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Anesthesia MM/TL > Neuro Anesthesia > Flashcards

Neuro Anesthesia Flashcards

1
Q

What are the signs/symptoms of ischemic optic neuropathy?

A

Painless visual loss within first 24-48 hours
Sluggish pupils
Visual field deficits

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2
Q

What are the risk factors for ION?

A 
Age over 50
Prone position 
Spine, cardiac, head/neck surgeries
Hypotension
Hemorrhage 
Anemia
Hemo dilution (don't give over 2L crystalloid)
HTN, diabetes, smoking
Male sex
Surgical time
Obesity
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3
Q

What is the pathophysiology of ION?

A

Ischemia to optic nerve leading to atonal destruction

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4
Q

What are the types of ION?

A

Anterior and posterior

Arteritic and non-arthritic

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5
Q

Which type of ION is more common after spine surgery?

A

Posterior

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6
Q

Which type of ION is more common after cardiac surgery?

A

Anterior

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7
Q

What are the treatment methods for ION.

A 
Acetazolamide 
Diuretics
Steroids
Transfusion
Position changes (avoid venous congestion)
Maintenance of bp
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8
Q

What does botulinum toxin do?

A

Inhibits release of Ach at NMJ causing flaccid paralysis by cleaving SNARE proteins

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9
Q

How does tetanus toxin travel?

A

Retrograde entering presynaptic neurons in the spinal cord

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10
Q

What is not associated with POVL?

A

Deliberate hypotension

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11
Q

What is the treatment for pneumocephalus?

A

Head of bed up, 100% FiO2, avoid maneuvers that increase ICP

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12
Q

How do you diagnose pneumocephalus?

A

CT scan

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13
Q

What are the hallmarks of autonomic hyperreflexia?

A

Hypertension and reflexive bradycardia

Other symptoms: sweating, piloerection, facial erythema, headache, nasal congestion, feeling of doom

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14
Q

What causes autonomic hyperreflexia?

A

Distention of a viscous in a patient with spinal cord lesion T7 or above.
- any noxious stimulation can trigger

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15
Q

What is the mechanism behind autonomic hyperreflexia?

A

The negative feedback from the CNS cannot mitigate the sympathetic stimulation below the lesion.

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16
Q

Why doesn’t autonomic hyperreflexia occur with lesions lower than T6?

A

Greater splanchnic ganglion receives innervation from T5-9 can buffer the response

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17
Q

What happens above the lesion in autonomic hyperreflexia?

A

Vasodilation –> flushing, nasal congestion, headaceh

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18
Q

How do you treat autonomic hyperreflexia?

A

Remove the stimulus
Deepen the anesthesia
Administer vasodilators: nifedipine, nitroglycerin, nitroprusside

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19
Q

What class of med should be avoided in autonomic hyperreflexia?

A

Beta blockers due to unopposed alpha stimulation

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20
Q

When does autonomic hyperreflexia syndrome occur in relation to the initial lesion?

A

3-4 weeks after when the spinal reflexes have returned.

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21
Q

Why should the patient with autonomic hyperreflexia by monitored for 7-10 days after the initial episode?

A

Because they are at a high rate of recurrence.

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22
Q

What are the predictors of postoperative mechanical ventilation in a MG patient?

A
  1. Pyridostigmine > 750 mg/day
  2. Vital capacity <2.9L
  3. NIF less than 20 cm H2O
  4. inability to clear secretion or produce a strong cough.
  5. Disease for more than 6 years
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23
Q

What is the leading predictor of postoperative mechanical ventilation in a MG patient?

A

Inability to clear secretions or produce a strong cough

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24
Q

What is the gold standard for estimating brain parenchyma temperature?

A

Jugular bulb temperature because of the proximity of the bulb to the brain

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25
Q

What must you do to ensure adequate cooling of brain in deep hypothermic circulatory arrest?

A

Run CPB for 20-30 minutes once goal blood temp is reached

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26
Q

What will be seen on intraventricular drain monitor when there is an acute increase in ICP?

A

A plateau wave (Lundberg’s A wave)

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27
Q

What is normal ICP?

A

5-13 mm Hg

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28
Q

What does P1 represent on ICP monitoring?

