Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharma Recall - Pharmacology > Ch 16 - Anesthetics - DONE > Flashcards

Ch 16 - Anesthetics - DONE Flashcards

1
Q

What are the two major of anesthetic classes

A
  • general

- local

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the route of administration and primary actions general anesthetics:

A

Given either:

  • inhaled
  • IV

They primarily have CNS effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the route of administration and primary actions local anesthetics:

A

Injected at the operative site to block nerve conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the stages of general anesthesia?

A
  • Stage I-Analgesia
  • Stage II-Excitement
  • Stage III-Surgical anesthesia
  • Stage IV-Medullary paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe Stage I-Analgesia of general anesthesia:

A
  • reduced sensation of pain

- the patient remains conscious and conversational

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe Stage II-Excitement of general anesthesia:

A
  • delirium and combative behavior ensue

- there is an increase in BP and respiratory rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe Stage III-Surgical anesthesia of general anesthesia:

A
  • the patient is unconscious, and regular respiration returns
  • there is muscle relaxation and decreased vasomotor response to painful stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe Stage IV-Medullary paralysis of general anesthesia:

A
  • respiratory drive decreases and vasomotor output diminishes
  • death may quickly ensue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does the pharmacokinetics of anesthesia affect these stages?

A
  • With slow-onset agents all four stages are discernible.

- Faster-acting agents allow for quicker progression through the stages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give example of slow-onset agent:

A
  • ether
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is induction of anesthesia?

A

The time from administration of a general anesthetic to the achievement of surgical anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is induction of anesthesia dependent on?

A

How fast the anesthetics reaches the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are the complications of anesthetics induction avoided?

A

An ultra-fast-acting, short-lived agent is given IV so that the patient will rapidly progress through the first and second stages of anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is recovery?

A

Simply, the reverse of induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does recovery depend upon?

A

How quickly the anesthetics are removed from the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

For inhaled anesthetics, what five factors influence the rate of induction?

A
  1. solubility
  2. pulmonary ventilation
  3. partial pressure of the inhaled agent
  4. alveolar blood flow
  5. arteriovenous concentration gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe how solubility affects the rate of induction:

A
  • The blood-gas partition coefficient is an index of solubility; a low coefficient implies relative insolubility.
  • An agent with a low solubility requires fewer molecules to raise the partial pressure and arterial pressure is achieved rapidly, which leads to faster induction.
  • Recovery likewise hastened when the anesthetic agent is discontinued.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe how the partial pressure of the inhaled agent affects the rate of induction:

A
  • An increased concentration in the inhaled air mixture leads to greater concentration at the alveoli and thus increase the partial pressure of the agent.
  • In clinical practice, a greater concentration is given initially to speed induction, and then it is reduced to a maintenance level.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does alveolar blood flow affect the rate of induction?

A

Increased flow allows for more rapid uptake of the agent and quicker effect on the CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe how the arteriovenous concentration gradient affects the rate of induction:

A

This is dependent of the agent by tissue.

  • A high rate and extent of tissue uptake will decrease the venous concentration of the anesthetic.
  • As a result, it will take longer time for the anesthetic concentration of arterial and venous blood to equilibrate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What factors influence tissue uptake of an anesthetic?

A

Anesthetic uptake is influenced by many of the same factors that influence transfer from the lung to the blood; tissue-blood partition coefficients rates of blood flow to the tissues, and concentration gradients are all important factors.

  • Highly perfused tissues (brain, heart, liver, kidneys, and splanchnic bed) will exert the greatest influence on arteriovenous concentration.
  • Skin and muscle undergo slow diffusion because these tissues are less richly perfused and thus exert less of an effect on arteriovenous concentration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the molecular mechanism of action for general anesthetics?

A

The mechanism is not clear.
- All anesthetics have common property of increasing treshold of action potentials and inhibiting the rapid increase in the membrane permeability to sodium ions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name 6 inhaled agents:

A
  1. Halothane
  2. Enflurane
  3. Isoflurane
  4. Desflurane
  5. Sevoflurane
  6. Nitrous oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is the potency of inhaled anesthetics defined and measured?

A

Using the concept of MAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is MAC

A

MAC is the minimum alveolar concentration of anesthetics necessary to eliminate movement among 50% of patients challenged by a standarized skin incision.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does MAC relate to potency?

A

The greater the MAC of an agent, the greater the concentration needed to provide anesthesia.
- Thus an agent with high MAC has low potency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Give an example of an agent with high MAC (=low potency):

A

Nitrous oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How can the MAC of any inhaled agent be reduced?

