Week 1 - Neurophysiology for Anesthesia Flashcards

1
Q

What is the purpose of Anesthesia?

A

To reduce anxiety – Anxiolysis
To relieve pain – Analgesia
To provide a stable surgical field – Paralysis
To produce Hypnosis (don’t want awareness)
Autonomic supression
Somatic suppression

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2
Q

Physiologic Patterns of Sleep and Wake

A

Wakefulness: norepinephrine, histamine, serotonin, dopamine, orexin
Non REM Sleep: firing decreases
REM Sleep: firing virtually quiescent

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3
Q

Anesthesia Affect on Sleep

A

Anesthetic effect on the thalamus resemble the naturally occurring thalamocortical inhibition characteristic of NREM sleep

Somnogens reduce amount of GA needed
Adenosinergic Antagonists increase amount of GA needed

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4
Q

Sites in the brain where anesthesia affects sleep

A

Thalamic Sites: during NREM sleep and anesthesia, the cortex is deprived of input (Thalamic Gates)

Hypothalamic Sites: histaminergic and orexenergic neurons in the hypothalamus stimulate the thalamus

Brainstem Sites: Locus Ceruleus, Mesopontine Tegentum, and VLPO stabilization

Limbic System: Hippocampus, medial septum, amygdala

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5
Q

Chemicals that Act at Synapses as Neurotransmitters (Table 3-2)

A

Glutamate — Oxytocin — Acetylcholine — Cholecystokinin — Norepinephrine — Gastrin — Glycine — GABA — Endorphins — Dopamine — Serotonin — Epinephrine — Histamine — Substance P — Vasopressin — Prolactin — Glucagon — Vasoactive intestinal Peptide

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6
Q

Inotropic Receptors vs Metabotropic Receptors

A

Ionotropic: ligand-gated ion channels that pass + or - ions and excite or inhibit

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

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7
Q

Glutamate?

A

Excitatory in the brain and spinal cord

KA, AMPA, NMDA ionotropic receptors
NDMA blocked by Mg at normal extracellular levels
Open NMDA allow Ca into the cell

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8
Q

GABA

A

Inhibitory primarily in the brain

GABAa - ionotropic (Chloride/Bicarb)
GABAb - metabotropic open K+ channels

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9
Q

Glycine

A

Inhibitory primarily in the spinal cord

Requires 3 glycine to activate Chloride channels
It is a co-agonist at the NMDA receptor

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10
Q

What type of receptors are the Acetylcholine Receptors in the CNS?

A

Nicotinic are ionotropic
Muscarinic are G protein coupled

ACh regulated wakefulness, attention, learning, and motivation

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11
Q

What is critical in memory formation and storage?

A

Alteration in the strength of neuronal connections

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12
Q

Phases of memory

A

Short-Term Memory - seconds to hours

Long-Term Memory - hours to months

Long-Lasting (months to lifetime)

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13
Q

What phase of memory do Benzodiazepines and IV Anesthetics affect?

A

Primarily long term memory storage or retrieval

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14
Q

At what MAC do volatile agents impair memory formation?

A

25% to 50%

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15
Q

What is Long Term Plasticity and what inhibits it?

A

A form of synaptic plasticity important in memory formation

Inhibited by barbiturates, benzodiazepines, propofol, and Isoflurane

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16
Q

What is a BIS monitor and its limitations?

A

Algorithmic EEG analysis – range 0-100

General Anesthesia = 40-60

Gives an indication of how “deep” under anesthesia the pt is

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17
Q

Limitations of a BIS monitor

A

Ketamine and N2O increase BIS (False high)
Neuromuscular blockers decrease BIS in awake pts (False low)
Multiple BIS sensors on same pt give different values
Low BIS values may result in a reduction in delivered anesthesia concentration and resulting awareness

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18
Q

Types of Procedures with Incidence of Awareness

A

Highest in OB
General Surgery with ETT (1%)
Cardiac Surgery (pure narcotic)
Trauma (shock and severe injury does not equal unconsciousness)

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19
Q

Reasons for Intraoperative Awareness

A
Equipment Failure
Inadequate Anesthesia
Patient Factors (age, health status, alcohol/drug use, obesity, pharmacokinetic/pharmacodynamic)
Inability to assess depth of anesthesia
Inappropriate anesthesia technique
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20
Q

Likely times for recall in anesthesia

A

Preinduction (light induction for various reasons)

After Intubation (paralyzed but not anesthetized)

Intraoperative (light anesthesia w/ paralysis, wakeup test well tolerated)

Postoperative (residual paralysis during emergence)

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21
Q

What are Guedels Signs and Stages?

