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Maximumpediatricdose=(weightofchildinlb÷150)×(maximumadultdoseinmg).
19. What should be considered when selecting a local anesthetic for children?
It is easy to exceed the maximum dose of local anesthetics with the pediatric patient.
• Articaineisnotrecommendedforchildrenyoungerthan4yearsold.
• Bupivacaineisnotrecommendedforchildrenyoungerthan12yearsold.
20. What effect does narcotic sedation have on the maximum pediatric dose of local
Amide local anesthetics and narcotics have a similar mechanism of action as both depress the central
21. What is the maximum amount of epinephrine or levonordefrin that can be admin-
The general recommendation for a patient with a history of cardiovascular disease is no more than
Previously,Clark’srulewasusedtocalculatethepediatricdrugdose.Theformulais:
It is now recommended to administer the local anesthetic based on the weight-dependent
maximumrecommendeddosemultipliedbythechild’sweight(Table 6-2). This calculated amount
should never be exceeded.
The maximum number of cartridges for the 30-lb child for the following anesthetics is:
2% Lidocaine with 1:100,000 epinephrine 2.6 cartridges
3%Mepivacaine 1.6 cartridges
Oftentimes, pediatric patients are treatment planned for multiple quadrant treatment such as
extractions of four primary molars. If all four teeth are to be extracted in one appointment, the practitioner has to be very careful with the amount of local anesthetic administered in each quadrant.
It is often habitual to administer a full cartridge (1.8 mL) for each injection site in the pediatric
patient. Remember, using large volumes of anesthetic in a child is not necessary! Children typically
have a decreased bone density compared to adults, thus smaller volumes of anesthetics can achieve
adequate pain control.
An anesthetic containing vasoconstrictors should be considered to limit the uptake of local
anestheticbythevasculatureandtherebydecreasesystemiceffects.Withvasoconstrictors,alarger
volumeofanestheticcanbeused.Whenworkinginonequadrantandtheprocedureisshort(less
then 30 minutes), “plain” local anesthetics are recommended. Always select a local anesthetic with
duration of action appropriate for the planned procedure as prolonged anesthesia in children can lead
to biting of the lip and tongue.
Generally, the safest local anesthetic to use in the pediatric patient is 2% lidocaine with
1:100,000 epinephrine. A conservative and easy method for remembering the pediatric dose of 2%
lidocainewithvasoconstrictoristouseonecartridgeforevery20lbsofthechild’sweight.Themaximumdoseshouldbebasedonthechild’sweight.
Note:
anesthetic?
nervous system. These drugs when used at the same time can have an additive effect, thereby
increasing the possibility of a toxic reaction. Narcotics can decrease the protein binding of local anesthetics, increasing the concentration of the local anesthetic in the bloodstream. Narcotics also cause
respiratory depression, hence elevating arterial carbon dioxide. Both of these effects will increase
central nervous system (CNS) sensitivity to convulsions.
It is advisable to use more conservative pediatric dosages of local anesthetics in pediatric
patients undergoing sedation with narcotics.
istered to a 70-kg patient with a history of cardiovascular disease?
0.04mg(40ug) of epinephrine or 0.20 mg (200 ug) of levonordefrin should be administered. Each
dental cartridge of 1:100,000 epinephrine contains 0.01 mg/mL of epinephrine; therefore no more
than two cartridges (3.6 mL) should be administered (total of 0.036 mg of epinephrine). Each dental
cartridge of 1:20,000 levonordefrin contains 0.5 mg/mL of levonordefrin; therefore no more than two
cartridges (3.6 mL) should be administered (Table 6-3).
Whentreatingapatientwithcoronaryarterydisease,theobjectiveistopreventincreasesin
heart rate. Increases in heart rate can decrease stroke volume and thereby decrease cardiac output.
A decreased cardiac output will diminish the amount of oxygenated blood flowing to poorly perfused
areas of the damaged pericardium.
Remember, this is a recommendation as maximal doses have not been established, and these
guidelines should be used for stable patients. In any case, each patient should have full vital signs
checked preoperatively to confirm a stable heart rate and blood pressure.
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Table 6-3. Maximum Allowable Vasoconstrictor for the Cardiac Patient
VASOCONSTRICTOR
CONCENTRATION
AND TYPE
VASOCONSTRICTOR
(MG/ML)
STANDARD DENTAL
CARTRIDGE
(MG/1.8 ML)
MAXIMUM
ALLOWED
CARTRIDGES
1:20,000 Levonordefrin 0.5 0.09 2
1:50,000 Epinephrine 0.02 0.036 1
1:100,000 Epinephrine 0.01 0.018 2
1:200,000 Epinephrine 0.005 0.009 4
Given that vasoconstrictors have a short elimination half-life and peak effects occur within
10 minutes, it is feasible to consider re-dosing another dental cartridge after 30 minutes if needed.
