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Neurology, Neurologic Anesthetic Physiology and Considerations > L&J Chp 28: Physiology, Pathophysiology, Anesthetic Management of Patients with Neurologic Disease > Flashcards

L&J Chp 28: Physiology, Pathophysiology, Anesthetic Management of Patients with Neurologic Disease Flashcards

1
Q

Electromyelography

A

-Measurement of electrical activity within the muscle

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2
Q

EMG recordings

A

Made with needle inserted into a muscle –> analysis of waveforms, firing rates of single or multiple motor units can give diagnostic information

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3
Q

Clinical applications of EMG

A
  • Diagnostic disorders of the spinal cord (acute disc herniation)
  • Disorders of peripheral nerves (traumatic neuropathies(
  • Disorders of the NMJ (myasthenia gravis)
  • Muscle disorders (myotonia, polymyositis)
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4
Q

Contents of the intracranial space

A
  • Brain tissue 80-85%
  • Cerebral blood volume (CBV) 5-8%
  • CSF (7-10%)
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5
Q

Intracranial pressure

A

Represents the pressure caused by brain tissue, cerebral blood volume, and CSF within the non-distensible cranial space

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6
Q

Monroe-Kelly Hypothesis

A

For ICP to remain normal, volume increase in any one of the three components must be matched by a decrease in another

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7
Q

Consequences of space-occupying brain tumors, TBI, subarachnoid hemorrhage

A

May all cause vasomotor paralysis, increase in ICP with subsequent decrease in CBF and impaired oxygen delivery

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8
Q

Rapidly increasing ICP

A

Arterial hypertension
Bradycardia
Respiratory irregularity

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9
Q

What is the response called for increased ICP?

A 
Vasomotor response
Cushing's response
Cushing's reflex 
Cushing reaction
Cushing's law 
Cushing's phenomenon 
Cushing's triad
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10
Q

Consequences of rapidly increasing ICP

A

-Cerebral herniation with brainstem compression, unconsciousness, subsequent death

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11
Q

Normal ICP

A

10-15mm Hg

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12
Q

Cerebral Perfusion Pressure Equation

A

MAP - ICP

why important to maintain normotension in these patients (>80 mm Hg)

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13
Q

Abnormal ICP

A

20-30mm Hg

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14
Q

What happens after TBI metabolically?

A
  • Brain may increase metabolic activity –> ramification of glutamate release, excitotoxicity
  • Euglycemic or hypoglycemic patients’ blood glucose concentrations may not allow for adequate substrate delivery to compensate for hypermetabolic brain –> metabolic crisis
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15
Q

Definition of a metabolic crisis

A
  • Simultaneous decrease in glucose below 0.7mmol/L
  • Increase in lactate-to-pyruvate ratio >40 in microdialyzate fluid
  • Why important to frequently measure serum glucose concentrations during neuroanesthesia as both severe hypo/hyperglycemia impact a patient outcome after brain injury
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16
Q

Cerebral blood flow autoregulation

A

-Multifactorial process that maintains constant CBF despite changes in systemic BP, CPP over wide range

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17
Q

CBF Autoregulation

A

Enables the brain to match blood supply with its metabolic demand both regionally and globally

  • -Usually intact during light planes of anesthesia
  • -Impaired/abolished during deep anesthesia
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18
Q

Effect of volatile anesthetic agents on CBF autoregulation

A

-Attenuate autoregulation up to a point when CBF becomes passively dependent upon CPP

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19
Q

Upper limit of flow autoregulation in a normotensive patient

A

MAP 130-150 mmHg

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20
Q

Lower limit of flow autoregulation in a normotensive patient

A

MAP 60 mm Hg

Decrease in MAP below lower limit results in CBF decrease and increase in arteriovenous oxygen difference

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21
Q

What happens above/below the limits of autoregulation?

A

CBF becomes flow-dependent

22
Q

CBF autoregulation: at a MAP of 40 mm Hg

A

Symptoms of cerebral ischemia including dizziness, hyperventilation, mental impairment occur

23
Q

T/F: CPP can decrease by approximately 30% before lower limit of autoregulation is reached

A

True

Rule of them useful clinically when planning management of a hypertensive/normotensive patient

24
Q

Brain function

A

Intimately related to cerebral perfusion, metabolism

25
Q

Characteristic features of cerebral metabolism

A
  1. High cellular energy demands utilizing ATP energy obtained from aerobic glucose oxidation
  2. No oxygen, minimal glucose and glycogen substrate reserves relative to consumption rates
  3. Low concentrations of high-energy phosphate compounds
26
Q

What is the brain dependent on?

A

-Adequate blood for minute-to-minute delivery of oxygen and glucose

27
Q

Normal cerebral metabolic rate for glucose

A

4.5mg/100g/min

Metabolic rate will be decreased during anesthesia, hypothermia, and/or hypercapnia

28
Q

How do volatile anesthetic agents affect the relationship btw CBF and CMRO2?

