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66 Cards in this Set

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2. What is the basic structure of local anesthetics?
2. Local anesthetics consist of a lipophilic end and a hydrophilic end connected by a hydrocarbon chain. The lipophilic end is an unsaturated benzene ring, and the hydrophilic end is a tertiary amine and proton acceptor. The bond that links the hydrocarbon chain to the lipophilic end of the structure is either an ester (---CO--) bond or an amide (-HNC-) bond. The local anesthetic is thus classified as either an ester or an amide local anesthetic.
3. Why are local anesthetics marketed as hydrochloride salts?
3. Local anesthetics are bases that are poorly water soluble. For this reason they are marketed as hydrochloride salts. The resulting solution is slightly acidic with a pH of about 6.
4. What are two differences between ester and amide local anesthetics that make classifying local anesthetics important?
4. The site of metabolism and the potential to produce allergic reactions differ between ester and amide local anesthetics, making this classification of local anesthetics important.
5. Name four ester local anesthetics.
s. The ester local anesthetics include procaine, chloroprocaine, cocaine, and tetracaine.
6. Name six amide local anesthetics.
6. The amide local anesthetics include lidocaine, mepivacaine, bupivacaine, etidocaine, prilocaine, and ropivacaine.
7. What is the mechanism of action Df local anesthetics?
7. Local anesthetics act by producing a conduction blockade of neural impulses in the affected nerve. This is accomplished through the prevention of the passage of sodium ions through ion selective sodium channels in the nerve membranes. The sodium channels are functionally inactivated by being maintained in the closed conformation. The inability of sodium ions to pass through their ion selective channels results in slowing of the rate of depolarization. As a result, the threshold potential is not reached and an action potential is not propagated in these nerves
8. Do local anesthetics most likely exert their action by working inside or outside the nerve membrane?
8. Local anesthetics are thought to exert their action on the nerve by binding to a specific receptor on the sodium ion channe~. The location of the binding site appears to be on the inner portion of the sodium channel. They may also alter odium permeability by blocking sodium channels near their external openings. This may explain why local anesthetics bind more rapidly and with a greater affinity to the receptors while the nerve is in the activated state. Regardless of the exact location of the binding site for the local anesthetic, the binding of local anesthetic to the receptor inactivates the sodium ion channel by preventing the flow of sodium ions through the channel.
9. How is the effect of a local anesthetic on the nerve terminated?
9. The conduction blockade produced by local anesthetic is completely reversible. Reversal of the blockade is spontaneous.
10. How is the resting membrane potential and the threshold potential altered in nerves that have been infiltrated by local anesthetic?
Neither the resting membrane potential nor the threshold potential is altered by local anesthetics.
11. What is the temporal progression of the interruption of the transmission of neural · impulses between the autonomic nervous system, motor system, and sensory system after the infiltration of a mixed nerve with local anesthetic?
11. The temporal progression of the interruption of the transmission of impulses is autonomic, sensory, and then motor nerve blockade. This yields a temporal progression of autonomic nef\Ous system blockade, then sensory nervous system blockade, followed by skeletal muscle paralysis.
13. What three characteristics are nerve fibers classified by? What are the three main nerve fiber types?
13. Fiber diameter, the presence or absence of myelin, and function are the three characteristics by which nerve fibers are classified. A, B, and C are the three main types of nerve fibers.
14. Which types of nerve fibers are myelinated? What is the function of myelin and how does it affect the action of local anesthetics?
14. The A and B nerve fiber types are myelinated. Myelin is composed of plasma membranes of specialized SchwaM cells that wrap around the axon during axonal growth. Myelin functions to insulate the axolemma, or nerve cell membrane, from the surrounling conducting media. It also forces the depolarizing current to flow through periodic intelTIlptions in the myelin sheath called the nodes of Ranvier. The sodium channels that are instrumental in nerve pulse propagation and conduction are concentrated at these nodes of Ranvier. Myelin increases the speed of nerve conduction and makes the nerve membrane more susceptible to local anesthetic-induced conduction blockade
15. How many consecutive nodes of Ranvier must be blocked for the effective blockade of the nerve impulse by local anesthetic?
15. At least three consecutive nodes of Ranvier must be exposed to adequate concentrations of local anesthetic for the effective blockade of nerve impulses to occur.