Remember to re-assess the vital signs before administration.
Vasoconstrictors should not be used in patients with uncontrolled blood pressure (>200/115),
uncontrolled hyperthyroidism, recent myocardial infarction, recent stroke, unstable angina, and
cardiac dysrhythmias.
22. Are there patients in whom vasoconstrictors should be avoided?
Generally, vasoconstrictors should be avoided in patients with active or recent (within 3 to 6 months)
cardiac abnormalities. These include recent myocardial infarction, unstable angina, and recent
cerebrovascularaccident.Patientswithactivedysrhythmias,especiallyventriculararrhythmias,are
sensitive to epinephrine, and the use of vasoconstrictors should be avoided. Other groups include
uncontrolled hyperthyroidism and patients with uncontrolled blood pressures.
Consultationwiththepatient’sphysicianisrecommendedifthehistoryofcardiovasculardisease
isunclear.Makesuretospecifythetypeandamountoflocalanesthetic/vasoconstrictoryouplan
to utilize when asking for the consultation. Remember, there is a balance between the risk in using
vasoconstrictors versus obtaining adequate pain control and hemostasis.
23. What are the clinical manifestations of local anesthetic toxicity?
Systemic toxicity is the result of elevated plasma levels of local anesthetics. It is usually a manifestation
of overdose or inadvertent intravascular injection. Toxicity from local anesthetics involves mostly the CNS
and the cardiovascular system. Classic early symptoms are perioral numbness, metallic taste, or tinnitus.
Because the CNS is generally more sensitive to the toxic effects of local anesthetics, it is usually
affected first. The manifestations are presented below, starting with early symptoms and progressing
to late symptoms for each system.
CNS:
• Light-headedness,tinnitus,perioralnumbness,confusion
• Muscletwitching,auditoryandvisualhallucinations
• Tonic-clonicseizure,unconsciousness,respiratoryarrest
Cardiac:
• Hypertension,tachycardia
• Decreasedcontractilityandcardiacoutput,hypotension
• Sinusbradycardia,ventriculardysrhythmias,circulatoryarrest
24. Which group of patients may accentuate the risk for local anesthetic toxicity?
The potential for local anesthetic toxicity is greatest in geriatric and pediatric patients. Older individu-
als generally metabolize drugs at a slower rate. A geriatric patient who takes multiple medications
may experience adverse drug reactions when lidocaine is administered. Cimetidine (Tagamet), a
histamine H2-receptor antagonist, inhibits the hepatic oxidative enzymes needed for metabolism,
thereby allowing lidocaine to accumulate in the circulating blood. This adverse reaction is seen only
withcimetidineandnotwithotherH2-receptorantagonists.Propranolol(Inderal),abeta-adrenergic
blocker, can reduce both hepatic blood flow and lidocaine clearance. Therefore, a local anesthetic
toxic reaction would not be expected with a routine injection of lidocaine in a patient who takes
cimetidine or propranolol, but it may result if high doses of lidocaine are given.
In addition, a possible additive adverse drug reaction exists with the combined administration of
local anesthetics and opioids in the geriatric and pediatric populations.
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25. What is methemoglobinemia, what are its causes and clinical manifestations, and
how can it be treated?
A hemoglobin deficiency occurring when hemoglobin has been oxidized to methemoglobin.
Oxidized hemoglobin cannot bind or carry oxygen. Excessive doses of prilocaine (above 600 mg) or
articaine (above 500 mg) may result in the accumulation of an oxidized metabolite, ortho-toluidine,
that is capable of allowing this conversion. Clinical manifestations include a decreased pulse
oximeter reading, cyanosis, and chocolate-colored blood in the surgical field. This condition can
be reversed with intravenous administration of 1 to 2 mg/kg of methylene blue over a 5-minute
period.
Benzocaine also has the potential to cause methemoglobinemia. It can be found in certain
topical liquids, gels, ointments, and sprays (e.g., Hurricaine, Cetacaine). Benzocaine preparations
should not be used in patients with a history of methemoglobinemia and in children <2 years of age.
Methemoglobinemiaformationcanoccurwithbenzocainedosesof15to20mg/kg.Benzocainegels
typicallycontain18%to20%benzocaine.Sprayscontaining14%to20%benzocainecandeliver
45to60mgofbenzocainein1second.Thesignsandsymptomsmayoccurwithinminutesorupto
2 hours after the use of benzocaine topical.
