Anesthesia Flashcards

1
Q

Define general anesthesia.

A

A reversible state of CNS depression, where the patient is in an amnestic state resulting in the loss of response to external stimuli and pain.

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2
Q

What are the five cardinal benefits of anesthesia?

A
  1. Sedation and reduction of anxiety.
  2. Lack of awareness and amnesia.
  3. Skeletal muscle relaxation.
  4. Suppression of undesirable reflexes.
  5. Analgesia.
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3
Q

Is there an anesthetic agent capable of achieving all five of the cardinal benefits of anesthesia?

A

No.

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4
Q

What are the two factors that determine the selection of anesthesia?

A
  1. Status of organ systems.
  2. Concomitant use of drugs.
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5
Q

How do anesthetic agents affect the cardiovascular system?

A

They suppress the cardiovascular system’s function.

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6
Q

Why must vasoactive substances sometimes be administered with anesthetics?

A

To counteract the cardiovascular suppression by anesthetics.

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7
Q

What cardiovascular conditions require careful consideration when selecting anesthesia?

A

Coronary artery disease.
Heart failure.
Dysrhythmias.
Valvular disease.
Any other cardiovascular diseases.

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8
Q

In what way do inhaled anesthetics impact the respiratory system?

A

They depress the respiratory system and reduce the ventilatory response to CO2.

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9
Q

How are anesthetics classified based on their effect on the airway?

A
  • Pungent (airway irritant).
  • Non-pungent.
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10
Q

Why are some anesthetics considered hepatotoxic and nephrotoxic?

A

Due to their damaging effects on the liver and kidneys due to the release of metabolites like fluoride and bromide from halogenated hydrocarbons.

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11
Q

Which nervous system conditions influence anesthesia selection?

A

Epilepsy.
Myasthenia gravis.
Neuromuscular disease.
Compromised cerebral circulation.

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12
Q

How does nitrous oxide affect pregnancy?

A

Causes aplastic anemia.

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13
Q

What fetal risks are associated with benzodiazepines during pregnancy?

A

Oral clefts and floppy baby syndrome (temporary hypotonia) in the fetus.

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14
Q

What are examples of muscle relaxants used in anesthesia?

A

NMJ blockers.
Curares.

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15
Q

What role do muscle relaxants play in anesthesia?

A

They aid in intubation during anesthesia.

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16
Q

What are examples of H2 blockers used in anesthesia?

A

Famotidine.
Rantidine.

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17
Q

How do H2 blockers contribute to the anesthesia process?

A

By reducing gastric acidity before anesthesia.

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18
Q

What are examples of barbiturates used in anesthesia?

A

Midazolam.
Diazepam.

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19
Q

What is the purpose of benzodiazepines in anesthesia?

A

Anxiolysis and amnesia.

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20
Q

How do barbiturates assist with anesthesia?

A

They help with smooth muscle induction and can lower the required dose of anesthetics.

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21
Q

What are examples of non-opioids used in anesthesia to provide analgesia?

A

Acetaminophen.
Celecoxib.

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22
Q

What are examples of opioids used in anesthesia to provide analgesia?

A

Fentanyl.

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23
Q

What is the role of antihistamines in anesthesia?

A

Prevent allergic reactions.

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24
Q

What are examples of serotonin antagonists used in anesthesia to provide analgesia?

A

Ondansetron.

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25
Q

How are serotonin antagonists used postoperatively in anesthesia?

A

To prevent postoperative nausea and vomiting.

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26
Q

What are examples of anti-cholinergic drugs used in anesthesia?

A

Glycopyrrolate.

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27
Q

What is the function of anticholinergic drugs in anesthesia?

A

They prevent bradycardia and fluid secretion into the respiratory tract during anesthesia.

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28
Q

What are the risks of coadministering drugs with anesthesia?

A

They can enhance undesirable effects like hypoventilation.

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29
Q

What are the three stages of anesthesia?

A
  1. Induction.
  2. Maintenance.
  3. Recovery.
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30
Q

What is induction?

A

The period of time from the onset of administration of the potent anesthetic to the development of effective surgical anesthesia.

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31
Q

What is maintenance?

A

The process of maintaining sustained surgical anesthesia.

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32
Q

What is recovery?

A

The time from discontinuation of administration of anesthesia until consciousness and protective physiologic reflexes are regained.

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33
Q

How is induction normally induced?

