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Anesthesia Pharm Exam 1 > Neurophysiology for Anesthesia > Flashcards

Neurophysiology for Anesthesia Flashcards

1
Q

What is the purpose of anesthesia?

A
  1. Reduce anxiety- anxiolysis
  2. Relieve pain- analgesia
  3. Provide a stable surgical field-paralysis
  4. Produce hypnosis
  5. Autonomic suppresion
  6. Somatic suppression
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2
Q

BIS monitor

A

poor mans EEG

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3
Q

Wakefulness

A
  • noradrenergic neurons in the locus creels
  • histaminergic neurons in the tuberomammillary nucleus
  • seroteneric neurons in the dorsal and median raphe nuclei
  • dopaminergic neurons in the periaqueductal gray matter
  • orexingeric neurons stimulate directly and support monoamingeric neurons
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4
Q

NREM sleep

A
  • firing decreases
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5
Q

REM sleep

A

-firing virtually quiescent

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6
Q

Anesthetic effects on the thalamus?

A

-resemble the naturally occurring thalamocortical inhibition characteristic of NREM sleep

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7
Q

Infusions of somnogens (adenosine) effects on general anesthesia?

A

-reduce the amount of general anesthetic needed

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8
Q

Infusions of theophylline (adenosinergic antagonist) effects on general anesthesia?

A

-increases the amount of general anesthesia needed

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9
Q

Thalamic sites during NREM sleep and anesthesia?

A
  • the cortex is deprived of input

- Thalamic Gates

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10
Q

Hypothalamic sites

A

-histaminergic and orexenergic neurons in the hypothalamus stimulate the thalamus

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11
Q

Brainstem Sites

A

-locus ceruleus, mesopontine tegentum and VLPO stabilization

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12
Q

Limbic System

A

-hippocampus, medial septum, amygdala

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13
Q

What doe GabaA, Glutamate, and Ach activate?

A

-Activate BOTH inotropic and metabotropic receptors

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14
Q

Ionotropic receptors

A

-Ligand-gated ion channels that pass (+) or (-) ions and excite or inhibit

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15
Q

Metabotropic receptors

A

-can be excited or inhibited by the same NTM depending on which type of G-protein is coupled to the transmitter

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16
Q

Glutamate

A
  • Excitatory in the brain and spinal cord
  • NMDA blocked by Mg2+ at normal extracellular levels
  • Open NMDA and allow Ca2+ into the cell
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17
Q

GABA

A
  • Inhibitory primarily in the brain
  • GabaA- ionotropic (Cl- and also HCO3-)
  • Gaba B- metabotroic (g proteins) open K+ channels
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18
Q

Glycine

A
  • Inhibitory primarily in the spinal cord
  • requires 3 glycine to activate Cl- channels
  • glycine is a co-agonist at the NMDA receptor
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19
Q

Nicotinic Acetylcholine receptors (nAChr)

A
  • located in the CNS
  • nicotinic are ionotropic
  • muscarinic are G protein
  • Ach regulates wakefulness, attention, learning and motivation
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20
Q

Benzodiazepines affect on anesthesia and memory

A
  • benzos and IV propofol primarily affect long term memory storage or retreival
  • volatile agents impair memory formation at 25-50% MAC in humans
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21
Q

LTP

A

-a form of synaptic plasticity important in memory formation, is inhibited by barbiturates, bentos, propofol, and isoflurane

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22
Q

Depth of anesthesia monitors: The BIS monitor

A
  • Algorithmic EEG analysis
  • Range 0-100
  • 40-60 recommended value for GA
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23
Q

Limitations of BIS monitor

A
  • ketamine and N2O increases BIS
  • BIS may decrease with NMB in awake patients
  • multiple BIS sensor on the same patients give different values
  • low BIS values may result in a reduction in delivered anesthesia concentration and resulting in awareness
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24
Q

Incidence of Awareness: Highest and Lowest areas

A
  • Highest in OB- .4-7%
  • lowest in General surgery w/ ETT- 1%
  • trauma and shock- 11-43%
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25
Q

Reasons for intraoperative awareness?

A
  1. Equipment failure
  2. Inadequate anesthesia
  3. Patient factors- alcohol use, drug use
  4. Inability to assess depth and anesthesia
  5. Inappropriate anesthesia technique
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26
Q

Likely times for recall?