Prilocaineismarketedasa4%solution.A4%solutioncontains72mgofprilocaine,witheight
cartridges needed to obtain 600 mg. The use of a benzocaine topical along with prilocaine will reduce
the maximum amount of injectable local anesthetic that can be used. In some countries other than the
United States and Canada, prilocaine is marketed as a 3% solution, which is less likely to cause an
excessive delivery of this local anesthetic.
EMLA(eutecticmixtureoflocalanesthetic)cream,usedpreoperativelybeforevenousaccess,
containsbothlidocaineandprilocaine.EMLAcreamshouldbeusedwithcautioninchildren,anditis
not recommended for use in children younger than age 12 months because of potential methemoglobinemia development.
26. A patient tells you he had an adverse reaction to local anesthetics in the past.
What are common adverse reactions, and how do you rule out allergic reactions?
Patientsoftenpresenttothedentalofceclaimingtheyareallergictolocalanesthetics.Common
reactions to rule out are vasovagal syncope (loss of consciousness/brief seizure) during administration/injection and or symptoms related to vasoconstrictors such as heart palpitations or nervousness/
excitability. True allergic reactions often can range from mild (rash or pruritus) to moderate (urticaria
or wheezing) or to critical (anaphylaxis or airway compromise).
Allergic reactions to local anesthetics have been reported. However, the reaction is most likely
attributed to preservatives (methylparaben) or antioxidants (sulfites) contained in the solutions.
Although the incidence is <1%, a thorough investigation is prudent. Allergies to the amides and ester
local anesthetics have been reported. Cross-reactivity is theoretically possible, thus a referral to an
allergist is recommended if a true allergy is suspected.
In the past, procaine (Novocaine) was a commonly used ester local anesthetic in dentistry but
now is no longer available in cartridges. Currently, benzocaine is a commonly used topical anesthetic
found in sprays and gels. Both procaine and benzocaine are metabolized to compounds resembling
PABA,whichisaknownallergen.
27. What types of local anesthetics can be used in the pregnant and lactating
patient?
Category B local anesthetics (see the following list) are recommended for the pregnant and lactating
patient. Local anesthetics can cross the placental barrier but are generally not harmful unless exces-
siveamountsareadministered.Amother’snormaltissuepHis7.4,whereasthefetushasapHof
approximately7.2.Anexcessiveamountoflocalanestheticcoulddangerouslylowerthefetus’spH
(ion trapping).
Category B Category C
Lidocaine Articaine
Prilocaine Bupivacaine
Etidocaine Mepivacaine
Note: Category C medications are not recommended unless the potential benefits warrant their use.
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28. To what components of a local anesthetic are patients most likely to be allergic?
Methylparaben, a bacteriostatic preservative, is found in multidose vials of local anesthetics. Oral
and maxillofacial surgeons that use multidose vials need to be cautious of potential allergic reactions.
Multidosevialsaremostlyencounteredintheemergencyroomandtheoperatingroom.Since1984,
methylparaben is no longer added to dental cartridges. Because the cartridge is intended to be used
as a single-dose vial, a preservative is not required.
Bisulfites are commonly used as preservatives at salad bars and in wines. Any local anes-
thetic cartridge containing a vasoconstrictor will have metabisulfite added as a preservative for the
vasoconstrictor.Patientswithknownbisulteallergiesneedtobegivenlocalanestheticswithout
vasoconstrictors.
Latex allergies should also be considered with the use of local anesthetics. The local anesthetic
itself contains no latex, but its container may. The needle-puncture diaphragm of dental cartridges
and multidose vials contains latex. The dental plunger of a dental cartridge may also contain latex. A
disposable, latex-free syringe is recommended for the latex-allergic patient. The anesthetic solution
may be drawn using a filtered needle or by removing the rubber diaphragm.
29. Why is your knowledge of local anesthetics so important?
Withthepossibleexceptionofanesthesiologists,dentalpractitioners,especiallyoralandmaxillofacial
surgeons, use local anesthetics most frequently. Therefore, a thorough understanding of the pharmacokinetics and pharmacodynamics of local anesthetics is essential.
30. Is there a method to reverse the clinical effects of local anesthetics?
Traditionally, the effects of local anesthetics would wear off over time. However, an alpha receptor
blocker, phentolamine mesylate (OraVerse, Septodont) has been approved in dental cartridges to
accelerate the reversal of soft tissue anesthesia. Although not fully understood, it is thought to cause
vasodilation in the identical site of the previous local anesthetic injection to increase absorption of the
anesthetic agents.