16. Which two nerve fiber types primarily function to conduct sharp and dull pain impulses? Which of these two nerve fibers is more readily blocked by local anesthetic?
16. The nerve fiber type A delta, which is myelinated, conducts sharp pain impulses. The nerve fiber type C, which is unmyelinated, conducts dull pain impulses. The large-diameter A delta type fiber appears to be more sensitive to blockade by local anesthetics than the smaller diameter C type fiber. This lends support to the theory that myelination of nerves has a greater influence than nerve fiber diameter on the conduction blockade produced by local anesthetics.
17. Which two nerve fiber types primarily function to conduct impulses that result in large motor and small motor activity?
17. The lerve fiber types A alpha and A beta, which are both myelinated, conduct motor nerve impulses, The nerve fiber type A alpha conducts large motor nerve impulses, and the nerve fiber type A beta conducts small motor nerve impulses.
18. Which nerve fibers are more readily blocked by local anesthetics than anv other nerve fiber?
18. Preganglionic type B fibers are more readily blocked by local anesthetics than any other nerve fiber. This is presumed to be due to a combination of its relatively small diameter and the presence of myelin.
19. How do local anesthetics diffuse through nerve fibers when deposited around a nerve? Which nerve fibers are blocked first as a result?
19. Local anesthetics diffuse along a concentration gradient from the outer surface, or mantle, of the nerve toward the center, or core, of the nerve. As a result, the nerve fibers located in the mantle of the nerve are blocked before those in the core of the nerve.
20. How are the neIVe fiters arranged from the mantle to the core in the dorsal nerve roots with respect to nerve diameter? How does this correlate with the apparent sensitivity to the effects of intrathecal local anesthetics between the small diameter and large diameter nerves of the dorsal nerve root?
20. Small-diameter nerve fibers are closer to the mantle, or nerve root surface, in dorsal nerve roots. Large-diameter nerves, conversely, are situated deep in the core of the dorsal nerve root. The diffusion path for local anesthetics is shorter to the mantle of the dorsal nerve root. In the case of dorsal nerve roots, this correlates to a shorter diffusion distance to the small diameter nerve fibers when local anesthetics are placed in the intrathecal space. The small diameter nerve fibers therefore appear to be more sensitive to local anesthetic blockade as a result of dorsal nerve root anatomy. This may explain the clinical finding of sensory nerve blockade occurring before motor nerve blockade with the onset of spinal anesthesia. In fact, the minimum concentration of local anesthetic (em) necessary for motor nerve blockade is twice that of sensory nerves.
21. How are the nerve fibers arranged from the mantle to the core in a peripheral nerve with respect to the innervation of proximal and distal structures? How does this correlate with the temporal progression of local anesthetic-induced blockade of proXimal and distal structures?
21. In a peripheral nerve the nerve fibers in the mantle most often innervate more proximal anatomic structures. The distal anatomic structures are more frequently innervated by nerve fibers near the core of the nerve. This physiologic orientamnervaleo oy nerve fibers near the core of the nerve. This physiologic orientamalgesia with subsequent progressive distal spread as local anesthetics diffuse more central core nerve fibers
22. Is the pKa of local anesthetics more than or less than 7.4?
22. The pKa of local anesthetics is more than 7.4. This means that the pH at which local anesthetics will exist divided equally between the ionized, cationic form, and nonionized form is greater than 7.4
23. At physiologic pH does most local anesthetic exist in the ionized or nonionized form? What fonn must the local anesthetic be in to cross nerve cell membranes?
23. Most local anesthetic exists in the ionized, hydrophilic form at physiologic pH. Local anesthetics must be in the nonionized, lipid-soluble form to cross the · lipophilic nerve cell membranes.,
24. Does local tissue acidosis create an environment for higher or lower quality local anesthesia? Why?
24. Local tissue acidosis is thought to be associated with a lower quality of local anesthesia. This is presumed to be due to an increase in the ionized fraction of the drug in an acidotic environment. Because the pKa of local anesthetics is greater than 7.4, it follows that when the pH is less than 7.4 a greater fraction of the local anesthetic will exist in the ionized form. This results in a decrease in the amount of local anesthetic available to cross nerve cell membJanes. (83;
25. What is the primary determinant of local anesthetic potency?
25. The primary determinant of the potency of a local anesthetic is its lipid solubility. (
26. After a local anesthetic has been absorbed from the tissues, what are the primary detenninants of local anesthetic peak plasma concentrations?