A
  1. Preinduction: defasciculating non depolarizing NMB prior to sux
  2. After intubation: paralyzed but not anesthetized
  3. Intraoperative
  4. Post operative
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27
Q

1858 Snow- 5 stages of narcotism

A

Evolved into 4 classifications:

  1. Analgesia
  2. Light anesthesia
  3. Surgical Anesthesia
  4. Overdose
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28
Q

1989- Magaw- details Snow’s 4 classifications with corresponding physiological events

A

-Described eye, muscle tone, respiratory, pulse caliber, and heart rate changes seen with each classification

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29
Q

1937- Guedel Signs and Stages

A
  • 4 stages with signs and planes
    1. Analgesia: regular small volume respirations
    2. Excitement: irregular respirations
    3. Anesthesia: (4 stages)
    4. Overdose: apnea
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30
Q

Guedels Stage I of Analgesia or Disorientation

A
  1. From beginning of induction of anesthesia to loss of consciousness
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31
Q

Guedels Stage II Excitement or Delirium

A
  1. From loss of consciousness to onset of automatic breathing
  2. Eyelash reflex disappears but other reflexes remain intact
  3. Pupils dilated but reactive, tearing, coughing, vomiting and struggling may occur
  4. Respiration can be irregular with breath-holding
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32
Q

Guedels Stage III Surgical Anesthesia

A
  1. Begins with the onset of regular respiratory pattern and ends with loss of respiration. Divided into 4 planes
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33
Q

Guedels Stage III- planes I and II

A

Plane I: from onset of automatic respiration to cessation of eyeball movements. Eyelid reflex is lost, swallowing reflex disappears, marked eyeball movement may occurring but conjunctival reflex is lost at the bottom of the plane

Plane II: from cessation of eyeball movements to beginning of paralysis of intercostal muscles. Laryngeal relax is lost, corneal reflex disappears, respirations are automatic and regular.

34
Q

Guedels Stage III: planes III and IV

A

Plane III: from beginning to completion of intercostal muscles paralysis, diaphragmatic respiration persists but respiratory intercostal paralysis occurs. Desired plane for surgery when NMB were not used

Plane IV- from complete intercostal paralysis to diaphragmatic paralysis (apnea)

35
Q

Guedels Stage IV

A
  • From stoppage of respiration till death
  • Anesthetic overdose causes medullary paralysis with respiratory arrest and vasomotor collapse
  • pupils are widely dilated and muscles are relaxed
36
Q

The BIS monitor:

A
  • Analysis of EEG under anesthesia
  • gives an indication of how deep anesthesia the patient is
  • may reduce the incidence of intraoperative awareness in high risk patients
  • 0= EEG silence
  • 100=expected fully awake patient
  • 40-60= level for general anesthesia
37
Q

Brain physiology: weight, and cardiac output?

A
  1. Weights= 1350 grams
    - 2% total body weight
    - 80% water= > 1000 ml
  2. Receives 12-15% of cardiac output
    - At rest, consumes oxygen at average rate of 3.5 ml oxygen per 100 G of brain tissue per minute (50 ml/min)
    - 20% of total body oxygen utilization
    - utilizes 25% of total body glucose
38
Q

Brain Energy Utilization

A
  1. Approx. 60% of brain’s energy consumption is used to support electrophysiologic function
  2. Maintenance of transmembrane ionic gradients: Na+/K+ ATPase pumps
  3. Synthesis, storage, release and repute of NTM
  4. Remainder of energy is used to maintain cellular homeostasis
39
Q

What does the brain absolutely require for sustained function?

A
  1. Brain absolutely requires oxygen and glucose for sustained function
  2. Glucose regenerates ATP by oxidative metabolism
  3. Brain has insignificant glycogen storage-
    - in complete absence of glucose, glycolysis could only be maintained by 5 minutes
    - anaerobic glycolysis provides very little ATP
40
Q

Delivery of Oxygen and Glucose to brain

A
  • brain’s high demand for oxygen and glucose must be met by adequate blood flow
  • space constraints imposed by noncompliant cranium and meninges require that blood flow cannot be excessive
41
Q

CBF is almost completely supplied by what?

A

-Internal carotid and vertebral arteries

42
Q

What do the vertebral arteries form?