Although unlikely to be useful in the surgical setting, this drug may have a role in the dental
office for routine procedures and patients wishing to have a faster return of function. OraVerse is
approved for use in patients 6 years of age and older and weighing more than 15 kg.
31. What are general concepts in the treatment of toxicity from local anesthesia?
If you suspect local anesthetic toxicity, the initial steps should be to stop the injection, ensure oxygen-
ation, stabilize the patient, and consider activating your emergency response team. Attention should
be paid to airway compromise, hypotension, dysrhythmias, and seizures.
Benzodiazepinesarethedrugsofchoiceforseizurecontrol.Propofolcanbeusedtocontrolseizures but has the risk of potentiating cardiovascular collapse. Cardiovascular support should include
fluid administration and vasopressors if needed.
Also available are lipid emulsions (Intralipid), which can reverse the cardiac and neurologic
effects of local anesthetic toxicity by extracting lipid soluble molecules from the plasma. These lipid
emulsions have been successful in treating toxicity, especially with bupivacaine, that is part of the
Advanced Cardiac Life Support (ACLS) support guidelines.
32. What are the common reasons for failure to obtain adequate local anesthesia
during the removal of a mandibular molar?
The inferior alveolar block has a high failure rate in dentistry. Here are some considerations to improve
the success rate when anesthetizing mandibular molars.
Technical considerations:
• Allowadequatetimefortheanesthetictotakeeffect.Sitthepatientinanuprightpositionafter
delivering the inferior alveolar block and wait an additional 5 to 10 minutes. This is difficult for the
oral and maxillofacial surgeon who is inherently impatient.
• Oftentheneedleisinsertedtoolowandtooanteriorontheramus.Considerre-administeringthe
local anesthetic at a higher level and deeper on the ramus.
• Adjustyourentrypositionandangleofentryfortheblock.Thereisasignicantdifferenceinsuc-
cess rates between the right and left inferior alveolar block, which is operator dependent.
Anatomic considerations:
• Considerinnervationsfromthemylohyoidnerveandanesthetizeaccordingly(lingualtotheman-
dibular second molar).
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• AdministeranothercartridgeofanestheticatthehighestlevelpossiblebyusingtheGow-Gates
technique (intraoral condylar injection) to anesthetize all branches of cranial nerve V3.
Physiologicconsiderations:
• ConsiderusingahigherpHanestheticsolution(onewithoutavasoconstrictor)tohelpovercomethe
acidity created by possible infection/inflammation.
• Alkalinize(buffer)youranestheticbyaddingsodiumbicarbonatetoyourlocalanestheticjustbefore
injecting.
• Usealargeramount(butdonotexceedthemaximumrecommendeddose)oflocalanestheticto
overcome the acidity created by the infection.
33. Is there an easy way to remember important data about lidocaine?
Yes. Because lidocaine is one of the safest and most commonly used local anesthetics, it is useful to
committomemorycertaininformationaboutthisdrug.Itsmolecularweightis234,itsproteinbinding
is56%,anditspKais7.8,sojustremember2,3,4,5,6,7,8.
BiBliography
AmericanAcademyofPediatricDentistry(AAPD):Guideline on use of local anesthesia for pediatric dental patients, Chicago
2009,AmericanAcademyofPediatricDentistry(AAPD).
Becker DE: Drug allergies and implications for dental practice, Anesth Prog60(4):188–197,2013.
Becker DE, Reed XL: Local anesthetics: review of pharmacological considerations, Anesth Prog59(2):90–101,2012.
Cummings DR, Yamashita DD,McAndrewsJP: Complications of local anesthesia used in oral and maxillofacial surgery,
Oral Maxillofac Surg Clin North Am23:369–377,2011.
GiovannittisJA,RosenbergMB,PheroJC:Pharmacologyoflocalanestheticsusedinoralsurgery,Oral Maxillofac Surg Clin
N Am25:453–465,2013.
Kumar S:Localanesthetics.InDukeJ, editor: Anesthesia secrets,ed4,Philadelphia,2010,Mosby.
MalamedSF: Handbook of local anesthesia,ed6,StLouis,2012,Mosby.
MastrelloCL, Abubaker AO, Benson KI: Local anesthetics. In Abubaker AO, Benson KI, editors: Secrets of oral and maxillofacial
surgery,ed2,Philadelphia,2007,Elsevier.
MoorePA: Adverse drug interactions in dental practice: interactions associated with local anesthetics, sedatives and
anxiolytics, J Am Dental Assoc130:541–554,1999.