A

By using the agent with conjunction with analgesics such as opioids or sedative hypnotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe Halothane:

A

The first of the halogenated volatile anesthetics to be developed halothane has been largely replaced by more modern agents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the clinical indications of Halothane?

A

Halothane is still used in the pediatric population because of its pleasant odor and lack of hepatotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Is Halothane metabolized?

A

ca. 20% is eliminated by metabolism; and the remainder is eliminated unchanged in expired air.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is Halothanes MAC?

A

0,75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the cardiovascular effect of Halothane?

A

Halothane sensitizes the myocardium to the effects of catecholamines (thus increasing the risk of arrythmias), decreases the heart rate and cardiac output, and leads to lowered BP and peripheral resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Are there any toxic effects associated with Halothane?

READ FOR MORE ON PAGE 105

A
  • hepatotoxicity

- malignant hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is malignant hyperthermia?

A

A potentially fatal reaction to any of the inhaled anesthetics, which results in:

  • hyperthermia
  • metabolic acidosis
  • tachycardia
  • accelerated muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is malignant hyperthermia treated?

A

With Dantrolene and cessation of the offending agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the clinical indication of Enflurane?

A

rapid induction of general anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Is Enflurane metabolized?

A

Ca. 2% of the agent is metabolized to a fluoride ion, which is then excreted in the kidneys. The rest is eliminated unchanged in the expired air.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is Enflurane´s MAC?

A

1,6%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are Enflurane´s cardiovascular effects?

A
  • decreases heart rate, BP, and peripheral resistance
  • it has a less sensitizing effect on the myocardium than does Halothane
  • can produce cardiac arrythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe the toxic effects of Enflurane?

A
  • The fluoride ion resulting from Enflurane´s metabolism can be nephrotoxic.
  • A decrease in the kidneys concentrating ability after prolonged exposure to Enflurane has been observed in patients with preoperative kidney insufficiency.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the clinical indications of Isoflurane?

A

general anesthetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Is Isoflurane metabolized?

A

Isoflurane is minimally metabolized; almost all of the drug is eliminated unchanged in the expired air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What si the MAC of Isoflurane?

A

1,4%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the cardiovascular effects of Isoflurane?

A
  • increases heart rate
  • does not effect cardiac output
  • can lower BP and reduce peripheral vascular resistance profoundly
  • does not sensitize the myocardium to catecholamines
  • does not induce arrythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the toxic effects of Isoflurane?

A

potential for malingant hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the clinical indications for Desflurane?

A

General anesthesia

48
Q

Does Desflurane udnergo metabolism?

A

Desflurane is eliminated unchanged in expired air

49
Q

What is Desflurane MAC?

A

6%

50
Q

What are Desflurane´s cardiovascular effect?

A

Its profile very similar to that of Isoflurane

51
Q

Are there toxic effects of Desflurane?

A

Potential for malignant hyperthermia

52
Q

What are the clinical indications of Sevoflurane?

A

General anesthesia

53
Q

Does Sevoflurane undergo metabolism?

A

A small percentage of this agent is metabolized to fluoride ion; the remainder is eliminated unchanged in the expired air

54
Q

What is the MAC of Sevoflurane?

A

2%

55
Q

Describe Sevoflurane´s cardiovascular effects:

A

It has a cardiac profile similar to that of Desflurane and Isoflurane

56
Q

What are the toxic effects of Sevoflurane?

A

Although metabolism of Sevoflurane produces a fluoride ion, it does not affect renal function like enflurane does.
- It has been hypothesized that because Sevoflurane is not metabolized in the kidney (as enflurane is), toxic effect do not occur.

57
Q

Laughing gas =

A

Nitrous oxide

58
Q

What are the clinical indications of Nitrous oxide?

A

Induction of general anesthesia

59
Q

How is Nitrous oxide administered?

A

Because of its low potency Nitrous oxide must be used in conjunction with other anesthetics (either inhaled or IV) for effective general anesthesia

60
Q

Is Nitrous oxide metabolised?

A

Nope!

61
Q

What is the MAC of Nitrous oxide?

A

100% - even if 100% Nitrous oxide was given to the patient, surgical anesthesia would not be achieved (and profound hypoxia would result)

62
Q

Are there cardiovascular effects after using Nitrous oxide?

A

Nitrous oxide minimally affects the cardiovascular system

63
Q

Name a major CI to the use of Nitrous oxide?

A

If Nitrous oxide is administered to patients who have closed air cavities (e.g pneumothorax), the gas will diffuse into the cavity and increase the pressure within it.

64
Q

What special consideration should be taken into account during the recovery phase?

A

Care must be taken to adequately oxygenate the patient, because Nitrous oxide will diffuse from the blood to the alveoli so quickly that it entirely replaces oxygen, which results in diffusion hypoxia

65
Q

What are the toxic effects of Nitrous oxide?