26. The rate of tissue distribution and the rate of clearance of the drug are the two primary detenninants of peak plasma concentrations of a local anesthetic after its absorption from tissue sites.
27. How are ester local anesthetics cleared?
27. Ester local anesthetics are cleared by hydrolysis by pseudocholinesterase enzymes in the plasma.
28. How are amide local anesthetics cleared?
28. Amide local anesthetics undergo degradation in the liver by hepatic microsomal enzymes. The metabolites are then excreted by the kidneys.
29. What percent of local anesthetic undergoes renal excretion unchanged?
29. Less than 5% of the injected dose of local anesthetic undergoes renal excretion unchanged. The low water solubility of local anesthetics limits their renal excretion
30. What are two organs that influence the potential for local anesthetic systemic toxicity?
30. The lungs and the liver both influence the potential for local anesthetic systemic toxicity. The ability of the lungs to extract local anesthetics from the circulation, or the first-pass pulmonary extraction of local anesthetic, influences systemic toxicity by preventing the accumulation of local anesthetics in the plasma. The liver also influences local anesthetic systemic toxicity, especially the amide local anesthetics that are metabolized by the liver. I
31. Which type of local anesthetic, the esters or the amides, is more likely to result in systemic toxicity? Why?
31. The administration of amide local anesthetics is more likely to result in systemic toxicity than the administration of ester local anesthetics secoooary to the mechanisms by which they are cleared. Amide local anesthetics are more slowly metabolized than the hydrolysis responsible for the clearance of ester local anesthetics. The slower metabolism of amide local anesthetics creates the potential for more sustained plasma concentrations, and thus the greater potential · for systemic toxicity.
32. Patients with atypical plasma cholinesterase are at an increased risk for what complication with regard to local anesthetics?
32. Patients with atypical plasma cholinesterase enzyme may be at an increased 2. Patients with atypical plasma cholinesterase enzyme may be at an increased Ester local anesthetics rely on plasma hydrolysis for their metabolism, which may be limited or absent in these patients.
33. What disease states may influence the rate of clearance of lidocaine from the plasma?
32. Patients with atypical plasma cholinesterase enzyme may be at an increased risk for developing excessive plasma concentrations of ester local anesthetics. Ester local anesthetics rely on plasma hydrolysis for their metabolism, which may be limited or absent in these patients.
34. Does lidocaine or its metabolites produce cardiac antidysrhythmic effects?
34. Both lidocaine and its metabolites possess cardiac antidysrhythmic effect
35. How does the addition of epinephrine or phenylephrine to a local anesthetic solution prepared for injection affect its systemic absorption? I
35. The addition of epinephrine or phenylephrine to a local anesthetic solution prepared for injection produces a local tissue vasoconstriction. This results in a slowing of the rate of s1stemic absor¢on of the local anesthetic.
36. How does the addition of epinephrine or phenylephrine to a local anesthetic solution prepared for injection affect its duration of action?
36. The addition of epinephrine or phenylephrine to a local anesthetic solution prepared for injection produces a local tissue vasoconstriction. This results in a prolonged duration of action of the local anesthetic by keeping the anesthetic solution in contact with the nerve fibers for a longer period of time.
37. How does the addition of epinephrine or phenylephrine to a local anesthetic solution prepared for injection affect its potential for systemic toxicity?
37. The addition of epinephrine or ph~n~ephrine to a local anesthetic solution prepared for injection causes a slower rate of systemic absorption and a prolonged duration of action. This increases the likelihood that the rate of metabolism will match the rate of absorption, resulting in a decrease in the possibility of systemic toxicity.
38. How does the addition of epinephrine or phenylephrine to a local anesthetic solution prepared for injection affect the rate of omet of anesthesia?
38. The addition of epinephrine or phenylephrine to a local anesthetic solution has · little effect on the rate of onset of anesthesia.
39. How does the addition of epinephrine or phenylephrine to a local anesthetic solution prepared for injection affect local bleeding?
39. The addition of epinephrine or phenylephrine to a local anesthetic solution decreases bleeding in the area infiltrated due to its vasoconstrictive properties.
40. What are some potential negative effects of the addition of epinephrine to a local anesthetic solution prepared for injection?
40. The systemic absorption of epinephrine in the local anesthetic solution may contribute to cardiac dysrhythmias or accentuate hypertension in vulnerable patients
41. Name some situations in which the addition of epinephrine to a local anesthetic solution prepared for injection may not be recommended.