MorganGE,MikhailMS,MurrayMJ:Localanesthetics.InMorganGE,MikhailMS,MurrayMJ, editors: Clinical anesthesiology,
ed4,NewYork,2005,McGraw-Hill.
Ogle OE,MajhoubiG: Local anesthesia: agents, techniques, and complications, Dent Clin North Am56:133–148,2012.
Reed KL,MalamedSF, Fonner AM: Local anesthesia part 2: technical considerations, Anesth Prog59(3):127–136,2012.
Stoelting RK,MillerRD: Local anesthetics. In Stoelting RK,MillerRD, editors: Basics of anesthesia,ed4,NewYork,2000,
Churchill Livingstone.
Wilburn-GooD, Lloyd LM:Whenpatientsbecomecyanotic:acquiredmethemoglobinemia,J Am Dental Assoc 130:
826–831,1999.
YagielaJA: Adverse drug interactions in dental practice: interactions associated with vasoconstrictors, J Am Dent Assoc
130:701–709,1999.
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Jason A. Jamali, A. Omar Abubaker
1. What are the different levels of sedations?
See Table 7-1.
2. How is an intravenous (IV) anesthetic agent used in anesthesia?
An IV anesthetic is a drug that is intravenously injected to induce unconsciousness at the beginning
of general anesthesia. At the same time, it allows rapid recovery after termination of its effect.
3. What are the properties of an ideal induction agent?
• Watersoluble,compatiblewithIVsolutions,andstableinaqueoussolution
• Rapidonsetandrecoveryofanesthesia(within1arm-braincirculationtime)
• Absenceofunwantedcardiovascularorneurologicsideeffects
• Anticonvulsant,antiemetic,analgesic,andamnesticproperties
• Itshouldnotimpairrenalorhepaticfunctionorsteroidsynthesis.
4. What are the commonly used intravenous anesthetic agents?
See Table 7-2.
5. What effect does age have on dosing of induction agents?
Withincreasingage,eliminationtimeandrenalclearancetimeincrease,resultinginlongerlasting
drug effects. Elderly patients are more sensitive to intravenous anesthetics; therefore dose reductions
are necessary in this group of patients.
6. What are the cardiovascular effects of commonly used induction agents?
See Table 7-3.
7. What are barbiturates?
Asderivativesofbarbituricacid,theyexhibitadose-dependentcentralnervoussystem(CNS)depres-
sion with hypnosis and amnesia. They are very lipid soluble, which results in a rapid onset of action.
Whenusedforinduction,theyproduceunconsciousnessinlessthan30seconds.
8. What are the pharmacologic effects of barbiturates?
Barbituratesmodulatetheinteractionofgamma-aminobutyricacid(GABA)withitsreceptors.GABA,
an inhibitory neurotransmitter, causes an increase in chloride concentration within the membranes of
postsynaptic neurons resulting in hyperpolarization. Barbiturates are capable of depressing the reticular activating system, which is important in maintaining wakefulness and medullary ventilatory centers
to decrease responsiveness to ventilatory stimulant effects of carbon dioxide. In addition, barbiturates
induce depression of the medullary vasomotor center, causing decreased sympathetic nervous system
impulsesfromautonomicganglia.Thisresultsindecreasesinbloodpressure(10to20mmHg)secondary to peripheral vasodilation. Finally, barbiturates are potent cerebral vasoconstrictors resulting in
decreasesincerebralbloodow,cerebralbloodvolume,andintracranialpressure(ICP).
9. What are the pharmacokinetics of barbiturates?
Maximaluptakeofbarbituratesbythebrainoccurswithin30secondsafterIVadministration.This
accountsfortherapid(1arm-braincirculation)inductionofanesthesia.Theredistributionofthese
drugs from the brain to inactive tissues, especially skeletal muscle and fat, results in prompt awakening. The elimination of barbiturates is dependent on hepatic function because less than 1% of the
administered dose is cleared unchanged by the kidneys.
