74. B. The response of the nerve to electrical stimulation depends on three factors: the

current applied, the duration of the current, and the position of the electrodes. These

factors can be modified in different ways to take advantage of the characteristic

features of the nondepolarizing neuromuscular blockade: fade and post-tetanic

facilitation with high-frequency stimulation. When stimulation is applied at a

frequency of ≥30 Hz, the mechanical response of the muscle is the fusion of

individual twitch responses. In the absence of neuromuscular-blocking drugs, no fade

is present and the response is sustained. During nondepolarizing block, the response

achieves a peak and then fades. Higher the frequency, more useful it is to detect

residual blockade, although sometimes there may be fade after stimulation with 100

Hz in the absence of a neuromuscular block. On the other hand, with train of four

when 2-Hz stimulation is used, the mechanical or electrical response decreases little

after the fourth stimulus, and the degree of fade is similar to that found at 50 Hz.

Problem with train of four is the difficulty to evaluate by visual or tactile means the

difference between the height of first and the fourth twitch. Irrespective of the

experience, it is difficult for anesthesiologists to detect train-of-four fade when actual

train-of-four ratio is 0.4 or greater, meaning thereby that residual paralysis may go

undetected. This shortcoming may be overcome, to some extent by applying two

short tetanic stimulations (three impulses at 50 Hz, separated by 750 ms), and by

evaluating the ratio of the second to the first response.

75. D. Guillain–Barré syndrome is the most common cause of acute flaccid paralysis.

It is an autoimmune disease triggered by bacterial or viral infection. Paralysis leads

to proliferation of extrajunctional acetylcholine receptors with risk of hyperkalemia if

succinylcholine is used. These patients may show a range of sensitivity to

nondepolarizing muscle relaxants from extreme sensitivity to resistance. Use of these

agents although is not contraindicated as long as caution is practiced in assuring

return of normal muscular power at the end of the procedure before extubation is

performed. If the circumstances allow, intrathecal opioids and epidural local

anesthetics may actually be a better way to provide anesthesia for these patients.

76. C. Sympathetic stimulation at the time of intubation may cause an exaggerated

sympathetic response and needs to be considered in this situation. Blockade of α

receptors by labetalol may be helpful under this condition, but its concomitant

blockade of β receptors may pose problem. Intense increase in the afterload

secondary to exaggerated release of norepinephrine may not be tolerated by the heart

that is inhibited by labetalol. Direct vasodilators like nitroglycerine and nitroprusside

are more suitable for this situation than a nonselective β-blocker agent. As ketamine

can stimulate sympathetic discharge, it is not an appropriate induction agent for this

patient. Ephedrine may also increase the release of norepinephrine from the stored

site and cause profound hypertension and cardiac dysrhythmias. Propofol does not

have any such action, and it is appropriate for use in this case. As mentioned earlier,

cocaine inhibits reuptake of norepinephrine into the presynaptic nerve, thus making it

accumulate in these nerve endings.

77. C. An acute of episode of cyanosis in a child with history of tetralogy of Fallot

signifies more right-to-left shunt because of decreased systemic vascular resistance.

Phenylephrine may be an appropriate agent for this situation, as it will increase the

systemic vascular resistance through its action on α1

receptors, thus decreasing the

shunt. As more blood flows through the lungs before returning to the heart, more

oxygen will be available to the peripheral tissues improving the cyanosis.

Oxygen in this situation may not be helpful as not enough of the blood is flowing

through the lungs. Other options also may help treat the primary problem. Children

with this condition learn to treat these episodes, called “tet spells,” by squatting

down, thus increasing their systemic vascular resistance and venous return to the

heart.

78. C. Clonidine has been in clinical use for over two decades now. It is a very potent

antihypertensive and is very useful to control high blood pressure in some patients

with a very resistant kind of disease. Unfortunately, oral dose requires repeated

doses, and omission of a dose, as will happen if a long surgical procedure was

scheduled, may lead to severe rebound hypertension. Availability of transcutaneous

patch has helped decrease this problem. A differential diagnosis in a patient with

hypertension in the recovery room should always include possibility of rebound

hypertension secondary to omission of a dose of an α agonist like clonidine.

Other antihypertensive agents mentioned in the question do not lead to rebound

hypertension, although hypotension during anesthesia associated with perioperative

use of drugs causing angiotensin-converting enzyme blockade can be difficult to

manage.

