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Spring '14 Pharmacology > Intro. to Anesthetic Drugs > Flashcards

Intro. to Anesthetic Drugs Flashcards

1
Q

Which type of anesthesia provides numbness to a small area, limited to where a local anesthetic is injected?

A

Local anesthesia

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2
Q

Which type of anesthesia includes spinals, epidurals, and peripheral nerve blocks that provide numbness to a large area?

A

Regional anesthesia

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3
Q

For which type of anesthesia does an anesthesia provider not need to be present for?

A

Local

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4
Q

What is meant by monitored care anesthesia (MAC)?

A

This is a billing term. It refers to the administration of IV sedation that needs to be monitored. Pt’s remain responsive and breathing with minimal assistance.

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5
Q

Which type of anesthesia puts the patient in a deep sleep where they typically lose consciousness and usually requires assisted ventilaton? The patient does not move in this state.

A

General anesthesia

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6
Q

Is propofol considered a general anesthetic?

A

Yes

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7
Q

What are some combination techniques of anesthesia?

A

Use a block with MAC, or block with general, etc.

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8
Q

Is it possible to administer a general anesthetic with only a nasal cannula for support?

A

Yes.

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9
Q

Define Minimal Sedation

A

Anxiolysis. Patient’s respond normally to verbal commands, cognitive function and coordination may be impaired, ventilatory and cardiovascular function are unaffected

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10
Q

Define Moderate sedation/ Analgesia

A

Conscious sedation. Patients respond purposefully to verbal commands, they may or may not require light tactile stimulation in addition. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained.

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11
Q

Define Deep Sedation/ Analgesia

A

Not easily aroused, respond purposefully after repeated/ painful stimulation. The ability to maintain a patent airway may be impaired. Cardiovascular function is usually maintained.

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12
Q

Which group of people may not be able to manage their cardiovascular state during deep sedation/ analgesia?

A

The elderly or people with compromised hearts

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13
Q

Describe General Anesthesia.

A

Patient is not arousable, even by painful stimulation. Ability to maintain ventilatory function is impaired. Requires assistance with airway. PPV may be required.Cardiovascular function may be impaired.

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14
Q

Which type of anesthesia gives you generalized reversible central nervous system depression?

A

General

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15
Q

Under general anesthesia do you have any sensory perception?

A

No

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16
Q

Under general anesthesia do you have loss of consciousness?

A

Yes

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17
Q

Under general anesthesia do you have recall of events?

A

Hopefully No

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18
Q

Under general anesthesia do you have immobility?

A

Yes

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19
Q

Do you have to give a muscle relaxant in every case?

A

No, they are not necessary in every general anesthesia case.

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20
Q

Do you get any muscle relaxation from the general itself?

A

Yes, some

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21
Q

Does general anesthesia suppress your autonomic nervous system?

A

Yes

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22
Q

Why would suppressing the autonomic nervous system in general anesthesia be good?

A

It decreases the stress response to surgery.

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23
Q

Why would suppressing the automonic nervous system in general anesthesia be bad?

A

Because it takes away the patients ability to respond to a low BP, they are dependent on us to fix that.

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24
Q

Does general anesthesia provide analgesia?

A

NO, anesthetics are hypnotics that cause amnesia. They have no analgesic properties…. except for one drug.

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25
Q

Which drug, used as an induction agent in general anesthesia is the only anesthetic that also has some analgesic properties?

A

Ketamine

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26
Q

Does general anesthesia cause anxiolysis?

A

Yes, but giving Versed pre-op is also a good idea to prevent pre-surgical anxiety.

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27
Q

What are the 7 types of medications typically given when delivering a general anesthesic. (think pre-op to the end of the case)?

A
  1. Pre-op anxiolytic with or without opiate 2. Induction drug (IV or inhaled) 3. Neuromuscular blockade 4. Inhalation drug or drip to maintain anesthetized state. 5. Opiates/ local anesthetics 6. antiemetic 7. Neuromuscular blockade reversal agent
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28
Q

Why do we give a pre-op medication or sedation?