10. What are the most commonly used barbiturates for induction of anesthesia?
Thiopentalsodium(Pentothal)isathiobarbiturateusuallypreparedasa2.5%solution.ThepHof
thiopentalis10.5.Wheninjectedintravenously,itcanbeirritating.Aninductiondoseof3to5mg/
kgproducesalossofconsciousnesswithin30secondsandrecoveryin5to10minutes.Becausethe
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Table 7-1. Continuum of Sedation
MINIMAL
SEDATION
Comment Anxiolysis Conscioussedation
Cognitive/
physical
coordination
Responsiveness Respondsnormally
Airway Unaffected Nointervention Intervention may
Spontaneous
ventilation
Cardiovascular
function
Table 7-2. Commonly Used Intravenous Anesthetic Agents
AGENT COMMENTS
Etomidate Anesthetic agent that provides hemodynamic stability. Excellent for compro-
Propofol Most popular anesthetic agent used in office anesthesia due to fast onset, short
Ketamine NMDAreceptorantagonism.Itcausesdissociativeanestheticstate.Itsusage
Midazolam Short-acting water-soluble benzodiazepam. Benzodiazepam carries anxiolysis,
Fentanyl Short-acting opioid that is used commonly with other anesthetic agents to
Dexmedetomidine It is a centrally acting alpha-2 agonist. It has a short half-life and good safety
to verbal commands
Unaffected Adequate Inadequate Inadequate
Unaffected Maintained Maintained Impaired
mised cardiac patient. Major side effect is adrenal suppression.
duration, and antiemetic property. Major disadvantage is its association with
myocardial depression and vasodilation.
hasgainedpopularityduetoitsuniquenessinprovidinganesthesia,amnesia,
and analgesia as a single agent. Major side effect is associated with its
sympathomimetic properties.
sedation, and amnesia properties. It also has minimal effect on cardiovascular system.
providesynergisticeffect.Opioid(exceptmeperidine)carriesvagolyticeffect
in high dose.
prole.Whengivenasanintravenousbolus,signicanthypotensioncanbe
observed due to activation of peripheral alpha-1 antagonist effect.
MODERATE
SEDATION
Drug-induced
depression of
consciousness
Purposeful
response to
verbal or tactile
stimulation
DEEP
SEDATION
Drug-induced
depression of
consciousness
Impaired
Purposeful
response following repeated or
painful
stimulation
berequired
GENERAL
ANESTHESIA
Drug-inducedloss
of consciousness
Unarousableeven
with painful
stimulus
Required
elimination half-life is 6 to 12 hours, patients may experience a slow recovery. After 24 hours, approxi-
mately28%to30%maybedetectableinthebody.Thiopentalisnotusedtomaintainanesthesia
because of accumulation in inactive tissues with repeated doses.
Methohexital(Brevital)issomewhatlesslipidsolubleandlessionizedatphysiologic
pHthanthiopental.ThepHis10.5.Aninductiondoseof1to2mg/kgproduceslossof
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Table 7-3. Cardiovascular Effects of Induction Agents
AGENT MAP HR SVR CO
Ketamine ++ ++ + +
Midazolam 0 0 0 0
Propofol – + – 0
Etomidate 0 0 0 0
Fentanyl 0 0 0 0
CO, Cardiac output; HR, heart rate; MAP, mean arterial pressure; SVR, systemic vascular resistance.
Modified from Duke J: Anesthesia secrets, ed 4.
consciousnessinlessthan20secondsandrecoveryin4to5minutes.Theeliminationhalf-lifeof
methohexital is 3 hours, which allows a clearance rate that is three to four times faster than that
of thiopental.
11. Why is propofol the best agent for outpatient anesthesia?
• Rapidinductionandrecovery
• Lowerincidenceofnauseaandvomiting
• Patientsregaincognitivefunctionquickly,whichleadstoashorterrecoveryperiod.
12. What are the properties of propofol?
Propofolisasedative-hypnoticthatworksviaGABApathwaystoproduceanesthesia(withoutanal-
gesia)witharelativelyrapidrecoverytime.Itmaybeusedasasedativeaswellasaninductionand
maintenance agent for general anesthesia. It has mostly supplanted the use of barbiturates given the
faster emergence during recovery.
• DecreasedcerebralbloodowandICP
• Myocardialdepression,decreasedsystemicvascularresistance(SVR),andhypotension(20%to
• Respiratorydepression
• Antiemeticproperties
Propofolshouldbeavoidedinpatientswithsoyandeggallergiesaswellaslipiddisorders.