A
  • -May uncouple tight relationship of CBF and CRMO2 –> resulting in an increased blood flow despite dose-dependent decrease in CRMO2
  • -Attenuate autoregulation –> may be lost at higher doses
29
Q

What are the consequences of losing auto regulation of CBF with CMRO2?

A

CBF is passively dependent on CPP

30
Q

Normal mean global CBF in humans

A

45-65mL/100g/min

31
Q

What are the two types of arteries that supply the cerebral hemispheres?

A
  1. conducting vessels

2. penetrating vessels

32
Q

Cerebral arteries: conducting arteries

A

Non-resistance vessels –> carotid, vertebral, occipital, spinal artery together with their major and minor branches

33
Q

Cerebral arteries: penetrating arteries

A

AKA nutrient arterioles –> enter brain parenchyma at right angles to surface vessels
Site of primary CBF regulation

34
Q

Even though the vessels receive automatic innervation…

A

neurogenic tone not essential to normal CBF regulation

35
Q

Why do cats with spring-held mouth gags have increased risk of post anesthetic neurological deficits, cortical blindness, or hearing deficits?

A

Maximally opened mouths in cats may be associated with disrupted CBF, reduced direct blood flow to the Reina or inner ear –> most likely caused by stretching of vasculature of maxillary artery and adjacent muscles including temporalis, masseter, pterygoid m

36
Q

Consequences of MAP increasing above the upper limit of auto regulation?

A
    • Blood flow exceeds ability of cerebral vasculature to constrict
    • Pronounced increases in CBF cause forced dilation of arterioles –> may be associated with disruption of the BBB, subsequent edema +/- hemorrhage
37
Q

Constancy of CBF

A

Achieved by active vascular response thus rendering CBF directly proportional to CPP, inversely proportional to cerebrovascular resistance (CVR)

38
Q

What happens when have an increase in perfusion pressure?

A

-Elicit arteriolar constriction

39
Q

What happens when have a decrease in perfusion pressure?

A

Arteriolar dilation

40
Q

CBF auto regulation results from…

A

Myogenic responses of smooth muscle cells of the arteriolar wall to stretch cause caused by distending transmural pressure rather than by activation of the autonomic nerve fibers of perivascular nerves

41
Q

Drainage of blood flow from the brain

A
  • Thin-walled, valveless cerebral veins drain blood into relatively thick-walled dural sinuses
  • Site of entry of cerebral vein into dural sinus anatomically presents relatively fixed orifice, physiologically presents significant resistance to flow
42
Q

Chronic cerebral arterial hypertension

A

–Cerebral vessels adapt to higher perfusion pressure by hypertrophy of the vessel wall –> displaces autoregulatory curve to the right

43
Q

Differences with chronically hypertensive patients

A
  • tolerate higher arterial pressure much better than normotensive patients
  • displacement of autoregulatory curve to the right means lower limit also shifted right –> increased risk of ischemia during systemic hypotension
  • Do not tolerate same acceptable lower limits (eg MAP 60-70) for arterial BP as normotensive patients
44
Q

Effect of hypovolemic hypotension on CBF autoregulation

A
  • CVR increases –> increased vessel tone displaces curve to the right
  • Increases lower limit of CBF auto regulation and lowest tolerated pressure
  • Brain ischemia develops at a higher perfusion pressure than during pharmacologically induced hypotension where CVR is decreased
45
Q

Effect of moderate changes in PaO2 (arterial hypoxemia, arterial hyperoxemia)

A

-Do not exert measurable influence on CBF

46
Q

At what PaO2 do we see increase in CBF?

A

50mm Hg or below
Same PO2 at which progressive brain tissue lactic acidosis appears so suggests hypoxia in CBF regulated by the periarteriolar pH

47
Q

T/F: anoxia or anoxia + hypercapnia can constitute a pronounced cerebral vasodilation may cause a fatal increase in ICP and mass displacement (brain herniation) in patients with space-occupying intracranial lesions

A

True

48
Q

Intracerebral Steal Syndrome

A

If CVR decreases in non-ischemic, normal regions of the brain (eg via isoflurane anesthesia), blood may be shunted away from the area of vasomotor paralysis

49
Q

Robin Hood Syndrome (inverse steal syndrome)

A

Increase in CVR in normal cerebral regions will shunt blood into areas of vasomotor paralysis

50
Q

What conditions cause inadequate cerebral perfusion and hypoxia? What are the consequences?

A

Pathologic conditions including transient cardiac arrest, traumatic brain injury, brain tumor, or meningitis

Will lead to severe tissue lactic acidosis, vasomotor paralysis, increased ICP

Neurology, Neurologic Anesthetic Physiology and Considerations (1 decks)

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