A

Stage I Analgesia or Disorientation

Stage II Excitement or Delirium

Stage III Surgical Anesthesia

Stage IV Overdose

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22
Q

Guedels Signs and Stages - Stage I

A

Analgesia or Disorientation

From beginning of induction of anesthesia to loss of consciousness

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23
Q

Guedels Signs and Stages - Stage II

A

Excitement or Delirium

From loss of consciousness to onset of automatic breathing

Eyelash reflex disappears but other reflexes remain intact, pupils dilated but reactive, tearing, coughing, vomiting and strugglilng may occur; respiration can be irregular with breath-holding

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24
Q

Guedels Signs and Stages - Stage III

A

Surgical Anesthesia

Begins with onset of regular respiratory pattern and ends with loss of respiration

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25
Q

Guedels Signs and Stages - Stage III Phane I

A

Onset of automatic respiration to cessation of eyeball movements

Eyelid reflex is lost, swallowing reflex disappears, marked eyeball movement may occur but conjunctival reflex is lost at the bottom at the bottom of the plane

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26
Q

Guedels Signs and Stages - Stage III Phane II

A

Cessation of eyeball movements to beginning of paralysis of intercostal muscles

Laryngeal reflex is lost although inflammation of the upper resp tract increases reflex irritability, corneal reflex disappears, secretion of tears increases, respiration is automatic and regular, movement and deep breathing as a response to skin simulation disappears

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27
Q

Guedels Signs and Stages - Stage III Phane III

A

From beginning to completion of intercostal muscle paralysis

Diaphragmatic respiration persists but there is progressive intercostal paralysis, pupils dilated and light reflex is abolished. Laryngeal reflex lost in plane II can still be initiated by painful stimuli arising from the dilatation of anus or cervix.

Desired plane for surgery when muscle relaxants were not used

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28
Q

Guedels Signs and Stages - Stage III Plane IV

A

From complete intercostal paralysis to diaphragmatic paralysis (apnea)

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29
Q

Guedels Signs and Stages - 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

30
Q

Pros and Cons of Guedels Signs and Stages

A

Good indicators of narcosis
Provide greater knowledge about the level of anesthesia (MAC provides boundaries)
Are important to know physiologic loss of reflexes related to level of anesthesia
Do NOT work well when using opioids and muscle relaxants

31
Q

What rate does a resting brain consume oxygen?

A

3.5 mL oxygen per 100g of brain tissue per minute (50mL/min)

Receives 12-15% of cardiac output

32
Q

What function is the brain’s energy utilized for?

A

Approx 60% of brain’s energy consumption is used to support electrophysiologic function (Maintenance of transmembrane ionic gradients (Na/K pump)
Synthesis, storage, release and reuptake of neurotransmitters)

Remainder of energy is used to maintain cellular homeostasis

33
Q

Energy Requirements of the Brain

A

Requires oxygen and glucose for sustained function

Glucose regenerates ATP by oxidative metabolism

Has insignificant glycogen storage - dependent on constant supply (maintained by adequate blood flow)

34
Q

What arteries supplies cerebral blood flow

A

Internal carotid and vertebral arteries

35
Q

What do the vertebral arteries form?

A

The single basilar artery

36
Q

What arteries form the circle of Willis?

A
Internal carotid arteries
Anterior Cerebral
Anterior Communicating
Posterior Communicating
Posterior Cerebral
Basilar
37
Q

What contains most of the cerebral blood volume?

A

Dural Sinuses

Passive recipient of “regulated” arterial inflow

38
Q

What is the normal cerebral metabolic rate (CMRO2)?

A

Remains stable between 3.0 and 3.8 mL /100g/min

39
Q

What is the global CBF at normocarbia?

A

45 to 65 mL /100g/min

40
Q

What is CBF-CMRO2 Coupling?

A

Blood flow is increased to areas of increased CMRO2 and vice versa

(normal brain will self regulate delivery of blood to areas that need it)

41
Q

When is CMRO2 decreased?

A

During sleep and coma

42
Q

When is CMRO2 increased?

A

Sensory stimulation
Mental tasks
Epileptic activity

43
Q

How does Hypothermia affect CMRO2?

A

It decreases by 6% to 7% for each 1 degree C reduction in temperature

Can cause complete suppression of EEG at 18 to 20 degrees C

Decreases rate of energy utilization associated with both electrophysiological function and maintenance of cellular integrity

44
Q

How does Hyperthermia affect CMRO2?

A

Between 37C and 42C both CBF and CMRO increase

Above 42*C a dramatic reduction in CMRO occurs (indicated threshold for the toxic effect of hyperthermia that may occur as a result of protein degradation

45
Q

What happens to EEG waves as body temperature decreases?

A

EEG waves flatten

46
Q

How to anesthetics affect CMRO2?

A

In general anesthetics decrease it with the exceptions of Ketamine and Nitrous Oxide

Increasing plasma concentrations of anesthetics beyond the level of initial EEG suppression does not further decrease CMRO

47
Q

What are the primary factors controlling CBF in the normal brain?

A

Carbon Dioxide (central)

Oxygen (peripheral)

Cerebral Perfusion Pressure

48
Q

How does PaCO2 affect CBF?

A

PaCO2 is the most potent physiologic determinant of CBF

CBF varies directly with PaCO (directly proportionate between 20 and 80) (Double CO2 - CBF doubles vice versa)

CBF changes 1 to 2 mL/100g/min for each 1 mmHg change in PaCO around normal PaCO

Above 80 = maximum vasodilation
Below 20 = maximal vasoconstriction

49
Q

What happens to CMRO2 when there is a PaCO greater than 80?

