Dentists possess a unique knowledge base and skill set that differs from anything else in medicine. They perform numerous complicated dental surgical procedures and also administer or prescribe anesthetics, analgesics, or sedation medications to nearly every patient they treat. Anesthesia and sedation in dentistry can have several forms. These include local anesthesia alone, oral and/or nasal sedation, intramuscular sedation, inhalation sedation (nitrous oxide), intravenous conscious sedation, intravenous deep sedation, total intravenous general anesthesia, inhalation general anesthesia, and inhalation general anesthesia with endotracheal intubation. Each of these anesthesia and sedation modalities requires a deep knowledge base with complex training and performance by qualified practitioners, as well as a thorough understanding of pharmacology. This chapter discusses how various sedation medications are administered, how they work, where they go when they enter the body, how they exert the desired sedation effects along with any undesired side effects, and how they are eliminated from the body. A technique for using the often-employed inhalational sedative nitrous oxide is described to further instruct the novice dental practitioners. A concise, yet comprehensive, review of the most commonly used medications administered in dentistry—local anesthetics—is presented along with potential complications from their use and management of these complications.
Introduction
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Anesthesia and sedation in dentistry can have several forms, including:
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Each of these modalities requires complex training and performance by qualified practitioners, as well as a thorough understanding of pharmacology.
This chapter only discusses local anesthesia, nitrous oxide, and medications used for mild/moderate sedation.
Metabolism
Plasma Protein Binding
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Protein binding can enhance or detract from a drug’s performance.
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As a general rule, agents that are minimally protein bound penetrate tissues better, but are excreted much more rapidly.
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Drugs may bind to a wide variety of plasma proteins, including albumin.
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The concentration of several plasma proteins can be altered by many factors including stress, surgery, liver or kidney dysfunction, inadequate nutrition, and pregnancy.
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Drugs bound to plasma proteins will not enter the liver readily to be metabolized or excreted, resulting in a longer drug half-life and elevated blood levels in the elderly whose plasma albumin contents are lower.
Routes of Administration
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Intranasal: direct delivery to the brain may be facilitated by the incomplete blood–brain barrier in the olfactory region.
Medications Utilized in Anesthesia/Sedation for Dental Patients
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Act as agonist on mu, delta, kappa, and sigma receptors in the central nervous system (CNS).
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Relieve pain without altering other senses (e.g., vision, hearing, touch).
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Synthetically modified morphine that is 100 times more potent.
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Cardiovascular system remains stable, but may see bradycardia.
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Best narcotic for asthmatic patients and patients with a history of nausea and vomiting.
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Can cause profound respiratory depression with deeper but infrequent breaths.
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Can cause chest wall rigidity if the administered dose is too potent and rapid.
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Stored in green medical gas cylinder tanks of varying sizes.
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Thirty percent or higher concentration of oxygen is recommended when delivering other pharmacologic agents to patients.
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Recommended for all medical emergencies except hyperventilation (see Chapter 13, Management of Medical Emergencies).
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Use with caution in patients with chronic obstructive pulmonary disease (COPD).
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Absolute contraindications: (1) Pregnancy (may cause spontaneous abortion according to some studies, though controversial), (2) otitis media, (3) congenital pulmonary blebs, (4) sinus blockage, (5) bowel obstruction, (6) nasal obstruction, (7) cystic fibrosis, (8) COPD.
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Relative contraindications: (1) Upper respiratory infection, (2) severe dental fear or anxiety, (3) patients with a prior bad experience or adverse reaction to nitrous oxide.
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Most flowmeters allow delivery of 30 to 70% nitrous oxide concentrations.
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May occur if the patient is permitted to recover from nitrous oxide sedation while breathing in only room air.
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Nitrous oxide from the bloodstream diffuses into the alveoli in the lungs diluting the oxygen concentration in the alveoli more rapidly than it can be replaced.
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This causes decreased oxygen blood saturation, resulting in hypoxia.
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Preventable via administration of high-concentration oxygen (100%) for at least 5 minutes during the recovery from nitrous oxide sedation. (1) 100% oxygen is almost five times more concentrated than the oxygen in room air (21%). (2) Allows for maintenance of adequate oxygen concentration in the alveoli.
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Patients with obstructive sleep apnea are sensitive to nitrous oxide and may benefit from lower concentrations of nitrous oxide.
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Technique for use of nitrous oxide:
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Inform patients that they “may feel like they are floating.”
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Inform patients that they “may feel tingling in their fingers and toes.”
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Onset of effect is usually 2 to 3 minutes after initiating flow of nitrous oxide.
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Low level nitrous oxide administration is usually sufficient for children.
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Medium level nitrous oxide administration is usually sufficient for most adults; maximum dose recommended for children.
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High level nitrous oxide administration (for certain adults who are unaffected at medium level).
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Maximum level nitrous oxide administration (for certain adults who are unaffected at high level).
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Procedure of administering nitrous oxide:
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Place monitors: (1) Pulse oximeter—continuous, (2) blood pressure cuff set to every 5 to 10 minutes.
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Turn flowmeter on to 6 to 8 L per minute oxygen (100%) before placing the nasal hood on the patient.
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Place the nasal hood on the patient ensuring that the size is appropriate and the fit is snug: (1) The patient should not feel air outflow on his/her eyes. (2) The patient should feel that he/she is getting enough air solely by breathing through their nose and nasal hood.
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Slowly initiate administering nitrous oxide by incrementally adjusting the nitrous oxide dial on the flowmeter: (1) Allow 2 to 3 minutes to take effect. (2) If the nitrous oxide level is too low, the patient will not experience the relaxant effects. (3) If the nitrous oxide level is too high, the patient may experience nausea, dysphoria, sleepiness, disorientation, or sweating.
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When the procedure is completed, turn off the nitrous oxide dial on the flowmeter and allow the patient to breathe 100% oxygen (6–8 L per minute) for at least 5 minutes: (1) This will prevent diffusion hypoxia and headache. (2) There is no need to slowly titrate down the nitrous oxide level when the procedure is completed.
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If the oxygen tank is empty or the tubing is not properly connected, the nitrous oxide will shut off (fail-safe mechanism).
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If the nitrous oxide tank is empty or the tubing is not properly connected, the oxygen will keep running (as long as there is oxygen in the tank).