Chapter 6 Intravenous Anesthetics
1. Name some examples of intravenous anesthetics. What are the potential clinical uses of intravenous anesthetics?
Propofol
2. What type of chemical structure is propofol?
3. What is the mechanism of action of propofol?
4. How is propofol cleared from the plasma?
5. What degree of metabolism does propofol undergo? How should the dose of propofol be altered when administered to patients with liver dysfunction?
6. What is the context-sensitive half-time of propofol relative to other intravenous anesthetics? What is the effect-site equilibration time of propofol relative to other intravenous anesthetics?
7. How does the emergence from a propofol anesthetic or propofol induction differ from the emergence seen with the other induction agents?
8. How does propofol affect the cardiovascular system?
9. How does propofol affect ventilation?
10. How does propofol affect the central nervous system?
11. How does propofol affect the seizure threshold?
12. What is the relationship between propofol and nausea and vomiting?
13. How is propofol administered for sedation?
14. How is propofol administered for maintenance anesthesia?
15. How can the pain associated with the intravenous injection of propofol be attenuated?
16. Why is asepsis important when handling propofol?
17. Which patients may be at risk for a life-threatening allergic reaction to propofol?
Barbiturates
21. Name some of the barbiturates. From what chemical compound are they derived?
22. What is the mechanism of action of barbiturates?
23. How are barbiturates cleared from the plasma?
24. What degree of metabolism do barbiturates undergo?
25. What is the context-sensitive half-time of barbiturates relative to other intravenous anesthetics? What is the effect-site equilibration time of barbiturates relative to other intravenous anesthetics?
26. How do methohexital and thiopental compare with regard to induction doses, duration of action, and clinical utility?
27. How do barbiturates affect the arterial blood pressure?
28. How do barbiturates affect the heart rate?
29. How do barbiturates affect ventilation?
30. How do barbiturates affect laryngeal and cough reflexes?
31. How do barbiturates affect the central nervous system? How do barbiturates affect an electroencephalogram?
32. How should thiopental be administered and dosed for cerebral protection in patients with persistently elevated intracranial pressures?
33. What are the various routes and methods for the administration of barbiturates in clinical anesthesia practice?
34. What are some potential adverse complications of the injection of thiopental?
35. What is the risk of a life-threatening allergic reaction to barbiturates?
Benzodiazepines
36. Name some of the commonly used benzodiazepines. What are some of the clinical effects and properties of benzodiazepines that make them useful in anesthesia practice?
37. What is the mechanism of action of benzodiazepines?
38. Where are benzodiazepine receptors located?
39. How does midazolam compare with diazepam with regard to its affinity for the benzodiazepine receptor?
40. How does water-soluble midazolam cross the blood-brain barrier to gain access to the central nervous system?
41. What is the effect-site equilibration time of benzodiazepines relative to other intravenous anesthetics? How do the context-sensitive half-times of the benzodiazepines compare?
42. How do benzodiazepines affect the cardiovascular system?
43. How do benzodiazepines affect ventilation?
44. How do benzodiazepines affect the central nervous system?
45. What are some clinical uses of benzodiazepines in anesthesia practice?
46. How do midazolam and diazepam compare with regard to time of onset and degree of amnesia when administered for sedation?
47. What are some advantages and disadvantages of benzodiazepines for use as induction agents?
48. How can the effects of benzodiazepines be reversed?
49. What organic solvent is used to dissolve diazepam into solution? What are some of the effects of this solvent?
Ketamine
51. What chemical compound is ketamine a derivative of? What is its mechanism of action?
52. How do patients appear clinically after an induction dose of ketamine?
53. What is the mechanism by which the effects of ketamine are terminated?
54. What are the induction doses for intravenous and intramuscular routes of administration of ketamine? What is the time of onset for the effect of ketamine subsequent to its administration?
55. How does ketamine affect the cardiovascular system?
56. How does ketamine affect ventilation?
57. How does ketamine affect skeletal muscle tone? How does this affect the upper airway?
58. How does ketamine affect the central nervous system?
59. What does the emergence delirium associated with ketamine refer to? What is the incidence? How can it be prevented?
60. What are some common clinical uses of ketamine?
61. What can the repeated administration of ketamine lead to? How is it manifest clinically?
Etomidate
63. What type of structure is etomidate? What is its mechanism of action?
64. How is etomidate cleared from the plasma?
65. What degree of metabolism does etomidate undergo?
66. What is the context-sensitive half-time of etomidate relative to other intravenous anesthetics? What is the effect-site equilibration time of etomidate relative to other intravenous anesthetics?