A

-single basilar artery, which along the internal carotids, provides input to the circle of willis

43
Q

In the event a major vessel becomes occluded, which structure permits collateral blood flow in the brain?

A

-Circle of Willis

44
Q

Veins draining from the brain?

A
  • thing and valveless
  • eventually converge to enter thick-walled non-elastic dural sinuses
  • contains most of the cerebral blood volume- passive recipient of regulated arterial inflow
45
Q

Sympathetic nervous supply to cerebral vessels:

A
  1. Originating in the locus coeruleus, superior cervical ganglia, and intermediolateral spinal cord.
46
Q

Parasympathetic nervous supply to cerebral vessels:

A
  1. Originating in sphenopalatine and otic ganglia
47
Q

Cerebral Metabolic Rate (CMRO2) remains stable between:

A
  • 3.0 and 3.8 ml per 100 grams per minute

- Maintained while asleep or while engaged in intense mental activity

48
Q

At normocarbia, global CBF is stable at:

A

-45 to 65 ml per 100 grams per minute

49
Q

CBF and CMRO2 Coupling

A
  • blood flow is increased to areas of increased CMRO2 and vice versa
  • mechanisms that mediate flow-metabolism coupling are not completely known
  • mediated by local by products: K+, lactate, adenosine, glutamate results in synthesis of N2O
  • nerve innervation
  • vascular factors
50
Q

Factors influencing CMRO2:

A
  1. Functional state: CMRO2 decreased by sleep and coma

2. CMRO2 is increased by sensory stimulation, mental tasks, epileptic activity

51
Q

Hypothermia influences CMRO2:

A
  1. CMRO2 decreases by 6-7% for each 1 degree C reduction in temperature
  2. Can cause complete suppression of EEG at about 10-20 degrees C
  3. Hypothermia decreases rate of energy utilization associated with both electrophysiological function and the maintenance of cellular integrity
52
Q

Hyperthermia influences CMRO2:

A
  • Between 37-43 degrees, C, CBF, CMR increase
  • Above 42 degrees, a dramatic reduction in CMRO2 occurs
  • indicates threshold for the toxic effect of hyperthermia that may occur as a result of protein degradation
53
Q

Anesthetics affect CMRO2:

A
  • decrease CMRO2

- ketamine and N2O are exceptions

54
Q

3 primary factors controlling CBF in the normal brain?

A
  1. Carbon Dioxide- central
  2. Oxygen- peripheral
  3. Cerebral perfusion pressure (CPP)
55
Q

PaCO2

A
  • most potent physiologic determinant of CBF is carbon dioxide
  • CBF varies directly with PaCO2: the H+ concentration in the ECF of the vascular smooth muscle mediates the response
  • CBF changes 1 to 2 ml/100g/min for each 1 mmHg change in PaCO2 around normal PaCO2
56
Q

CBF is directly proportionate to PaCO2 between tensions:

A

-20 and 80 mm Hg

57
Q

Doubling the normal PaCo2 to 89 mmHg will:

A

-double the CBF

58
Q

Above 80 mmHg there is a plateau which reflects maximum _____________

A
  • vasodilation
59
Q

At PaCO2 greater than 80 mmHg, what happens to CMRO2?

A
  • a reduction in CMRO2 occurs reflecting the anesthetic effect of extreme hypercarbia
60
Q

When reducing the normal PaCO2 to one-half (20 mmHg) what happens to the CBF?

A
  • it will half the CBF

- decreasing it below 20 mmHg, has no effect due to maximal vasoconstriction

61
Q

The brain can compensate and tolerate a 50% decrease in CBF without ischemic changes, however, the extreme alkalosis can produces what?

A
  • extreme alkalosis produces a leftward shift of the oxyhemoglobin dissociation curve which may induce brain ischemia
62
Q

How long does it take for CBF to normalize?