A
  • bone marrow depression with prolonged administration

- high concentrations may cause neuropathies

66
Q

What are the classes of IV anesthetics?

A
  • barbiturates
  • benzodiazepines
  • opioids
  • dissociative agents
67
Q

Ultra-short-acting barbiturates example:

A

Thiopental

68
Q

What are the clinical indications for the use of Thiopental?

A
  • Thiopental is used for the induction of anesthesia in combination with inhaled anesthetics.
  • It has a rapid onset of action, with unconsciousness occuring 15-30 seconds after administration.
69
Q

What is the mechanism of action of Thiopental?

A
  • Thiopental binds the GABAa receptor which results in prolonged opening of the chloride channel.
  • The neuron´s membrane is thus hyperpolarized, which creates a reduction in neuronal excitability.
70
Q

What phenomenon is responsible for Thiopental fast onset of action and short duration?

A

Thiopental has high lipid solubility and thus crosses the blood-brain barrier very quickly.
- However the drug just as quickly diffuses out of the brain and other highly vascularized organs, and is rapidly redistributed to muscle, fat, and other body tissues, which accounts for its short duration.

71
Q

Is Thiopental metabolised?

A

Yes.

  • Metabolism (in the liver) occurs more slowly than redistribution.
  • Nearly 99% of the metabolised drug; thus after large doses (especially continuous infusion), recovery can be very slow.
72
Q

What are the cardiovascular effects of Thiopental?

A

Thiopental reduces BP and cardiac output, but it does not affect peripheral resistance.

73
Q

Describe the respiratory rate after the use of Thiopental:

A

Thiopental depresses the respiratory center of the brain and blunts the response to CO2 and hypoxia.
- This effect on cerebral blood makes Thiopental a desirable agent in patients who have cerebral edema.

74
Q

What are the effects of Thiopental on the cerebral blood flow?

A
  • decreases blood flow

- oxygen consumption in the brain

75
Q

Are there any side effects with the use of Thiopental?

A
  • may induce laryngospasm and bronchiospasm
  • exacerbate acute intermittent porphyria by inducing the synthesis of hepatic δ-aminolevulinic acid synthase (thiopental has precipitated pophyric crisis)
76
Q

Name some benzodiazepines:

A
  • midazolam
  • diazepam
  • lorazepam
77
Q

Describe the clinical uses of benzodiazepines:

A
  • preoperative surgery
  • intraoperative sedation for procedures not requiring analgesia
  • As a apart of balanced anesthesia
78
Q

Give examples of intraoperative sedation for procedures not requiring analgesia:

A
  • colonoscopy

- cardioversion

79
Q

Balanced anesthesia def:

A

using several agents simultaneously to obtain surgical anesthesia

80
Q

What is the mechanism of action of benzodiazepines?

A

Benzodiazepines binds GABA receptors, which results in reduced neuronal excitability.
- These drugs have a much slower onset of action than do the barbiturates.

81
Q

Why is midazolam used as a preanesthetic medication?

A

Midazolam produces antegrade amnesia, which calms the patient

82
Q

Antegrade amnesia def:

A

loss of memory of events after administration of the drug

83
Q

Why is midazolam also the preferred benzodiazepine for induction and maintenance of anesthesia?

A

Midazolam has a shorter onset of action, greater potency, and more rapid elimination when compared to other benzodiazepines

84
Q

What are the side effects of benzodiazepine?

A
  • Alone, benzodiazepines can cause moderate circulatory and respiratory depression.
  • If used with opioids, cardiovascular collapse and respiratory arrest can occur.
85
Q

Are there other uses for benzodiazepine?

A

benzodiazepine is used to control seizures and in the alcohol withdrawal process to control symptoms

86
Q

Is there a benzodiazepine antagonist?

A

Flumazenil antagonizes the CNS depression caused by benzodiazepine

87
Q

Give examples of opioids:

A
  • fentanyl

- morphine

88
Q

What are the clinical indications for opioids?

A

Opioids are used as general anesthetics in patients undergoing cardiac surgery or other major surgeries for which cardiac reserve is limited.

89
Q

Why is fentanyl used more than morphine?

A
  • greater potency

- less impact on respiratory drive

90
Q

What are the side effects of opioids?

A
  • IV opioids can cause chest wall rigidity , which makes ventilation more difficult.
  • Postoperative respiratory depression can occur.
  • Intraoperative awareness with unpleasant postoperative recall may occur.
91
Q

Is there an opioids antagonist?

A

Naloxone reverses the respiratory and CNS effects of opioids

92
Q

What is Innovar?