A

Patient comfort, decrease anxiety, prevent aspiration, antibiotics per surgeon request.

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29
Q

Should the induction agent be IV or inhaled?

A

either

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30
Q

Why do we give neuromuscular blockade?

A

To facilitate intubation, optimize surgical conditions

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31
Q

Should the maintenance anesthetic be IV or inhaled?

A

You can use either

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32
Q

Why do we give opiates or local during the case?

A

to minimize physiological effects of pain, to decrease post op pain and promote comfort at emergence.

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33
Q

Can patients still have pain under general anesthesia?

A

Yes, which can cause tachycardia, cortisol release, and other physiological things that we don’t want happening.

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34
Q

Why do we give an antiemetic in general anesthesia cases?

A

inhaled agents and opiates both have the side effect of nausea.

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35
Q

Do we always have to give a neuromuscular blockade reversal?

A

No, if enough time has passed the neuromuscular blocker will have decreased enough to be insignificant to inhibit a patient’s ability to breathe.

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36
Q

What are the 5 pharmacological effects of Benzodiazepines?

A
  1. anxiolysis 2. sedation 3. anterograde amnesia 4.anticonvulsant actions 5. muscle relaxation, spinal level
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37
Q

What is meant by anterograde amnesia?

A

Amnesia that lasts from the moment you give the drug

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38
Q

What is meant by muscle relaxation at the spinal level when speaking of Benzos?

A

Benzos specifically relax the muscles of the back. They are commonly used for patients with chronic back pain.

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39
Q

What is the prototype benzodiazepine?

A

Valium

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40
Q

What 2 things do benzodiazepines do?

A
  1. potentiate binding of GABA to GABA-a receptor. 2. Increases GABA potency 3 fold.
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41
Q

What does the effect on GABA by benzodiazepines do at the neuromuscular junction?

A

Increases Cl- influx, hyperpolarizes, decrease neuronal excitability.

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42
Q

What are 5 things you would use benzos for in the anesthesia setting?

A
  1. Pre-medication, 2. IV sedation, 3. General anesthetic induction (rare) 4.General anesthetic maintenance (rare) 5. Post-op anxiolysis
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43
Q

Do benzodiazepines cause a decrease in ventilation?

A

Yes,the severity is dependent on dose.

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44
Q

Do hypoventilation and hypoxemia occur after a benzo is given?

A

Yes.

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45
Q

What should you consider if you are giving an opiod with a benzo?

A

hypoxemia and hypoventilation are enhanced with opiods and benzos.

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46
Q

Do benzos decrease SVR?

A

when given at induction doses they do, but not usually.

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47
Q

Are benzos OK to give to pregnant women?

A

No. They have iatrogenic effects on the baby and can cause anomolies.

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48
Q

Opiods act on what type of receptors?

A

Mu

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49
Q

Where are Mu-opioid pain receptors located?

A

brainstem, spinal cord, and peripheral tissue

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50
Q

What are the pharmacological effects of opioids?

A

Supraspinal and Spinal analgesia. Activation of endogenous pain suppression system. Agonist at stereospecific opioid pain receptors- activates pain modulating systems.

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51
Q

Do opioids act a pre or post synaptic sites?

A

both

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52
Q

If an opioid binds at an opioid receptor what happens to neurotransmission?

A

it is decreased

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53
Q

How exactly is neurotransmission decreased at the synaptic site?

A

Increased K+ conductance, creates hyperpolarization. Ca++ channel inactivation, and immediate decrease in neurotransmitter release.

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54
Q

What do benzos do to Cl-

A

increase Cl- influx and hyperpolarize

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55
Q

What do opioids do to K+

A

Increase K+ influx and hyperpolarize.

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56
Q

What effects do opiods have on K+ and Substance P?

A

decreases both of them

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57
Q

Name 4 uses of opiods in anesthesia.

A
  1. Pre-medication 2.Intra-operative pain management (IV, epidural, or spinal) 3.General anesthesia in high doses 4.Post-op pain management
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58
Q

Would you want to give an opioid as pre-med in addition to a benzo?

A

No, the combination of the two could cause hypoventilation to the point of apnea.

