Many diagnostic and minor therapeutic surgical procedures can be performed without general anesthesia using sedation-based anesthetic techniques. In this setting, regional or local anesthesia supplemented with midazolam or propofol and opioid analgesics (or ketamine) may be a more appropriate and safer approach than general anesthesia for superficial surgical procedures. This anesthetic technique is known as monitored anesthesia care, abbreviated as MAC, and should not be confused with the minimal alveolar concentration for the comparison of potencies of inhaled anesthetics (see text and Box: What Does Anesthesia Represent & Where Does It Work?). The technique typically involves premedica-tion with intravenous midazolam to produce anxiolysis, amnesia, and mild sedation, followed by a titrated, variable-rate propofol infusion (to provide moderate to deep levels of sedation). A potent opioid analgesic or ketamine may be added to blunt pain associ-ated with the injection of local anesthesia and the procedure itself. Another approach, used primarily by nonanesthesiologists, is called conscious sedation. This technique produces alleviation of anxiety and pain with less alteration to the level of conscious-ness by using smaller doses of sedative medications. In this state, the patient retains the ability to maintain a patent airway and is responsive to verbal commands. A wide variety of intravenous anesthetic drugs can be used in conscious sedation (eg, diaz-epam, midazolam, propofol). Use of benzodiazepines and opioid analgesics (eg, fentanyl) in conscious sedation protocols has the advantage of being reversible by the specific receptor antagonist drugs (flumazenil and naloxone, respectively). MAC or conscious sedation can be used to supplement regional anesthesia techniques such as peripheral nerve blocks or neuraxial anesthesia. A specialized form of sedation is occasionally required in the intensive care unit (ICU), when patients are under severe stress and require mechanical ventilation for prolonged periods. In this situation, sedative-hypnotic drugs and low doses of intra-venous anesthetics may be combined. Recently, dexmedetomi-dine has become a popular choice for this indication. Deep sedation is similar to a light state of general anesthe-sia characterized by decreased consciousness from which the patient is not easily aroused. The transition from deep sedation to general anesthesia is fluid and can be difficult to define. Because deep sedation is accompanied by loss of verbal respon-siveness, protective airway reflexes, and the ability to maintain a patent airway, this state may be indistinguishable from general anesthesia. A practitioner with expertise in airway management (anesthesiologist or nurse anesthetist) must be present. Intravenous agents used in deep sedation protocols mainly include the sedative-hypnotics propofol and midazolam, some-times in combination with potent opioid analgesics or ketamine, depending on the level of pain associated with the surgery or procedure.
Anesthetics Glutamate or ACh Action potential Postsynaptic neuron nACh receptor NMDA receptor B Presynaptic neuron Ca2+ Ca2+ Mg2+ Ca2+ Mg2+ Mg2+Na+ Ca2+ Na+ Ca2+ Ca2+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Anesthetics GABA or Glycine Action potential A Presynaptic neuron Mg2+ Ca2+ Ca2+ Postsynaptic neuron Glycine receptor channelK+ K+ K+ K+ K+K+K+ K+ K+ Cl– Cl– Cl– Cl– Cl– Cl– Cl– Cl– Cl–Cl– Cl– GABAA receptor FIGURE 25–1 Putative targets of anesthetic action. Anesthetic drugs may (A) enhance inhibitory synaptic activity or (B) diminish excitatory activity. ACh, acetylcholine; GABAA, γ-aminobutyric acid-A.