A

With an IV anesthetic like propofol, which produces unconsciousness within 30-40 seconds after injection.

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34
Q

How is anesthesia induction involved in children with children without IV access?

A

With non-pungent agents, such as halothane or sevoflurane.

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35
Q

How is general anesthesia maintained?

A

By the administration of volatile anesthetics, which offer good control over the depth of anesthesia.

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36
Q

Why are IV anesthetics used in induction of anesthesia not used to maintain the anesthetic activity?

A

Due to their short duration of action.

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37
Q

What is the process that predominates the process of recovery from anesthesia?

A

Redistribution from the site of action rather than the metabolism of the anesthetic.

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38
Q

What are the four stages of anesthesia?

A

Stage I - Analgesia.
Stage II - Excitement.
Stage III - Surgical anesthesia.
Stage IV - Medullary paralysis.

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39
Q

What is done to shorten the excitement stage of anesthesia?

A

A rapid acting agent, such as propofol, is given IV before inhalation anesthesia is administered.

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40
Q

How is the development of severe medullary paralysis, depression of the respiratory of vasocenters, coma, and death avoided in anesthesia?

A

Through continuous careful monitoring.

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41
Q

How does the anesthetic concentration in inspired air affect the rate of induction and recovery of anesthetics?

A

Increased inspired anesthetic concentration results in increased alveolar anesthetic concentration and increased rate of anesthetic transferring to the blood (increased rate of induction of anesthesia).

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42
Q

How does the relative solubility of the anesthetic in blood affect the rate of induction and recovery of anesthetics?

A

The solubility of the anesthetic in blood is inversely related to the induction and recovery of anesthesia.

So agents with higher solubility in blood have a slow induction rate and slow recovery rate, whereas agents with lower solubility in blood have a faster induction rate and a faster recovery rate.

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43
Q

What is the blood:gas solubility coefficient?

A

It defines the relative affinity of anesthetic for blood compared to air.

The lower it is, the more potent the anesthetic.

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44
Q

Rank the solubility of anesthetic agents according to the blood-gas solubility coefficient.

A

Halothane (slow) > Enflurane > Isoflurane > Sevoflurane > Desflurane > Nitrous Oxide (fast)

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45
Q

How does the pulmonary blood flow affect the rate of induction and recovery of anesthetics?

A

Increased cardiac output is correlated with increased pulmonary blood flow and more removal of the agent from the alveoli, thereby slowing the rate of increase in arterial tension and slowing induction.

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46
Q

How does the pulmonary ventilation affect the rate of induction and recovery of insoluble anesthetics?

A

Changes in minute ventilation have little influence on induction with insoluble agents in the blood, as the alveolar concentration is always high.

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47
Q

How does the pulmonary ventilation affect the rate of induction and recovery of soluble anesthetics?

A

Soluble agents show significant increases in alveolar tension with increased minute ventilation.

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48
Q

What are inhalation anesthetics most commonly used for?

A

The maintenance of anesthesia after induction of anesthesia by IV agent.

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49
Q

What are the two subtypes of inhalation anesthetics?

A

Gas anesthetics.
Liquid volatile anesthetics.

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50
Q

What is an example of a gas anesthetic?

A

Nitrous oxide.

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51
Q

What are examples of liquid volatile anesthetics?

A

Halothane.
Sevoflurane.
Desflurane.
Isoflurane.

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52
Q

How can the depth of anesthesia be rapidly altered?

A

By changing the concentration of the drug.

Increased anesthetic concentration increases the transfer of the drug to the blood.

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53
Q

What is the therapeutic index of inhalation anesthetics?

A

Very narrow. Generally from 2 to 4., so they should be monitored carefully.

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54
Q

Do inhalation anesthetics have an antagonist?

A

No.

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55
Q

What are the general safety features of inhalation anesthetics?

A

They are generally nonflammable and nonexplosive, with the exception of ether.

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56
Q

How do inhalation anesthetics affect cerebrovascular resistance?

A

They decrease it, which leads to increase perfusion of the brain.

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57
Q

What effect do inhalation anesthetics have on bronchial smooth muscle and how is this beneficial?

A

Inhalation anesthetics can cause bronchodilation, which can be particularly useful for patients with wheezing and status epilepticus.

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58
Q

How is the potency of inhaled anesthetics defined?

A

As the minimum alveolar concentration (MAC).

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59
Q

How is MAC expressed?

A

The percentage of gas in a mixture required to achieve anesthetic immobility.

