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550 Pharm > Intro to Anesthetics > Flashcards

Intro to Anesthetics Flashcards

1
Q

Local anesthesia

A

provides numbness to a small area limited to where LA is injected

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2
Q

Regional anesthesia

A

epidural, spinal, peripheral nerve blocks; provides numbness to much larger areas then LA

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3
Q

Monitored anesthesia care

A

uses sedatives and other agents
doses low enough that patients remain responsive and breathe w/o assistance
Utilized during simple procedures and minor surgery

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4
Q

General anesthesia

A

deep state of sleep where the patient loses consciousness and sensation and usually requires assisted ventilation

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5
Q

Combined techniques

A

MAC & local/regional;
regional and general
etc

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6
Q

Anxiolysis

A

Minimal sedation
patients respond normally to verbal commands.
Cognitive fx and coordination may be impaired, ventilatory and cardiovascular functions are unaffected

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7
Q

Conscious sedation/ Moderate sedation/analgesia

A

Patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation.
No interventions are required to maintain a patent airway and spontaneous ventilation is adequate
Cardiovascular fx is usually maintained

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8
Q

Deep sedation/ analgesia

A

not easily aroused, respond purposefully following repeated/ painful stimulation. The ability to independently maintain ventilatory fx and patent airway may be impaired
Cardio fx usually maintained

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9
Q

General anesthesia

A

Not arousable, even w/ painful stimulation
Ability to independently maintain ventilatory fx impaired. Requires assistance in maintaining patient airway; pos pressure ventilation may be required
Cardio fx may be impaired

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10
Q

What is General anesthesia? What are some qualities of it?

A 
Generalized, reversible CNS depression
no sensory perception
loss of consciousness
no recall of events
immobility
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11
Q

What are some other potential effects of GA and adjuncts?

A

muscle relaxation
suppression of autonomic reflexes
analgesia
anxiolysis

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12
Q

What are the 7 types of medication used in GA w/ an ETT Template?

A
  1. Pre-op medications/sedation
  2. Induction drug: IV or inhalation
  3. NMB
  4. Inhalational drug: may be IV
  5. Opiods/LAs, etc
  6. Antiemetic
  7. NMB reversal
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13
Q

Why are pre-op sedation and other meds given before GA w/ an ETT template?

A

patient comfort
reduce anxiety
prevent aspiration
Abx per surgeon request

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14
Q

Why is NMB given w/ GA?

A

to facilitate intubation

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15
Q

Why are opiods and LAs given w/ GA?

A

to minimize physiological effects of pain and to promote comfort at emergence

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16
Q

What are the 5 pharmacologic effects of Benzodiazepines?

A
  1. Anxiolysis
  2. Sedation
  3. Anterograde amnesia
  4. Anticonvulsant actions
  5. Muscle relaxation (spinal level)
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17
Q

what is the prototype benzo?

A

Diazepam

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18
Q

How do benzos fundamentally work?

A

Potentiates binding of GABA to GABA A receptor

Increases GABA potency x3

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19
Q

Benzos increase _________ influx, cause _________ of the membrane potential and ________ neuronal excitability.

A

Cl-
hyperpolarization
decrease

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20
Q

What are 5 ways that benzos are used in anesthesia? Which ones are rare?

A 
pre-medication
IV sedation
GA induction (rare)
GA maintenance (rare)
post-op anxiolysis (rare)
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21
Q

Benzos cause a __________________ in ventilation. They can cause enhanced _________ & ________ in the presence of opiods.

A

dose dependent decrease

hypoxemia & hypoventilation

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22
Q

If used at induction dosage, benzos can cause what?

A

decrease in SVR

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23
Q

W/ benzos, __________ decreases, especially in the presence of hypovolemia.

A

BP

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24
Q

Can you use benzos in pregnant patient?

A

no; they cause anomalies in fetus

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25
Q

Opioids provide ____________ & _______________ analgesia by activation of the ______________ pain suppression system

A

supraspinal
spinal
endogenous

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26
Q

Opioids act by activating pain-modulating systems by acting as _____________ at _______________ receptors

A

agonists

stereospecific opioid receptors

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27
Q

Do opioids act at pre or post synaptic sites?

A

both

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28
Q

What tissues/organs do opioids act at?

A

brainstem
spinal cord
peripheral tissues

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29
Q

What occurs when opioids bind to a receptor?

A

decreased neurotransmission

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30
Q

Opioids cause increased _______ conductance and ______ of the membrane. The __________ channes are inactivated and there is an immediate __________ in neurotransmitter release.

A

K
hyperpolarization
Ca
decrease

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31
Q

What are some common uses of opioids in anesthesia? What is the prototype?

A 
pre-medication
intra-op pain management ( IV, epidural, spinal)
GA (high doses)
post-op pain management
prototype: Morphine
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32
Q

What are some adverse effects and precautions for use of opioids?