79. C. Postoperative nausea and vomiting (PONV) is one of the most disliked side

effects of anesthesia and surgery. Efforts to treat it sometimes lead to troublesome

side effects which look alarming at the time of presentation but are easy to treat.

Dystonic reactions, including tardive dyskinesia, torticollis (commonly called

oculogyric crisis), dysphagia, and excessive salivation, are some of the

manifestations of this pseudoparkinsonian syndrome. Butyrophenones,

phenothiazines, gastrointestinal prokinetics, and lithium are some of the etiologic

agents.

Although promethazine can cause these reactions, the incidence is much lower

than with metoclopramide. Granisetron is a 5-HT3

-receptor antagonist similar to

ondansetron. The 5-HT3

-receptor antagonists have become the most frequently

administered prophylaxis and treatment for PONV due to their efficacy. Central

nervous symptoms occur in less than 8% of patients treated with this group of drugs.

Intravenous diphenhydramine provides excellent relief of these neurologic symptoms.

80. A. Repeated administration of ketamine may necessitate increased dose to achieve

the same effect. This phenomenon could partly be explained by the fact that chronic

administration of ketamine stimulates the liver enzymes that metabolize it. It exerts

its primary anesthetic and analgesic action through NMDA receptor, although it is

found to interact with many other receptors in the central nervous system. Primary

site of metabolism of ketamine is liver. It is not significantly bound to plasma

proteins and thus is readily available for distribution into the tissues.

81. C. Etomidate cannot be used as an infusion because of its suppressive action on

the adrenal gland; otherwise, it would be an ideal sedative agent for procedure that

needs moderate sedation as it does not depress respiration even when used in

induction doses. It is a potent cerebral vasoconstrictor and causes decrease in

cerebral metabolism as well as cerebral blood flow. In comparison to thiopental it

increases the excitatory spikes on the EEG and is a good agent for anesthesia for

electroconvulsive therapy and mapping for seizure focus if EEG activity needs to be

facilitated. An administered dose of etomidate is almost completely metabolized by

the liver, and very little of the parent molecule is found in the urine.

82. D. Gabapentin has become a first-line treatment for neuropathic pain. This action is

not mediated through GABA receptors as would be expected from the name. Instead,

it modulates voltage-gated calcium channels which get activated in an injured nerve.

Inhibition of this channel leads to decreased influx of calcium into the nerve cell,

decreasing neuronal transmission responsible for causing pain.

Gabapentin has not been found to interact directly with NMDA receptor.

Gabapentin’s role in treatment of neuropathic pain has not been linked with any

interaction with sodium channel.

83. D. Lipid solubility of a local anesthetic is most closely related to its potency, while

pKa determines the onset of action. As a result, more lipid-soluble local anesthetics

like tetracaine and bupivacaine are more potent (needing less dose) than less lipidsoluble local anesthetics like lidocaine. The pH at which the charged and uncharged

forms of the drug exist in equal concentration is pKa

. As it is the uncharged form that

crosses the neuronal membrane, local anesthetics with a pKa

farther from the

physiologic pH have more of the drug in ionized (charged) form delaying their onset

of action. This is not the only determinant of the onset of action, though

chloroprocaine has a very short onset of action despite having a pKa of 8.7. Reason

is that the quantity of the drug injected is so high with chloroprocaine that more of its

molecules are available in its uncharged form despite the low percentage of the drug

found in uncharged form. Protein-binding of the local anesthetic determines its

duration of action as the receptors are proteins, and a drug with a higher affinity for

protein will latch on to these receptors longer than a drug with less affinity for

protein-binding. Intrinsic property of a drug to cause vasodilatation causes the drug

to get absorbed in the systemic circulation, reducing its duration of action at the site

of injection compared to a local anesthetic which causes vasoconstriction.

84. A. Etomidate is a carboxylated imidazole. It resembles midazolam in its

pharmacokinetics, in that it is water soluble in acidic form and would be useless as

an induction agent, except that it changes its characteristics in the body and becomes

lipid soluble on exposure to physiologic pH. Unlike propofol, it is not useful for

sedation of the patients in the ICU because of its action on adrenal glands. It inhibits

11-β-hydroxylase, thus causing inhibition of conversion of cholesterol to cortisol.