A

P1 = percussion wave, arterial pulsation

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29
Q

What does P2 represent on ICP monitoring?

A

Tidal wave and it represents incranial compliance

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30
Q

What does P3 represent?

A

The dicrotic wave and it represents aortic valve closure

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31
Q

What is a normal ICP waveform?

A

P1 > P2 > P3

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32
Q

What does it mean if P2 becomes higher than P1?

A

Reduced intracranial compliance

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33
Q

What are B and C waves?

A

correspond to changes in ICP with respiration and arterial blood pressure
***no clinical significance

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34
Q

What strategies can be employed to prevent a hyperkalemic periodic paralysis episode?

A

Maintaining normal body temperature
Dextrose containing K-free fluids
Decreasing serum potassium concentrations to low normal
regional

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35
Q

What are the potential triggers of hyperkalemic periodic paralysis?

A 
Hyperkalemia (metabolic acidosis)
Potassium rich meals
Rest after exercise
Stress
Succinylcholine
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36
Q

What is hyperkalemic periodic paralysis?

A

Mutations in the voltage gated sodium channel in skeletal muscle that interfere with channel inactivation leading to prolonged depolarization and subsequent myotonia, membrane desensitization and paralysis.

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37
Q

What is the goal CPP in a patient with TBI?

A

50-70 mm Hg

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38
Q

What cerebral artery is being evaluated by TCD?

A

Middle cerebral

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39
Q

What does TCD detect intraoperatively during carotid endarterectomy?

A

Embolization in more than 90% of patients

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40
Q

What are isonation windows?

A

Areas of the skull where the bone is less dense and therefore more amenable to US penetration.

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41
Q

What does the mean flow velocity following clamping of the carotid artery correlate with in CEA?

A

the degree of cerebral ischemia

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42
Q

What percentage of mean flow velocity indicates ischemia?

A

<40% of the preclamped mean flow velocity

Severe = <15%

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43
Q

What do volatile agents do to CMRO2 and CBF in a dose dependent manner?

A

Uncouple the CMRO2 and CBF - cause a decrease in CMRO2 while increase CBF the higher the MAC

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44
Q

What affects somatosensory evoked potentials?

A

Anemia
Hyper/hypothermia
Hypoxia

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45
Q

How much will dropping a patient’s PaCO2 by 1 mm Hg effect the CBF?

A

It will decrease CBF by 1-2 ml/100g/min

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46
Q

At what PaCO2 does local ischemia start?

A

PaCO2 of 25 mm Hg

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47
Q

What arterey is SSEP a poor monitor of?

A

The ASA because it gives blood supply to the motor portions.

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48
Q

How does the somatosensory pathway get to the brain?

A

Through the dorsal columns to the thalamus and cortex

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49
Q

Where does the lateral funiculus lie?

A

In the anterior portion of the spine

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50
Q

What does the lateral funiculus supply?

A

Sensory portion to LE

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51
Q

What are the considerations in neurofibromatosis?

A
  1. Altered responses to neuromuscular blocking agents
  2. Neurofibromas in the airway that can cause obstruction
  3. Cervical spine abnormalities, scoliosis
  4. Intracranial tumors
  5. Endocrine disorders: pheo, medullary thyroid CA, hyperparathyroidism
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52
Q

When is vasospasm suspected on TCD?

A

When flow velocity of the MCA is > 120cm/s

or FVMCA: FVICA ratio is larger than 3

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53
Q

What is the mechanism behind neurogenic pulmonary edema within a few hours of TBI?

A

Massive sympathetic discharge

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54
Q

What are the clinical manifestations of neurogenic pulmonary edema?

A

Rapid onset

Intraalveolar hemorrhage

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55
Q

What is unique about brainstem auditory evoked potentials?

A

They are most resistant to anesthetic technique

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56
Q

Contralateral or bilateral changes in the BAEP recordings indicates what?

A

Changes in global physiology and blood supply to the auditory pathway

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57
Q

What is the path of stimulus to terminal recording of a somatosensory evoked potential?

A

Peripheral nerve –> dorsal root ganglia –> posterior spinal cord –> (decussation at the cervicomedullary jxn) medial lemniscus –> thalamus –> cortex

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58
Q

What does a decrease in amplitude or increase in latency of SSEP indicate?