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60
Q

What does MAC indicate?

A

It indicates the concentration needed to prevent movement in response to surgical incision in 50% of subjects.

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61
Q

What is the relationship between MAC and the potency of anesthetics?

A

A smaller MAC value indicates a more potent anesthetic (such as sevoflurane, isoflurane, and halothane), while a larger MAC indicates a less potent agent (such as nitrous oxide).

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62
Q

How does lipid solubility affect the potency of an anesthetic?

A

The more lipid-soluble an anesthetic is, the higher the fat:gas partition coefficient and the lower the MAC value, which corresponds to higher potency.

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63
Q

What factors can increase MAC, making the patient less sensitive to anesthetics?

A
  • Hyperthermia.
  • Increased CNS catecholamines (due to drugs like ephedrine and amphetamine).
  • Chronic ethanol abuse can also increase MAC.
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64
Q

Which drugs that increase CNS catecholamines and thus increase MAC, making the patient less sensitive to anesthetics?

A

Ephedrine.
Amphetamine.

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65
Q

What factors can decrease MAC, making the patient more sensitive to anesthetics?

A
  • Increased age.
  • Hypothermia.
  • Pregnancy
  • Sepsis.
  • Acute ethanol intoxication.
  • Concurrent administration of IV anesthetics.
  • α-2 adrenergic receptor agonists like clonidine and dexmedetomidine.
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66
Q

Give two examples of α-2 adrenergic receptor agonists that make the patient more sensitive to anesthetics (i.e., decrease MAC)?

A

Clonidine.
Dexmedtomidine.

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67
Q

What is the primary effect of intravenous anesthetics on the induction of anesthesia?

A

The rapid induction of anesthesia.

68
Q

Is there a specific receptor identified for the action of general anesthetics?

A

No.

69
Q

What are the main targets for inhalation anesthetic action?

A

The main targets for inhalation anesthetics are:
1) increasing the sensitivity of GABA receptors to GABA.
2) increasing the activity of glycine receptors in the spinal motor neurons.
3) blocking the excitatory postsynaptic currents of the nicotinic and glutamate receptors.

70
Q

What are the key characteristics of Halothane as an anesthetic?

A

Halothane is a prototype anesthetic that is non-explosive and allows for rapid induction and quick recovery compared to previous anesthetics, despite having a high blood:gas partition coefficient which generally leads to slower induction and recovery than the newest anesthetics.

71
Q

What are the therapeutic uses of Halothane?

A

Halothane is used as a potent anesthetic often coadministered with nitrous oxide, opioids, or local anesthetics due to its relatively weak analgesic properties. It causes uterine and skeletal muscle relaxation (useful in obstetric when uterine relaxation is indicated) and is a bronchodilator and non-pungent, making it suitable for patients with airway problems.

72
Q

Why is Halothane considered suitable for children?

A

Halothane is considered suitable for children due to its low hepatotoxicity in the pediatric population and its pleasant odor which makes administration easier.

73
Q

What are the pharmacokinetics and potential hepatotoxic effects of Halothane?

A

Halothane is metabolized to tissue-toxic hydrocarbons like trifluoroethanol and bromide ions, which can cause hepatic necrosis. Symptoms of this include anorexia, nausea, vomiting, and possible signs of hepatitis. Therefore, Halothane anesthesia should not be repeated at intervals of less than 2-3 weeks to avoid such effects.

74
Q

What are the cardiac effects associated with Halothane use?

A

Halothane can cause myocardial depression, leading to reduced cardiac output and hypotension. It also has vagomimetic effects that can cause atropine-sensitive bradycardia and may sensitize the heart to arrhythmias.

75
Q

What is malignant hyperthermia and how is it related to Halothane?

A

Malignant hyperthermia is a life-threatening condition characterized by severe muscle contraction, increased skeletal muscle oxidative metabolism, and an overwhelming increase in body temperature, which can lead to death if not treated immediately. It can be triggered by Halothane.

76
Q

How does Halothane compare to similar anesthetics in terms of renal or hepatic damage?

A

Halothane is more likely to induce renal or hepatic damage than similar general anesthetics. However, changes in renal function induced by Halothane are fully reversible.

77
Q

What are the induction and recovery characteristics of Isoflurane?

A

Isoflurane allows for rapid induction and recovery due to its low blood solubility.

78
Q

Why does Isoflurane have a low MAC value and why is it not used for inhalation induction?