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59
Q

As an example of the size of dose you would need, how much fentanly would you need to give if using it as a general anesthetic?

A

50-100mcg/kg HUGE doses

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60
Q

Which drug is the prototype opioid?

A

Morphine

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61
Q

Name 7 adverse effects of opiods.

A
  1. Bradycardia 2. Respiratory Depression 3. Miosis 4. Urinary retention 5. Constipation 6. Physical dependence 7. Sedation
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62
Q

Opioids with have a ________ effect if given with other medications that cause sedation.

A

Synergistic

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63
Q

According to Dr. E. Synergistic means:

A

1+1 = 3

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64
Q

What sort of respiratory depression do you see with opioids?

A

a decreased respiratory rate but an increased volume.

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65
Q

Is opioid induced bradycardia a bad thing?

A

Not always, we like bradycardia in the cardiac OR

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66
Q

Which class of drugs are considered the ‘classic’ induction agents?

A

Barbiturates

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67
Q

How do the barbiturates work?

A

They decrease the rate at which GABA dissociates from its receptor which increases the duration of GABA activated Cl- channel opening,enhances GABA activity. Basically, once GABA is bound, it makes it hold on tight.

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68
Q

The structure of barbiturates _______ the structure of GABA.

A

mimics GABA at the receptor causing direct activation of Cl- channels.

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69
Q

Barbiturates produce functional __________ of the post synaptic neuron.

A

inhibition

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70
Q

What effects do barbiturates have on the reticular activating system (RAS)?

A

Depresses it, causing sleep.

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71
Q

What is the prototype barbiturate?

A

Thiopental

72
Q

What are the 4 main uses of barbiturates in anesthesia?

A
  1. Sedation and hypnosis, 2. cerebral protection 3. anti-seizure 4. general anesthetic
73
Q

How would barbiturates give you cerebral protection?

A

by decreasing cerebral blood flow and cerebral metabolic oxygen consumption.

74
Q

Which is the better anti-seizure drug, a barbiturate or a benzo?

A

barbiturate.

75
Q

Would using a barbiturate in patients with increased ICP and/or focal brain ischemia be good or bad?

A

Good. Barbiturates decrease Cerebral metabolic Oxygen (CMO2) consumption

76
Q

What is the “hang-over effect”?

A

Caused by thiopental and barbiturates, they have a long half life and stay in the plasma for a long time.

77
Q

What happens to the patient’s preload when given barbiturates?

A

It drops. Depression of the medullary vasomotor center and decreased sympathetic outflow from the CNS causes peripheral vasodilation and hence a drop in preload.

78
Q

What happens to systolic BP and HR in the patient who has received a barbiturate?

A

Drop in BP (peripheral vasodilation) and increased in HR (compensatory)

79
Q

If the sympathetic nervous system is not intact or the patient is already hypovolemic or large doses are given to decrease ICP, what cardiovascular effects can occur from giving a barbiturate?

A

Significant decrease in BP and myocardial depression

80
Q

Do barbiturates cause ventilatory depression?

A

Yes, the patient will likely stop breathing.

81
Q

What happens if you give barbiturates into an artery?

A

gangrene and nerve damage.

82
Q

What happens to liver enzymes with chronic barbiturate use?

A

they become elevated

83
Q

Which barbiturate is the most potent inducer of liver enzyme increase?

A

Phenobarbitol

84
Q

Which important medications would you need to be careful of if giving your patient a barbiturate?

A

barbiturates increase the metabolism of oral anticoagulants, phenytoin, TCAs, corticosteroids, and Vitamin K.

85
Q

What effect do barbiturates have on heme?

A

accelerated production of heme by enzyme D- aminolevulinic acid synthetase

86
Q

Because of it’s effects on heme, barbiturates should be avoid in patients with?

A

porphyria

87
Q

Are allergies to barbiturates common?

A

No, only 1 in 30,000 but allergic reactions are associated with a high mortality!

88
Q

Do barbiturates cross the placenta?

A

Yes, readily

89
Q

What is the classification of propofol?

