Neuroanesthesia Flashcards

1
Q

What are the stimulation and response sites for SSEPs and MEPs?

A

SSEPs:
Stimulation - median nerve
Response - scalp electrodes over sensory cortex

MEPs:
Stimulation - scalp electrodes over motor cortex
Response - EMG in abductor pollicis brevis

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2
Q

What is normal ICP?

A

15 mm Hg or less

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3
Q

What is the equation for cerebral perfusion pressure (CPP)?

A

CPP = MAP - (the greater of CVP or ICP)

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4
Q

What is the ideal EtCO2 range for reduction in ICP? What PaCO2 does it reflect?

A

EtCO2 of 25 to 30 mm Hg, which reflects a PaCO2 of 30 to 35 mm Hg

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5
Q

Describe cerebral blood flow autoregulation? What are its limits?

A

The intrinsic ability of the cerebral vasculature to adjust resistance to maintain constant CBF over a wide range of MAPs

Autoregulation occurs from 60 to 160 mm Hg
- Above or below this range, CBF is pressure dependent

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6
Q

How do changes in PCO2 effect CBF?

A

For every 1 mm Hg change in PCO2, CBF will change by 1mL/100g/min in the same direction

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7
Q

What is autonomic hyperreflexia? Where is the transection usually located? What anesthetic technique is preferred? How is it treated?

A

Autonomic hyperreflexia is a disorder of sympathetic dysinhibition seen after spinal cord transection

  • Stimulation below the level can result in generalized vasoconstriction and hypertension
  • Bradycardia can occur secondary to activation of baroreceptor reflexes

Above lesion, parasympathetic predominantly - flushing and sweating
Below lesion, sympathetic predominantly - pale, cool, and goosebumps

About 85% of pts have transection above T6

Anesthetic technique should involve deep general or spinal/epidural with local anesthetic

Treatment of acute episode is with alpha-antagonists and vasodilators
- beta-blockers should not be used

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8
Q

What is the normal cerebral metabolic rate for oxygen per minute?

A

3.5 mL/100 g brain tissue

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9
Q

Order (most to least) of neuromonitoring sensitivity to interference from anesthetics

A

Visual evoked potentials
Somatosensory evoked potentials
Brainstem auditory evoked responses

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10
Q

What are the most sensitive monitors for venous air embolism?

A

TEE is the gold standard

Precordial doppler is the most sensitive non-invasive monitor
- can detect as little as 0.25 mL of air

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11
Q

What is normal cerebral blood flow? What is the critical low value?

A

Normal CBF is 50cc/100g tissue/min

The critical low value is 20cc/100g tissue/min, under which EEG changes begin to occur

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12
Q

How does ischemia effect autoregulation? What is the difference between intracerebral steal syndrome and Robin Hood syndrome?

A

During focal cerebral ischemia, ischemia areas of the brain are unable to participate in autoregulatory changes of vessel resistance

Intracerebral steal syndrome occurs with hypercarbia, when normal vessels vasodilate shunting blood away from the unchanged ischemic area

Robin Hood syndrome is reverse steal caused by hypocarbia, when normal vessels constrict shunting blood to the “poor” ischemic areas

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13
Q

What is the treatment for venous air embolism?

A
Flood the field and pack the wound
100% O2
Jugular venous compression
Aspirate air through central line
Place pt head down and in left lateral position
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14
Q

Describe the Glascow Coma Scale

A
Motor response:
Obeys commands - 6
Localizes stimulus - 5
Withdraws from pain - 4
Flexion posture - 3
Extension posture - 2
No response - 1
Verbal response:
Oriented - 5
Confused - 4
Inappropriate - 3
Incomprehensible - 2
No response - 1
Eye opening:
Spontaneous - 4
To speech - 3
To pain - 2
Nothing - 1
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15
Q

What is neurogenic pulmonary edema?

A

NPE is pulmonary edema caused by massive sympathetic discharge after neurologic/spine injury

Occurs in up to 20% of pts with severe head injury

Typically develops within 4 hours of inciting event

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16
Q

How do the following agents effect CMRO2, CBF, and ICP?

  • Volatile anesthetics
  • Nitrous oxide
  • Xenon
  • Propofol
A

Volatiles decrease CMRO2, increase CBF, and increase ICP

N2O increases CMRO2, CBF, and ICP
- Increase in CBF can be blunted by the simultaneous administration of IV or volatile anesthetics

Xenon decreases CMRO2, but increases both CBF and ICP

Propofol decreases CMRO2, CBF, and ICP

17
Q

What are the physiologic effects of ECT?

