Transcript Analgesics. Anesthetic and Neuromuscular Blocking Agents

Pain Management
What is pain?


A protective mechanism to warn of
damage or the presence of disease
Part of the normal healing process
Managing pain can be a challenge.
Discussion
What are the
classifications of pain?
Discussion
What are the classifications of pain?
Answer
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Acute
Chronic
 Nonmalignant
 Malignant
Pain Management
Acute Pain
 Associated with trauma or surgery
 Easier to manage by treating the
cause
 Has a beginning and an end
Pain Management
Chronic Pain
 No end to the pain
 Patients may have a sense of
helplessness and hopelessness
 Affects different aspects of life
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Physical
Psychological
Social
Spiritual
Pain Management
Chronic Nonmalignant Pain
 Cause may be diagnosed or
undiagnosed
 Pain lasts for more than 3 months
 Patients may have signs and
symptoms of depression
Pain Management
Chronic Malignant Pain
 Accompanies malignant disease
 Often increases in severity with
disease progression
Major Sources of Pain
Source
Area
Involved
Characteristics
Treatment
Somatic
body
framework
throbbing,
stabbing
narcotics,
NSAIDS
Visceral
kidneys,
intestines,
liver
Nerves
aching,
throbbing,
sharp, crampy
burning,
numbing,
tingling
narcotics,
NSAIDS
Neuropathic
antidepressants,
anticonvulsants
Sympathetically overactive no pain should nerve blockers
Mediated
sympathetic be felt
system
Pain Transmission
Tissue injury causes the release of:
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Bradykinin
Histamine
Potassium
Prostaglandins
Serotonin
These substances stimulate nerve
endings,
starting the pain process.
Pain Transmission
There are two types of nerves
stimulated:
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
“A” fibers
and
“C” fibers
Pain Transmission
“A” Fibers
“C” Fibers
Myelin sheath
Large fiber size
Conduct fast
Inhibit pain
No myelin sheath
Small fiber size
Conduct slowly
Facilitate pain
transmission
transmission
Dull and
nonlocalized
Sharp and
well-localized
Pain Transmission

Types of pain related to proportion
of
“A” to “C” fibers in the damaged
areas
Pain Transmission
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These pain fibers enter the spinal
cord
and travel up to the brain.
The point of spinal cord entry is the
DORSAL HORN.
The DORSAL HORN is the location
of the “GATE.”
Pain Transmission
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This gate regulates the flow of
sensory impulses to the brain.
Closing the gate stops the impulses.
If no impulses are transmitted to
higher centers in the brain, there is
NO pain perception.
Pain Transmission
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Activation of large “A” fibers
CLOSES gate
Inhibits transmission to brain

Limits perception of pain
Pain Transmission
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Activation of small “B” fibers OPENS
gate
Allows impulse transmission to brain

Pain perception
Pain Transmission
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Gate innervated by nerve fibers
from brain, allowing the brain some
control over gate
Allows brain to:
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Evaluate, identify, and localize the pain
Control the gate before the gate is
open
Pain Transmission
“T” cells

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Cells that control the gate have a
threshold
Impulses must overcome threshold to be
sent
to the brain
Pain Transmission
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Body has endogenous
neurotransmitters
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Enkephalins
Endorphins
Produced by body to fight pain
Bind to opioid receptors
Inhibit transmission of pain by
closing gate
Pain Transmission
Rubbing a painful area with massage
or liniment stimulates large sensory
fibers

Result:
 GATE closed, recognition of pain
REDUCED
 Same pathway used by opiates
Pain Management
Narcotic
 Pain-modulating chemical derived
from opium or is synthetically
produced
 Also called opioid
 Causes insensibility or stupor
 Mainly effects on CNS and GI tract
 Lesser effects on peripheral tissues
Pain Management
Natural Opioids
 Endorphins, enkephalins, and dynorphins
 Produced by the brain in response to pain
stimuli
 When receptors are activated
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causes decreased nerve transmission
sensation of pain is diminished
Opioids bind to these same receptors
Discussion
What are the three
effects of narcotics?
Discussion
What are the three effects of
narcotics?
Answer
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