Patients experiencing sepsis or hemorrhage, and who might require an intact cortisol

response, would be at risk if etomidate is administered to them. Even a single dose

may lead to a prolonged depressant effect (4–8 hours) on the adrenal gland. As

propofol is a substituted isopropyl phenol, it is very dissimilar in its chemical

structure to etomidate. Like other induction agents, awakening from an induction

dose of etomidate is secondary to redistribution of the drug. Liver metabolism of

etomidate is very complete but not fast enough that that action will lead to awakening

from an induction dose of this agent.

85. A. Clopidogrel binds to ADP receptors on the surface of platelets. This action

leads to inhibition of activation, aggregation, and degranulation of platelets.

Clopidogrel modifies the ADP receptor irreversibly, resulting in its inhibition for the

lifetime of the platelet, which is up to 7 days. So recommendation from ASRA is to

avoid performing a neuraxial block for 7 days even if only a single therapeutic dose

of clopidogrel was used by the patient. Clopidogrel may cause neutropenia,

thrombotic thrombocytopenic purpura, and hepatic dysfunction but has not been

associated with pancytopenia.

86. C. NMDA receptors have been documented in the spinal cord, and epidural

ketamine does have some analgesic action but much less than morphine. Of all the

anesthetics available, ketamine maintains the muscle tone the most, and so it does not

decrease the duration of action of nondepolarizing neuromuscular-blocking agents.

Although in vivo ketamine has been shown to maintain the stroke volume, in vitro

studies with isolated myocardial cell show that ketamine leads to decrease in the

force of contraction of myocardial cell. In vivo finding is explained by the ability of

ketamine to stimulate sympathetic system, which counteracts its myocardial

depressant action. This action of ketamine can get unmasked in a patient with chronic

congestive heart failure, that is, already using maximum sympathetic activity to

maintain his or her cardiac output. Ketamine does not decrease the amplitude of the

cortical sensory–evoked potentials.

87. A. True allergic reaction to a local anesthetic is very rare, but is more common

with ester local anesthetics compared with amide local anesthetics. Procaine is the

only ester local anesthetic among the choices given in this question. All others are

amides. So it is probably from procaine.

88. A. Lidocaine has been in use for treating a myriad of pain conditions involving

neuropathic pain. Although primary mechanism of its analgesic action may be

through blockade of the sodium channel, it acts on many other channels including

calcium and G-protein–coupled receptors. So the mechanism of its analgesic action

may be more complicated than simple blockade of sodium channel. Although

lidocaine has been found to inhibit NMDA receptor in supra clinical levels,

activation of this receptor would not lead to analgesia.

89. D. Belladonna alkaloids found in the nature sometimes lead to manifestations of

anticholinergic syndrome. Factors that need to be taken into consideration for

treatment of this condition include whether there is CNS involvement or not. In this

case, it seems that manifestations of CNS involvement are obvious. Neostigmine,

pyridostigmine, and edrophonium have quaternary ammonium ion in their chemical

structure, making them unable to cross the blood–brain barrier. Physostigmine being

a tertiary compound is able to cross this barrier and is able to antagonize the central

actions of these anticholinergic agents.

90. D. Many physiologic factors and medications are associated with potentiation of

action of neuromuscular blockers. Calcium channel blockers like verapamil lead to

decreased sarcoplasmic concentration of calcium, which may potentiate the muscle

weakness as well as prolong the duration of action of neuromuscular-blocking agents.

Carbamazepine was originally used as anticonvulsant but has been found to be

useful in many other conditions. It is not associated with prolonged action of

neuromuscular-blocking agents.

Many antibiotics, notably aminoglycosides, prolong the actions of these drugs,

but clindamycin is safe to use and has not been shown to have any deleterious effect

when used concomitantly with drugs like vecuronium.

91. C. Remifentanil is metabolized by nonspecific esterases found in blood and

tissues. This metabolism is so rapid that action of remifentanil is terminated without

the need for redistribution or hepatic extraction. There is no accumulation of the drug

in patients with renal failure. Elimination half-life (6 minutes) is not prolonged even

after a prolonged infusion. Hypothermia during cardiac bypass does prolong its

elimination time up to 20%.

92. C. Dexmedetomidine is an α2

-agonist, which acts centrally to inhibit sympathetic

nervous system activity. Clonidine belongs to the same group of medicines.

