sedation in dentistry Flashcards

1
Q

Proper patient selection includes?

A

patient’s wants and needs
patient assessment
risk stratification

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2
Q

What is minimal sedation (anxiolysis)?

A

A minimally depressed level of consciousness where the patient can independently maintain an airway and respond normally to stimulation and verbal commands.

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3
Q

How does minimal sedation affect cognitive function and coordination?

A

It may modestly impair

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4
Q

Does minimal sedation affect ventilatory and cardiovascular functions?

A

No

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5
Q

What is moderate sedation/analgesia?

A

A drug-induced depression of consciousness where patients respond purposefully to verbal commands, either alone or with light tactile stimulation.

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6
Q

Can patients under moderate sedation independently maintain an airway?

A

Yes

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7
Q

Does moderate sedation affect cardiovascular function?

A

Usually, it maintains cardiovascular function.

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8
Q

What characterizes deep sedation/analgesia?

A

A drug-induced depression of consciousness where patients cannot be easily aroused but respond purposefully following repeated or painful stimulation.

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9
Q

Can patients under deep sedation independently maintain ventilatory function?

A

may be impaired, and patients may need assistance.

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10
Q

How does deep sedation affect cardiovascular function?

A

Cardiovascular function is usually maintained.

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11
Q

What characterizes general anesthesia?

A

A drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation.

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12
Q

What is enteral sedation?

A

Any technique of administration in which the agent is absorbed through the gastrointestinal tract or mucosa.

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13
Q

What is parenteral sedation?

A

A technique of administration in which the drug bypasses the gastrointestinal tract (intramuscular, intravenous, intranasal, submucosal, or subcutaneous routes).

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14
Q

What is inhalation sedation?

A

A technique of administration in which a gaseous or volatile agent, including nitrous oxide (N2O), is introduced into the pulmonary tree and its primary effect is due to absorption through the pulmonary bed.

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15
Q

What factors determine the depth of sedation?

A

Drug & dosage
Patient’s comfort level
Type of procedure
Patient’s medical condition
Clinician’s experience

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16
Q

What are the pre-operative requirements for sedation?

A

Health History Questionnaire
Review of Systems
Focused Physical Exam
Pre-operative Preparation (Labs/Imaging)
Assessment/Risk Stratification
Doctor-Patient Bond

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16
Q

Which patients are typically selected for elective procedures during preoperative assessment?

A

Healthier patients classified as ASA I or II.

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17
Q

What is the focus of the cardiovascular assessment during preoperative evaluation?

A

Clinical Predictors
Functional Capacity
Surgical Risk

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18
Q

Why is it important to assess for cardiopulmonary disease in a focused history?

A

may accentuate hemodynamic/respiratory depression caused by sedatives and analgesics.
May require decreased drug dosages.
EKG monitoring may be warranted.

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19
Q

Why is it important to assess hepatic or renal abnormalities in a focused history?

A

may impair drug metabolism, leading to altered sensitivity and prolonged duration of action for sedatives/analgesics.

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20
Q

Why is it important to consider medication interactions in a focused history?

A

Medication interactions between a patient’s routine medications and sedatives/analgesics can alter normal drug responses.

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21
Q

Why must patient allergies be documented during the focused history?

A

To avoid administering medications that could trigger allergic reactions.

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22
Q

How does alcohol or illicit substance abuse affect sedation?

A

Chronic use may increase tolerance to sedatives/analgesics, while acute use can have additive or synergistic effects with sedative medications.

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22
Q

How does tobacco use impact sedation procedures?

A

Tobacco use increases airway irritability and the risk of bronchospasm during sedation.

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23
Q

Why is it important to ask about prior adverse reactions to anesthesia or sedation?

A

A history of adverse reactions may indicate an increased risk during future sedation procedures.

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24
Q

The patient undergoing conscious sedation should have a
thorough airway assessment focusing on

A

airway class (mallampati score)
mouth opening
thyromental distance (distance from chin to thyroid)
range of motion of the neck

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25
Q

Mallampati Score classes

A

Predicts difficulty in intubation

Class I: soft palate, uvula, fauces, pillars visible (grade 1)
Class II: soft palate, uvula, fauces (grade 2)
Class III: soft palate, uvula, base of uvula visible (mod difficult) (grade 3)
Class IV: only hard palate visible (severe difficult) (grade 4)

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25
Q

What are the Intra-operative Monitoring?