A

Isoflurane has a low MAC value due to its high lipid solubility, making it a potent anesthetic. It’s not typically used for inhalation induction because it can cause a severe cough reflex and has a pungent smell.

79
Q

How does Isoflurane affect the cardiovascular system?

A

Isoflurane has a good cardiovascular profile as it does not induce cardiac arrhythmias, preserves cardiac output, does not sensitize the heart to catecholamines (making it a better choice for patients with CVD), dilates coronary arteries, and can be beneficial for patients with ischemic heart disease. However, it does produce dose-dependent hypotension due to peripheral vasodilation.

80
Q

What adverse effect is associated with the metabolism of Isoflurane?

A

Isoflurane produces halogenated metabolites which can lead to hepatotoxicity.

81
Q

What are the onset and recovery times like for Desflurane, and how does this relate to its use in surgeries?

A

Desflurane has a very rapid onset and recovery due to its low blood solubility, making it the volatile anesthetic with the lowest solubility and a popular choice for outpatient surgery.

82
Q

Why is Desflurane not used for inhalation inductions?

A

Desflurane is pungent and can irritate the airway, potentially causing laryngospasm, coughing, and excessive secretions, similar to Isoflurane. Therefore, it is not used for inhalation inductions.

83
Q

How does Desflurane affect vasodilation and cardiac output?

A

Desflurane produces greater vasodilation with minimal effect on cardiac output, making it a better choice for patients with cardiovascular diseases (CVDs).

84
Q

What is required for the administration of Desflurane due to its physical properties?

A

Due to its high volatility, Desflurane must be delivered using a special vaporizer.

85
Q

How is Desflurane metabolized and what does this mean for tissue toxicity?

A

Desflurane undergoes minimal degradation as it is eliminated unchanged through the lungs, which means tissue toxicity is rare.

86
Q

What characterizes the induction process with Sevoflurane?

A

Sevoflurane allows for rapid induction due to its rapid onset and recovery, attributed to its low blood solubility.

87
Q

Why is Sevoflurane often chosen for inhalation induction in pediatric patients?

A

Sevoflurane has low pungency and does not cause airway irritation, making it suitable for inhalation induction in pediatric patients and often the first choice for this purpose.

88
Q

What makes Sevoflurane a preferred anesthetic in cardiac surgery?

A

Sevoflurane is preferable for cardiac surgery because it produces greater vasodilation with minimal effect on cardiac output, making it a good option for patients with cardiovascular diseases (CVDs).

89
Q

What is the metabolic fate of Sevoflurane and its implication for nephrotoxicity?

A

Sevoflurane is metabolized by the liver into two metabolites, including fluoride, resulting in minimal nephrotoxicity.

90
Q

What is the common name for Nitrous Oxide and how is it characterized as an analgesic?

A

Nitrous Oxide is commonly known as laughing gas and is characterized as a potent analgesic.

91
Q

Why is Nitrous Oxide usually combined with another anesthetic?

A

Although Nitrous Oxide is a potent analgesic, it is a weak anesthetic, so it is typically combined with another anesthetic to produce pain-free anesthesia.

92
Q

What are the respiratory and muscular effects of Nitrous Oxide?

A

Nitrous Oxide is non-irritating (non-pungent), does not depress respiration (acts as a bronchodilator), and does not produce muscle relaxation.

93
Q

What is the solubility of Nitrous Oxide in blood and how does it affect induction and recovery?

A

Nitrous Oxide is poorly soluble in blood, allowing for very rapid induction and recovery times.

94
Q

What is diffusion hypoxia and how is it prevented when using Nitrous Oxide?

A

Diffusion hypoxia occurs because Nitrous Oxide diffuses rapidly from blood back to alveoli, diluting oxygen. To prevent this, Nitrous Oxide must be combined with at least 20% oxygen.

95
Q

How does Nitrous Oxide affect the cardiovascular system and cerebral blood flow?

A

Nitrous Oxide has moderate to no effect on the cardiovascular system and does not significantly increase cerebral blood flow.

96
Q

What is the hepatotoxic potential of Nitrous Oxide compared to other inhalation anesthetics?

A

Nitrous Oxide is the least hepatotoxic of the inhalation anesthetics as it is eliminated unchanged by the lungs.

97
Q

Why is Nitrous Oxide contraindicated in pregnancy?

A

Nitrous Oxide is contraindicated in pregnancy due to the risk of causing hematologic complications, including aplastic anemia.