Analgesia
Sedation
Euphoria and Dysphoria
Opioid Analgesics
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Pain relievers that contain opium,
derived from the opium
poppy
or
chemically related to opium
Narcotics: very strong pain relievers
Poppy
Papaver
rhoeas L.
1.
2. Papaver
somniferum L.
1
2

Opioid drugs are used primarily for the
treatment of pain. Some of the CNS
mechanisms that reduce the
perception of pain also produce a state
of well-being or euphoria. Thus, opioid
drugs also are taken outside of medical
channels for the purpose of obtaining
the effects on mood. This potential for
abuse has generated much research on
separating the mechanism of analgesia
from that of euphoria in the hope of
eventually developing a potent
analgesic that does not produce
euphoria.
The
major risk for abuse or addiction occurs in
patients complaining of pain with no clear physical
explanation or with evidence of a chronic disorder
that is not life threatening. Examples are chronic
headaches, backaches, abdominal pain, or peripheral
neuropathy. Even in these cases, an opioid might be
considered as a brief emergency treatment, but longterm treatment with opioids is not advisable. In those
relatively rare patients who develop abuse, the
transition from legitimate use to abuse often begins
with patients returning to their physician earlier than
scheduled to get a new prescription or visiting
emergency rooms of different hospitals complaining
of acute pain and asking for an opioid injection.
Opioid Analgesics
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codeine sulfate
meperidine HCl (Demerol)
methadone HCl (Dolophine)
morphine sulfate
propoxyphene HCl
Opioid Analgesics
Three classifications based on their
actions:
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Agonist
Agonist-antagonist
Partial agonist
Opioid Analgesics: Site of action
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Large “A” fibers
Dorsal horn of spinal cord
Opioid Analgesics:
Mechanism of Action
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Bind to receptors on inhibitory
fibers, stimulating them
Prevent stimulation of the GATE
Prevent pain impulse transmission
to the brain
Mechanism of action
Opioids act at the Mesolimbic Dopaminergic
System
=> Reward Center of the Brain.
Inhibit the release of GABA at the VTA

Inhibition of inhibition of Dopamine neurons

DA activity
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Opiates concentrate in the VTA,
nucleus accumbens, caudate
nucleus and thalamus.
The opiates bind to opiate receptors
that are concentrated in areas
within the reward system.
The action of opiates in the
thalamus contributes to their ability
to produce analgesia
Opioid Analgesics:
Mechanism of Action
Three types of opioid receptors:
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Mu
Kappa
Delta
Opioid Analgesics: Therapeutic Uses
Main use: to alleviate moderate to
severe pain

Opioids are also used for:
 Cough center suppression
 Treatment of constipation
Subtypes of opioid receptors
mu
Analgesia, depression of breathing, euphoria,
addiction development, sedative effect,
depression of contents mocing through
digestive tract, miosis
kappa
Analgesia, sedative eefect, psychotomimetic
action
delta
Analgesia, euphoria, behaviour chnages
sigma
Mania, increasing of breathing frequency,
hallucinations, midriasis
Opioid Analgesics: Side Effects
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Euphoria
Nausea and vomiting
Respiratory depression
Urinary retention
Diaphoresis and flushing
Pupil constriction (miosis)
Constipation
Opiate Antagonists
naloxone (Narcan)
naltrexone (Revia)
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Opiate antagonists
Bind to opiate receptors and prevent a
response
Used for complete or partial reversal of
opioid-induced respiratory depression
Opiates: Opioid Tolerance
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A common physiologic result of
chronic opioid treatment
Result: larger dose of opioids are
required
to maintain the same level
of
analgesia
Opiates: Physical Dependence