A

Cortex ischemia

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59
Q

What does jugular bulb venous monitoring measure?

A

Direct cerebral oxygenation and global cerebral oxygen metabolism by measuring jugular venous oxygen sat and arterial-jug venous oxygen content differences.

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60
Q

What does SSEP measure?

A

MCA so can detect subcortical sensory cortex response to peripheral sensory nerve stimulation

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61
Q

What does internal carotid stump pressures reflect?

A

Collateral flow back-pressure in the circle of Willis originating from the contralateral carotid artery.
Detect hypoperfusion at pressures <50 mm Hg
***cannot detect emboli

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62
Q

What is EEG used for in CEA?

A

Monitoring for cerebral ischemia and for selective shunting during CEA

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63
Q

What is the pathogenesis of tetanus?

A

Inhibition of neurotransmitter release from inhibitory neurons in the CNS. Happens by cleavage of a protein component of synaptic vesicles, synaptobrevin II which prevents release of inhibitory NTs

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64
Q

What is the pathogenesis of botulism?

A

Inhibition of NT release for NMJ at alpha motor neurons

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65
Q

What is the pathogenesis of polio?

A

Destruction of cells in the CNS, particulary the spinal cord

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66
Q

What can cause exacerbations of MS?

A

Postpartum period
Spinal anesthesia
Hyperthermia

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67
Q

How can you decrease the incidence of myalgia after succinylcholine administration?

A

Calcium gluconate pretreatment (stabilizes celular membranes)
Lidocaine pretreatment
Perioperative vit C (stabilizes endothelial cells)

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68
Q

AT what point in CBF does irreversible brain damage begin to occur?

A

6-12 ml/100g/min

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69
Q

At what point in CBF does ischemia of brain begin to occur?

A

20 ml/100g/min

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70
Q

What is average CBF in the normal brain?

A

50 ml/100g/min

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71
Q

What is the ischemic penumbra?

A

The time period in which membrane failure and neuronal death can be prevented.
May be hours!

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72
Q

How much does CBF changes with 1 degree Celsius change in temperature?

A

5-7%

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73
Q

What does an entropy monitor do?

A

Processes the EEG signal with a publicly known algorithm that primarily measures the degree of disorder or variability within the EEG signal.

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74
Q

What are the CNS differences in the elderly

A
  1. BBB is more permeable
  2. Loss of brain volume that is not uniform
  3. Decrease in neuronal density that is not uniform
  4. Regional reductions of NTs
  5. Reduction of blood flow and oxygen consumption in gray matter
  6. Decreased CSF volume
  7. Decreased response to hypoxia/hypercarbia
  8. Higher pain thresholds
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75
Q

What are the changes of neuraxial anesthesia in the elderly?

A

Larger spread due to more epidural permeability, lower CSF volume and space.

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76
Q

What is the desired endpoint for barbiturate infusion during an open aneurysmal clipping?

A

Burst suppression

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77
Q

What are delta waves on EEG indicative of?

A

deep coma, anesthesia or encephalopathy

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78
Q

What are theta waves on EEG indicative of?

A

Encephalopathy

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79
Q

What are alpha waves on EEG indicative of?

A

Awake, but eyes closed

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80
Q

What are beta waves on EEG indicative of?

A

Wakefulness

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81
Q

What should not be used as an anesthetic technique in a patient with T1?

A

Spinal anesthesia with opioid only because it will not prevent autonomic hyperreflexia

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82
Q

What is complication not commonly seen with a sitting craniotomy?

A

POVL

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83
Q

What is the most worrisome complication of sitting craniotomy?

A

VAE because noncollapsible venous channels such as venous sinuses can be violated during surgery and air is entrapped in them due to negative pressure gradient between the surgical site and the heart.

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84
Q

Who is at the highest risk for developing tension pneumocephalus?

A

Posterior fossa or cervical dural incisions in the seated position due to possible air trapping and tracking cephalad in the higher regions of the brain

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85
Q

What position can decrease the risk of pneumocephalus?

A

The “ski-jump” position where the patient is in some reverse T and the neck slightly flexed so the occiput is level with or slightly below the level of the neck.