13. What are the pros and cons of using dexmedetomidine (Percedex) over traditional
Dexmedetomidineisacentrallyactingalpha-2agonist.Itsshorthalf-life,fastonset,andlimited
14. What are the pharmacologic properties and side effects of etomidate?
Etomidate(Amidate)isacarboxylatedimidazolederivative.Aninductiondoseof0.2to0.5mg/kgIV
15. What is ketamine, and how does it exert its physiologic action?
Ketamine,aphencyclidine(PCP)derivative,is10timesmorelipidsolublethanthiopental,enabling
The systemic effects include:
30%reduction)
anesthetic agents?
effects on the respiratory system make it a great anesthetic alternative. Studies have also suggested
abetteremergenceprole(i.e.,delirium)thanpropofol.Themajordisadvantageswithdexmedetomidine
are the relative high cost compared with generic propofol and midazolam and its association with
hypotensionwhengiveninbolusdoseintravenously.Itssedationdoseis0.2to0.7mcg/kg/hr.
producesrapidinductionofanesthesiathatlasts3to12minutes.TheCNSeffectsaredosedependent,andrecoveryofpsychomotorskillsisequaltothatofthiopental.Rapidawakeningresultsfrom
redistribution and nearly complete hydrolysis to inactive metabolites. Because etomidate produces
no noticeable cardiovascular changes, it is used in patients with limited cardiac reserve. In addition,
etomidatedecreasescerebralbloodowandICP.Likemethohexital,itactivatesseizurefoci.
Side effects include venoirritation with rapid infusion, involuntary skeletal muscle movements,
and a high incidence of nausea and vomiting. Also, etomidate suppresses adrenocortical function for
upto8hoursafteradministration.Duringthistime,theadrenalcortexisunresponsivetoadrenocorticotropichormone(ACTH).
ittocrosstheblood-brainbarrier(BBB)quickly.Itproducesdissociativeanesthesia,whichcanbe
seenonelectroencephalogram(EEG)asdissociationbetweenthethalamusandlimbicsystem.
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RapidCNSdepressionwithhypnosis,sedation,amnesia,andintenseanalgesiaoccursin30to
60secondsafterIVadministration.Theanestheticinductiondosesare1to2mg/kgIV,witheffects
lasting5to10minutes,or10mg/kgintramuscular(IM),whichactsin2to4minutes.Aketamine
dartcontains4mg/kg.
IM can be administered to uncooperative patients to facilitate completion of short procedures.
16. What are the pharmacologic effects and side effects of ketamine?
Ketamine is highly lipid soluble, is rapidly redistributed to muscle and fat, and undergoes extensive
hepatic metabolism to a weakly active metabolite, norketamine. Ketamine stimulates the cardiovascular system, increasing the heart rate, blood pressure, and cardiac output. In patients with ischemic
heartdisease,ketaminemayadverselyincreasemyocardialoxygenrequirements.Inaddition,ketamine produces bronchial smooth muscle relaxation because of sympathetic stimulation, which may
be beneficial in patients with bronchospasm or asthma. Airway secretions are increased by ketamine,
creating the need for anticholinergics such as glycopyrrolate in the preoperative period. Ketamine
isapotentcerebralvasodilatorandwillincreaseICPinpatientswithintracraniallesions.Finally,
emergence from ketamine anesthesia may be associated with unpleasant auditory, visual, and out-ofbody illusions that can progress to delirium. It is recommended that benzodiazepines or droperidol be
administered either preoperatively or after induction to decrease the incidence of emergence delirium.
17. What are the dosages for ketamine?
Route/Anesthetic Type Dosage
IV induction 1-2mg/kg
IV sedation 0.25-0.75mg/kg
IM ketamine dart 4mg/kg
18. What are the onset and duration of ketamine when administered via IV versus IM
route?
Onset 30-60seconds 2-4 minutes
Duration 10-15minutes 30-60minutes
19. What are the clinical uses for benzodiazepines?
• Preoperativemedication
• Intravenoussedation
• Inductionofanesthesia
Anterograde amnesia, minimal depression of ventilation and the cardiovascular system, and sedative
properties make benzodiazepines favorable preoperative medications.
20. Where in the CNS do benzodiazepines exert their amnestic effects?
These effects occur at benzodiazepine receptors, which are found on postsynaptic nerve endings in
theCNS.BenzodiazepinereceptorsarepartoftheGABAreceptorcomplex.TheGABAreceptorcomplex consists of two alpha subunits, to which benzodiazepines bind, and two beta subunits, to which
GABAbinds.Achlorideionchannelexistsinthemiddleofthereceptorcomplex.Benzodiazepines
enhancethebindingofGABAtobetasubunits,whichopensthechlorideionchannel.Chlorideions
flow into the neuron, hyperpolarizing it and inhibiting action potentials.
21. What clinical properties make benzodiazepines good preoperative medications?
At lower doses, only anxiolysis is obtained. Anterograde amnesia, sedation, and anxiolysis are pro-
duced at higher concentrations. At this concentration, patients are conscious and can maintain their
own airway but will not remember events during surgery. Finally, at even higher concentrations, benzodiazepines will produce unconsciousness, although they are not complete anesthetics. A complete
general anesthetic produces the effects already mentioned plus analgesia, control of the autonomic
nervous systems, and occasionally muscle relaxation. Benzodiazepines do not provide analgesia, and
they should not be used alone to produce general anesthesia. They are best used in low doses to
supplement inhaled or intravenous anesthetics to provide amnesia.