A

Elevations in CBF and ICP

Long- and short-term memory loss

Initial increase in parasympathetic stimulation

  • increased secretions
  • bradycardia
  • asystole

Quickly followed by increased sympathetic stimulation

  • hypertension
  • tachycardia
  • ST segment and T wave changes
18
Q

What methods are available for CNS monitoring during carotid endarterectomy? What can they detect?

A

Carotid stump pressures
- can detect global ischemia but not emboli

EEG
- can detect global ischemia but not emboli

SSEPs
- can detect even subcortical ischemia

Transcranial doppler
- can detect emboli but not ischemia

19
Q

What are the requirements for the determination of brain death?

A

Evaluation by two physicians
No other causes that could mimic brain death
Coma with absent brainstem reflexes
Lack of respiratory drive by apnea testing
- if apnea testing can not be performed, confirmatory testing (cerebral perfusion scintigraphy) is necessary

20
Q

Describe the timing of the morbidity/mortality of SAH? Are there any predictors of outcome? What is the treatment?

A

Re-bleeding can occur in the first 48 hours
Vasospasm can occur 3-7 days after initial event

Higher admission hemoglobin has been associated with decreased cerebral ischemia and improved outcomes

Traditional treatment involved Triple H therapy, but studies have not proven benefit

  • hypertension
  • hemodilution
  • hypervolemia

Calcium channel blockers (Nimodipine) can improve outcome and decrease cerebral infarction

Chemical angioplasty can also be used to treat vasospasm

21
Q

What physiologic changes can negatively impact SSEP monitoring?

A

Hypotension
Hypo-/Hyper-thermia
Hypoxia
Anemia

Acid-base status does not affect SSEPs

22
Q

What is Cushing’s Triad? What causes it?

A

Cushing’s Triad:

  • Hypertension
  • Bradycardia
  • Breathing alterations

Caused by brainstem compression, usually due to surgical manipulation or severe cerebral edema

23
Q

What is jugular bulb venous oxygen saturation (SjVO2)?

A

SjVO2 is a monitoring modality which can assess the oxygen extraction of brain tissue

Values represent the balance between global cerebral oxygen supply and demand
- focal ischemia cannot be assessed

24
Q

Which fluids should be avoided during surgery for an intracranial aneurysm and why?

A

Hypotonic solutions - may worsen cerebral edema

Glucose containing solutions - may exacerbate neuronal injury

25
Q

What drug should be avoided in a patient with myotonic dystrophy?

A

Succinylcholine

- known precipitating factor for myotonia

26
Q

What are the differences between Myasthenic Syndrome (Lambert-Eaton) and Myasthenia Gravis?

A

Myasthenic Syndrome (Lambert-Eaton)

  • Dysfunction of presynaptic calcium channels leading to decreased release of Ach
  • Muscle weakness improves with use
  • Muscle pain is common; reduced DTRs
  • Associated with small cell lung cancer
  • MORE sensitive to both succinylcholine and non-depolarizing NMBs

Myasthenia Gravis

  • Destruction of postsynaptic Ach receptors
  • Muscle weakness worsens with use
  • No muscle pain; normal DTRs
  • Associated with thymoma
  • Resistant to succinylcholine; MORE sensitive to non-depolarizing NMBs
27
Q

What factors can predict increased likelihood of the need for postoperative mechanical ventilation in patients with Myasthenia Gravis?

A

Risk Factors:

  • Duration of disease over 72 months (6 years)
  • History of chronic respiratory disease (ie. asthma or COPD)
  • Pyridostigmine dose over 750mg/day
  • Vital capacity of less than 2.9 liters
28
Q

Describe the potential causes of postoperative visual loss

A

Ischemic optic neuritis (ION)

  • occurs due to hypoperfusion or decreased oxygen delivery to the optic nerve
  • presents with painless visual loss and impaired color vision

Retinal artery occlusion

  • occurs due to external compression, retrobulbar hemorrhage, or embolism
  • presents with painless visual loss and “cherry red macula”

Acute angle glaucoma

  • occurs due to increased IOP from blockade of aqueous humor outfow
  • presents with painful and red globe, blurry vision, headache, N/V