Dexmedetomidine actually sometimes is used to treat spasm observed in cerebral

palsy patients. Its effect in opioid-induced rigidity is not well studied. Decay time of

the serum levels of dexmedetomidine after a short duration of infusion is very fast,

but if it used for longer time, for example, 10 hours, as it is sometimes used in

intensive care unit setting, the sedative action may take a long time to dissipate.

Dexmedetomidine decreases systemic vascular resistance, and that is one of its

mechanism by which it may cause a decrease in blood pressure.

93. D. Myotonia is characterized by continued involuntary contraction of a group of

muscles. So once triggered, muscles fail to relax. Myotonic dystrophy is the most

common form. Succinylcholine can cause severe hyperkalemia and is contraindicated

in this condition. Nondepolarizing muscle relaxants may not be able to reverse this

spasm. As neostigmine can also trigger myotonic episode, its use for reversal of

muscle relaxants is not indicated. For that reason, it is prudent to avoid using longeracting nondepolarizing agents that may require reversal agents.

Hypothermia can trigger this condition, so precautions need to be taken to avoid

it during any anesthetic. Best treatment to relieve the spasm is to inject local

anesthetic into the muscle.

94. C. Administration of anticholinesterase agents to reverse the action of

nondepolarizing agent allows the acetylcholine levels to build up not only in

neuromuscular junction of the skeletal muscle but also at the level of muscarinic

receptors. That leads to the problem of bradycardia if not effectively

counterbalanced by administration of an anticholinergic agent. Finding the best

combination of these agents is of great importance to an anesthesiologist. Older

anticholinesterase agent edrophonium causes the cholinesterase activity to increase in

cardiac muscarinic receptors, while neostigmine was found to have additional direct

action on these cardiac receptors. Despite that finding, neostigmine-induced

bradycardia is effectively prevented by administration of anticholinergic agent

compared with edrophonium, where this effect is not as predictable. Another factor to

consider is the onset of action of these drugs. Atropine and edrophonium are very

fast-acting, while neostigmine and glycopyrrolate are slower in onset. As a result, if

glycopyrrolate is injected to counteract the cholinergic response induced by

edrophonium, the chance of development of bradycardia is greatest with this

combination, as glycopyrrolate will take much longer and may not reverse all of the

cholinergic effect produced by edrophonium.

95. D. Carcinoid syndrome can be precipitated in the operating room when the

carcinoid tumor is manipulated by the surgeon. Cause is the release of massive

amount of hormones made by the carcinoid tumor into the systemic circulation. Signs

and symptoms during anesthesia may include flushing of head, neck, and upper

thorax, bronchospasm, and hypo or hypertension. Many carcinoid tumors contain

somatostatin receptors: a gastrointestinal regulatory peptide that reduces the

production and release of gastro pancreatic hormone. Somatostatin infusion can

avoid and treat the manifestation of this syndrome in the perioperative period. A

synthetic analogue: octreotide is used more often in contemporary practice. It is

recommended to be started 2 weeks prior to the scheduled surgery and continued in

the postoperative period. Ketamine is not indicated in this condition, as it may

increase the sympathetic nervous system discharge and worsen the situation.

Sevoflurane is helpful to treat bronchospasm acutely but is not specific for this

condition and may not be potent enough to treat bronchospasm induced by these

hormones. Dexamethasone is not indicated for the acute treatment of bronchospasm,

as its onset of action measures in hours and not in minutes.

96. D. This patient seems to be in hypovolemic shock. Body’s response to such a state

is to redirect the intravascular volume to vital organs like brain and heart by causing

peripheral vasoconstriction through activation of the sympathetic system. Thiopental

is a known vasodilator. Mechanism of this action includes barbiturate-induced

depression of the medullary vasomotor center and decreased CNS outflow from the

CNS. This vasodilatation will cause peripheral pooling of blood. This may cause

catastrophic drop in blood pressure, which this patient may not be able to tolerate.

Metabolism of thiopental by the liver is slow and does not contribute appreciably to

the termination of effect of this drug. Thiopental does have negative inotropic effects

on the heart, although this effect is normally masked by baroreceptor-mediated

responses.

