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151908065-Anesthesiology-Ppt

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ANESTHESIOLOGY
(LOCAL ANESTHESIA)
DEFINITION:
• Anesthesia – temporary loss of
sensation(including the loss of sensation to
touch, pressure, proprioception, and loss of
motor function) either with the patient
conscious or unconscious.
• Analgesia – temporary loss of pain
sensation
• Regonal(local) analgesia- temporary
loss of pain sensation over a portion of
anatomy without loss of consciousness.
Pain and nerve conduction
Pain- an unplesant sensation
usually iniated by a noxious
stimulus and transmitted over
a specialized neural network
where it is interpreted as pain.
Theories of pain conduction:
1.Specificity theory- descartes in1644.
2.pattern/summation theory-goldscheider in
1894.
3.Gate control theory-melzack and wall in 1965
a. Information about presence of pain from an
injury from peripheral nerves of the brain.
b. These info either facilitated or inhibited by
larger peripheral nerves that also carry info
about innocuous event (temp,pressure)
c. ascending control system originating from
the brain modulated the excitability of cells
that transmit info about injury.
Nerve conduction
Step 1 resting potential- 70- -90 mv in the
inside of the cell because of the relative
impermiability of the nerve membrane to
Na+ ions and the action of the Na+ pump.
Step 2 presence of stimulus (action
potential)
a. Slow depolarization
b. Threshold potential or firing potential -50-60mv .
c. Rapid depolarization
Step 3 repolarization- resting potential
• Absolute refractory period- the return to
the resting (step 1 and 2) wherein the
nerve cannot be stimulated.
• Relative refractory period- when the
imbalance returns to the resting state
wherein a greater stimulus is needed to
stimulate the nerve.
• “All or non law” of nerve conduction-the
stimulus should be strong enough to reach
the threshold potential to stimulate the
nerve.
Dual nature of pain
• Pain perception- physioanatomical process
• Pain reaction- psychophysiological process
affected by: a. emotional state
b. fatigue
c. age
d. race and nationality
e. sex
f. fear and apprehension
g. socio economic status
Methods of pain control:
1.removing the cause
2.Blocking the pathway of painful
impulses- local anesthesia
3.Raising the pain threshold- sedation
anesthesia
4.Cortical depression- general anesthesia
5.Using psychosomatic methodshypnotism
WHAT IS LOCAL
ANESTHESIA?
is any technique to induce the absence
of sensation in part of the body, generally
for the aim of inducing local analgesia,
that is, local insensitivity to pain, although
other local senses may be affected as
well. It allows patients to undergo surgical
and dental procedures with reduced pain
and distress.
*drugs that have a little or no
irritating effects when injected in to
the tissue and that will temporarily
interrupt conduction when
absorbed into the nerves tissue
The following terms are often used
interchangeably:
*Local anesthesia, in a strict sense,
is anesthesia of a small part of the body such as a
tooth or an area of skin.
*Regional anesthesia is aimed at
anesthetizing a larger part of the body such
as a leg or arm.
*Conduction anesthesia is a
comprehensive term, which encompasses a
great variety of local and regional
anesthetic techniques.
LOCAL
ANESTHETIC
A local anesthetic is a drug that causes reversible
local anesthesia and a loss of nociception. When it
is used on specific nerve pathways (nerve block),
effects such as analgesia (loss of painsensation)
and paralysis (loss of muscle power) can be
achieved. Clinical local anesthetics belong to one of
two classes: aminoamide and aminoester local
anesthetics. Synthetic local anesthetics are
structurally related to cocaine. They differ from
cocaine mainly in that they have no abuse potential
and do not act on the sympathoadrenergic system,
i.e. they do not producehypertension or
local vasoconstriction, with the exception
of Ropivacaine and Mepivacaine that do produce
Properties of ideal
anesthetics
1.Action must be reversible
2.non-irritating to tissues
3.Low degree of systemic toxicity
4.Rapid onset and sufficient duration
5.Potency sufficient enough to produced
complete analgesia without the use of
harmful concentrated solution.
6.Suffiecient penetrating properties
7.Free for producing allergic reactions
8.Stable in solution and undergo
biotransformation readily.
9.Sterile and capable of sterilization
Groups of local anesthesia
I. ESTER GROUP
A. Benzoic acid ester
1.cocaine
2.benzocaine
B.PABA ESTERS
1.procaine (novocaine)
2. tetracaine (pontocaine)
3.propoxycaine(ravocaine)
II. AMIDE GROUP (anilide derivatives)
1.bupivacaine(marcaine)
2.etidocaine (duranest)
3.lidocaine (xylocaine)
4.mepivacaine(carbocaine)
5.prilocaine(citanest)
Benzocaine (ester)
Mepivacaine (Polocaine/Carbocaine)
Procaine (ester)
Bupivacaine (Marcaine)
Composition of local anesthesia
1. Aromatic lypophilic group
2. Intermediate chain
containing ester and amide
group
3. Hydrophilic secondary or
tertiary amino group
MODE OF ACTION OF LA
LA drugs (weak base and not soluble in water)--- add
HCI (strong acid) --- create LA salts --- LA solution--contain free base (RN) which are lipophilic and
cations (RHN+) which are hydrophilic
pKa- dissociation constant or measure of the affinity
of a substance to H+ ions
LA salt--- injected to tissues--- cation loses H+--alkaloidal base--- penetrates nerve membrane—
free bases attract H+ ions inside the nerve
membrane --- theories of regional anesthesia--- Na+
cannot enter the nerve--- nerve stabilize--- no
conduction
VASOCONTRICTOR
The vasodilation activity of local anesthetics produce an
increased rate of absorption. This results in decreased
effectiveness, short duration of anesthesia, and a
higher risk of toxicity. Bleeding in the area of injection
is increased. Vasoconstrictors are clinically useful in
counteracting these effects. Vasoconstrictors are added
to local anesthetics to decrease the absorption of the
drug and prolong the anesthetic effect that produces
anesthesia that is more profound. The vasoconstrictor
also serves to reduce the risk of toxicity because it is
more slowly absorbed by the circulatory system. The
length of the procedure, desired level of hemostasis, and
the medical health of the patient must all be considered
when selecting an appropriate vasoconstrictor.