A

● Oxygen Saturation (normal = 100%)
● Vitals: RR, HR, BP
● Level of Response/consciousness
● EKG
● End tidal CO2 (capnography)

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26
Q

What is End Tidal CO2 (capnography) and its normal range?

A

The maximal concentration of CO2 at the end of respiration (exhalation).
35-45 mmHg

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27
Q

Should oxygen be administered to all patients undergoing sedation?
Can the oxygen delivery rate or mode be adjusted?

A

Yes

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28
Q

What is the initial oxygen flow rate for sedation patients?

A

Begin at 2L/min via nasal cannula.

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29
Q

When should a baseline respiratory assessment be made?

A

Prior to administration of drugs and at least every 15 minutes thereafter.

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30
Q

What should be recorded during respiratory monitoring?
How can respiration adequacy be assessed?

A

Respiratory rate and observations of spontaneous ventilation/airway patency.
By auscultation and observing the chest rise and fall.

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31
Q

How often should BP and heart rate be assessed during sedation?

A

2-3 minutes after administering any drug, when the patient’s condition changes, and at least every 15 minutes.

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32
Q

When is EKG monitoring recommended?

A

For patients with cardiac disease or those at risk for dysrhythmias.

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33
Q

How should the level of consciousness be monitored during sedation?

A

By frequently assessing the patient’s response to commands or light tactile stimuli using the sedation scale.
Document every 15 mins

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33
Q

Equipment sedation procedures?

A

●Self inflating bag and mask
●Oxygen – 2 outlets
●Suction (working )
●Pharmacologic antagonists
●Emergency equipment – airway kit (age appropriate
● Broselow tape) crash cart, defibrillator

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34
Q

Major Drugs Classes

A

● Benzodiazepines
● Opioids
● Barbiturates
● Ketamine
● Propofol
● Volatile Agents

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35
Q

What effects do benzodiazepines produce?

A

Sedation, anxiolysis, and amnesia.

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36
Q

Do benzodiazepines provide analgesia?

A

No

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37
Q

What is the mechanism of action of benzodiazepines?

A

They act on GABA receptors in the brain.

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38
Q

What is GABA?

A

GABA is the major inhibitory neurotransmitter in the CNS.

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39
Q

Name some examples of benzodiazepines.

A

Midazolam, diazepam, lorazepam, and alprazolam.

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40
Q

What adverse effects can benzodiazepines cause?

A

Dose-related respiratory depression, hypotension, and tachycardia, especially in the elderly.

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41
Q

What happens when midazolam is administered rapidly?

A

It is particularly likely to produce apnea.

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42
Q

Are benzodiazepines generally safe during pregnancy?

A

No, they are generally contraindicated in pregnancy.

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43
Q

What side effect can diazepam and lorazepam cause?

A

Thrombophlebitis

44
Q

How does the potency of midazolam compare to diazepam?

A

Midazolam is 3-4 times more potent than diazepam. (10 mg diazepam = 2.5-3 mg midazolam)

45
Q

How does the potency of lorazepam compare to diazepam?

A

Lorazepam is 5 times more potent than diazepam. (10 mg diazepam = 2 mg lorazepam)

46
Q

What types of agents can be used to provide sedation and analgesia?

A

A variety of agents, including opioids and other sedative medications, can be used for sedation and analgesia.

47
Q

When are opioids primarily used in sedation?

A

Opioids are primarily used when analgesia is required for painful procedures.

48
Q

Why is combinational use of different classes of medication beneficial in sedation?

A

Combinational use can help decrease individual drug toxicity.

49
Q

What effects do opioids provide?

A

Opioids provide analgesia, some sedation, alterations of mood and perception, and depress cough reflexes.

50
Q

How do opioids affect the heart?

A

minimal cardiac effect.

51
Q

Where do opioids exert their agonist actions?

A

Opioid receptors concentrated in the CNS

52
Q

Why are opioids rapidly distributed to tissues?

A

Because they are highly lipid-soluble.

53
Q

What can happen when opioids accumulate in fat reservoirs?