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86
Q

How much total body oxygen does the brain consume?

A

20%

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87
Q

What is average CMRO2?

A

3-3.8 ml/100 g/min or 50 ml/min

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88
Q

Where is CMRO2 greatest in the brain?

A

The gray matter of the cerebral cortex

89
Q

What is total CBF in adults?

A

750 ml/min (15-20% of CO)

90
Q

What flow rate of CBF is associated with cerebral impairment?

A

20-25 ml/100g/min

91
Q

What is the normal global CBF rate?

A

50 ml/100g/min

92
Q

What flow rate of CBF is associated with isoelectric EEG?

A

15-20 ml/100 g/min

93
Q

What CBF rate is associated with irreversible damage?

A

10 ml/100 g/min

94
Q

What is normal velocity of the MCA?

A

55 cm/sec

95
Q

What does the Lindegaard ratio tell you?

A

Distinguishes between vasospasm and hyperemic blood flow

MCA velocity 3X the velocity of the ICA = vasospasm

96
Q

What are the indirect measures of adequate CBF and brain tissue oxygen delivery?

A

TCDs
Near Infrared spectroscopy (primarily reflects cerebral venous oxygen saturation)
Brain tissue oximetry (through Clark electrode in a bolt)
Microdialysis (analyzes cerebral lactate, NTs, glucose, inflammatory medidators)

97
Q

What is normal brain tissue oxygen tension?

A

20-50 mm Hg

98
Q

What is normal CPP?

A

80-100 mm Hg

99
Q

What CPP is associated with an isoelectric EEG?

A

25-40 mm Hg

100
Q

At what range of MAP is CPP unchanged?

A

60-160 mm Hg

101
Q

At what MAP is the BBB disrupted?

A

150-160 mm Hg

102
Q

At what temperature does brain injury begin to occur?

A

42 C

103
Q

At what temperature is the EEG isoelectric?

A

20 C

104
Q

How much does CBF change by degree in temperature?

A

5-7%

105
Q

How much CSF is made per hour in adult?

A

21 ml/hr

106
Q

How much total CSF is there in an adult?

A

150 ml

107
Q

How does the CSF flow?

A

Lateral ventricles –> foramina of Monroe (intraventricular) –> third ventricle –> fourth ventricle –> cerebellomedullary cistern –> subarachnoid spaced

108
Q

Where is the foramin of Monroe?

A

Between the lateral and third ventricles

109
Q

Where is the cerebral aqueduct of Sylvius?

A

Between the third and fourth ventricle

110
Q

Where is foramen of Magendie?

A

Fourth ventricle to cisterna magna?

111
Q

Where is foramen of Luschka?

A

Fourth ventricle to cisterna magna

112
Q

Where is the CSF absorbed?

A

Arachnoid granulations over the cerebral hemispheres to the cerebral venous sinuses

113
Q

What is the tonicity of CSF?

A

Isotonic with lower potassium, bicarb and glucose than plasma
(Choroid plexus actively secrete Na)

114
Q

How are perivascular and interstitial protein returned to the blood?

A

By absorption of CSF

no lymphatics in CNS

115
Q

What are the major compensatory mechanisms for rises in ICP?

A
  1. Movement of CSF from brain to spinal cord compartment
  2. Increase CSF absorption
  3. Decrease CBV mainly via venous sinuses
  4. Decrease CSF production
116
Q

What drugs/medications decrease CSF production?

A 
Acetazolamide
Isoflurane
Lasix
Steroids
Spironolactone
117
Q

How much does CBV increase with each 1 mm Hg increase in PaCO2?

A

By 0.05 ml/100 g

118
Q

What are the four herniation site?

A
  1. Cingulate gyrus under falx cerebri
  2. Uncinate gyrus under tentorium cerebelli
  3. Cerebellar tonsils thru foramen magnum
  4. Any area under a defect in the skull (transcalvarial)
119
Q

What do all the volatile agents do to CBF?

A

Increase it, thereby increasing ICP

120
Q

What do all volatile agents do to CMR?

A

Decrease it

121
Q

Which anesthetics decrease CMRO2, CBF and ICP?

A 
Propofol
Etomidate
Lidocaine
Barbiturates
BZDs
122
Q

Which volatile agent has the greatest effect on CBF?