A

Bradycardia (direct effect)
respiratory depression ( decreased RR, increased TV)
Miosis
Urinary retention
Physical dependence
Sedation (in higher doses, synergistic w/ other drugs)
Don’t give together w/ benzos unless already in the OR=will cause person to stop breathing

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33
Q

What neurotransmitter do barbituates affect?

A

GABA

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34
Q

What are 3 ways barbituates affect GABA?

A
  1. decrease the rate at which GABA dissociates from its receptor: increases the duration of GABA activated Cl- channel opening (enhances GABA activity)
  2. Mimics GABA at the receptor (direct activation of Cl- channels)
  3. Produces functional inhibition of the post-synaptic neuron
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35
Q

What part of the brain do barbituates depress? What is the prototype?

A

RAS (reticular activating system)

Thiopental

36
Q

What are some uses of barbituates?

A

sedation and hypnosis
cerebral protection
anti-seizure (more effective then benzos)
Anesthetic uses: induction of GA in patients w/ increased ICP and/or focal brain ischemia

37
Q

Barbituates cause a ___________ effect.

A

hang over

38
Q

Barbs cause depression of the ______________ in the brain which leads to decreased _______ outflow, peripheral __________ and decreased ___________

A

medullary vasomotor center
SNS
vasodilation
preload

39
Q

If using barbs and SBP drops, will the HR increase to compensate? Do barbs cause ventilatory depression?

A

yes

yes

40
Q

When will you see significant decreases in BP and myocardial depression w/ barbs?

A

if SNS not intact OR
hypovolemia OR
large doses given to reduce ICP

41
Q

What can happen if you inject a barbituate intraarterially?

A

gangrene/ nerve damage

42
Q

What causes more preload reduction, barbs or propofol?

A

propofol

43
Q

What can chronic use of barbs cause? What does this mean to you as a CRNA?

A

hepatic enzyme induction:

patient will eat up the meds you give them, you will have to increase your dosing and/or frequency

44
Q

Barbs cause the increase in metabolism of what meds?

A 
oral anticoagulants
phenytoin
TCAs
corticosteroids
Vit K
45
Q

What are some other adverse effects and precautions of barbs?

A
  • accelerated production of heme by stimulation of the enzyme: D-aminolevulinic acid sythetase: avoid in pts w/ porphyria
  • allergy is rare but deadly (1:30,000)
  • readily crosses placenta
46
Q

How is propofol classified? What is it supplied as?

A

nonbarbituate IV anesthetic

supplied as: 1% solution in egg, soy, glycerol base

47
Q

What type of preservatives can be in propofol?

A

Sodium metabisulfite vs. EDTA (etylenediamine tetraacetic acid)

48
Q

How does propofol affect GABA? What receptor does it affect? What subunit?

A

potentiates binding of GABA to GABA “A” receptor
B1 subunit
It also decreases the rate of dissociation of GABA from the receptor

49
Q

Propofol increases ___________ influx, causes _________ of the membrane and __________ neuronal activity.

A

Cl-
hyperpolarizatoin
decreased

50
Q

What are some pharmacological effects of propofol?

A 
dose dependent sedation & hypnosis
antiemetic
antipuritic
anticonvulsant
attentuation of bronchoconstriction (usually related to patient not being deep enough)
51
Q

What are some anesthetic uses of propofol?

A 
IV sedation
induction of GA
maintenance of GA  (TIVA)
part of balanced tecnique for maintenance of anesthesia
antiemetic (small doses)
52
Q

Propofol causes dose dependent _______________, __________________, & ___________

A

ventilatory depression
myocardial depression
vasodilation

53
Q

propofol causes myocardial depression by decreasing what 3 things? How does HR respond?

A

SV, CO, SVR
HR remains unchanged (cant compensate)
possibility for bradycardia related death

54
Q

What are some other adverse effects of propofol?

A

myoclonus
pain on injection
lipidemia w/ LT infusion
infection and bronchospasm

55
Q

What happens on the pre-synaptic side of the NMJ?

A
  1. AP = depolarization of nerve terminal
  2. Ca channels open
  3. Ca diffuses down gradient to nerve terminal
  4. Ach spills out into synaptic cleft
56
Q

What happens at the post-synaptic side of the NMJ?

A
  1. ACh binds at nicotinic receptors
  2. After both receptor spots bond to, channels open and Na & Ca diffuse into cell and K diffuses out
  3. motor end plate depolarizes
  4. AP is created
  5. Skeletal muscle contracts
57
Q

Describe the ACh receptor

A
  • 5 protein subunits
  • Central core for cation channeling
  • ACh must bind to both “a” subunits in order for the core to open
  • “A” subunits are the site of agonism and antagonism
58
Q

What kind of drug is Succinylcholine?

A

depolarizing NMB

59
Q

What is the mechanism of action of succs?