The physiologic adaptation of the
body to
the presence of an opioid
Opiates: Psychological Dependence
(addiction)
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A pattern of compulsive drug use
characterized by a continued
craving for
an opioid and the need to use the
opioid
for effects other than pain relief
Opiates

Opioid tolerance and physical
dependence are expected with longterm opioid treatment and should
not be confused with psychological
dependence (addiction).
Opiates

Misunderstanding of these terms
leads to ineffective pain
management and contributes to the
problem of undertreatment.
Opiates

Physical dependence on opioids is
seen when the opioid is abruptly
discontinued or when an opioid
antagonist is administered.
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Narcotic withdrawal
Opioid abstinence syndrome
Opiates
Narcotic Withdrawal Opioid
Abstinence Syndrome
 Manifested as:

anxiety, irritability, chills and hot
flashes, joint pain, lacrimation,
rhinorrhea, diaphoresis, nausea,
vomiting, abdominal cramps, diarrhea
Opioid Analgesics:
Nursing Implications
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Before beginning therapy, perform a
thorough history regarding
allergies, use of other
medications,health history, and
medical history.
Obtain baseline vital signs and I &
O.
Assess for potential
contraindications and drug
interactions.
Opioid Analgesics:
Nursing Implications

Perform a thorough pain
assessment, including nature and
type of pain, precipitating and
relieving factors, remedies, and
other pain treatments.

Assessment of pain is now being
considered
a “fifth vital sign.”
Opioid Analgesics:
Nursing Implications
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Be sure to medicate patients before
the pain becomes severe as to
provide adequate analgesia and
pain control.
Pain management includes
pharmacologic and
nonpharmacologic approaches. Be
sure to include other interventions
as indicated.
Opioid Analgesics:
Nursing Implications
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Oral forms should be taken with
food to minimize gastric upset.
Ensure safety measures, such as
keeping side rails up, to prevent
injury.
Withhold dose and contact physician
if there is a decline in the patient’s
condition or if VS are abnormal—
especially if respiratory rate is
below 12 breaths/minute.
Opioid Analgesics:
Nursing Implications
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Follow proper administration
guidelines for IM injections,
including site rotation.
Follow proper guidelines for IV
administration, including dilution,
rate of administration, and so forth.
CHECK DOSAGES CAREFULLY
OPIOIDS or NARCOTICS
B. Acute Toxicity/Overdose
1.Disruption of central
sympathetic activity.
control
of
peripheral
Brainstem  Respiratory depression  DEATH
 Circulatory depression  BP
Pupils constricted (miosis), (may be dilated with
meperidine or severe hypoxia)
Nausea and Vomiting
Pulmonary edema
Reflexes 
OPIOIDS or NARCOTICS
2. CNS depression
Drowsiness  Sedation  Coma
3. CNS abnormal neuronal activity
Convulsions -- with propoxyphene or
meperidine
OPIOIDS or NARCOTICS
Treatment of
overdose:
acute
toxicity
and
Naloxone. Opioid antagonist, used to block
the actions of opioids in a life-threatening
situation of opioid overdose. Given IV.
Short half-life (1-2hrs). It precipitates
withdrawal.
Methadone. Used in the detoxification
process. It causes a less pronounced
euphoria and less severe withdrawal.
OPIOIDS or NARCOTICS
C. Withdrawal
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Most severe withdrawal of all drugs of
abuse.
Onset related to time-effect curve and t½
of narcotic.
Not life threatening, no convulsions, no
delirium, no disorientation.
Opiate Withdrawal
6-8 hr =>drug seeking behavior, restless,
anxious.
8-12 hr => Pupils dilated (mydriasis),
reactive to light; increased pulse rate; blood
pressure;
yawning;
chills;
rhinorrhea;
lacrimation;
piloerection/
gooseflesh; sweating; restless sleep.
48-72 hrs (peak) => All of the above plus
muscular weakness, aches (cramps) and
twitches; nausea, vomiting and diarrhea;
temperature; respiratory rate; heart rate
and blood pressure; dehydration.
Treatment of Sympathetic effects during withdrawal.
ANS EFFECTS