67. How does etomidate affect the cardiovascular system?
68. How does etomidate affect ventilation?
69. How does etomidate affect the central nervous system?
70. How does etomidate affect the seizure threshold?
71. What are the endocrine effects of etomidate?
72. What are some potential negative effects associated with the administration of etomidate?
Dexmedetomidine
73. What type of structure is dexmedetomidine?
74. What is the mechanism of action for dexmedetomidine?
75. What are some common clinical uses for dexmedetomidine?
76. What are the typical doses for dexmedetomidine when used as infusion in the operating room?
77. How does dexmedetomidine affect the cardiovascular system?
78. How does dexmedetomidine affect the respiratory system?
79. What are the effects of dexmedetomidine on cerebral blood flow?
Answers*
1. Examples of intravenous anesthetics include the barbiturates, benzodiazepines, opioids, etomidate, propofol, ketamine, and dexmedetomidine. These drugs can be used as induction agents or, in combination with other anesthetics, for the maintenance of anesthesia. (100)
Propofol
2. Propofol is a lipid-soluble isopropyl phenol formulated as an emulsion. The current formulation consists of 1% propofol, soybean oil, glycerol, and purified egg phosphatide. (100, Figure 9-1)
3. The mechanism by which propofol exerts its effects is not fully understood, but it appears to be in part via the gamma-aminobutyric acid (GABA) activated chloride ion channel. Evidence suggests that propofol may interact with the GABA receptor and maintain it in an activated state for a prolonged period, thereby resulting in greater inhibitory effects on synaptic transmission. Propofol also inhibits the NMDA subtype of the glutamate receptor, which may contribute to its CNS effects. (101)
4. Propofol is cleared rapidly from the plasma through both redistribution to inactive tissue sites and rapid metabolism by the liver. (100-101)
5. Propofol is extensively metabolized by the liver to inactive, water-soluble metabolites, which are then excreted in the urine. Less than 1% of propofol administered is excreted unchanged in the urine. The metabolism of propofol is extremely rapid. Patients with liver dysfunction appear to rapidly metabolize propofol as well, lending some proof that extrahepatic sites of metabolism exist. This has been further supported by evidence of metabolism during the anhepatic phase of liver transplantation. (100)
6. The context-sensitive half-time refers to the time required to pass for the concentration of a particular drug to reach 50% of its peak plasma concentration after the discontinuation of its administration as a continuous intravenous infusion for a given duration. The context-sensitive half-time of a drug depends mostly on the drug’s lipid solubility and clearance mechanisms. The continuous infusion of propofol rarely results in cumulative drug effects. After the continuous administration of propofol for several days for sedation in the intensive care unit the discontinuation of the infusion resulted in the rapid recovery to consciousness. The lack of cumulative effects of propofol illustrates that the context-sensitive half-time of propofol is short. The effect-site equilibration time refers to the interval of time required between the time that a specific plasma concentration of the drug is achieved and a specific effect of the drug can be measured. The effect-site equilibration time reflects the time necessary for the circulation to deliver the drug to its site of action, such as the brain. The rapid administration of an induction dose of propofol results in unconsciousness in less than 30 seconds, illustrating its rapid effect-site equilibration time. (100-101, Figure 9-3)
7. After the administration of propofol, patients experience a rapid return to consciousness with minimal residual central nervous system effects. Patients who are to undergo brief procedures or outpatient surgical patients may especially benefit from the rapid wake-up associated with propofol anesthesia. Propofol also tends to result in the patient awakening with a general state of well-being and mild euphoria. Patient excitement has also been observed. Hallucinations and sexual fantasies have been reported to have occurred in association with the administration of propofol. (101)
8. The administration of an induction dose of propofol results in a profound decrease in systolic blood pressure greater than any other induction agent. This effect of propofol appears to be primarily due to vasodilation, which is dose dependent. Unlike the barbiturates, the heart rate is usually unchanged with the administration of propofol. Propofol may selectively decrease sympathetic nervous system activity more than parasympathetic nervous system activity. In fact, propofol inhibits the normal baroreceptor reflex such that profound bradycardia and asystole have occurred in healthy adults after its administration. (102)
9. The administration of an induction dose of propofol (1.5 to 2.5 mg/kg) almost always results in apnea through a dose-dependent depression of ventilation in a manner similar to, but more prolonged than, that of thiopental. The apnea that results appears to last for 30 seconds or greater and is followed by a return of ventilation that is characterized by rapid, shallow breathing such that the minute ventilation is significantly decreased for up to 4 minutes. Propofol causes a greater reduction in airway reflexes than any other induction agent, making it a better choice as the sole agent for instrumentation of the airway. (102)
10. The administration of propofol results in decreases in intracranial pressure, cerebral blood flow, and cerebral metabolic oxygen requirements in a dose-dependent manner. In patients with an elevated intracranial pressure, the administration of propofol, however, may be accompanied by undesirable decreases in the cerebral perfusion pressure. (101-102)
11. The effects of propofol on the seizure threshold are controversial. The administration of propofol has resulted in seizures and opisthotonos and has been used to facilitate the mapping of seizure foci. Propofol has also been used to treat seizures. High doses of propofol can result in burst suppression on the electroencephalogram. Excitatory effects that cause muscle twitching are not uncommon, but do not indicate seizure activity. (102)
12. Propofol appears to have a significant antiemetic effect, given the low incidence of nausea and vomiting in patients who have received a propofol anesthetic. In addition, propofol administered in subhypnotic doses of 10 to 15 mg has successfully treated both postoperative nausea and vomiting and nausea in patients receiving chemotherapy. (102)
13. Propofol may be administered for sedation through a continuous intravenous infusion at a rate of 25 to 75 μg/kg/min. At these doses, propofol will provide sedation and amnesia without hypnosis. Because of the pronounced respiratory depressant effect, propofol, even for sedation, should only be administered by individuals trained in airway management. (102)
14. Propofol may be administered for maintenance anesthesia through a continuous intravenous infusion at a rate of 100 to 200 μg/kg/min. The clinician may use signs of light anesthesia such as hypertension, tachycardia, diaphoresis, or skeletal muscle movement as indicators for the need to increase the infusion rate of propofol. For procedures lasting more than 2 hours, the use of propofol for maintenance anesthesia may not be cost effective. (102)
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