This document discusses the pharmacology of local anesthesia. It defines local anesthesia as drug-induced reversible blockade of nerve conduction in a specific part of the body without altering consciousness. It describes the ideal properties of local anesthetics and classifies them based on their chemical structure as esters or amides. The document discusses the mechanism of action of local anesthetics in blocking nerve conduction and their pharmacokinetics of absorption, distribution, metabolism and excretion. It also covers the systemic effects, interactions, contraindications and proper use of local anesthetics.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
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1. Pharmacology of Local AnAesthesia
Dr.SalehBakry
AssistantProfesorofOralandMaxilofacial Surgery
2.
3. Local Anaesthesia
1. DEFINITION:
Local anaesthesia is drug-induced reversible
local blockade of nerve conduction in a specific
part of the body that does not alter
consciousness.
4. 2. Properties of ideal local anesthesia
• Reversible action.
• Non-irritant.
• No allergic reaction.
• No systemic toxicity.
• Rapid onset of action.
• Sufficient duration of action.
• Potent.
• Stable in solutions.
• Not interfere with healing of tissue.
• Have a vasoconstrictor action or compatible
with VC.
• Not expensive
6. 3. structural classification of local anaesthetics
1- Aromatic (lipophilic) portion: composed of benzene
ring, enable local anesthetic solution to diffuse
through lipid rich nerves.
2- Amine (hydrophilic) portion: enable anesthesia to
diffuse through interstitial tissues.
3- intermediate chain portion: connect between
lipophilic and hydrophilic portions and divides local
anesthesia into two chemical classes, ester and amide
type.
Local anesthetics without a hydrophilic part are not
suitable for injection but are good for topical
anesthetics e.g.10% benzocaine, 5% Lidocaine.
7. Esters vs Amides
Ester
• Ester linkage is more easy broken
• Less stable in solution
• Cannot be stored for long time
• Metabolism of most esters
results in the production of para
aminobenzoate (PABA)
which is associated
with allergic reaction.
Amide
• Not broken easy
• More stable in solution
• Stored for long time
• Amides, very rarely cause
allergic phenomena
8. STRUCTURE OF LOCAL ANESTHETICDRUG
• Most of the local anesthetic drugs are tertiary
amines, N≡R (basic active analgesic radical).
• These are generally found in the market in the
form of the watery solution of their acid salts,
usually a hydrochloride salt, which provides
acidic medium for storage of tertiary amine.
N≡R + HCl → R=NHCl ↔ R=NH+ + Cl-
Hydrochloride salt Cation Anion
9. • This local anesthetic salt is dissolved in sterile
water or saline.
• In this solution it exists simultaneously as
uncharged molecules RN called (base) and
positively charged molecules RNH+ called
(cation)
RNH+ ↔ RN + H+
Cation base
• RNH+ is responsible for binding to the protein
receptor site in sodium channel for nerve
conduction blockage.
• RN is responsible for diffuse and penetration
through lipid nerve sheath membrane.
10.
11.
12. 4. PH of the surrounding tissues andL.A
• Lower PH acidic medium (high conc of H+) →
most anesthetic solution exists in cationic
form:
RNH+ > RN + H+
• Higher PH alkaline medium (decrease conc of
H+) → more free base which produce action:
RNH+ < RN + H+
13. 5. PKa or dissociation constant of the agent
• All local anaesthetic agents are weak bases,
meaning that they exist in two forms: unionised
(RN) and ionised (RNH+).
• The pKa of a weak base defines: the pH at which
both forms exist in equal amounts.
• PKa is a measure of a molecule's affinity for
hydrogen ions (H+) i.e. it is the liability to form
cation RNH+.
If PKa = PH → RNH+ = RN
If PKa > PH → RNH+ > RN
If PKa < PH → RN > RNH+
14. • All local anesthetics have PKa values >7.4
• PKa of amide 7.6-8.1 & PKa of ester are higher.
• Pka determine onset of action of anesthesia.
• Protein binding determine duration of action.
15. • When PKa of agent (7.3) = PH of solution or
tissue 7.3
50% of drug in cationic form RNH+ and 50% of
drug in base form RN
• When PKa high as procaine 9.1 > PH of
solution or tissue 7.3 Results in RNH+ > RN
The end result poor anesthetic action because too
small amount of RN base diffuse through a nerve
membrane sheath onset of anesthesia
prolonged 14-18 minutes.
16. • When PKa low 6.5 < PH of solution or
tissue 7.3 Results in RNH+ < RN
The end result very large number of base
molecules RN is formed which are able to
diffuse through nerve sheath and produce
rapid onset of action about 2-4 minutes.
17. Local analgesics are not so
effective in infected tissues,
this may be due to:
• Inflammatory vasodilatation
flushing the analgesic away from
the site of injection.
• Pus lowers the PH and thus
inhibits the liberation of active
analgesic radical
20. A. According to chemical structure
Local anesthetics are classified into 2 groups:
• the ester group and the amide group.
• The classification is based on the chemical structure
of the intermediate chain.
• Commonly used amides include: lidocaine,
Mepivacaine.
• Commonly used esters include: tetracaine,
procaine, cocaine.
• There are third group know as Quinoline which
include Centbucridine.