98
Q

What is the primary effect of intravenous anesthetics on the induction of anesthesia?

A

Intravenous anesthetics cause the rapid induction of anesthesia.

99
Q

What is the preferred method of anesthesia induction in most settings?

A

The preferred method of anesthesia induction in most settings is intravenous, except for pediatric anesthesia where inhalation is commonly used.

100
Q

How can IV anesthetics be administered during longer procedures?

A

IV anesthetics may be administered as infusions to help maintain anesthesia during longer procedures.

101
Q

What is a secondary use of IV anesthetics at lower doses?

A

At lower doses, IV anesthetics may be used to provide sedation.

102
Q

What is the analgesic potency of Thiopental and Methohexital?

A

Thiopental and Methohexital are potent anesthetics but weak analgesics.

103
Q

Why do Thiopental and Methohexital enter the CNS quickly?

A

Their high lipid solubility allows them to quickly enter the CNS and depress function.

104
Q

What has replaced Thiopental and Methohexital as induction agents and why?

A

Propofol has largely replaced Thiopental and Methohexital as induction agents due to its fast onset of action.

105
Q

What duration of action do Thiopental and Methohexital have?

A

They are ultrashort-acting barbiturates.

106
Q

What respiratory side effects may Thiopental and Methohexital cause?

A

Thiopental and Methohexital might cause laryngospasm and bronchospasm if used for anesthesia, making them contraindicated in asthma.

107
Q

What cardiovascular effect can Thiopental and Methohexital have?

A

They may produce hypotension.

108
Q

What is the role of Propofol in anesthesia?

A

Propofol is an IV sedative/hypnotic used in the induction or maintenance of anesthesia.

109
Q

How fast is the onset of anesthesia with Propofol?

A

The induction of anesthesia with Propofol is very rapid, typically occurring within 30-40 seconds.

110
Q

Why is recovery from Propofol anesthesia typically rapid?

A

Plasma levels of Propofol decline rapidly, allowing for a quick recovery due to the redistribution of the drug.

111
Q

What occasional side effects can Propofol have on the CNS?

A

While Propofol facilitates CNS depression, it can occasionally cause excitatory phenomena such as muscle twitching, spontaneous movement, and hiccups.

112
Q

What effects does Propofol have on blood pressure and intracranial pressure?

A

Propofol decreases blood pressure and reduces intracranial pressure due to systemic vasodilation.

113
Q

Why can Propofol lead to respiratory depression?

A

Propofol leads to respiratory depression primarily due to its inhibitory effects on the central nervous system, which can dampen the respiratory drive.

114
Q

In what context is Propofol commonly used at lower doses?

A

Propofol is commonly infused in lower doses to provide sedation for outpatient procedures.

115
Q

Why is the incidence of postoperative nausea and vomiting low with Propofol?

A

The low incidence of postoperative nausea and vomiting with Propofol may be related to its antiemetic properties and the fact that it is less likely to stimulate the chemoreceptor trigger zone.

116
Q

What feeling does Propofol produce in patients?

A

Propofol produces a feeling of euphoria in some patients.

117
Q

How does the CNS depressant effect of Propofol compare to other anesthetics?

A

Propofol is considered a less potent CNS depressant compared to other anesthetics.

118
Q

Which intravenous anesthetic has Propofol replaced as a first-choice induction agent?

A

Propofol has replaced thiopental as the first choice for anesthesia induction.

119
Q

Why is Propofol typically prepared in a viscous or milky emulsion formulation?

A

Propofol is poorly soluble in water, which leads to its preparation in a viscous formulation that can cause pain at the IV injection site, or in a milky emulsion formulation that has an increased chance of bacterial contamination.

120
Q

What is the solution to the problems associated with Propofol’s formulations?

A

The preparation of Fospropofol, a water-soluble prodrug of Propofol, presents less problems than lipid-formulated Propofol.

121
Q

How is Fospropofol related to Propofol in terms of pharmacological effects?

A

Fospropofol is metabolized into Propofol in the body, and the pharmacological effects of Fospropofol are attributed to Propofol.

122
Q

What is the primary effect of Etomidate and does it have any analgesic activity?

A

Etomidate is an IV anesthetic with hypnotic effects and lacks analgesic activity.

123
Q

What are the benefits of using Etomidate for anesthesia?