41. The addition of epinephrine to a local anesthetic solution may not be recommended in patients with unstable angina pectoris, cardiac dysrhythmias, uncontrolled hypertension, or uteroplacental insufficiency. The addition of epinephrine to a local anesthetic solution is not recommended for intravenous anesthesia or for peripheral nerve block anesthesia in areas that may lack collateral blood flow, such as the digits or the penis
42. What are 3 potential negative side effects associated with the adninistration of local anesthetics?
42. Potential negative side effects associated with the administration of local anesthetics include systemic toxicity, neurotoxicity, and allergic reactions
42. What are some potential negative side effects associated with the administration of local anesthetics?
42. Potential negative side effects associated With the administration of local anesthetics include systemic toxicity, neurotoxicity, and allergic reactions. (
43. What is the most common cause of local anesthetic systemic toxicity?
43. L)cal anesthetic systemic toxicity occurs as a result of excessive plasma concentrations of a local anesthetic drug. The most common cause of local anesthetic systemic toxicity is accidental intravascular injection of local anesthetic solution during the performance of a nerve block
44. What are the factors that influence the magnitude of the systemic absorption of local anesthetic from the tissue injection site
44. The magnitude of the systemic absGrption of local anesthetic from the tissue injection site is influenced by the pharmacologic profile of the local anesthetic, the total dose injected, the vascularity of the injection site, and the inclusion of a vasoconstrictor in the local anesthetic solution.
45. From highest to lowest, what is the relative order of peak. plasma concentrations of local anesthetic associated with the following regional anesthetic procedures: bra· chial plexus, caudal, intercostal, epidural, sciatic/femoral?
45. The relative order from highest to lowest of peak plasma concentrations of local anesthetic associated with regional anesthesia is intercostal nerve block, caudal block, epidural, brachial plexus, and sciatic/femoral.
46. Which two organ systems are most likely to be affected by excessive plasma concentratilns of local anesthetic?
46. The central nervous system and cardiovascular system are most likely to be affected by excessive plasma concentrations of Local anesthetic
47. What are the initial and subsequent manifestations of central nervous system toxicity due to increasingly excessive plasma concentrations of local anesthetic?
47. The initial manifestations of central nervous system toxicity due to excessive plasma concentrations of local anesthetic include lightheadedness and dizziness. fhese symptoms are then followed by alterations in visual and auditory sensations, such as difficulty focusing, vertigo, and tinnitus, and may proceed to symptoms of disorientation, restlessness, and slurred speech. With progressively increasing concentrations of local anesthetic in the plasma, symptoms may progress to manifestations of central nervous system excitation, such as facial and extremity muscular twitching and tremors. Finally, tonic-clonic seizures, apnea, and death can follow.
48. What is a possible pathophysiologic mechanism for seizures that result from excessive plasma concentrations of local anesthetic?
48. Local anesthetic drugs in excessive plasma concentrations sufficient to cause seizures are believd to initially depress inhibitory pathways in the cerebral cortex. This allows for the unopposed action of excitatory pathways in the central nervous system, which manifests as seizures. As the concentration of local anesthetic in the plasma increases, there is subsequent inhibition of both excitatory and inhibitory pathways in the brain. Ultimately this leads to generalized global central nervous system depression.
49. What are some potential adverse effects of local anesthetic-induced seizures? What is the treatment of local anesthetic-induced seizures?
49. Potential adverse effects of local anesthetic-induced seizures are arterial hypoxentia, metabolic acidosis, and the pulmonary aspiration of gastric contents. The mainstay of the treatment of local anesthetic-induced seizures, as with all seizures, is aimed toward supporting the patient while attempting to abort the seizure with anticonvulsant drugs. Supplemental oxygen should be administered. The patient's airway may need to be secured with a cuffed endotracheal tube if
50. What is the indication for and disadvantage of the administration of neuromuscular blocking drugs for the treatment of seizures? .