A

A nonbariburate intravenous agent (hint: any induction agent that isn’t a barbiturate will be classified as this)

90
Q

How is propfol supplied?

A

1% solution of egg, soy, and glycerol base (nice medium for bacteria so use alcohol wipes)

91
Q

What substance is added to propofol to decrease the risk of infection?

A

EDTA

92
Q

What type of preservative is used in propofol?

A

sodium metabisulfate (used instead of EDTA in some)

93
Q

How does propofol work, pharmacologically?

A

It potentiates binding of GABA to GABA-a receptor (Beta 1 subunit), it decreases the rate of dissociation of GABA from the receptor once it is bound

94
Q

What effect does propofol have at the synanpse?

A

By inceasing GABA at the receptor, Cl- influx is increased, hyperpolarization occurs, and a decrease in neuronal excitability occurs.

95
Q

Name 4 pharmacological effects of propofol.

A
  1. Dose dependent sedation and hypnosis 2. antiemetic 3.antipruritic 4. anticonvulsant
96
Q

Can propofol be used to decrease ICP?

A

Yes

97
Q

Does propofol have an effect on bronchoconstriction?

A

Yes, propofol attenuates bronchoconstriction, usually the patient is not under deep enough, so deepen your anesthetic to fix this.

98
Q

How should asthmatics be managed under anesthesia?

A

Asthmatics should be kept very deep or they will respond with bronchoconstriction. Asthmatics respond to almost any irritation with bronchoconstriction.

99
Q

What are 5 main uses for propofol in anesthesia?

A
  1. IV sedation 2. Induction of general anesthesia 3. maintenance of general anesthesia 4. As part of a balanced technique for maintenance of anesthesia (with things like ketamine and fentanyl) 5. as an antiemetic in small doses.
100
Q

Does propofol affect ventilation?

A

Yes, it depresses it but this is dose dependent

101
Q

Does propofol affect cardiovascular tone?

A

Yes, this is also dose dependent but propofol will drop SV, CO, and SVR

102
Q

Will a patient receiving propofol become tachycardic?

A

They shouldn’t. Even in the setting of decreased BP, it is thought that propofol inhibits baroreceptors thereby preventing a compensatory increase in HR when BP falls.

103
Q

Can a patient on propofol become bradycardic?

A

Yes, 1.4 in 100,000 patients will die from bradycardia related to propofol.

104
Q

Can propofol cause myoclonus?

A

Yes, especially in young, muscular men, and especially if you give it fast.

105
Q

Why did my patient get tachycardic when I first pushed the propofol?

A

Pain. Propofol hurts when injected. You should give lidocaine IV before pushing it. But even that doesn’t always take away the pain.

106
Q

With long term infusion of propofol you have to be monitor for?

A

lipidemia

107
Q

Can propofol cause infection?

A

Yes. the soy and egg base make a great medium for bacteria.

108
Q

Can propofol cause bronchospasm?

A

Yes, especially with some of the sulfates they put in as preservative.

109
Q

At the neuromuscular junction, what are the 4 pre-synaptic events as they occur in chronological order?

A
  1. An action potential depolarizes the nerve terminal 2. Ca channels open 3. Ca diffuses down a gradient to the nerve terminal 4. AcH spills out into the synaptic cleft
110
Q

At the neuromuscular junction, what are the 5 post synaptic events in chronological order?

A
  1. AcH combines with nicotinic receptors, 2. after both nicotinic receptors occupied channels open, Na and Ca diffuse into the cell and K+ diffuses out. 3.Motor end plate depolarizes 4. Action potential created 5. Skeletal muscle contracts
111
Q

How many protein subunits are on the ACH receptor?

A

**5 ** 2 alpha, 2 beta, and 1 gamma

112
Q

The central core of the receptor is for:

A

cation channeling

113
Q

AcH must bind to __________ to open the core.

A

Both alpha receptors

114
Q

Alpha subunits are the site of ________ and _________.

A

agonism and antagonism

115
Q

What is the classification of succinylcholine?

A

A depolarizing neuromuscular blockade agent

116
Q

What is the mechanism of action of succinylcholine?