A

The benefits of Etomidate include rapid induction and recovery, and little to no effect on the heart and circulation, making it useful for patients with coronary artery disease or cardiovascular dysfunction.

124
Q

What are the common adverse effects of Etomidate?

A

Etomidate can cause pain, nausea, vomiting, and excitatory phenomena such as involuntary movements.

125
Q

Why can Etomidate cause a decrease in plasma cortisol and aldosterone levels, and how does this affect its usage?

A

Etomidate inhibits the enzyme 11-β-hydroxylase, leading to decreased cortisol and aldosterone levels. Because of this, Etomidate is not recommended for long-term use, such as continuous infusion, since it can increase mortality.

126
Q

What type of anesthetic is Ketamine and what analgesic property does it have?

A

Ketamine is a short-acting, non-barbiturate anesthetic with good analgesic properties.

127
Q

What is the dissociated state induced by Ketamine characterized by?

A

Ketamine induces a dissociated state where the patient remains conscious, may appear to be awake, but does not feel pain.

128
Q

How does Ketamine interact with CNS receptors and affect respiratory function?

A

Ketamine interacts with the N-methyl-D-aspartate (NMDA) glutamate receptor. It is an inhibitory neurotransmitter but also activates the respiratory centers and causes bronchodilation.

129
Q

What effects does Ketamine have on the cardiovascular system?

A

Ketamine stimulates the central sympathetic outflow, which causes an increase in blood pressure and cardiac output. It’s beneficial for patients with hypovolemic or cardiogenic shock, asthma, or when cardiac depression is undesirable, but it should not be used alone in heart failure patients.

130
Q

How is Ketamine metabolized, and what should be considered in patients with liver impairment?

A

Ketamine is metabolized in the liver, but small amounts can be excreted unchanged. The dose of Ketamine should be reduced in patients with liver impairment.

131
Q

Why is Ketamine not preferred in certain patients due to its effect on cerebral blood flow?

A

Ketamine increases cerebral blood flow, which is why it is not preferred in patients with increased intracranial pressure or those at risk for cerebral hemorrhage.

132
Q

What are the potential psychological disadvantages of using Ketamine?

A

Ketamine can induce postoperative hallucinations, often referred to as “nightmares,” particularly in adults. It also has a potential for abuse.

133
Q

Why are Benzodiazepines used in conjunction with anesthetics?

A

Benzodiazepines are used with anesthetics to sedate the patient, providing anxiolysis and amnesia, which can make the overall anesthesia process smoother and less stressful.

134
Q

Which Benzodiazepine is most commonly used for anesthesia and why?

A

Midazolam is the most commonly used Benzodiazepine for anesthesia due to its rapid onset and short duration, making it suitable as a preoperative medication and for brief therapeutic procedures.

135
Q

What are the alternatives to Midazolam and their onset/duration characteristics?

A

Diazepam and Lorazepam are alternatives to Midazolam, with slower onsets and longer durations of action.

136
Q

How do Benzodiazepines affect memory and anxiety during anesthesia?

A

All three Benzodiazepines mentioned (Midazolam, Diazepam, Lorazepam) facilitate amnesia and have anxiolytic and sedative actions by enhancing the inhibitory effects of neurotransmitters, particularly GABA.

137
Q

What is the effect of Benzodiazepines on cardiovascular and respiratory function, contributing to their safety profile?

A

Benzodiazepines have minimal cardiovascular and respiratory depressant effects, which contributes to their safety in anesthetic procedures.

138
Q

Why are opioids commonly used with anesthetics?

A

Opioids are used with anesthetics due to their potent analgesic properties, which are effective both intraoperatively and postoperatively.

139
Q

What makes fentanyl and its congeners commonly used opioids in anesthesia?

A

Fentanyl and its congeners, such as sufentanil and remifentanil, are commonly used because they induce analgesia more rapidly and are significantly more potent than morphine.

140
Q

How can opioids be administered during anesthesia?

A

Opioids can be administered intravenously, epidurally, or intrathecally.

141
Q

Are opioids effective amnesics?

A

No, opioids are not considered good amnesics.

142
Q

What side effects can opioids cause during anesthesia?

A

Opioids can cause hypotension, respiratory depression (especially with large doses of fentanyl), muscle rigidity, and postanesthetic nausea and vomiting.

143
Q

How can the effects of opioids be reversed?

A

Opioid effects can be antagonized by naloxone.

144
Q

What are the primary uses of neuromuscular blockers in anesthesia?