A

Halothane

At concentrations > 1%, it abolishes autoregulation

123
Q

Which volatile agent has the greatest effect on CMR?

A

Isoflurane (50%)

124
Q

How can you blunt the response of CBF and CMR to volatiles?

A

With hyperventilation/hypocapnia as the response of the cerebral vasculature to CO2 is retained with volatile agents

125
Q

What is luxury perfusion?

A

The combination of a decrease in neuronal metabolic demand with an increase in CBF

126
Q

What may happen with volatile agents?

A

You can get circulatory steal phenomenon due to increase blood flow to normal areas but not in ischemic areas where the arterioles are already maximally dilated.

127
Q

How does isoflurane affect CSF?

A

It increases it absorption

128
Q

How does halothan affect CSF?

A

It impedes its absorption

129
Q

Which volatile agent produces the least cerebral vasodilation?

A

Sevoflurane

130
Q

How much do barbs decrease CMR and CBF?

A

They decrease it in a dose-dependent manner until isoelectricity on EEG. This is about 50% of CMR and CBF

131
Q

What are the CNS effects of barbs?

A
  1. Dose dependent decrease in CBF and CMR
  2. More decrease in CMR than CBF so get more metabolic supply than demand
  3. Uniform decrease in CMR
  4. Absorption of CSF
  5. Robin hood steal phenomenon - redistribute blood flow to ischemic areas
  6. anticonvulsant
132
Q

What are the CNS effects of opioids?

A

Little effect on CBF, CMR, and ICP

133
Q

Which opioids increase seizures?

A

Alfentanil

Meperidine

134
Q

Why is morphine a poor choice for neuroanesthesia?

A

Low lipid solubility

Prolonged sedative effects

135
Q

What are the CNS effects of etomidate?

A
  1. Nonuniform decreases in CMR (more in cortex, than brainstem which may explain its greater hemodynamic stability)
136
Q

In what patients should etomidate be avoided?

A

History of epilepsy

137
Q

How does ketamine offer neuroprotective effects?

A

During times of increased glutamate concentrations as during brain injury

138
Q

What is the principal advantage of lidocaine in neuroanesthesia?

A

It decreases CBF without causing hemodynamic effects

139
Q

Which adrenergic receptors have the greater effect on the brain when the bbb is disrupted?

A

Beta 1 –> increase CMR and CBF

140
Q

What does alpha 2 agonist due in the brain?

A

Cause vasoconstriction

141
Q

When do vasopressors increase CBF?

A

Only when MAP is outside of the cerebral autoregulation curve

142
Q

How can NMBs affect CMR and CBF?

A

HTN and histamine-mediated cerebral vasodilation

143
Q

What is the pathophysiology of cerebral ischemia?

A

Intracellular K decreases while intracellular Na and Ca increase.
Increased intracellular Ca results in activation of lipases, proteases which results in FFA and COX and Lipoxygenase activities –> prostaglandins and leukotrienes –> cell injury

144
Q

What happens in reperfusion?

A

Tissue damage due to formation of oxygen-derived free radicals

145
Q

Which volatiles do not cause electrical silence?

A

Sevo
Des
Nitrous

146
Q

What does nitrous cause on EEG?

A

High amplitude activation

147
Q

Which IV anesthetics produce isoelectricity?

A

Propofol, barbs, etomidate

148
Q

What does ketamine produce on EEG?

A

High amp theta followed by high amp gamma and low amp beta

149
Q

What do somatosensory evoked potentials test the integrity of?

A

The spinal dorsal columns and sensory cortex

150
Q

What are short latency evoked potentials from?

A

The nerve stimulated or the brain stem

151
Q

What are long latency evoked potentials from?

A

The cortex

152
Q

What are motor evoked potentials good for assessing?

A

The anterior spinal cord perfusion (aortic surgery)

153
Q

What is vasogenic edema?

A

Most common

Follows disruption of bbb

154
Q

What is cytotoxic edema?

A

From metabolic insults such as hypoxia

Results from failure of brain cells to actively extrude sodium causing progressive cellular swelling

155
Q

What is interstitial edema?

A

Results from obstructive hydrocephalus and entry of CSF into the brain interstitium.

