISOtonic, & ISOoncotic. If dehydrated, restore volume
  • Give hourly maintenance & replace U/O
  • Replace blood when Hct 25-30% (depending on status & hx)
  • Mannitol may be given after the dura is opened
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15
Q

Discuss positioning in neurosurgery (in general).

A
  • Most common: supine, semi-sitting, lateral & prone
  • 100%O2 prior to turn & remember to reconnect all monitors!
  • Watch for hypoTN with sicker pts. Possibly turn agent down/off
16
Q

If neurosurgery in the supine position, use caution to…

A

Avoid extreme head rotation that can obstruct jugulars or vertebrals

17
Q

If neurosurgery in the prone position, one should…

A
  • watch eyes for risk of BLINDNESS

- Check ALL pressure points

18
Q

What are the relative contraindications to the sitting position?

A
  • pt with ventriculo-atrial shunt
  • an awake, un-anesthetized pt demonstrating cerebral ischemia in the upright pstn (cerebral vascular dx, coronary dx)
  • CAD with CHF with Right atrial P> Left atrial P, or patent foramen ovale
19
Q

What are the complications of sitting pstn?

A
  • Circulatory instability
  • VAE
  • Quadriplegia
  • Head, neck, and tongue edema
  • Compressive peripheral neuropathy
20
Q

How is ventilation managed during neurosurgery?

A
  • Obtain baseline ABG to aproximate PaCO2 with etCO2 readings
  • Routine hyperventilation is NO LONGER recommended
  • Maintain PaCO2 30-32 mmHg
21
Q

Which drugs treat “tight brain?”

A
  • Boluses or transfusions of thiopental, etomidate, propofol, or narcotic
  • Diuretics
22
Q

What is the most sensitive NON-invasive monitor for VAE?

A

Precordial Doppler (still a standard modality)

23
Q

What are the anesthetic implications of stereotactic -assisted procedures?

A
  • Pts are often sedated & local anesthesia is used to apply the localizing frame
  • Sedation is omitted if IICP or altered LOC
  • Awake FOB may be safest, intubation is hard with frame in place
  • Avoid hypocapnea during GA to prevent shifting of the brain
24
Q

What are the anesthetic implications for endovascular procedures?

A
  • Typically off-site, GA
  • Make sure ventriculostomy bag stays level, doesn’t overflow, & stays open (per surgeon request)
  • Keep lines on pt’s left side, out of the way of rotating fluoroscopy heads
  • maintain etCO2 30-32 to prevent vasospasm, keep paralyzed, maintain BP within 20% of baseline
  • Heparanize to ACT of 200 secs if coiling, 300 secs for stents
  • If CTscan, keep paralyzed and run penthothal gtt if ordered
25
Q

What are some vasospastic techniques?

A
  • Keep MAP >75, normal etCO2
  • 3 H’s: Hypervolemia, Hypertonic, Hyperoncotic (modify fluids for pt tolerance)
  • Nicardipine gtt: Mix 50mg/250ml, run at 0.5-2.2mg/hr. Increase to 5-15mg/hr for acute hypertensive crisis
  • Nicardipine increases ICP by increasing CBF & decreased CPP
26
Q

What can we do to prevent vision loss associated with prone and sitting cases?

A
  • use Foam headrests, check eyes (& document) at least every 20 mins, ProneView Mirror
  • Head neutral in relation to the back
  • Keep SBP w/in 20% of baseline, pressors PRN
  • Avoid head-down pstng, Reverse Trendelenburg if possible
  • Mayfield head clamp avoids compression of the globe
27
Q

What are the mechanisms of vision loss associated with prone & sitting cases?

A

Ischemic Optic Neuropathy (ION)-Most common.
-Possible causes: Low BP; Blood loss, anemia, or hemodilution; increased intraocular pressure; abnormal autoregulation of the optic nerve circulation; vasopressors, systemic vascular disease
Central retinal artery occlusion-Less common. d/t diret compression in spine surgery

28
Q

Identify the pathophysiology of an aneurysm.

A

Aneurysm is caused by an abnormal, localized dilation of the intracranial arteries.

29
Q

Identify the pathophysiology of SAH.

A
  • A bleed between the pia and arachnoid layers

- Most common cause: rupture of cerebral aneurysm

30
Q

Identify the pathophysiology related to AVMs.

A

Similar to aneurysms. A “tangling” of thin-walled abnormal vessels without an intervening capillary bed.
-Congenital disorder. Arteries fow directly into veins

31
Q

Identify the pathophysiology of carotid atherosclerosis.

A

Vascular plaques eventually occlude or rupture the vascular lumen in the internal carotid artery