A

6-8 hours

  • CSF pH gradually returns to normal due to retention of bicarb
  • acute normalization of PaCO2 can lead to CSF acidosis or alkalosis
63
Q

Below a PaO2 of 60, CBF:

A
  • CBF increases rapidly
  • vasodilation is secondary to acidic metabolic products like lactic acid
  • “oxygen sensor” for the brain in the rostral ventrolateral medulla- stimulation of the RVM results in an increase in CBF and not in CMRO2
64
Q

Autoregulation: in normal individuals CBF is constant at

A
  • a CPP of 50 mmHg to 150 mmHg

- CPP= MAP- ICP or CVP

65
Q

Autoregulation is due to myogenic mechanisms in smooth muscle:

A
  • increased pressure produces increased stretch on the muscle and it responds with contraction (and vice versa)
66
Q

Intracranial Pressure volumes:

A
  1. Brain= 80%
  2. Blood= 12%
  3. CSF= 8%
    - Skull is rigid, increase anything increase in ICP*
67
Q

A CPP above 150 mmHg results in:

A
  • hypertensive encephalopathy due to BBB disruption, edema, and ischemia
68
Q

A CPP below 50 mmHg results in:

A
  • maximal vasodilation and CBF becomes pressure dependent
69
Q

Cerebral Steal:

A
  • stealing of blood from 1 area of the brain to another
  • in ischemic brain regions, blood vessels are maximally dilated
  • if vasodilation occurs due to hypercapnia or other vasodilators, the normal adjacent brain regions get vasodilator and receive increased flow
  • stealing flow from the ischemic area that needs it
70
Q

Inverse Cerebral Steal:

A

-vasoconstriction caused by hypocapnia or an anesthetic agent such as Na+- thiopental causes an increase in blood flow to ischemic regions

71
Q

Benzodiazepines effect on CBF

A
  • all cause a reduction in CBF due to a decrease in CVR and CMRO2
  • reduction in CBF and CMRO2 is less than that observed with other IV anesthetics

-Flumazenil reverses these effects and may increase CBF and CMRO2 above pre-midas and should be used with caution in patients with impaired intracranial compliance

72
Q

Barbiturates effect on CBF

A
  • barbs decrease both CBF and CMRO2
  • incremental doses of pentathol may decrease CBF and CMRO2 by 55-60%
  • has a direct vasoconstrictive effect
  • appears to be due to influx of calcium into vascular smooth muscles
  • causes a decrease in CBF and ICP
73
Q

Propofol effects on CBF

A
  • resemble effects of barbiturates
  • decreases CBF and CMRO2, and may also decrease ICP particularly when combined with hyperventilation
  • no direct cerebral vascular effects
  • may cause hypotension which can cause decreased CPP
74
Q

Etomidate effects on CBF

A
  • resembles thiopental in its effects on CBF and CMRO2
  • causes minimal hemodynamic suppression, even in high doses
  • high incidence of myoclonus- may be misinterpreted as a seizure
  • adrenal cortical suppression: intracranial mass patients are usually on high dose steroids
75
Q

Ketamine effects on CBF:

A
  • causes a significant increase in CBF and ICP but has lesser effects on CMRO2
  • should be avoided in patients at risk of high ICP
76
Q

N2O effects on CBF:

A
  • has little effect on CMRO2
  • when used alone with oxygen N2O s a potent vasodilator and may increase ICP
  • when combined with barbs, narcotics, volatile agents or hypocarbia it has little or no effect on CBF and ICP
77
Q

Volatile Anesthetics

A
  • all cause a dose related increase in CBF and a decrease in CMRO2
78
Q

Halothane

A
  • potent cerebral vasodilator and can cause increased ICP
  • hyperventilation to a PaCO2 of 25 mmHg will abolish this effect
  • potential for halothane induced cerebral toxicity with end expiration concentrations exceeding 2.3%
79
Q

Enflurane

A
  • is a less potent cerebral vasodilator than halothane but is a more potent suppressor of CMRO2
  • when administered at concentrations greater than 1.5 MAC it has a capacity to induce seizures (especially when combined with hypocapnia)
80
Q

Isoflurane

A
  • when compared to halothane & enflurane, it has the least potent cerebral vasodilator and the MOST potent depressant of CMRO2
  • does not increase CBF at doses less than 1-1.5 MAC
81
Q

Desflurane

A
  • does not adversely affect ICP
  • dose dependent increase in CBF and decrease in CMRO2 at least up to 2 MAC
  • rapid onset and emergence
82
Q

Sevoflurane

A

-like iso it causes little or no increase in ICP at concentrations up to 1.5 MAC
-cerebral autoregulation has been found to be intact at concentrations below 1 Mac
-

Anesthesia Pharm Exam 1 (4 decks)

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