156
Q

What does vasogenic edema often respond to?

A

Corticosteroids

157
Q

How does furosemide lower the ICP?

A

By removing intracellular water from normal brain tissue

Decreasing formation of CSF

158
Q

How does mannitol lower ICP?

A

By increasing serum osmolality (300-315 mOsm/L = goal)

159
Q

What are the detrimental effects of mannitol?

A

Pulmonary edema due to transiet increase in intravascular volume
Vasodilation
Expand hematomas by osmotic diuresis of the normal brain tissue around it

160
Q

Who should mannitol be avoided in?

A

Elderly patients
Intracranial aneurysms
AVMs
ICH/IVH

161
Q

What position are frontal, temporal and parieto-occipital craniotomies performed in?

A

Supine

162
Q

What are posterior fossa tumors associated with?

A

Obstructive hydrocephalus through the fourth ventricle or cerebral aqueduct of Sylvius

163
Q

What should you think of first if you have an abrupt circulatory change during a posterior fossa surgery?

A

Brain stem injury to respiratory center

164
Q

What are the risks of sitting position?

A
  1. Excessive neck flexion - swelling of upper airway due to decreased venous drainage
  2. Pneumocephalus (delayed awakening, neurologic dysfunction)
  3. VAE -
165
Q

Where does a precordial doppler sit?

A

Right of the sternum between 3rd and 6th ribs

166
Q

What are the signs of VAE?

A
  1. Decreased ETCO2 due to increased dead space and decreased CO
  2. Reappearance or increase of NO2 in expired gases
  3. Mill wheel murmur
  4. Hypotension
167
Q

What are the steps of treating a VAE?

A
  1. Notify surgeon to flood surgical field with saline, bone wax or wet gauze
  2. Turn off nitrous oxide and turn up O2 to 100%
  3. Open fluids to increase intravascular volume and CVP
  4. Bilateral jugular vein compression
  5. Head down position
168
Q

What does anesthetic management of a patient with head trauma entail?

A

PaCO2 30-35
CPP 110-160 mm Hg
Avoid vasodilators until cranium is opened
Use volume and alpha agonism for hypotension

169
Q

What is DIC due to head trauma usually due to?

A

The release of large amounts of brain thromboplastin

170
Q

What is the pathophys of autonomic hyperreflexia?

A

No inhibitory signals can reach below the level of the lesion so you get unopposed vasoconstriction (HTN, MI, arrythmias) and SNS effects below the lesion and exaggerated PSNS effects above the lesion

171
Q

What are the best anesthetic techniques to limit autonomic hyperreflexia?

A

Spinal or epidural

Deep

172
Q

What is contraindicated in elevated ICP in patients with head trauma?

A

High dose glucocorticoids because they increase mortality

173
Q

What is triple H therapy?

A

HTN, hypervolemia, hemodilution

174
Q

How quickly should acute hypernatremia be fixed?

A

At a rate of 1-3 mmol/hr with max of 12 meQ per day

175
Q

How quickly should chronic hypernatremia be fixed?

A

0.5 mmol/hr

176
Q

What is clofibrate?

A

Hypolipidemic agent that causes release of ADH used as outpatient for central DI.

177
Q

What is chlorpropamide?

A

An oral hypoglycemic agent which stimulates ADH release used for as outpatient med for central DI.

178
Q

What is the treatment for central DI?

A

Free water replacement

DDAVP

179
Q

What is better nasal or IV DDAVP?

A

Nasal because it lasts longer and has fewer pressor side effects

180
Q

What does etomidate do to seizure duration?

A

Increases it

181
Q

What does caffeine do to seizure duration?

A

Increases it

182
Q

What is grade I on Hunt Hess?

A

Asymptomatic or mild headache

183
Q

What is grade II on Hunt Hess?

A

Severe headache

Nuchal rigidity

184
Q

What is grade III on Hunt hess?

A

Drowsiness, confusion, or focal deficit

185
Q

What is grade IV on Hunt Hess?

A

Stupid

Hemiparesis

186
Q

What is grade V on Hunt hess?

A

Coma

Decerebrate posture

187
Q

What is mild TBI defined by?

A

GCS of 13 or higher

188
Q

What is moderate TBI defined by?