A

Neuromuscular blockers are used to abolish reflexes for tracheal intubation and provide muscle relaxation during surgery.

145
Q

What is the mechanism of action for neuromuscular blockers?

A

Neuromuscular blockers work by blocking nicotinic acetylcholine receptors at the neuromuscular junction.

146
Q

Can you name some commonly used neuromuscular blockers?

A

Common neuromuscular blockers include cisatracurium, pancuronium, rocuronium, succinylcholine, and vecuronium.

147
Q

Do local anesthetics cause unconsciousness?

A

No, local anesthetics do not cause unconsciousness.

148
Q

How are local anesthetics applied and what is their primary function?

A

Local anesthetics are applied or injected to block nerve conduction of sensory impulses from the periphery to the CNS.

149
Q

What is the mechanism of action of local anesthesia?

A

Local anesthesia prevents action potentials by blocking sodium ion channels, which are necessary for the transient increase in permeability of the nerve membrane to sodium that is required for an action potential. This action results in the loss of sensation from the source of stimulation to the brain, leading to a loss of sensation in a limited region of the body.

150
Q

Which local anesthetic compounds are most widely used?

A

The most widely used local anesthetic compounds are bupivacaine, lidocaine, mepivacaine, procaine, ropivacaine, and tetracaine. Lidocaine is probably the most commonly used among these.

151
Q

Why can’t some local anesthetics be used systemically, and which local anesthetic is an exception to this rule?

A

Some local anesthetics cannot be used systemically due to poor absorption. However, lidocaine is an exception and is used systemically as an antiarrhythmic agent.

152
Q

How is Prilocaine metabolized and what is a potential side effect?

A

Prilocaine is metabolized in the plasma and kidneys, and one of its metabolites may lead to methemoglobinemia, which is a condition with an increased level of methemoglobin that decreases the blood’s ability to carry oxygen.

153
Q

Why should Mepivacaine not be used in obstetric anesthesia?

A

Mepivacaine is contraindicated in obstetric anesthesia due to its toxicity to neonates.

154
Q

What factors are most important in influencing the onset and duration of action of local anesthetics?

A

The pH of the tissue and the pKa of the drug are the most important factors influencing the onset and duration of local anesthetics.

155
Q

How does physiologic pH affect local anesthetics?

A

At physiologic pH, local anesthetics are charged ionized, which is the active form that interacts with sodium channels to inhibit their function.

156
Q

How can the pH of infection sites affect local anesthetic action?

A

The pH may drop in sites of infection, causing the onset of local anesthetic action to be delayed or even prevented.

157
Q

What does a low pKa indicate about a local anesthetic and its form at physiological pH?

A

A low pKa indicates that the local anesthetic is a weak base and will exist in a predominantly uncharged form at physiological pH.

158
Q

What does a high pKa indicate about a local anesthetic and its form at physiological pH?

A

A high pKa indicates that the local anesthetic is a strong base and will exist in a predominantly charged form at physiological pH.

159
Q

What effect do local anesthetics have on blood vessels, and how does this affect their duration of action?

A

Local anesthetics cause vasodilation, which leads to rapid diffusion of the drug from the site of application and a shorter duration of action when these drugs are administered alone.

160
Q

What is the benefit of adding epinephrine to local anesthetics?

A

Adding the vasoconstrictor epinephrine to local anesthetics decreases the rate of local anesthetic diffusion and absorption, which minimizes systemic toxicity and increases the duration of action at the applied site.

161
Q

What happens if a patient is allergic to one ester-type local anesthetic?

A

An allergy to one ester-type local anesthetic usually rules out the use of another ester, because the allergenic component is the breakdown product para-aminobenzoic acid, which is common to all esters upon metabolism.

162
Q

Does an allergy to one amide-type local anesthetic rule out the use of another amide?

A

No, an allergy to one amide-type local anesthetic does not necessarily rule out the use of another amide, as their metabolic pathways may differ.

163
Q

Can a patient be allergic to components in local anesthetics other than the active drug?

A

Yes, a patient may be allergic to other compounds in the local anesthetic, such as preservatives found in the vials.

164
Q

Which local anesthetics belong to the amide group?

A

The amide group includes Lidocaine, Mepivacaine, Bupivacaine, Etidocaine, and Prilocaine.

165
Q

Which local anesthetics belong to the ester group?

A

The ester group includes Cocaine, Procaine, Chloroprocaine, and Tetracaine.