Anestesia

Question 1

1. What are the three major categories of anesthetic technique?

Answer 1

Anesthetic techniques are generally grouped into three major categories: general anesthesia, regional anesthesia, and monitored anesthesia care (MAC). (213)

Question 2

2. What four components are part of the clinically accepted definition of general anesthesia?

Answer 2

The four components are immobility, amnesia, analgesia, and the absence of harm to the patient (i.e., minimal adverse physiologic effects such as respiratory depression and hypotension). (213)

Question 3

3. What are the four levels on the continuum of sedation, as defined by the American Society of Anesthesiologists? Describe them in terms of patient responsiveness, airway maintenance, spontaneous ventilation, and cardiovascular homeostasis.

Answer 3

The ASA sedation continuum includes: Minimal sedation (patient responds briskly to verbal stimulus with no effect on airway or cardiovascular function); Moderate sedation (patient responds purposefully to verbal or tactile stimulation, with maintained airway and usually stable cardiovascular function); Deep sedation (patient requires repeated or painful stimulation to elicit a response, may have inadequate spontaneous ventilation requiring airway intervention, though cardiovascular function is usually maintained); and General anesthesia (complete absence of responsiveness, inadequate spontaneous ventilation necessitating airway management, and potential impairment of cardiovascular homeostasis). (214)

Question 4

4. Which of the four levels on the sedation continuum might an anesthesia provider encounter during monitored anesthesia care?

Answer 4

During MAC, the provider may encounter any level—from minimal to deep sedation—and must be prepared to escalate care to general anesthesia if needed. (214)

Question 5

5. What major factors go into the choice of anesthetic technique?

Answer 5

The choice of anesthetic technique depends on surgical requirements, the patient’s comorbidities, and patient preferences, balancing risks and benefits for optimal safety and recovery. (214)

Question 6

6. What are some perioperative roles of peripheral nerve blockade and neuraxial anesthesia besides surgical analgesia?

Answer 6

Beyond providing surgical analgesia, these techniques can reduce postoperative pain, decrease the risk of chronic pain development, and potentially reduce intraoperative blood loss. (215)

Question 7

7. How is “preventive analgesia” defined?

Answer 7

Preventive analgesia is defined as analgesia that lasts longer than 5.5 half-lives of the administered analgesic, thereby preventing central sensitization and reducing postoperative pain. (215)

Question 8

8. What is preoxygenation? Why is it performed prior to anesthesia induction?

Answer 8

Preoxygenation, or denitrogenation, is the replacement of nitrogen in the functional residual capacity with oxygen. This creates an oxygen reservoir that reduces the risk of hypoxemia during periods of apnea between induction and controlled ventilation. (216)

Question 9

9. By what drug administration routes may induction of general anesthesia occur?

Answer 9

General anesthesia may be induced via inhalation (using volatile anesthetics) or intravenously, and sometimes both techniques are used concurrently (e.g., inhaled induction in children to establish IV access, followed by IV hypnotics). (216)

Question 10

10. What is the most common high-potency volatile anesthetic gas used for inhaled induction of anesthesia, and why?

Answer 10

Sevoflurane is most commonly used for inhaled induction because of its high potency, low pungency, and relatively low lipid solubility, which facilitate a rapid and smooth onset of anesthesia. (216)

Question 11

11. When is a rapid sequence induction (RSI) technique used? What differentiates an RSI from a standard intravenous induction?

Answer 11

RSI is used for patients at high risk for aspiration (e.g., full stomach, reflux). It is characterized by the immediate sequential administration of a hypnotic and a neuromuscular blocking drug with no mask ventilation, and often the application of cricoid pressure. (217)

Question 12

12. Why is mask ventilation not performed in a true RSI? What defines a modified RSI?

Answer 12

In a true RSI, mask ventilation is avoided to prevent gastric insufflation and the risk of aspiration. In a modified RSI, gentle positive-pressure ventilation with low inspiratory pressures (typically less than 20 cm H2O) may be used if necessary. (217)

Question 13

13. How is cricoid pressure achieved? How efficacious is cricoid pressure?

Answer 13

Cricoid pressure is applied by exerting approximately 30 newtons (about 7 pounds) of force on the cricoid cartilage to occlude the esophagus. Although traditionally standard, its efficacy in preventing aspiration has been questioned in recent studies. (217)

Question 14

14. What airway management technique is considered safest in a cooperative patient at high risk for difficult or impossible intubation?

Answer 14

Awake fiberoptic intubation is considered the safest technique in cooperative patients at high risk for difficult intubation, as it allows maintenance of consciousness, spontaneous ventilation, and airway reflexes until the airway is secured. (217)

Question 15

15. What technique is used to achieve endotracheal intubation in a patient at risk for both aspiration of gastric contents and difficult or impossible intubation?