50. The administration of paralyzing doses of a rapidly acting neuromuscular blocking drug may be necessary to facilitate intubation of the trachea during a seizure. The administration of a neuromuscular blocking drug with prolonged paralytic effects during a seizure may be indicated when benzodiazepines and barbIturates have not been effective in stopping the seizure activity. The advantage of neuromuscular blocking drugs for this purpose is twofold. First, it decreases the contribution of motor activity to the formation of lactic acid and metabolic acidosis. Second, it facilitates controlled hyperventilation of the lungs to offset potentially life-threatening metabolic acidosis and to facilitate the delivery of oxygen to the lungs. The disadvantage of neuromuscular blockade is that, although it aborts the peripheral seizure activity, it does not alter the abnormal cerebral electrical activity. The cerebral electrical activity should therefore be monitored by an electroencephalogram in patients who have had neuromuscular blocking drugs administered during seizure activity
51. Is the cardiovascular system more or less susceptible to local anes1hetic toxicity than the central nervous system?
51. The cardiovascular syrtem is less susceptible to local anesthetic toxicity than the central nervous system. That is, the dose of local anesthetic required to result in central nervous system toxicity is less than the dose of local anesthetic uired to result in cardiotoxicity.
52. What are two mechanisms by which local anesthetics produce hypotension?
52. Two mechanisms by which local anesthetics produce hypotension include the direct relaxation of peripheral vascular smooth muscle and direct myocardial depression.
53. What is the mechanism by which local anesthetics exert their cardiotoxic effects? How is this manifested on the electrocardiogram?
53. Local anesthetics exert their cardiotoxic effect directly through the blockade of sodium ion channels in the myocardium. This blockade of sodium channels results in an increase in the conduction time throughout the heart. Local anesthetics also produce a dose-dependent negative inotropic effect. Clinically, these may result in a decreased cardiac output. With extremely elevated levels these may re9.llt in a decreased cardiac output. With extremely elevated levels tations of local anesthetic-induced cardiotoxicity on an electrocardiogram in- . elude a prolongation of the PR interval and widening of the QRS complex
54. How is the relative cardiotoxicity between local anesthetic agents compared? What is the relative cardiotoxicity between lidocaine, bupivacaine, and ropivacaine?
54. The relative cardiotoxicity between local anesthetic agents is made through a comparison of the cardiovascular collapse to central nervous system toxicity ratio. This ratio compares the concentration of drug required to produce cardiovascular collapse relative to the dose required to produce central nervous
55. How does bupivacaine differ from lidocaine with respect to their cardiotoxic effects? What is a potential explanation for the differing effects of bupivacaine and lidocaine on the heart?
" 55, Bupivacaine is more cardiotoxic than lidocaine per dose administered to achieve ! a given anesthetic effect. The injection of an accidental intravenous bolus of bupivacaine can result in precipitous hypotension, cardiac dysrhythrnias, and I atrioventricular heart block. The risk of cardiotoxicity from bupivacaine appears to be greater than it otherwise would have been if epinephrine had been added . I or if the patient was on beta-I'.drenergic blockade therapy. The toxicity to the heart caused by bupivacaine is also qualitatively different than that caused by lidocaine in several ways. Filst, bupivacaine may induce ventricular arrhythmias and ventricular fibrillation with its rapid intravenous administration, whereas lidocaine is unlikely to. Second, cardiovascular resuscitation after cardiovascular collapse induced by bupivacaine is more difficult to achieve than after cardiovasculM collapse induced by lidocaine.
56. What is the maximum recommended concentration of bupivacaine to be administered for obstetric epidural anesthesia? Why?
56. The maximum recommended concentration of bupivacaine to be administered for epidural anesthesia in obstetrics is 0.5%. This recommendation comes as a result of numerous cardiotoxic reactions that have occurred with the administration of 0.75% bupivacaine to this patient population. It is possible that elevated levels of progesterone associated with pregnancy increase the sensitivity of the myocardium to the cardiotoxic effects of bupivacaine as well.
57. Why is ropivacaine unique among local anesthetics?
57. Ropivacaine is unique from all other local anesthetics because it is prepared as I a levoisomer rather than a racemic mixture. Ropivacaine was developed in response to the cardiotoxic effects of bupivacaine. Ropivacaine appears to cause less persistent myocardial depression than bupivacaine. In addition, the reversal of cardiotoxicity with aggressive cardiopulmonary resuscitation appears to result Ire favorable outcome! with ropivacaine than bupivacaine in animal studies.
58. The administration of which local anestheic has been associated with methemoglobinemia? What is the mechanism by which this occurs? How can it be treated?