97. D. Patients with valvular heart disease are sometimes extremely sensitive to abrupt

changes in the heart rate. High-dose fentanyl has been shown to cause bradycardia

through its effect on the vagus nerve. To some extent, this may be desirable in a

patient with stenotic valvular lesion. In case of regurgitant lesions, this may lead to

critical decrease in cardiac output. In order to counteract this bradycardia action of

the fentanyl, some anesthesiologists like to use a muscle relaxant that causes

tachycardia. Pancuronium and an older nondepolarizing muscle-relaxant gallamine

were used for this purpose. Effect of pancuronium on the heart rate is elicited at the

level of sinoatrial node by blockade of the muscarinic receptors. On the other hand,

effect of fentanyl that caused bradycardia was more through central nuclei of the

vagus nerve. Carotid baroreceptors and β adrenergic receptor are not involved in

induction of tachycardia noticed after administration of pancuronium.

98. D. Different surgical techniques are used to suture the donor heart to the cuff of the

recipient heart. In any case, donor sinoatrial (SA) node is severed of its autonomic

nervous system connections. As a result, all of the drugs that use SA node and

normal conduction system of the heart to produce their cardiac effects fail to produce

their effects in a transplanted heart. Although α1

receptors are found in the heart,

their stimulation with phenylephrine is not associated with chronotropic effects.

Only drugs that are able to directly stimulate the adrenergic receptors found in

the myocardium are useful in treating bradycardia in a transplanted heart.

Isoproterenol being a direct β1 stimulant is the drug of choice to treat an episode of

bradycardia under these circumstances.

99. C. Propofol infusion syndrome was first described in pediatric intensive care units,

but quite a few adult cases have been reported now. Earliest sign of syndrome is

metabolic acidosis because of impairment oxidative phosphorylation in the

mitochondria, anaerobic metabolism, and accumulation of lactic acid. Cardiac

dysfunction is also an early sign, which manifests early on as bradycardia, and rightheart block is very common. Rhabdomyolysis is a hallmark of this condition, and

free myoglobin precipitates in the renal tubules, leading to kidney failure. In an

established case, the mortality rate is extremely high, in excess of 80%. Higher

cumulative dose of propofol over a relatively longer period of time seems to be

associated with higher incidence of this condition. This has led to a drop in the

popularity of this drug in the pediatric intensive care setting.

100. C. Generally, cerebral blood flow is related to cerebral metabolic rate with factors

that decrease cerebral metabolic rate decrease the cerebral blood flow. This coupling

effect is preserved during anesthesia, but the degree of the coupling may be altered

by anesthetic agents where inhalational agents have relatively higher cerebral blood

flow for any degree of cerebral metabolic rate. This variation is different for different

inhalational agents and also at different doses of the same agent. At 1.5 MAC, the

overall effect of desflurane is cerebral vasodilatation and increased blood flow.

Although nitrous oxide has been shown to have species-specific action on

cerebral vasculature, it is clear that in humans, it is a cerebral vasodilator with

potential of increasing the cerebral blood flow and intracranial pressure. Phenytoin is

an anticonvulsant, which has many central nervous system effects but has not been

shown to be a cerebral vasodilator. Pentothal decreases cerebral metabolic rate and

is known to preserve the normal coupling between the metabolism and blood flow.

So administration of this agent will decrease the cerebral blood flow.

101. A. Anaphylactic reaction during anesthesia is estimated to occur between 1 in

5,000 and 1 in 25,000 cases. Neuromuscular-blocking drugs seem to be the most

common agents causing this reaction. Incidence is far too low to determine the

relative frequency of occurrence with individual neuromuscular blocker. Latex,

antibiotics, and induction agents are much less common etiologic agents in

anesthesia. Opioids extremely rarely cause anaphylactic reactions.

Spinal and Epidural Anesthesia

Thomas Halaszynski

1. A spinal neuraxial anesthetic was given 20 minutes earlier to a 28-year-old G3P2

parturient scheduled for repeat cesarean section. Alcohol swab exam revealed that

she has lost temperature sensation up to T2 level. At what level do you anticipate

the block will reach to provide adequate pain control?

A. T2

B. T3

C. T4

D. T5

2. You have just administered a bolus of 2% lidocaine (25 mL) through an epidural

catheter that has been working well for labor analgesia in preparation for emergency

cesarean section for fetal distress in an otherwise-healthy 35-year-old woman.