Answer 15

Awake fiberoptic endotracheal intubation is used in these high-risk patients, as it enables the patient to maintain spontaneous ventilation and protective airway reflexes until intubation is confirmed. (217)

Question 16

16. What advantages do potent volatile anesthetics offer as a maintenance drug?

Answer 16

Potent volatile anesthetics are easy to titrate, suppress autonomic responses to surgical stimuli, provide a degree of muscle relaxation, and allow for continuous monitoring of end-tidal anesthetic concentrations, which correlate with the depth of hypnosis. (217)

Question 17

17. What are the drawbacks of potent volatile anesthetics?

Answer 17

Drawbacks include a higher incidence of postoperative nausea and vomiting, emergence agitation (hyperreactivity), and potential hypotension from myocardial depression and peripheral vasodilation. (217)

Question 18

18. What differentiates nitrous oxide from the potent volatile anesthetics?

Answer 18

Nitrous oxide differs in that it produces less vasodilation and cardiac depression, has inherent analgesic properties, and due to its low blood solubility, offers rapid onset and offset. However, its low potency means it cannot be used as a sole anesthetic agent. (217)

Question 19

19. What are the advantages and disadvantages of propofol as an anesthetic maintenance drug, compared with potent volatile anesthetics?

Answer 19

Propofol offers advantages such as reduced postoperative nausea and smoother emergence with less coughing or laryngospasm, and it is suitable for procedures requiring an open airway. However, it requires reliable IV access, lacks a means for real-time serum concentration measurement, and carries a risk of intraoperative awareness if the infusion is interrupted. (217)

Question 20

20. Name some procedural and patient requirements for successful regional anesthesia as the sole anesthetic technique.

Answer 20

Successful regional anesthesia requires that the surgical site is amenable to a regional block (e.g., peripheral nerve or neuraxial block) and that the patient is cooperative and capable of providing informed consent. (218)

Question 21

21. Why might regional or neuraxial anesthesia be particularly desirable for patients with severe systemic disease?

Answer 21

For patients with severe systemic disease, regional or neuraxial anesthesia is desirable because it avoids the systemic effects of general anesthesia, such as cardiovascular depression and unpredictable pharmacokinetics in organ dysfunction. (218)

Question 22

22. What are some options available to the anesthesiologist in the event that a peripheral nerve block is attempted but surgical anesthesia is not accomplished?

Answer 22

If a peripheral nerve block is inadequate, options include supplementing the block with local anesthetic infiltration, administering IV analgesics and sedatives, postponing the surgery to reattempt the block, or converting to general anesthesia. (218)

Question 23

23. List some pharmacologic and nonpharmacologic methods of providing sedation and anxiolysis during monitored anesthesia care (MAC).

Answer 23

Pharmacologic methods include the use of propofol, opioids, and benzodiazepines; nonpharmacologic methods include video or audio distraction and verbal reassurance. (218)

Question 24

24. What are common manifestations of respiratory depression from oversedation?

Answer 24

Respiratory depression from oversedation typically presents as upper airway obstruction, hypoventilation, and resultant hypoxemia. (218)

Question 25

25. What is the atmospheric impact of potent volatile anesthetics and nitrous oxide?

Answer 25

Potent volatile anesthetics and nitrous oxide are greenhouse gases that deplete ozone; although desflurane has the highest global warming potential by volume, nitrous oxide is particularly impactful due to its high usage concentrations. (219)

Question 26

26. What are techniques to minimize the environmental impact of inhaled anesthetics?

Answer 26

Techniques include reducing fresh gas flow (low-flow or closed-circuit anesthesia), using total intravenous anesthesia (TIVA) when possible, selecting volatile agents with lower environmental impact (e.g., sevoflurane or isoflurane), and utilizing scavenging systems to capture waste anesthetic gases. (219)

Question 27

1. Is anesthetic neurotoxicity limited to pediatric patients?

Answer 27

Preclinical reports clearly demonstrate a neurotoxic effect of anesthetic drugs at all stages of neurodevelopment – from the fetus through the aged – indicating that anesthetic neurotoxicity is not limited to pediatric patients. (176)

Question 28

2. Is the issue of anesthetic neurotoxicity a recent finding?

Answer 28

No. Abnormal behavior related to general anesthesia was reported as early as the 1950s in both children and the elderly, and halothane toxicity was noted in rodents in the 1960s. (176)

Question 29

3. Has any regulatory agency commented on the issue of anesthetic neurotoxicity?

Answer 29

Yes. The FDA held open hearings and on December 14, 2016, issued a cautionary perspective warning that repeated or lengthy use of general anesthetic and sedation drugs in children under 3 years or in pregnant women during the third trimester may affect brain development. (176)

Question 30

4. What are the primary receptors that are the targets of anesthetic drugs and the purported cellular intermediaries for the reported toxicity in preclinical reports?