A

binds to nicotinic receptors, channels open, motor end plate depolarizes, single contraction occurs. Succinylcholne is not metabolized by normal acetylcholinesterases so channels stay open until succs. diffuses back into circulation. Further action potentials cannot be initiated.

117
Q

What are the anesthetic uses of succinylcholine?

A

Neuromuscular blockade to optimize intubating conditions, rapid sequence induction, treatment of life threatening laryngospasm

118
Q

Does succinylcholine cause cardiac dysrhythmias?

A

Yes! Especially in children. They can brady right down to asystole. You must give atropine with succinylcholine if you use it in a child.

119
Q

What electrolyte disturbance will you see with succinycholine?

A

Hyperkalemia. Especially in burns, trauma, nerve damage, neuromuscular disease, and renal failure.

120
Q

Is there any pain associated with succinylcholine?

A

Yes, you can have muscle pain and fasiculations

121
Q

What effect does succinylcholine have on ICP?

A

increases

122
Q

What effect does succinylcholine have in IOP?

A

increases

123
Q

What is a major concern with succinycholine that you should watch for?

A

Succinylcholine is a potent triggering agent of malignant hyperthermia.

124
Q

If patients report a family history of difficulty with anesthesia, what should you immediately be thinking?

A

This patient may have an atypical acetylcholinesterase, which would make succinycholine dangerous if not fatal. Without proper acetycholinesterases, succinylcholine will not break down and the pt. will stay paralyzed for a very long time.

125
Q

What drug classification does vecuronium fall into?

A

it is a non-depolarizing muscle relaxant; it is a monoquaternary aminosteroid

126
Q

What is the mechanism of action of vecuronium?

A

It is a competitive antagonist at pre and post neuromuscular junction nACH receptors

127
Q

What does vecuronium do at the receptor site?

A

Occupies alpha subunits of ACH receptor without inducing a conformational change, so an action potential cannot be initiated

128
Q

How long does vecuronium last?

A

45 minutes to an hour

129
Q

What are the anesthetic uses of vecuronium?

A

Facilitiate endotracheal intubation, optimize surgical conditions.

130
Q

Vecuronium has long unpredicable effects with which disease states?

A

Liver and kidney disease, neuromuscular disease, hypothermia and electrolyte imbalances

131
Q

Can vecuronium be given with aminoglycosides?

A

Yes but aminoglycosides are metabolized through similar pathways so you may see a prolonged effect of vecuronium in patients on aminoglycosides.

132
Q

Is vecuronium ok to use in burn patients?

A

Burn patients tend to be resistant to the effects of vecuronium

133
Q

After giving a neuromuscular blocking agent, you should be aware of ____________

A

residual neuromuscular blockade.

134
Q

There is thought to be a higher risk for ____________ if inadequate general anesthesia is given in additon to neuromuscular blockade.

A

recall

135
Q

What class is isoflurane?

A

Inhaled anesthetic, halogenated methyl ethyl ether

136
Q

Is the mechanism of action for inhaled anesthetics different than with IV anesthetics?

A

Yes, very much so, and beyond the scope of this lesson

137
Q

Does the lipid solubility of the inhaled agent have any signficant importance?

A

Yes, lipid solubility determines onset, duration, etc.

138
Q

How are inhaled agents eliminated?

A

Almost entirely by the lungs, they are minimally metabolized by the kidney and liver.

139
Q

What is the prototype inhaled agent?

A

Isoflurane

140
Q

What are the pharmacological effects and anesthetic uses of isoflurane?

A

It is a bronchodilator. It is also a general anesthetic and causes sedaton, hypnosis, and partial muscle relaxation, can be used in the induction and maintenance of anesthesia.

141
Q

Which inhaled agent is usually used in the induction of anesthesia?

A

sevoflurane

142
Q

What are the respiratory effects of isoflurane?

A

Respiratory depression. Higher RR but lower volumes

143
Q

Inhaled anesthetic agents have the opposite effect on ventilation as opioids do, which is which?

A

opioids: decreased RR, higher volumes inhaled agents: higher RR, lower volumes. Both may be inadequate to maintain oxygenation.