58. The administration of prilocaine has been associated with methemoglobinemia I in a dose-dependent manner. It appears that this effect specific to prilocaine
59. What is the nature of the neurotoxicity produced by chloroprocaine? What is the mechanism by which this occurs?
59. The administration of chloroprocaine has been associated with neurotoxicity when administered at recommended doses. Its administration in the subarachnoid space has resulted in prolonged motor and sensory deficits. CWoroprocaine is the only local anesthetic that has been shown to have this effect, and it is not recommended for administration in the subarachnoid space or for intravenous regional anesthesia as a result. the mechanism by which these effects have occurred appears to be due to a combination of the low pH of 3.0 of the local anesthetic sobtion and to sodium bisulfite, an antioxidant included in the preparation of cWoroprocaine. Newer preparations of chloroprocaine do not contain sodium bisulfite
62. What is the allergenic potential of local anesthetics? What are the potential causes of an allergic reaction to local anesthetics?
62. Less than 1% of all adverse reactions to local anesthetics are believed to be true allergic reactions. When a true allergic reaction to a local anesthetic is suspected to have occurred, full documentation should be made in the chart regarding the dose and route of local anesthetic administered and the reaction that occurred. A true allergic reaction might yield a rash, laryngeal edema, hypotension, and/or bronchospasm. In contrast to this, the accidental intravenous injection of an epinephrine-containing local anesthetic solution may result in a vasovagal response manifested by hypotension, syncope, tachycardia, or bradycardia. There are two potential causes of an allergic reaction due to local anesthetics. First, a metabolite of the ester local anesthetics, para-aminobenzoic acid, may induce an allergic reaction. Esters are more likely than amides to cause allergic reactions on this basis. Second, the preservative methylparaben used in some commercial preparations of both arnides and esters may also have antigenic potential
65. What are some clinical uses of lidocaine that make it unique among the local anesthetics?
65. Clinical uses of lidocaine that make it unique among the local anesthetics include its use intravenously to prevent or treat cardiac ventricular dysrhythmias, to attenuate pressor responses associated with intubation of the trachea, to I prevent or treat increases in the intracranial pressure, and to minimize coughing during intubation or extubation of the trachea. Li~ocaine, as well as tetracaine, may be used topically on the mucous membranes of areas such as the nose, mouth, or tracheobronchial tree
66. What is unique to cocaine with respect to its use as a local anesthetic?
66. Cocaine is unique to all other local anesthetics by producing topical anesthesia and vasoconstriction. The mechanism for this is the inhibition of norepinephrine · reuptake into postganglionic nerve endings. This property of cocaine is useful when topically preparing the nasal mucosa for a nasal intubation, which has the potential of nasal hemorrhage. Vasoconstriction of the coronary arteries is a risk of the topical administration of cocaine. The abuse potential of cocaine is also a disadvantage of this drug. (
67. Name some possible manifestations of cocaine-induced cardiovascular effects. How should these effects be treated?
I 67. Manifestations of cocaine-induced cardiovascular effects may include coronary artery vasoconstriction, myocardial ischemia, cardiac dysrhythmias, or hypertension. The hypertension induced by cocaine has resulted in cerebral vascular accidents. The administration of cocaine with epinephrine, or in the presence of volatile anesthetics that sensitize the myocardium to catecholamines, may augment these potential effects of cocaine. The cardiovascular effects of cocaine may be treated by titrating esmolol to the desired heart rate, typically less than 100 beats per minute. A concern with the administration of beta-adrenergic blockers to these patients is the possible exacerbation of coronary artery vasospasm. Nitroglycerin may be administered to treat myocardial ischemia
68. Which two local anesthetics may be used for topicial anesthesia?
68. Tetracaine and lidocaine may be used as topical anesthetics
69. What is eutectic mixture of local anesthetics (EMLA)?
69. Eutectic mixture of local anesthetics (EMLA) is a topical anesthetic cream that consists of lidocaine 2.5% and prilocaine. EMLA cream requires 45 to 60 minutes to exert its peak effect. (8
70. Which eight local anesthetics may be used for local infiltration?
70. Procaine, chloroprocaine, lidocaine, mepivacaine, bupivacaine, ropivacaine, eti· docaine, and prilocaine may be used for local infiltration anesthesia. (88
71. Which two local anesthetics may be used for intravenous regional anesthesia?
71. Lidocaine and prilocaine may be used for intravenous regional anesthesia.