Clonidine
2-AR
NA
NE
SN
DA
LC
VTA
VTA
Motivational:
Pleasure
Reward
Euphoria
Used to block
autonomic signs
and symptoms of
withdrawal:
 cramps
 nausea
 vomiting
 tachycardia
 sweating
 hypertension
D. Treatment of Addiction
Medical Detoxification
A
process
whereby
individuals
are
systematically withdrawn from addicting
drugs in an inpatient or outpatient setting,
typically under the care of a physician.
Detoxification is sometimes called a distinct
treatment
modality
but
is
more
appropriately considered a precursor of
treatment, because it is designed to treat
the acute physiological effects of stopping
drug use.
OPIOIDS or NARCOTICS
Severity of Withdrawal
Heroin
Methadone
Naltrexone
TIME
OPIOIDS or NARCOTICS
Detoxification or Maintenance treatment
a. Methadone
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Used for the sequential detoxification and maintenance
treatment of opiate dependence.
b. LAAM (L--acetyl methadol, methadyl acetate).
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Structurally similar to methadone.
Longer-acting opiate.
Taken orally in liquid form, lasts 72 hrs (visits 3 X a week).
“Take home" medication.
c. Buprenorphine
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Partial opioid agonist which substitutes for low doses of
opioids but antagonizes at high doses.
Can be administered sublingually every 24-48 hrs as an
alternative to methadone
OPIOIDS or NARCOTICS
d. Naltrexone
Opiate Antagonist
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Causes precipitated abstinence.
Use only for long-term maintenance of abstinence.
Long half-life, oral, 3 times a week.
Major problem in detoxification and maintenance of
abstinence is the motivational component of the CNS
effect, which is responsible for the “drug craving”
sensations, also conditional dependence and social
factors play an important role.
Opioid Analgesics:
Nursing Implications
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Constipation is a common side effect
and
may be prevented with adequate fluid
and
fiber intake.
Instruct patients to follow directions
for administration carefully, and to
keep a
record of their pain experience and
response to treatments.
Patients should be instructed to
Opioid Analgesics:
Nursing Implications
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Patients should not take other
medications or OTC preparations
without checking with their
physician.
Instruct patients to notify physician
for signs of allergic reaction or
adverse effects.
Opioid Analgesics:
Nursing Implications
Monitor for side effects:
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Should VS change, patient’s
condition decline,
or pain continue, contact physician
immediately.
Respiratory depression may be
manifested by respiratory rate of
less than 12/min, dyspnea,
diminished breath sounds, or
shallow breathing.
Opioid Analgesics:
Nursing Implications
Monitor for therapeutic effects:
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Decreased complaints of pain
Increased periods of comfort
With improved activities of daily living,
appetite,
and sense of well-being
Pain Management
Effects of Narcotics
 Analgesia
Reduce pain from most sources
Pain Management
Effects of Narcotics
 Analgesia
Reduce pain from most sources
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Sedation
Decrease anxiety and cause drowsiness
Pain Management
Effects of Narcotics
 Analgesia
Reduce pain from most sources
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Sedation
Decrease anxiety and cause drowsiness
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Euphoria and Dysphoria
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Can cause feelings of well-being and
disquiet or restlessness
Potential for tolerance and dependence
Pain Management
Patient-Controlled Analgesia Pump
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Patient controls (within limits) when
and how often medication is
administered
Allows for better pain control
Pain Management
Analgesic Ladder
1. Onset of mild to moderate pain
Administer acetaminophen (APAP)
or an NSAID
Pain Management
Analgesic Ladder
1. Onset of mild to moderate pain
Administer acetaminophen (APAP) or an
NSAID
2. Adequate relief is not achieved
in Step 1
Administer NSAID plus a “weak”
opioid (codeine)
Pain Management
Analgesic Ladder
1. Onset of mild to moderate pain
Administer acetaminophen (APAP) or an
NSAID
2. Adequate relief is not achieved in
Step 1
Administer NSAID plus a “weak” opioid
(codeine)
3. Adequate relief is not achieved
in Step 2
Administer a strong opioid
(morphine)
Pain Management
Chronic opioid therapy has a low risk
of addiction when used appropriately.
Discussion
What is the difference
between addiction and
dependence?
Pain Management