A

They may produce long-lasting effects.

54
Q

Where are opioids metabolized?

A

In the liver.

55
Q

How are some active metabolites of opioids excreted?

A

Through the kidneys.

56
Q

Why are elderly patients more sensitive to opioids?

A

They have decreased hepatic or renal function and increased fat-soluble drug depots, requiring reduced doses.

57
Q

Why are pediatric patients more sensitive to opioids?

A

Due to their immature blood-brain barrier and renal function.

58
Q

How does the potency of meperidine compare to morphine?

A

Meperidine is 10 times less potent than morphine.

58
Q

How does the potency of hydromorphone compare to morphine?

A

Hydromorphone is 10 times more potent than morphine.

59
Q

How does the potency of fentanyl compare to morphine?

A

Fentanyl is 100 times more potent than morphine.

60
Q

What is a potential side effect of fentanyl when administered rapidly?

A

Fentanyl may cause chest wall and glottic rigidity, making manual ventilation difficult.

61
Q

Why should meperidine be used cautiously in patients with renal or hepatic disease?

A

Meperidine can cause seizure risk due to the accumulation of its active metabolite, normeperidine.

62
Q

How do barbiturates work within the central nervous system?

A

Barbiturates enhance GABA effects, depress the sensory cortex, and alter cerebellar function.

63
Q

What functions do barbiturates affect in the central nervous system?

A

Barbiturates depress sensory cortex and alter cerebellar function.

64
Q

What are two examples of barbiturates used in sedation?

A

Sodium pentothal and methohexital.

65
Q

Do barbiturates provide analgesia?

66
Q

What are some adverse effects of barbiturates?

A

Respiratory depression/apnea
Laryngospasm, bronchospasm
Tachycardia and hypotension
CNS depression or excitation
Twitching & myoclonus (often mistaken for seizures)

67
Q

Why should barbiturates be used cautiously in certain patients?

A

Cautioned in patients with hepatic/renal disease, congestive heart failure, or hypovolemia.

67
Q

Why are barbiturates not commonly used anymore?

A

They frequently produce deep sedation and have a long duration.
Should only be used by those with privileges in deep sedation.

68
Q

What risk does ketamine carry?

A

Increased risk of deep sedation; should only be used by those with privileges in deep sedation.

69
Q

How does ketamine work to create a “trance-like” state?

A

It induces functional dissociation between the cortical and limbic systems, leading to sensory isolation.

70
Q

What is ketamine’s primary effect as a pain reliever?

A

It prevents cortical interpretation of noxious stimuli, making it a potent pain reliever.

71
Q

What is the effect of ketamine on the CNS and myocardial function?

A

Ketamine produces CNS stimulation and inhibits catecholamine uptake, overcoming direct myocardial depressant effects.

72
Q

What side effects can ketamine cause?

A

Nystagmus, vocalizations, and myoclonus.

73
Q

What effects does ketamine produce?

A

Sedation, amnesia, and analgesia.

74
Q

How can the adverse effects of dreams and delirium caused by ketamine be minimized?

A

By co-administering small doses of midazolam.

75
Q

What adverse effects can ketamine cause during sedation?

A

Dreams and delirium.

76
Q

What is the mechanism of action (MOA) of ketamine?

A

NMDA receptor antagonist.

77
Q

What is the onset of action for ketamine when administered through IV or IM

A

IV: Approximately 1 minute.
IM: 10-20 minutes.

78
Q

How long does it take for the baseline level of consciousness to return after a single IV dose of ketamine?

A

Approximately 15 minutes.

79
Q

What is the mechanism of action (MOA) of propofol?

A

It mediates activity at the GABA receptor in the CNS by “slowing channel closing.”

80
Q

Does propofol have analgesic properties?

A

No, propofol has no analgesic properties but does produce sedation and amnesia.

81
Q

What are the negative cardiac effects of propofol?

A

It may cause a drop in heart rate and blood pressure by 20%.

82
Q

Is propofol contraindicated in any specific patients?

A

Yes, it is contraindicated in patients with egg and soy allergies.

83
Q

How is propofol distributed and eliminated in the body?

A

Propofol is widely distributed in the body and is eliminated via the hepatic and pulmonary systems.

84
Q

Does propofol require dosage adjustments for patients with hepatic or renal disease?

A

No, no dosage adjustments are necessary for patients with hepatic or renal disease.

85
Q

In which patients should the dose of propofol be reduced?

A

Reduced doses should be considered in the elderly, hypovolemic patients, or those receiving other narcotics/sedatives to prevent hypotension.

86
Q

What type of agent is a volatile agent?

A

A volatile agent is an inhalation agent commonly used in general anesthesia.

87
Q

What is the mechanism of action (MOA) of volatile agents?

A

The MOA is unknown, but it is believed that multiple receptors may be involved.

88
Q

What is a common negative effect of volatile agents?

A

Volatile agents can have a negative cardiac effect.

89
Q

Which volatile agent is the most potent and has the longest duration?

A

Isoflurane is the most potent and has the longest duration among the volatile agents.

89
Q

Do volatile agents have the same onset of action, metabolism, and duration?

A

No, different volatile agents have different onset of action, metabolism, and duration.

90
Q

Name some common volatile agents used in anesthesia

A

Isoflurane
Desflurane
Sevoflurane
Nitrous Oxide

91
Q

slide 60

92
Q

What are some minor complications of sedation?

A

Pain
Nausea and vomiting (up to 30% of patients)
Sore throat and laryngeal damage
Thrombophlebitis (e.g., from Diazepam)

93
Q

What are major complications of sedation due to excessive/inappropriate use of agents?

A

Respiratory depression
Cardiovascular collapse

94
Q

How should respiratory depression be managed during sedation?

A

Provide airway support
Jaw thrust/chin lift
Oral/nasal airways
Intubation/cricothyrotomy

95
Q

How should cardiovascular complications be managed during sedation?

A

Maintain adequate circulation
Discontinue agents with negative cardiac effects
Administer sympathomimetic medications (Ephedrine, Phenylephrine, Atropine)
For angina, use Nitroglycerin
Follow BLS protocols for cardiac arrest

96
Q

What is the mechanism of action of naloxone?

A

Naloxone is an opioid antagonist that binds to CNS opioid receptors to displace opioid agonists.

97
Q

What does naloxone reverse?

A

It reverses respiratory depression and sedation associated with opioids.

98
Q

What is a consideration when using naloxone?

A

Naloxone may be displaced from CNS receptors by additional doses of opioid.

99
Q

What is the half-life of naloxone?

A

Naloxone’s half-life is approximately 30 minutes.

100
Q

How does the half-life of naloxone compare to opioids?

A

Opioids have a half-life of 4-6 hours, which is much longer than naloxone’s half-life.

101
Q

What should be done after administering naloxone due to its short half-life?

A

Patients should be monitored for a longer period to watch for recurrent respiratory depression. Additional doses of naloxone may be required.

101
Q

How long should a patient be monitored after the last dose of naloxone?

A

Patients should be monitored for one hour after the last dose of naloxone.

102
Q

What happens if naloxone reverses the entire analgesic effect of narcotics?

A

Naloxone may cause severe pain if the entire analgesic effect of narcotics is reversed.

103
Q

What are the effects of over-administration of naloxone?

A

Over-administration can lead to tachycardia, hypertension, severe pain, nausea & vomiting, and even pulmonary edema due to sympathetic outflow.

104
Q

What is the mechanism of action of flumazenil?

A

Flumazenil binds to GABA receptors in the CNS to reverse the effects of benzodiazepines.

105
Q

What can displace flumazenil from its receptors?

A

Additional administration of benzodiazepines (BZDs) may displace flumazenil from receptors.

106
Q

What effects does flumazenil reverse?

A

Flumazenil reverses sedation, respiratory depression, paradoxical agitation, and causes cessation of amnesia following its administration.

107
Q

How long is the half-life of flumazenil compared to benzodiazepines (BZDs)?

A

Flumazenil has a half-life of about 45 minutes, whereas the half-life of BZDs may be greater than 12 hours.

108
Q

How long should patients be monitored after receiving flumazenil?

A

Patients should be monitored for 1 hour after the last dose of flumazenil.

109
Q

What risk is associated with flumazenil in patients with underlying disorders?

A

Flumazenil may precipitate seizures (sz) in patients with an underlying seizure disorder.