A

GCS of 9-12

189
Q

What are the triggers for hypokalemic periodic paralysis?

A

Dextrose fluids, high sodium foods, ingestion of carbs, exercise, insulin, stress, hyperthermia

190
Q

What are the hallmarks of hypokalemia periodic paralysis?

A

10-20 years of age, gets proximal muscle weakness with age,

Autosomal dominant alteration in cation channels

191
Q

What is adenosine used for in aneurysmal clipping?

A

Circulatory arrest for 30-45 seconds

During acute hemorrhage

192
Q

What are the goals laid out by the American Association of Neurosurgeons for patient with head trauma?

A

ICP < 20-25 mm Hg
MAP > 80
PaO2 > 95
CPP > 60

193
Q

What drug is used to prevent paralysis episode in both hypo and hyperkalemic periodic paralysis?

A

Acetazolamide

194
Q

What are the treatments for hyperkalemia periodic paralysis?

A

Beta blockers
Acetazolamide
K-wasting diuretics

195
Q

What are the treatments for hypokalemic periodic paralysis?

A

Acetazolamide

K-sparing diuretics

196
Q

What metabolic derangement can cause exacerbation of MS?

A

Hyperthermia because increased temperature blocks conduction of demyelinated nerves

197
Q

Where should PaCO2 and CPP be kept in a TBI patient?

A

35-40 mm HG and 50-70 mm Hg respectively

198
Q

What are the ST changes on ECG in SAH associated with?

A

Catecholamine release causing subendocardial ischemia

199
Q

What is the path of stimulus to terminal of a motor evoked potential?

A

Lower limb cortex –> internal capsule–> brainstem –> corticospinal tract –> peripheral nerve

200
Q

What is the path of stimulus of an auditory evoked potential?

A

Cochlea –> CN VIII –> cochlear nucleus –> inferior colliculus –> auditory cortex

201
Q

What is the path of stimulus of visual evoked potential?

A

retina –> optic nerve –> optic chiasm –> optic trat –> superior colliculus –> visual cortex

202
Q

What anti-epileptic can be used in central DI?

A

Carbamazepine because it sensitizes the collecting tubule to ADH

203
Q

What does demeclocycline do?

A

Antagonizes ADH at tubule inducing DI. Used in SIADH

204
Q

What is the correct pathway for eccrine swear gland innervation?

A

SNS preganglionic –> (via Ach) nicotinic –> SNS post ganglionic –> (Ach) muscarinic receptors

205
Q

What organ has no postganglionic fibers?

A

Adrenal glands

206
Q

How much does CMRO2 decrease for every 1 degree in temperature?

A

6 % with proportional changes in CBF

207
Q

At what PaO2 does CBF become affected?

A

50 mm Hg

208
Q

Where are the eccrine glands?

A

All over the body

209
Q

What do eccrine glands do.

A

Provide cooling via sweating

210
Q

Where are the apocrine glands?

A

Arm pits and perianal region

211
Q

What are the clinical manifestations of neurogenic shock?

A

Unopposed vagal tone : Bradycardia, hypo tension from loss of cardiac accelerator fibers

Paradoxical shallow breaths indicate a lesion between C4-C7

212
Q

What is the Bainbridge reflex?

A

When the heart rate increases due to stretch receptors in the atrial wall

213
Q

What causes inhibition of acetylcholine at the NMJ?

A

Botulinum toxin

214
Q

What areas do not contain the bbb?

A

Circumventricular areas and areas that regulate the ANS (area postrema, pineal gland, lamina terminals, median eminence, neurohypophysis)

215
Q

What are the risk factors for intraoperative awareness?

A

TIVA with NMB
< MAC 0.7
Use of nitrous
Use of NMBs

216
Q

Which gas is associated with the least amount of intraoperative awareness?

A

Isoflurane

217
Q

Which gas is associated with the most intraoperative awareness?

A

Nitrous oxide

218
Q

Why should you not push the CPP above 70?

A

Risk of ARDS

219
Q

What is the response to stimulation in a paralyzed nerve compared to a normal nerve?

A

It is exaggerated due to extrajunctional Ach receptors

Anesthesia MM/TL (36 decks)

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