Dependence
Physical and emotional reliance on a drug

Addiction
Compulsive disorder
Pain Management
Symptoms of Addiction
 Preoccupation with drugs
 Refusal of medication tapers
 Strong preference for a specific opioid
 Decrease in ability to function
 Medication is typically not taken as
prescribed
 Have a tendency to visit many different
doctors and pharmacies in order to get
the drug(s)
Narcotic
Dispensing Issues
Warning!
Pharmacy technicians have a legal
and moral responsibility to alert
pharmacist of suspected abuse and
addiction.
Pain Management
Patients are more successful
overcoming addiction if withdrawal
symptoms are handled appropriately.
Drug List
Addiction Treatment

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
buprenorphine (Buprenex, Subutex)
buprenorphine-naloxone
(Suboxone)
methadone (Dolophine)
methadone (Dolophine)

Uses

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
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Detoxification
Maintenance of narcotic addiction
Dispensed in clinics or in hospitals
Binds to opiate receptors without
giving a euphoric feeling
Pain Management
Combinations of narcotics and
nonnarcotics is common.
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Enhances relief
Facilitates use of lower doses
Decreases side effects
Narcotic Analgesics
Varying dose requirements due to
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Severity of pain
Individual response to pain
Patient’s age and weight
Presence of concomitant disease
NON-NARCOTIC
ANALGESICS
Types of action of non-narcotic
analgesics
Analgesic
Antipyretic
Anti-inflammatory
(except paracetamol)
Mechanism of action of non-narcotic
analgesics
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depression of cyclooxygenases activity
decreasing of prostaglnadins synthesis in
peripheral tissues and in central nervous
system
decreasing of sensitivity of nervous endings
and depression of transduction of nociceptive
impulses on the level of CNS structures
pain-relieving action of non-narcotic analgesics
is partly connected with their anti-inflammatory
activity
Indications for administration of
non-narcotic analgesics
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headache
toothache
radiculitis
neuritis, neuralgias
myositits, myalgia
arthritis, arthralgia
pain,
connected
with
pelvic
organs
(dysmenorrhea)
for potentiation of their action – combinations
paracetamol with codein,
analgin with dimedrol, analgin with codein
Acetylsalicylic acid
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


Blocks
cyclooxygenase
irreversably
As
a
pyrolytic
and
analgesic drug – 0,25 and
0,5 g per time
As an antiinflammatory –
3-4 g per day (for
arthritis,
myocarditis,
подагрі,
pleuritis,
bronchitis
For
prophylaxis
of
thrombus-formation
(in
case of ischemic heart
disease, thrombophlebitis
etc.) – day dose – 80-100
mg
Analgin
(metamizol-sodium)
Baralgin (maxigan, spazgan, spazmalgon,
trigan)
analgin+pitophenon hydrochloride+pheniverinium bromide
 Ampoules
tablets
suppositories
 Analgesic
and
spasmolytic
activity
Acetaminophen



analgesic and pyrolytic drug
maximal effect if the drug is
introduced orally – after 2 hours, lasts
approximately for 4 hours
in case of durable administration of
big doses – damaging of liver and
kidneys,
production
of
methemoglobin
Acetaminophen