Shortly after administration of lidocaine, the patient complains of nausea, and you

notice that her heart rate has decreased from 99 to 38 bpm. The most likely cause is

A. Anaphylactic reaction to lidocaine

B. Pneumothorax

C. Epidural level is higher than T4

D. Amniotic fluid embolus

3. Contraindication(s) for neuraxial blockade include(s)

A. Severe aortic stenosis

B. Severe bleeding tendency

C. Existing severe hypotension

D. All of the above

4. During epidural placement using a midline approach, the epidural needle penetrates

all the following anatomical layers, except

A. Ligamentum flavum

B. Subarachnoid membrane

C. Supraspinous ligament

D. Intraspinous ligament

5. Major benefits of a neuraxial block in a Whipple procedure include all the following,

except

A. Decreases the incidence of atelectasis

B. Leads to earlier return of GI function

C. Decreases the risk of urinary retention

D. Reduces the risk of pulmonary embolism or deep-vein thrombosis

6. The correct statement for human neuraxial anatomy is

A. Adult spinal cord ends at L2

B. Spinal cord in children ends at L3

C. The dural sac and subarachnoid space in adults end at S1

D. The dural sac and subarachnoid space in children end at S2

7. Blood supply to the human spinal cord includes all of the following, except

A. Blood supply to the spinal cord is from a single anterior spinal artery and two

posterior spinal arteries

B. The anterior spinal artery supplies the anterior two-thirds of the spinal cord, and

the posterior spinal arteries supply the posterior one-third

C. Anterior spinal artery originates from the vertebral artery

D. Posterior spinal artery originates from the posterior cerebral artery

8. The principal site of action of local anesthetics placed into the epidural space is the

A. Spinal cord

B. Nerve roots

C. Epidural space

D. Subarachnoid space

9. Lidocaine and epinephrine are commonly used together when testing epidural

anesthesia because

A. Lidocaine injection (3 mL of 1.5%) intravascularly will induce local anesthetic

toxicity such as perioral numbness

B. Intrathecal injection of epinephrine will result in a high spinal

C. Intrathecal injection of lidocaine can cause a low-level spinal anesthesia with

some degree of motor block

D. Intravascular injection of epinephrine (typically 15 μg/3 mL) can cause

hypertension more than tachycardia

10. As an adjuvant in epidural anesthesia, epinephrine can

A. Prolong duration of blockade

B. Improve the quality of blockade

C. Decrease the peak plasma levels of local anesthetic concentration

D. All of above

11. Factors that can affect the level of an epidural anesthetic include

A. Patient weight, amount of local anesthetic injected, patient position

B. Patient height, amount of local anesthetic injected, patient position

C. Patient age, amount of local anesthetic injected, patient position

D. B and C

12. Addition of sodium bicarbonate to epidural local anesthetics may accelerate the

onset of blockade with all of the local anesthetics, except

A. Lidocaine

B. Chloroprocaine

C. Mepivacaine

D. Bupivacaine

13. Factors influencing the level of spinal anesthesia achieved include all of the

following, except

A. Baricity of anesthetic solution

B. Patient age

C. Volume of anesthetic solution injected

D. Patient gender

14. All of the following factors may influence the spinal level achieved during spinal

anesthesia, except

A. Drug dose

B. Needle direction

C. Patient position at the time and immediately following injection

D. Patient weight

15. Complications from neuraxial blockade may include all of the following, except

A. Radiculopathy

B. Anterior spinal artery syndrome

C. Arachnoiditis

D. Constipation

16. Neuraxial block complications using local anesthetics alone include all of the

following, except

A. Post–dural puncture headache

B. Urinary retention

C. Postoperative cognitive dysfunction

D. High spinal anesthesia

17. Spinal anesthesia was performed on a 25-year-old healthy male for ureter stent

placement. A total of 1.5 mL of 5% preservative-free lidocaine in 7.5% dextrose was

injected intrathecally after being mixed with CSF. There was evidence of free CSF

flow before and after injection. The surgery was performed in the lithotomy position

and was uneventful, but the patient complained of severe buttock pain in the post–

anesthesia care unit. A neuro exam was negative for sensory and motor deficits. The

most likely diagnosis is

A. Spinal hematoma

B. Spinal abscess

C. Transient neurological symptoms

D. Radiculopathy

18. You are consulted as to when a patient would be an appropriate candidate for a

neuraxial block following administration of the following anticoagulant medications

(patient does not have any other coagulopathies, and does not take other medications

that could influence coagulation). The most correct statement is

A. Last dose of ticlopidine (Ticlid) 7 days ago

B. Last dose of clopidogrel (Plavix) this morning

C. Last dose of abciximab (ReoPro) 24 hours ago

D. Last dose of eptifibatide (Integrilin) 12 hours ago

19. You performed an epidural anesthetic for an elective open–abdominal aneurysm

repair. You are asked to advise the surgeon when it would be considered safe to

administer intraoperative intravenous heparin:

A. Not at all

B. One hour after epidural placement

C. Two hours after epidural placement

D. Four hours after epidural placement

20. A higher-than-expected spinal level achieved or greater dermatomal spread of local

anesthetic can be associated with all of the following clinical situations, except

A. Pregnancy

B. Ascites

C. Elderly

D. Female gender

21. Commonly used spinal anesthesia adjuvants include all the following, except

A. Morphine

B. Clonidine

C. Dexmedetomidine

D. Ephedrine

22. A 75-year-old female with ovarian cancer is scheduled for total abdominal

hysterectomy/bilateral salpingo oophorectomy and tumor debulking. A thoracic

epidural anesthesia was performed using a test dose of 1.5% lidocaine with

1:200,000 epinephrine injected through the epidural Tuohy needle that resulted in no

evidence of adverse sequelae. An epidural catheter was then threaded through the

needle followed by evidence of negative aspiration through the catheter. A total of

10 mL 0.5% bupivacaine was administered through the epidural catheter. Thirty

seconds later, the patient became agitated and complained of lightheadedness,

tinnitus, and feeling faint, but still able to move all of her extremities. Her BP

decreased from 150/70 to 100/45 mm Hg and her HR decreased from 85 to 55 bpm.

The patient maintained spontaneous breathing throughout with an oxygen saturation

(SpO2

) of 95%. The most likely diagnosis is

A. Local anesthetic systemic toxicity (LAST)

B. High epidural anesthesia

C. Total spinal anesthesia

D. Anaphylactic reaction

23. All of the following local anesthetic systemic toxicity (LAST) treatment measures

should be performed when caring for a patient who may be experiencing toxicity,

except

A. Stop epidural medication administration

B. Support the airway with 100% oxygen

C. Administer intravenous epinephrine according to ACLS protocols

D. Administer an intralipid bolus and continuous infusion

24. You have just placed a lumbar epidural for labor analgesia at L3–L4 interspace in a

34-year-old G2P1 woman of 39 weeks’ gestation. The patient is 6-feet tall and

weighs 300 pounds. Two hours later, you are called for an emergency cesarean

section on the woman. The minimum amount of 2% lidocaine you would need to

administer through the epidural catheter in order to achieve a T4 level is

A. 5 mL

B. 10 mL

C. 20 mL

D. 30 mL

25. The correct statement regarding caudal anesthesia is

A. Caudal anesthesia is essentially sacral epidural anesthesia

B. Caudal anesthesia can only be performed in pediatric population

C. A caudal anesthesia catheter should be positioned without penetrating the

sacrococcygeal ligament

D. The younger the child, the less likely you are to experience an intrathecal

injection

26. You just placed a thoracic epidural in a morbidly obese female (5’1” and 350 lb).

You quickly administer a total of 20 mL 0.5% bupivacaine through the epidural

catheter. As you reposition the patient from the sitting to the supine position, the

patient complains of shortness of breath, bilateral arm weakness, and nausea. Her HR

has decreased from a baseline of 98 to 41 bpm, and her systolic blood pressure has

decreased from a baseline of 140s to 70s mm Hg. The most likely cause is

A. Accidental intravascular injection of local anesthetic

B. Local anesthetic systemic toxicity

C. A high epidural block

D. Anaphylactic reaction to local anesthetic or latex

27. The most likely reason for dyspnea in a patient experiencing the effects of a high

neuraxial blockade is

A. Phrenic nerve palsy when the neuraxial level reaches T3–T5

B. Patient is experiencing an anxiety attack

C. Medullary hypoperfusion

D. Congestive heart failure

28. In the situation of a high spinal anesthetic, which of the following drug is

pharmacodynamically considered the least useful in controlling hypotension

A. Ephedrine

B. Atropine

C. Phenylephrine

D. Epinephrine

29. During performance of lumbar epidural anesthesia for labor analgesia, you

experience free-flowing cerebrospinal fluid (CSF) from the advancing 17G Tuohy

epidural needle. The epidural needle is removed and a second attempt is

successfully performed with an epidural catheter placed at a different level. Which

of the following you would not recommend for the patient to practice in the next 72

hours?