Answer 30

Most anesthetic and sedative drugs act as agonists at γ-aminobutyric acid (GABA) receptors, as antagonists at N-methyl-D-aspartate (NMDA) glutamate receptors, or as a combination of both; both receptor types have been implicated in anesthetic-induced developmental neurotoxicity. (177)

Question 31

5. What are the neurodevelopmental processes that are impaired with exposure to anesthetic drugs?

Answer 31

Exposure to anesthetic drugs impairs neurogenesis, neuronal morphogenesis, migration, synaptogenesis, and remodeling, processes that are critical for normal neurodevelopment. (177)

Question 32

6. How does the developmental stage of the GABAergic neuron affect its excitatory state?

Answer 32

In the immature brain, GABA acts as an excitatory neurotransmitter due to the predominance of the NKCC1 transporter that increases intracellular chloride; the switch to the mature inhibitory state occurs with the expression of the KCC2 transporter starting around the 15th postnatal week in term human infants, not completing until about 1 year of age. (177)

Question 33

7. Does neuronal apoptosis always impair neurodevelopment?

Answer 33

Not necessarily. Neuronal apoptosis is a normal part of neurodevelopment that eliminates redundant or improperly connected neurons; however, excessive apoptosis induced by anesthetic drugs can contribute to neurodevelopmental deficits. (178)

Question 34

8. Is there an age-dependent impact on dendritic development after exposure to anesthetic drugs?

Answer 34

Yes. In very young animal models, anesthetic exposure decreases synapse and dendritic spine density, whereas in slightly older animals it may increase dendritic spine formation; the implications of these divergent effects remain unclear. (178-179)

Question 35

9. What is the preclinical link between anesthesia and Alzheimer disease in older animal models?

Answer 35

Preclinical reports have shown that exposure to anesthesia, particularly isoflurane, can lead to increased accumulation of β-amyloid and tau proteins in rodent brains, suggesting a potential link with Alzheimer disease pathology. (179)

Question 36

10. Neonatal rat pups exposed to volatile anesthetics have been shown to develop learning deficits. Which interventions mitigate this adverse outcome?

Answer 36

Interventions such as exposure to an enriched environment, exercise, and administration of agents like lithium, estrogen, erythropoietin, melatonin, or dexmedetomidine have been shown to mitigate anesthetic-induced neurobehavioral deficits in neonatal animal models. (179–180)

Question 37

11. What are the three factors that increase the development of neuronal cell death in neonatal laboratory animals exposed to anesthetic drugs?

Answer 37

The development of neuronal cell death is increased by high doses of anesthetic drugs, prolonged exposure duration, and vulnerability due to the specific developmental stage of the brain. (180)

Question 38

12. Recent retrospective reports detected neurocognitive deficits after exposure to surgery and anesthesia. What are the drawbacks of these investigations?

Answer 38

These retrospective studies are subject to confounding factors such as the effects of surgery itself and underlying comorbid conditions, making it difficult to isolate the impact of anesthetic exposure on neurocognitive outcomes. (180)

Question 39

13. Are there any prospective reports that examine the impact of surgery and anesthetic at an early age on subsequent neurocognitive function?

Answer 39

Yes. Prospective studies such as the GAS and PANDA trials have been conducted; while the GAS study’s interim 2-year follow-up did not show neurocognitive differences between general and regional anesthesia, further long-term assessments are ongoing, and some smaller studies have shown subtle deficits in long-term recognition memory. (181)

Question 40

14. Are there any other perioperative factors that can impair subsequent neurocognitive function?

Answer 40

Yes. Factors such as maternal deprivation, hypoglycemia, hypoxia, hypotension, and hypocarbia during the perioperative period can adversely affect the developing brain and contribute to neurocognitive deficits. (181)

Question 41

15. Parents are in your office for surgery and want to know the long-term risks of general anesthesia for their 6-month-old infant. They have concerns about the possible neurocognitive effects of general anesthesia and are contemplating a regional anesthetic rather than a general anesthetic. What is your advice to them?

Answer 41

Based on current evidence, including the GAS study which did not show a significant neurocognitive difference between general and regional anesthesia, you can advise that while concerns are understandable, current prospective data do not conclusively demonstrate that general anesthesia leads to long-term neurocognitive deficits in infants. (181)