144
Q

What are the cardiac effects of isoflurane?

A

Depression of CV. Decrease CO and BP, these agents cause vasodilation

145
Q

What is a potentially serious consequence of any inhaled anesthetic?

A

Malignant hyperthermia

146
Q

What are 4 things that happen in MH?

A
  1. Ca channel interference 2. muscle rigiditiy 3. increased temperature 4. Increased CO2
147
Q

What is the first thing we will notice in MH?

A

CO2 starts rising for no apparent reason.

148
Q

Is muscle rigidity a good indicator of MH?

A

No, if you have given a neuromuscular blocker, you won’t be able to tell.

149
Q

Is there an increased risk of aspiration with isoflurane?

A

Yes, inhaled agents abolish your airway reflexes

150
Q

Are there any environmental concerns with inhaled anesthetics?

A

Yes, be aware of them in the OR, you can cause OR pollution and anesthetize everyone in the room.

151
Q

What is MAC, in reference to inhaled anesthetics?

A

Mean Alveolar Concentration. One MAC of a volatile anesthetic is the dose at which 50% of patients won’t move in reponse to a noxious stimulus.

152
Q

MAC is used to?

A

describe potency, it tells us how much of a specific gas to administer

153
Q

What is the MAC of isoflurane?

A

1.2%

154
Q

If the patient is on 100% O2, and I add 1.2% of Isoflurane, what concentration of gases is my patient getting?

A

98.8% Oxygen and 1.2% isoflurane

155
Q

Can nitrous reach 100% potency?

A

No, nitrous will never reach 100% potency. It is the only inhaled agent that will not.

156
Q

What is the MAC of nitrous?

A

104%

157
Q

A local anesthetics action is by blocking which impulse?

A

block impulse conduction during the depolarization phase of the action potential

158
Q

Local anesthetic blockade is caused by the inhibition of _____ ions

A

sodium; sodium channel blockade.

159
Q

Blockade only occurs when the Na channels are in the__________ state.

A

inactivated, closed.

160
Q

Which drug is the prototype local anesthetic?

A

Lidocaine

161
Q

What is the pharmacological effect of local anesthesia?

A

Blocks afferent nerve transmission to produce analgesia and anesthesia without loss of consciousness.

162
Q

Does local anesthesia cause autonomic blockade?

A

Yes

163
Q

Does local anesthesia cause somatic sensory blockade?

A

Yes

164
Q

Does local anesthesia cause somatic motor blockade?

A

Yes

165
Q

What is the classification of Lidocaine?

A

Amide local anesthetic

166
Q

There are 2 general categories of local anesthetics, they are the:

A

Amides and the Esters (remember one eyed esters, Esters have only one “i” in their spelling)

167
Q

They typical local anesthetic molecule consists of 3 parts, they are?

A
  1. Lipophilic head, 2. intermediate chain 3. hydrophilic tail
168
Q

The lipophilic head of the local anesthetic molecule is an:

A

aromatic ring

169
Q

The intermediate chain is made of either a _______ or a ___________.

A

amide (NH) or ester (COO-)

170
Q

The hydrophilic tail is made of a ______________.

A

Tertiary amine

171
Q

One of the biggest adverse effects/ precautions we need to take with local anesthetics is?

A

CNS toxicity.

172
Q

What are the signs/ symptoms of CNS toxicity?

A

circumoral tongue numbness, tinnitus, vision changes, dizziness, slurred speech, restlessness, seizure- followed by CNS depression, apnea, hypotension

173
Q

What are some of the cardiac effects of local anesthetic toxicity?

A

CV is more resistant to the toxic effects than the CNS is. But hypotension, myocardial depression, reduced SVR and CO may occur.

174
Q

Which local anesthetic is known to cause arrythmias, AV heart block, hypotension, and cardiac arrest?

A

Bupivacaine

175
Q

What happens with cocaine overdose?

A

Massive sympathetic outflow, coronary vasospasm, MI, dysrhythmias including V-fib.

Spring '14 Pharmacology (6 decks)

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