Tablets
Suppositories
Syrups
Soluble tablets
Capsules
Acetaminophen
Panadol (Acetaminophen)
Ketorolak (ketanov)




according to analgesic activity it prevails
over
effect
of
acetylsalicylic
acid,
indometacin
and
equals
to
opioid
analgesics
moderate anti-inflammatory, pyrolytic
and anti-aggregant effects
high effectiveness in case of pain in
postoperative period, in oncology, during
child delivery, traumas, colics
intramuscular introduction
NOT indicated
for chronic pain syndrome
Ketoprophen (ketonal)



strong
analgesic,
antiinflammatory
and
pyrolytic
agent
administered
in
case
of
arthroses
and
arthritis,
ancilizing spondilitis, pain of
different
genesis
(after
surgeries, in case of traumas,
painful menstruations etc.)
administered
orally,
intramuscularly, in forms of
suppositories and ointments
TRAMADOL
Analgesic activity is not
weaker than activity of
morphine
In case of intravenous
administration effect develops
after 5-10 min, if
administered orally – after
30-40 min, action lasts for
3-5 hours.
ADMINISTRATION OF TRAMADOL
surgery, traumatology, gynecology,
neurology, urology, oncology
For all kinds of acute and chronic pain
of moderate and considerable
intensity, including postoperative,
traumatic pain
neuralgias
diagnostic
and
therapeutic
interventions
oncologic pathology
Anesthesia
Goals of Balanced
Anesthesia
 Amnesia
Anesthesia
Goals of Balanced
Anesthesia

Amnesia
 Adequate
Muscle
Relaxation
Anesthesia
Goals of Balanced
Anesthesia


Amnesia
Adequate Muscle Relaxation
 Adequate
Ventilation
Anesthesia
Goals of Balanced
Anesthesia



Amnesia
Adequate Muscle Relaxation
Adequate Ventilation
 Pain
Control
Types of Anesthesia
General
Local
Types of Anesthesia
General
 Local
Discussion
What are some of the
indicators used to assess
general anesthesia?
Discussion
What are some of the indicators
used to access general anesthesia?
Answer: Blood pressure,
hypervolemia, oxygen level,
pulse, respiratory rate, tissue
perfusion, urinary output
General Anesthesia
Preanesthetic Medications




Control sedation
Reduce postoperative pain
Provide amnesia
Decrease anxiety
General Anesthesia
Malignant Hyperthermia

Side effect of anesthesia
Fever of 110°F or more
 Life threatening


Treatment: dantrolene (Dantrium)
Warning!
Always check
expiration date.
Drug List
Inhalant Anesthetics





desflurane (Suprane)
enflurane (Ethrane)
halothane
isoflurane (Forane)
nitrous oxide
Inhalant Anesthesia Side Effects
 Causes
reduction in blood
pressure
 May cause nausea and
vomiting
nitrous oxide




Causes analgesia only; no
amnesia or relaxation
May be given alone or may be
given with more powerful
anesthetics to hasten the
uptake of the other agent(s)
Commonly used for dental
procedures
Rapidly eliminated
desflurane (Suprane)


Has rapid onset and recovery
Often used in ambulatory
surgery
General Anesthesia


Often dispensed by IV drip
Very lipid soluble
Drug List
Injectable Anesthetics







etomidate (Amidate)
fentanyl (Duragesic, Sublimaze)
fentanyl-droperidol
ketamine (Ketalar)
morphine
propofol (Diprivan)
sufentanil (Sufenta)
Drug List
Injectable Anesthetics
Barbituates
 methohexital (Brevital)
 thiopental (Pentothal)
Benzodiazepines
 diazepam (Valium)
 lorazepam (Ativan)
 midazolam (Versed)
propofol (Diprivan)


Used for maintenance of
anesthesia, sedation, or
treatment of agitation
Has antiemetic properties




Drowsiness
Respiratory depression
Motor restlessness
Increased blood pressure
Injectable Anesthesia
Dispensing Issues
Warning!
Diprivan (anesthetic) and Diflucan
(antifungal) may be confused.
This mix-up could be life-threatening.
fentanyl