A

Innovar is a combination of Fentanyl and Droperidol.

- When used with Nitrous oxide, Innovar porduces neuroleptanesthesia

93
Q

Neuroleptanesthesia def:

A

combined analgesia and amnesia

94
Q

What are the clinical indications of Propofol?

A

Induction of anesthesia

95
Q

What are the pharmacological characteristics of Propofol?

A
  • Ultra-fast-acting drug with pharmacodynamics similar to those of Thiopental
  • High lipid solubility
  • Very quick distribution to highly vascularized sites (e.g. the brain)
  • Rapid diffusion back into the blood, with subsequent redistribution.
96
Q

Why is Propofol preferred over Thiopental for induction of anesthesia?

A
  • Rate of onset very similar to Thiopental
  • Recovery is quicker, with patients able to ambulate sooner than with other IV anesthetics.
  • Patients report less nausea and emesis
  • No cumulative effect from Propofol administration or delayed recovery after prolonged administration.
97
Q

How is Propofol metabolized?

A

It is rapidly metabolized by the liver and other extrahepatic enzymes (10 times more quickly than Thiopental)

98
Q

What are the side effects of Propofol?

A
  • Hypotension
  • Negative inotropic effects
  • Pain at the site of injection
  • Apnea
99
Q

Does Propofol have any other uses?

A

Propofol is often used in the critical care settings as a continuous infusion to provide prolonged sedation

100
Q

What are the clinical indications for Ketamine?

A

Ketamine, because of its unique cardiovascular effects, is used in trauma cases where cardiovascular support is necessary.
- It is also used in children undergoing painful procedures (dressing changes of burns) or to facilitate cooperation during radiographic procedures

101
Q

What is the mechanism of action of Ketamine?

A

Ketamine produces dissociative anesthesia characterized by catatonia, amnesia, and analgesia without the actual loss of consciousness

102
Q

What are the cardiovascular effects of Ketamine?

A
  • Ketamine is unique in that it produces cardiovascular stimulation, with HR, arterial BP, and CO all usually significantly increased.
  • Ketamine stimulates the sympathetic nervous system, which causes the release of catecholamines
103
Q

Is Ketamine used in head trauma cases?

A

No, because it increases the cerebral blood flow, oxygen consumption, and intracranial pressure.

104
Q

What are the side effects of Ketamine?

A
  • can cause an emergence phenomenon consisting of disorientation, sensory and perceptual illusion, and vivid, often unpleasant dreams.
105
Q

What can be done to reduce the phenomenon that occurs when taking Ketamine?

A

Use of Diazepam 5-10 min before Ketamine administration.

106
Q

Are there other routes of administrating Ketamine?

A
  • IM

- IV

107
Q

What are the two types of local anesthetics?

A

The two classes are determined by the bond linking the lipophilic portion of the molecule with the hydrophilic components

  • ester bond, or
  • amide bond
108
Q

Name the ester anesthetics:

A
  • cocaine
  • benzocaine
  • procaine
  • tetracaine
109
Q

Name the amide anesthetics:

A
  • lidocaine
  • mepivacaine
  • bupivacaine
  • prilocaine
110
Q

How does the metabolism of ester and amide anesthetics differ?

A
  • Esters are more rapidly metabolised by blood and tissue esterase, which gives them short half-lives.
  • Amides are metabolised by hepatic microsomal enzymes, which results in longer half-life.
111
Q

What is the mechanism of action of local anesthetics?

A

These agents block the nerve conduction by inhibiting the voltage-gated sodium channels of the neuronal membrane

112
Q

Which nerve fibers are the most sensitive to local anesthetics?

A
  • Small, unmyelinated fibers that conduct pain, temperature, and autonomic activity that are affected first.
  • With increasing concentrations of anesthetic, pain fibers (C and A fibers) are first affected, then sensory fibers (A fibers), and last motor neurons (A fibers)
113
Q

What are the clinical indications for local anesthetics?

A

Used for:

  • Surface anesthesia
  • Nerve blocks
  • Spinal and epidural anesthesia
  • Lidocain is also a potent antiarrythmic
114
Q

How is the duration of local anesthetics increased?

A

Adding epinephrine to local anesthetics reduces blood flow to the anesthetized area, thus decreasing the absorption of the drugs and enhancing their duration of action

115
Q

What are the side effects of local anesthetics?

A

Systemic effects of local anesthetics occurs with high doses of the drug:

  • CNS disturbances (light-headedness, sensory distrubances, convulsion, coma, and even death at high doses)
  • Cardiovascular effects (myocardial depression and hypotension except for cocaine, which causes vasoconstriction and hypertension)

Pharma Recall - Pharmacology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions