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pharmacoloy/pain control > sedation in dentistry > Flashcards

sedation in dentistry Flashcards

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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
Why is it important to ask about prior adverse reactions to anesthesia or sedation?
A history of adverse reactions may indicate an increased risk during future sedation procedures.
24
The patient undergoing conscious sedation should have a thorough airway assessment focusing on
airway class (mallampati score) mouth opening thyromental distance (distance from chin to thyroid) range of motion of the neck
25
Mallampati Score classes
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)
25
What are the Intra-operative Monitoring?
● Oxygen Saturation (normal = 100%) ● Vitals: RR, HR, BP ● Level of Response/consciousness ● EKG ● End tidal CO2 (capnography)
26
What is End Tidal CO2 (capnography) and its normal range?
The maximal concentration of CO2 at the end of respiration (exhalation). 35-45 mmHg
27
Should oxygen be administered to all patients undergoing sedation? Can the oxygen delivery rate or mode be adjusted?
Yes
28
What is the initial oxygen flow rate for sedation patients?
Begin at 2L/min via nasal cannula.
29
When should a baseline respiratory assessment be made?
Prior to administration of drugs and at least every 15 minutes thereafter.
30
What should be recorded during respiratory monitoring? How can respiration adequacy be assessed?
Respiratory rate and observations of spontaneous ventilation/airway patency. By auscultation and observing the chest rise and fall.
31
How often should BP and heart rate be assessed during sedation?
2-3 minutes after administering any drug, when the patient’s condition changes, and at least every 15 minutes.
32
When is EKG monitoring recommended?
For patients with cardiac disease or those at risk for dysrhythmias.
33
How should the level of consciousness be monitored during sedation?
By frequently assessing the patient’s response to commands or light tactile stimuli using the sedation scale. Document every 15 mins
33
Equipment sedation procedures?
●Self inflating bag and mask ●Oxygen – 2 outlets ●Suction (working ) ●Pharmacologic antagonists ●Emergency equipment – airway kit (age appropriate ● Broselow tape) crash cart, defibrillator
34
Major Drugs Classes
● Benzodiazepines ● Opioids ● Barbiturates ● Ketamine ● Propofol ● Volatile Agents
35
What effects do benzodiazepines produce?
Sedation, anxiolysis, and amnesia.
36
Do benzodiazepines provide analgesia?
No
37
What is the mechanism of action of benzodiazepines?
They act on GABA receptors in the brain.
38
What is GABA?
GABA is the major inhibitory neurotransmitter in the CNS.
39
Name some examples of benzodiazepines.
Midazolam, diazepam, lorazepam, and alprazolam.
40
What adverse effects can benzodiazepines cause?
Dose-related respiratory depression, hypotension, and tachycardia, especially in the elderly.
41
What happens when midazolam is administered rapidly?
It is particularly likely to produce apnea.
42
Are benzodiazepines generally safe during pregnancy?
No, they are generally contraindicated in pregnancy.
43
What side effect can diazepam and lorazepam cause?
Thrombophlebitis
44
How does the potency of midazolam compare to diazepam?
Midazolam is 3-4 times more potent than diazepam. (10 mg diazepam = 2.5-3 mg midazolam)
45
How does the potency of lorazepam compare to diazepam?
Lorazepam is 5 times more potent than diazepam. (10 mg diazepam = 2 mg lorazepam)
46
What types of agents can be used to provide sedation and analgesia?
A variety of agents, including opioids and other sedative medications, can be used for sedation and analgesia.
47
When are opioids primarily used in sedation?
Opioids are primarily used when analgesia is required for painful procedures.
48
Why is combinational use of different classes of medication beneficial in sedation?
Combinational use can help decrease individual drug toxicity.
49
What effects do opioids provide?
Opioids provide analgesia, some sedation, alterations of mood and perception, and depress cough reflexes.
50
How do opioids affect the heart?
minimal cardiac effect.
51
Where do opioids exert their agonist actions?
Opioid receptors concentrated in the CNS
52
Why are opioids rapidly distributed to tissues?
Because they are highly lipid-soluble.
53
What can happen when opioids accumulate in fat reservoirs?
They may produce long-lasting effects.
54
Where are opioids metabolized?
In the liver.
55
How are some active metabolites of opioids excreted?
Through the kidneys.
56
Why are elderly patients more sensitive to opioids?
They have decreased hepatic or renal function and increased fat-soluble drug depots, requiring reduced doses.
57
Why are pediatric patients more sensitive to opioids?
Due to their immature blood-brain barrier and renal function.
58
How does the potency of meperidine compare to morphine?
Meperidine is 10 times less potent than morphine.
58
How does the potency of hydromorphone compare to morphine?
Hydromorphone is 10 times more potent than morphine.
59
How does the potency of fentanyl compare to morphine?
Fentanyl is 100 times more potent than morphine.
60
What is a potential side effect of fentanyl when administered rapidly?
Fentanyl may cause chest wall and glottic rigidity, making manual ventilation difficult.
61
Why should meperidine be used cautiously in patients with renal or hepatic disease?
Meperidine can cause seizure risk due to the accumulation of its active metabolite, normeperidine.
62
How do barbiturates work within the central nervous system?
Barbiturates enhance GABA effects, depress the sensory cortex, and alter cerebellar function.
63
What functions do barbiturates affect in the central nervous system?
Barbiturates depress sensory cortex and alter cerebellar function.
64
What are two examples of barbiturates used in sedation?
Sodium pentothal and methohexital.
65
Do barbiturates provide analgesia?
No
66
What are some adverse effects of barbiturates?
Respiratory depression/apnea Laryngospasm, bronchospasm Tachycardia and hypotension CNS depression or excitation Twitching & myoclonus (often mistaken for seizures)
67
Why should barbiturates be used cautiously in certain patients?
Cautioned in patients with hepatic/renal disease, congestive heart failure, or hypovolemia.
67
Why are barbiturates not commonly used anymore?
They frequently produce deep sedation and have a long duration. Should only be used by those with privileges in deep sedation.
68
What risk does ketamine carry?
Increased risk of deep sedation; should only be used by those with privileges in deep sedation.
69
How does ketamine work to create a "trance-like" state?
It induces functional dissociation between the cortical and limbic systems, leading to sensory isolation.
70
What is ketamine’s primary effect as a pain reliever?
It prevents cortical interpretation of noxious stimuli, making it a potent pain reliever.
71
What is the effect of ketamine on the CNS and myocardial function?
Ketamine produces CNS stimulation and inhibits catecholamine uptake, overcoming direct myocardial depressant effects.
72
What side effects can ketamine cause?
Nystagmus, vocalizations, and myoclonus.
73
What effects does ketamine produce?
Sedation, amnesia, and analgesia.
74
How can the adverse effects of dreams and delirium caused by ketamine be minimized?
By co-administering small doses of midazolam.
75
What adverse effects can ketamine cause during sedation?
Dreams and delirium.
76
What is the mechanism of action (MOA) of ketamine?
NMDA receptor antagonist.
77
What is the onset of action for ketamine when administered through IV or IM
IV: Approximately 1 minute. IM: 10-20 minutes.
78
How long does it take for the baseline level of consciousness to return after a single IV dose of ketamine?
Approximately 15 minutes.
79
What is the mechanism of action (MOA) of propofol?
It mediates activity at the GABA receptor in the CNS by "slowing channel closing."
80
Does propofol have analgesic properties?
No, propofol has no analgesic properties but does produce sedation and amnesia.
81
What are the negative cardiac effects of propofol?
It may cause a drop in heart rate and blood pressure by 20%.
82
Is propofol contraindicated in any specific patients?
Yes, it is contraindicated in patients with egg and soy allergies.
83
How is propofol distributed and eliminated in the body?
Propofol is widely distributed in the body and is eliminated via the hepatic and pulmonary systems.
84
Does propofol require dosage adjustments for patients with hepatic or renal disease?
No, no dosage adjustments are necessary for patients with hepatic or renal disease.
85
In which patients should the dose of propofol be reduced?
Reduced doses should be considered in the elderly, hypovolemic patients, or those receiving other narcotics/sedatives to prevent hypotension.
86
What type of agent is a volatile agent?
A volatile agent is an inhalation agent commonly used in general anesthesia.
87
What is the mechanism of action (MOA) of volatile agents?
The MOA is unknown, but it is believed that multiple receptors may be involved.
88
What is a common negative effect of volatile agents?
Volatile agents can have a negative cardiac effect.
89
Which volatile agent is the most potent and has the longest duration?
Isoflurane is the most potent and has the longest duration among the volatile agents.
89
Do volatile agents have the same onset of action, metabolism, and duration?
No, different volatile agents have different onset of action, metabolism, and duration.
90
Name some common volatile agents used in anesthesia
Isoflurane Desflurane Sevoflurane Nitrous Oxide
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92
What are some minor complications of sedation?
Pain Nausea and vomiting (up to 30% of patients) Sore throat and laryngeal damage Thrombophlebitis (e.g., from Diazepam)
93
What are major complications of sedation due to excessive/inappropriate use of agents?
Respiratory depression Cardiovascular collapse
94
How should respiratory depression be managed during sedation?
Provide airway support Jaw thrust/chin lift Oral/nasal airways Intubation/cricothyrotomy
95
How should cardiovascular complications be managed during sedation?
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
What is the mechanism of action of naloxone?
Naloxone is an opioid antagonist that binds to CNS opioid receptors to displace opioid agonists.
97
What does naloxone reverse?
It reverses respiratory depression and sedation associated with opioids.
98
What is a consideration when using naloxone?
Naloxone may be displaced from CNS receptors by additional doses of opioid.
99
What is the half-life of naloxone?
Naloxone's half-life is approximately 30 minutes.
100
How does the half-life of naloxone compare to opioids?
Opioids have a half-life of 4-6 hours, which is much longer than naloxone's half-life.
101
What should be done after administering naloxone due to its short half-life?
Patients should be monitored for a longer period to watch for recurrent respiratory depression. Additional doses of naloxone may be required.
101
How long should a patient be monitored after the last dose of naloxone?
Patients should be monitored for one hour after the last dose of naloxone.
102
What happens if naloxone reverses the entire analgesic effect of narcotics?
Naloxone may cause severe pain if the entire analgesic effect of narcotics is reversed.
103
What are the effects of over-administration of naloxone?
Over-administration can lead to tachycardia, hypertension, severe pain, nausea & vomiting, and even pulmonary edema due to sympathetic outflow.
104
What is the mechanism of action of flumazenil?
Flumazenil binds to GABA receptors in the CNS to reverse the effects of benzodiazepines.
105
What can displace flumazenil from its receptors?
Additional administration of benzodiazepines (BZDs) may displace flumazenil from receptors.
106
What effects does flumazenil reverse?
Flumazenil reverses sedation, respiratory depression, paradoxical agitation, and causes cessation of amnesia following its administration.
107
How long is the half-life of flumazenil compared to benzodiazepines (BZDs)?
Flumazenil has a half-life of about 45 minutes, whereas the half-life of BZDs may be greater than 12 hours.
108
How long should patients be monitored after receiving flumazenil?
Patients should be monitored for 1 hour after the last dose of flumazenil.
109
What risk is associated with flumazenil in patients with underlying disorders?
Flumazenil may precipitate seizures (sz) in patients with an underlying seizure disorder.

pharmacoloy/pain control (36 decks)

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