2. Local anesthetic: Produce loss of sensation to pain in a specific area
of the body without the loss of consciousness
3. In 1884, Carl Koller an ophthalmologist used the first local anesthetic on a
patient with glaucoma.
Koller continued his cocaine experiments on himself and prepared a paper for
the Heidelberg Ophthalmological Society to demonstrate the technique which
published in October 1884.
Koller became addicted to the drug through self-experimentation
Carl Koller
1857-1944
4. ¢ Limit influx of sodium, thereby limiting
propagation of the action potential
4
5. ¢ Local anesthetics block the conduction in peripheral
nerves, that inhibited the nerve to excite.
¢ The anesthetics reversibly binds to sodium channels and
inactivates the sodium channels.
¢ The sodium unable to influx through these channels and
depolarizes the nerve cell membranes, and fail to produce
impulses along the way.
¢ As a result, the nerve loses depolarization and the capacity
to create the impulse, the patient loses sensation in the
area supplied by the nerve.
5
6. ¢ Two classes of local anesthetics:
Amino amides
Amino esters
Esters:--Metabolized in plasma
Amides:--Metabolized in liver
¢ Esters
Cocaine , Chloroprocaine , Procaine, Tetracaine
¢ Amides
Bupivacaine , Lidocaine, Ropivacaine, Mepivacaine
7.
8. ¢ All local anaesthetics are weak bases.
¢ Chemical structure of local anaesthetics have an amine
group on one end & an aromatic ring on the other.
¢ Amine end is hydrophilic (soluble in water)
¢ Aromatic end is lipophilic (soluble in lipids)
9. LIDOCAINE
— In 1940, the first modern local anaesthetic agent was
lidocaine, trade name Xylocaine
— cause little allergic reaction.
— Sets on quickly and produces a desired anaesthesia effect for
several hours
— It’s accepted broadly as the local anaesthetic in United
States & worldwide today.
10. ¢ Procaine is the first derivative of cocaine, also known
as the first synthetic local anaesthetic drug
¢ Trade name is Novocaine®
11. LA are administered as very dilute solutions which can be
expressed as parts of active drug per 100 parts of solution
(grams percent)
Ex.: 2% solution =
2 grams = 2000mg_ = 20 mg
100 cc’s 100 cc’s 1 cc
12. FACTORS AFFECT THE REACTION OF LOCAL
ANAESTHETICS
¢ Lipid solubility
Increasing the lipid solubility leads to faster nerve
penetration, block sodium channels, and speed up the
onset of action.
¢ pH influence
Usually at range 7.6 – 8.9
Lower pH, solution more acidic, gives slower onset of action.
13. ¢ Vasoconstrictors
Vasoconstrictor is a substance used to keep the
anaesthetic solution in place at a longer period and
prolongs the action of the drug
15. ¢ The amount of dose also varied based on the type of
solution used and the presence of vasoconstrictor
¢ Maximum dose for an individual is usually between 70mg
to 500mg(lidocaine 4-7 mg/kg & bupivacaine 2-3mg/kg)
16. TOXICITY
Some common toxic effects:
Light headedness
Shivering or twitching
Seizures
Hypotension (low blood pressure)Numbness
Tinnitus
17. LOCAL ANAESTHETICS - ALLERGY
¢ True allergy is very rare
¢ Most reactions are from ester class
¢ Patient reports of “allergy” are frequently due
to previous intravascular injections
18. TISSUE TOXICITY
• Tissue toxicity is Rare
• Can occur if administered in high enough
concentrations (greater than those used clinically)
• Usually related to preservatives added to solution
19. LOCAL ANAESTHETICS - DURATION
Determined by rate of elimination of agent from site
injected
Factors include lipid solubility, dose given, blood flow at
site, addition of vasoconstrictors (does not reliably
prolong all agents)
Some techniques allow multiple injections over time
to increase duration, e.g. epidural catheter
20.
21. Rendering a specific area of the body.
For Example, Foot, arm, lower extremities
22. REGIONAL ANESTHESIA -
USES
n Provide anesthesia for a surgical procedure
n Provide analgesia post-operatively or during labor and
delivery
n Diagnosis or therapy for patients with chronic pain
syndromes
26. Overdose reaction is occurring when the drug
access to the circulatorysystem.
Normally there is constant absorption of the drug
from its site of admission into the circulatory
system and a steady removal from the blood by
the liver.
27. Use aspirationsyringe.
Use a needle no smaller than 25gauge.
Aspirate in at least two planes before injection.
Slow inject the anaesthetic.
29. ¢ Reassure the patient.
¢ Basic Emergency Management
i.e. ABC
¢ Administer oxygen
¢ Monitor and record vital signs
¢ IV anticonvulsants (diazepam5
mg/min. or midazolam
¢ 1mg/min.)
¢ Vasopressor and IV fluid is
recommended for management
of hypotension.
31. 3. Generalized Anaphylaxis
§ Skin reactions
§ Smooth muscle spasm
(gastrointestinal, genitourinary
tracts and bronchospasm)
§ Respiratory distress.
§ Cardiovascular collapse.
Treatment of the entire reaction
may be terminated rapidly, but
hypotension and laryngeal edema
may persist for hours to days.
33. Respiratory reaction:
(Bronchospasm)
¢ Administer oxygen at flow 5-6 litersmin
¢ Epinpherine 0.3 IM or Bronchodilator “albuterol”
¢ Observation for 1 hour.
¢ IM histamine blocker
¢ Medical consultation
34. Generalized Anaphylaxis :
(unconscious patient)
¢ Administer oxygen
¢ Monitor vital signs, recorded every 5 min
¢ Summon medical assistance
¢ Epinpherine 0.3 IM, dose repeated 10-15 min
¢ IM histamine blocker
¢ Corticosteroid IM or IV