IV IM
• Maintenanceofanesthesia
• Suppressionofseizureactivity
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22. What benzodiazepines are most commonly used as amnestics in anesthesiology?
• Induction of anesthesia: Midazolam(mostcommon)
• Inductionofanesthesia:Lorazepam
• Inductionofanesthesia:Diazepam
23. What are the properties and pharmacokinetics of midazolam?
Midazolam is prepared as a water-soluble compound that is transformed into a lipid-soluble compound
byexposuretothepHofblooduponinjection.Thisuniquepropertyofmidazolamimprovespatientcomfort during administration. This also prevents the need for an organic solvent such as propylene glycol
(venoirritation),whichisrequiredfordiazepamandlorazepam.Midazolamisthemostlipidsolubleofthe
threeand,asaresult,hasarapidonsetandarelativelyshortdurationofaction.(SeeTable 7-4.)
24. What is the antagonist for benzodiazepines?
Flumazenil,acompetitiveantagonist,giveninincrementsof0.2mgIVevery60seconds,willreverse
unconsciousness, sedation, respiratory depression, and anxiolysis. Flumazenil has a rapid onset with
thepeakeffectoccurringinabout1to3minutes.Theeffectofumazenillastsforabout20minutes,
and resedation may occur.
25. What is the concept of context-sensitive half-time and its relevance to opioids?
Context-sensitivehalf-timeisthetimerequiredfor50%reductionintheplasmaconcentrationofa
drug on termination of a constant infusion. This time is determined by both elimination and redistribution, and it varies considerably as a function of infusion duration for commonly used opioids.
26. What is the mechanism of action of opioids?
Opioidsactasagoniststhroughcomplexinteractionswithmu,delta,andkappareceptorsintheCNS.
Supraspinally, mu receptors are responsible for analgesia, euphoria, miosis, nausea and vomiting, urinary
retention,depressionofventilation,andbradycardia.Deltaandkappareceptorsareactiveatthespinal
level, mediating spinal analgesia, sedation, and miosis. In addition, opioids may act presynaptically to inter-
ferewiththereleaseofneurotransmitterssuchasacetylcholine,dopamine,norepinephrine,andsubstanceP.
27. How are opioids used clinically?
Usesincludeprovisionofanalgesiabeforeoraftersurgery,synergisticeffectswithinhaledanesthetics
beingusedformaintenanceofanesthesia,inductionandmaintenanceofanesthesia(particularlyin
patientswithseverecardiacdysfunction),andinhibitionofreexsympatheticnervoussystemactivity.
Usually,opioidsareadministeredintermittentlyinlowerdosesduringmaintenanceofanesthesiaor
ascontinuousinfusionstoaugmentinhaledanesthetics.Often,smalldosesoffentanyl,sufentanil,or
alfentanil are administered just before direct laryngoscopy and tracheal intubation to attenuate blood
pressure and heart rate responses evoked by these stimuli.
28. What are the pharmacologic effects of opioids?
Opioidsarecardiac-stabledrugs.Inmanysettings,opioidsareusedastheprincipalanestheticagentfor
cardiac anesthesia because of their hemodynamic stability; however, they do lack an amnestic effect.
At the same time, opioids can cause a dose-dependent bradycardia resulting from vagal stimulation in
the medulla. In contrast, meperidine will cause tachycardia because it is structurally similar to atropine
andelicitsatropine-likeeffects.Opioidsactonthemedullaryventilatorycenterstoproducerapidand
sustained dose-dependent depression of ventilation. This is characterized by increases in the resting
PaCO2anddecreasedresponsivenesstotheventilatorystimulanteffectsofcarbondioxide.IntheCNS,
opioids do not produce unconsciousness reliably. They do, however, stimulate dopamine receptors in the
Table 7-4. The Properties and Pharmacokinetics of Midazolam
DRUG DOSAGE ONSET
Midazolam (IV-sedation) 0.01-0.1mg/kg 0.5-2minutes 2 hours
Midazolam (IV-induction) 0.1-0.3mg/kg
Diazepam IV 2-10mgprn 1-3 minutes 20-90hours
Lorazepam IV 2-4 mg prn 1-5minutes 10-20hours
ELIMINATION
HALF-LIFE
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