*Epinephrine and levonordefrin (neocobefrin) are the most commonly used
vasoconstrictors in dentistry.
*Epinephrine is sensitive to heat and can be
inactivated if left too warm for too long.
*Epinephrine is available in concentrations
of 1:50,000 for better hemostasis.
Epinephrine is contraindicated in
patients with
• blood pressure over 200 torr systolic or 115 torr
diastolic,
• uncontrolled hyperthyroidism,
• severe cardiovascular disease including less than 6
months after a myocardial infarction or
cerebrovascular accident
• daily episodes of angina pectoris or unstable angina
• cardiac dysrhythmias despite appropriate therapy
• medicated with -blocker, monoamine oxidase
inhibitors, or tricyclic antidepressants; or general
anesthesia with a halogenated anesthetic like
halothane, methoxyflurane, or ethrane.
Why is Epinephrine a perfect
vasoconstrictor?
Epinephrine, also known as adrenaline is a naturally
occurring hormone and a neurotransmitter. Epinephrine
is a perfect vasoconstrictor because it is produced
naturally by the body as adrenaline, occasionally called
the "fight or flight hormone". If it enters the normal
circulation, it can cause an increased heart rate and
stronger heart beatwith a feeling of anxiety, besides
causing a constriction of blood supply. So, it increases
heart rate, constrictsblood vessels, dilates air passages
and participates in the acute stress response of the
sympathetic nervous system, one of the three parts of
the autonomic nervous system. These side
effects describe for the "rush" that some people feel after
getting an anesthetic shot.
What is the concentration of
vasoconstrictor in Anesthesia?
• The concentration of vasoconstrictor in any given carpule of anesthesia
is represented by a ratio of vasoconstrictor per mL of solution. For
instance, a solution may be labeled as 1:100,000. This concentration
represents 1000mg/100,000mL or 0.01mg/mL, or 1 gram per 100 Liters. A
1:1000 solution translates to 1 mg vaoconstrictor per mL of solution, or 1
gram per Liter. Most anesthetic solutions contain the minimum amount of
anesthesia required to constrict local blood vessels and extend the action
of the anesthetic. A few, however, contain a higher concentration
of vasoconstrictor for use in controlling bleeding for specific purposes,
such as periodontal surgery. For instance, general purpose lidocaine
contains epinephrine in the amount of 1/100,000 for producing deep,
extended anesthesia. On the other hand, lidocaine also comes with
epinephrine at twice the normal concentration (1/50,000) used mostly by
periodontists who need to control gingival bleeding during surgery.
What is the advantage of anesthetics
that don't have a vasoconstrictor?
• The majority of anesthetic solutions have added vasoconstrictor. Only
two, mepivicaine and prilocaine are sold with or without vasoconstrictor.
Mepivicaine and prilocaine have the advantage of producing only minor
vasodilation and, though both are short acting without their
vasoconstrictor added. However, they still produce
sufficient anesthesia for short procedures. The most important
advantage of using an anesthetic without a vasoconstrictor is that there
are virtually no interactions with other drugs the patient may be taking.
• Also, carpules that do not contain vasoconstrictor do not contain
preservatives either. This is a vital point, because it is most often the
preservatives, and not the anesthetics themselves which play a role in
allergic reactions. There has never been a recognized case of allergy to
the modern amine based anesthetics themselves; nevertheless, many
people are allergic to the preservatives linked with the vasoconstrictor.
What is the disadvantage of
anesthetics that don't have a
vasoconstrictor?
• The use of vasoconstrictor has a disadvantage. These
naturally occurring hormones are not very stable, and
must be stabilized by the addition of an acidic
preservative. The presence of the preservative can
lower the PH of the anesthetic solution to the range of
3.8 to 5.0, thus reducing the amount of the neutral
basic radical (RN) and slowing the beginning of action
of the anesthetic. This effect is, however not
particularly major, and anesthesiawith vasoconstrictor
is a very popular choice among practitioners when
other medical considerations authorize its use.
Are vasoconstrictors safe?
The use of vasoconstrictor in dentistry has been proven to be
very safe for approximately all patients. Actually, the use of
vasoconstrictor is highly recommended due to the increase in
effectiveness and prolonged existence of dental anesthesia.
There are no absolute contraindications to the use
of vasoconstrictors in dental local anesthetics, as epinephrine
is an endogenously produced neurotransmitter. According to
the American HeartAssociation and the American Dental
Association, the characteristic concentrations
of vasoconstrictors present in local anesthetics are not
contraindicated with cardiovascular disease so long as
preliminary objective is accomplished, the agent is injected
gradually, and the smallest effective dose is offered.
THE END
SUBMITTED TO: DR. NAPOLEON NAVARETTE
SUBMITTED BY: BACTON,AMOR D.
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