Dosage Forms




IV (Sublimaze)
patch (Duragesic)
lozenge (Actiq) for children
Used extensively for open-heart
surgery due to lack of cardiac
depression
Benzodiazepines



Used for induction, short
procedures, and dental procedures
Useful in controlling and preventing
seizures induced by local
anesthetics
midozolam (Versed)



fastest onset of action
greatest potency
most rapid elimination
Antagonist Agents
Antagonist agents reverse
benzodiazepine and narcotic
overdose.
Drug List
Antagonist Agents



flumazenil (Romazicon)
nalmefene (Revex)
naloxone (Narcan)
flumazenil (Romazicon)


Antagonizes benzodiazepines by
competing for receptor site
Used for complete or partial
reversal
naloxone (Narcan)


Competes for opiate receptor sites
Has a shorter duration of action
than narcotics, so it must be given
repeatedly
Neuromuscular Blocking Agents

Causes immediate skeletal muscle
relaxation.




Short Duration
Intermediate Duration
Extended Duration
Used to facilitate endotracheal
intubation.


Allows for easier insertion of endotracheal
tube.
Keeps airway open.
Drug List
Neuromuscular Blocking
Agents







atracurium (Tracrium)
cisatracurium (Nimbex)
mivacurium (Mivacron)
pancuronium
rocuronium (Zemuron)
succinylcholine (Quelicin)
vecuronium (Norcuron)
Neuromuscular Blocking Agents
Dispensing Issues
Warning!



Very expensive
Be conscious of storage
requirements
Store away from look-alike and
drugs
succinylcholine (Quelicin)




Often called “sux.”
Only depolarizing agent. All others
work as competitive antagonists to
ACh receptors.
Persistent depolarization at motor
endplate.
Causes sustained, brief period of
flaccid skeletal muscle paralysis.
Reversal of Neuromuscular Blocking
Agents


Increases the action of acetylcholine
by inhibiting acetylcholinesterase
Used for reversal of nonpolarizing
agents
Drug List
Anticholinesterase Agents



edrophonium (Enlon)
neostigmine (Prostigmin)
pyridostigmine (Mestinon)
Types of Anesthesia
 General
Local
Local Anesthesia
Relieves pain without altering
alertness or mental function.
Local Anesthesia
Variety of Dosage Forms






Topical
Superficial injection (infiltration)
Nerve block
IV
Epidural
Spinal
Discussion
Local anesthetics are
classified by their
chemistry into two classes.
What are they?
Discussion
Local anesthetics are classified by
their chemistry into two classes.
What are they?
Answer


Esters
Amides
Local Anesthesia
Esters



Short acting
Metabolized in the plasma and tissue
fluids
Excreted in urine
Local Anesthesia
Amides



Longer acting
Metabolized by liver enzymes
Excreted in urine
Drug List
Local Anesthesia
Esters
 benzocaine (Americaine)
 chloroprocaine (Nesacaine)
 dyclonine (Cēpacol Maximum Strength)
 procaine (Novocain)
 tetracaine (Cēpacol Viractin, Pontocaine)
Drug List
Local Anesthesia
Amides
 bupivacaine (Marcaine)
 levobupivacaine (Chirocaine)
 lidocaine (L-M-X, Solarcaine, Xylocaine)
 lidocaine-epinephrine (Xylocaine w/
Epinephrine)
 lidocaine-prilocaine (EMLA)
 mepivacaine (Carbocaine)
Discussion
What functions are lost
with local anesthetics?
Discussion
What functions are lost with local
anesthetics?
Answer





Pain perception
Temperature
Touch sensation
Proprioception
Skeletal muscle tone
Discussion
Under what conditions
would a local anesthetic
be used over a general
anesthetic?
Discussion
Under what conditions would a local
anesthetic be used over a general
anesthetic?
Answer: It is chosen
when a well-defined area
of the body is targeted.