A
  • binds to nicotinic receptors: channels open and motor end plate depolarizes
  • single contraction occurs
  • not metabolized by true acetylcholinesterases
  • channels stay open until succs diffuses back into circulation
60
Q

What can not occur when succs is bound to the receptor?

A

further APs cannot be initiated

61
Q

What is the pharmacologic effect/anesthetic use of succs?

A

NMB

  • optimize intubating conditions
  • rapid sequence
  • treatment of life-threatening laryngospasm
62
Q

What are some adverse effects and precautions w/ succs?

A
  • cardiac dysrhythmias (esp. w/ kids; mix w/ atropine)
  • Hyperkalemia
  • muscle pains, fasciculations
  • increased ICP, IOP
  • potent MH triggering agent
  • avoid in pts. w/ atypical acetylcholinesterase (won’t wake up for a few days bc they can’t metabolize the drug)
63
Q

When is there an increased risk of hyperkalemia in succs?

A 
burns
trauma
nerve damage
neuromuscular disease
RF
64
Q

What type of drug is Vecuronium?

A

non-depolarizing muscle relaxant

monquaternary aminosteroid

65
Q

How does vec work?

A

it is a competitive antagonist at pre & post NMJ nACH receptors

66
Q

Vecuronium occupies __________ subunits of ________ receptors without a inducing a __________ change.
With Vec at the receptor, ____ can not be initiated

A

alpha
ACh
conformational
APs

67
Q

What is vec used form?

A

muscle relaxation/ paralysis:

  • facilitated ET intubation
  • optimize surgical conditions
68
Q

When can vec have a prolonged or unpredictable effect?

A

liver & kidney disease
neuromusc disease
hypothermia, e- imbalances
use of abx: aminoglycosides (metabolized similarly)

69
Q

When is there risk for resistance of vec?

A

burn patients

70
Q

What must you be on the look out for in all patients who are on muscle relaxants/paralytics? Why?

A
  • residual NMB in all patients

- In theory, at higher risk for recall if inadequate GA given

71
Q

What kind of drug is Isoflurane?

A

inhalational anesthetic; halogenated methyl ethyl ether

72
Q

How does Isoflurane work?

A

Very different from IV drugs: don’t need to know specifics for this lecture!

73
Q

What determines onset, duration of action, etc. of inhalational agents? How are they eliminated?

A
  • lipid solubility

- almost entirely by lungs

74
Q

What are some pharmacological effects and anesthetic uses of isoflurane?

A

bronchodilator
GA: sedation, hypnosis, partial muscle relaxation
-induction (usually sevo only)
-maintenance

75
Q

How does isoflurane affect respiratory, cardio, and airway?

A

Respiratory: depression–> higher rates, lower volumes (opposite of opioids)
Cardio: depression–> decreased CO & BP, vasodilation (direct CV depressants)
Airway reflexes are abolished

76
Q

What are some s/s of MH?

A

Ca channel interference
muscle rigidity
increased temp
increased CO2

77
Q

What else can inhaled agents cause?

A

OR pollution

78
Q

What are the 2 different types of MAC?

A
  1. Monitored anesthesia care
  2. Mean Alveolar Concentration: describes potency
    - of a voltatile anesthetic: how much is needed to make 50% of patients not respond to a noxious stimulus
    - how much gas to admin
79
Q

What is the MAC of isoflurane? How much would they get if they were also on 100% O2?

A

1.2%

they would get 98.8% O2 and 1.2% iso

80
Q

What is the only inhaled agent that will not provide 100% anesthesia by itself? What is its MAC?

A

N2O

104%

81
Q

What is the mech of action of Local anesthetics? What is the prototype?

A

-block impulse conduction during depolarization phase of AP
-inhibits influx of Na (Na channel blockade)
-Blockade ONLY occurs when Na channels are in the inactivated closed state
Lidocaine

82
Q

What is the pharmacologic effect of LAs?

A

block AFFERENT nerve transmission to produce analgeis and anesthesia w/o loss of consciousness
-autonomic, somatic sensory, somatic motor blockade

83
Q

What is the class of lidocaine?

A

Amide: local anesthetic

84
Q

What is the typical structure of an LA?

A

They are either amides or esters:
lipophilic molecule w/ lipophilic head (aromatic ring), intermediate chain withe either amide (NH) or ester (COO-) and hydrophilic tail (tertiary amine)

85
Q

What are some s/s of LA toxicity in the CNS?

A 
circumoral/tongue numbness
tinnitus
vision changes
dizziness
slurred speech
restlessness
seizure followed by CNS depression, apnea, hypotension
86
Q

What are some s/s of LA toxiticy in cardio system?

A

MORE RESISTANT TO TOXIC EFFECTS THAN CNS?
hypotension, myocardial depression, reduced SVR & CO
Bupivicaine: arrythmias, AV heart block, hypotension, and arrest
Cocaine: massive SNS outflow, coronary vasospasm, MI, dysrhythmias including V-fib

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