A

a reduction in CMRO occurs reflecting the anesthetic effect of extreme hypercarbia (why pts become unresponsive)

50
Q

How long to changes in CBF last?

A

CBF returns to normal over a period of 6 to 8 hours

51
Q

How does PaO2 below 60 affect CBF?

A

Below a PaO2 of 60, CBF increases rapidly

“Oxygen Sensor” - located in the rostral ventrolateral medulla (stimulation results in an increase in CBF and not in CMRO)

Increased PaO has little effect on CBF

52
Q

What range of cerebral perfusion pressure is CBF constant (Autoregulation)?

A

50 mmHg to 150 mmHg

CPP = MAP - ICP or CVP (whichever is greater)

53
Q

What happens when CPP is above 150 mmHg?

A

it results in hypertensive encephalopathy due to BBB disruption, edema, and ischemia

54
Q

What happens when CPP is below 50 mmHg?

A

it results in maximal vasodilation and CBF becomes pressure dependent

55
Q

What direction does hypertension shift the curve?

A

To the Right

Limits the safe level for reduction CPP
Following successful treatment of HTN, curve returns to control levels

56
Q

What is Cerebral Steal?

A

Stealing of blood from one area of the brain to another

In ischemic brain regions, blood vessels are maximally dilated - if vasodilation occurs due to hypercapnia or other reasons, the normal adjacent brain regions get vasodilated and receive an increased flow - Stealing flow from the ischemic area that needs it

57
Q

What is Inverse Cerebral Steal?

A

Robin Hood effect

Vasoconstriction caused by hypocapnia or an anesthetic agent such as Sodium-Thiopental causes an increase in blood flow to ischemic regions

58
Q

How do benzodiazepines affect CBF and CMRO2?

A

All cause a reduction in CBF due to a decrease in CVR and CMRO2
Induction dose of midazolam (0.15mg/kg) causes 40% decrease in CBF
Fall in CBF not associated with any cerebral ischemia

Flumazenil reverses these effects and may increase CBF and CMRO2

59
Q

How do barbiturates affect CBF and CMRO2?

A

Decrease in both CBF and CMRO

Incremental doses of pentathol may decrease CBF and CMRO by 55-60%

Has a direct vasoconstrictive effect (appears to be due to influx of calcium into VSM)

60
Q

How does Propofol affect CBF and CMRO2?

A

Decreases both CBF and CMRO

May also decrease ICP particularly when combined with hyperventilation

No direct cerebral vascular effects (affects the vessels that supply the brain instead)

May cause hypotension which can cause decreased CPP

61
Q

How does Etomidate affect CBF and CMRO2?

A

Decreases both CBF and CMRO

Causes minimal hemodynamic suppression, even in high doses

High incidence of myclonus
Causes adrenal cortical suppression

62
Q

How does Ketamine affect CBF and CMRO2?

A

Causes significant increase in CBF and ICP but has lesser effects of CMRO

Should be avoided in pts at risk of high ICP

63
Q

How does Nitrous Oxide affect CBF and CMRO2?

A

Has little effect on CMRO
When used alone with oxygen it is a potent vasodilator and may increase ICP
When combined with barbiturates, narcotics, volatile agents, or hypocarbia it has little or no effect on CBF and ICP

64
Q

How do volatile anesthetics affect CBF and CMRO2?

A

All cause a dose related increase in CBF and a decrease in CMRO

65
Q

How do volatile anesthetics affect cerebral autoregulation?

A

Dose-dependent depression of cerebral autoregulation

As does gets higher autoregulation decreases eventually going away

66
Q

How does Halothane affect ICP?

A

It is a potent cerebral vasodilator and can cause increased ICP (hyperventilation to CO2 of 25 will abolish this effect)

potential for halothane induced cerebral toxicity with end expiration concentrations exceeding 2.3%

67
Q

How does Enflurane affect CMRO?

A

it is less potent cerebral vasodilator than halothane but is more potent suppressor of CMRO

when administered at concentrations greater than 1.5 MAC it has a capacity to induce seizures (especially when combined with hypocapnia)

68
Q

How does Isoflurane affect CBF and CMRO2?

A

Least potent cerebral vasodilator and the Most potent depressant of CMRO (when compared to halothane/enflurane)

Does not increase CBF at doses less than 1 to 1.5 MAC

69
Q

How does Desflurane affect CBF and CMRO2?

A

In clinically used concentrations in humans it does not adversely affect ICP

Dose dependent increase in CBF and decrease in CMRO at least up to 2 MAC (same as isoflurane)

Has advantage of rapid onset and emergence

70
Q

How does Sevoflurane affect CBF and CMRO2?

A

It causes little to no increase in ICP at concentrations up to 1.5 MAC

Cerebral autoregulation has been found to be intact at concentrations below 1 MAC

There is no evidence of acute tolerance or cerebral toxicity after prolonged exposure to higher concentrations

71
Q

What kind of amnesia do benzodiazepines produce?

A

Anterograde Amnesia