21. B. ACCORDING TO TIME OF ACTION
1. SHORT DURATION (pulpal anesthesia approximately 30 minutes)
• Lidocaine HCl 2%
• Mepivacaine HCl 3%
• Prilocaine HCl 4% (by infiltration)
2. INTERMEDIATE DURATION (pulpal anesthesia approximately 60
minutes)
• Articaine HCl 4% + epinephrine 1:100,000 and 1:200,000
• Lidocaine HCl 2% + epinephrine 1:50,000 and 1:100,000
• Mepivacaine HCl 2% + levonordefrin 1:20,000
• Mepivacaine HCl 2% + epinephrine 1:100,000
• Prilocaine HCL 4% + epinephrin 1:200,000
22. 3. LONG DURATION (pulpal anesthesia approximately 90+
minutes)
• Bupivacaine HCl 0.5% + epinephrine 1:200,000
• Etidocaine 1.5% with epinephrin
23.
24. 7. ELECTROPHYSIOLOGYAND
ELECTROCHEMISTRY OF NERVE
CONDUCTION
The function of nerve is to carry messages from
one part of the body to another in the form of
electrical action potential called IMPULSES
initiated by chemical, mechanical, thermal or
electrical stimuli.
25. • In a resting nerve, the electrical resistance
keeps sodium, potassium and chloride ions
from flowing into the axons.
• Nerve has a resting electrical potential (-70 mv)
where the inside or axoplasm has a negative
electrical potential and the outside is positive.
27. STEP 1
• When the nerve is stimulated, the membrane
become transiently permeable to sodium ions
which across the neural membrane through
special pores in the membrane called sodium
channel depolarization.
• This called threshold potential or firing
threshold.
28. • The electrical potential is then reversed resulting
in the inside of the nerve being electrically
positive and the outside negative (+40 mv).
29. STEP 2
• This is a phase of Repolarisation.
• Electrical potential gradually becomes more
negative in respect to the outside until -70mv is
achieved.
31. 1. Specific receptor theory:
• L.A. binds to specific receptors on Na+ channels
→↓ permeability to Na+ → prevent nerve
condition.
32. 2. Membrane expansion theory:
• L.A. penetrates the cell membrane of the nerve
cell → expand some critical regions in the
membrane → decrease of Na+ channel diameter
→ prevent nerve conduction.
33. 3. Calcium displacement theory:
• Ca++ ions are displaced from receptor sites →↓
permeability to Na+ → prevent nerve
conduction.
34. • 4. Acetylcholine theory:
• L.A. interfere with acetylcholine at synaptic
function → prevent nerve conduction.
35. 5. Physiological theory:
• L.A. interfere with nerve metabolism → no
energy production → prevents nerve
conduction.
6. Mechanical or reversible coagulation theory:
• L.A. dissolve in the lipid contents of nerve
tissues → temporary coagulation → prevent
nerve impulses conduction.
7. Electrical potential theory (Surface charge
theory):
• L.A. agent makes nerve fibers positively charged
→ prevent nerve conduction.
37. The following sequence is proposed mechanism
of action of LA:
1. Displacement of calcium ions from the sodium
channel receptor site
2. Binding of local anesthetic molecule to this
receptor site
3. Blockade of sodium channel
38. 4. Decrease in sodium conductance
5. Depression of rate of electrical depolarization
6. Failure to achieve the threshold potential level
8. Conduction blockade…
39.
40. 10. PHARMACOKINETICS Of LOCAL
ANESTHETICS
Pharmacokinetics describes the processes by
which drugs are absorbed, distributed,
metabolized and excreted by the body.
41. A. Uptake
• The rate of absorption of the local anesthetic
into the blood is related to:
A. Vasoactivity of the drug
• Most local anesthetics produce varying degrees
of vasodilatation.
• Procaine is the most potent vasodilator.
• Cocaine is the only local anesthetic that
produces vasoconstriction.
42. • 3% mepivacaine has very slight vasodilating
property so it can be used if vasoconstrictor is
contraindicated.
• mepivacaine has vasoconstrictor action this could
be related to the pyridine ring which incorporated in
its molecule and also pyridine ring is found in
cocaine.
• The clinical significance of vasodilatation:
– Increases blood flow to the site which in turn
increases the rate of absorption of the local
anesthetic into the blood, with the subsequent
decrease in the duration of anesthesia.
– Increases toxicity.
– Decreases duration of pain control (decrease
effect of anesthesia)
43. B. Vascularity of the injection site
• Increased vascularity at the site of injection
results in a more rapid absorption of the local
anesthetic.
• This most notable in areas of infection and
inflammation.
44. B. Distribution
• Once absorbed into the blood, L.A agents are
distributed throughout the body to all tissues.
• Highly perfuse organs (with increased blood
supply) as brain, liver, kidney, lung, spleen
initially have height levels of anesthesia.
• Skeletal muscles contain greatest percentage of
L.A because it constitutes the largest mass
tissues.
45. The blood level of local anesthetic is influenced
by:
– Rate of absorption of the local anesthetic into
the blood. ( increase in this rate, increase
anesthetic blood Level )
– Rate of distribution of the drug to the tissues.
( decrease in this rate, increases anesthetic
blood Level)
– Rate of elimination of the drug (decrease in
this rate, increases anesthetic blood Level).
46. C. Biotransformation
• Ester L.A are hydrolysed in the plasma by
enzyme pseudocholine esterase
• Amide La. are biotransferred in the liver
(detoxification), Prilocain is detoxicated in the
lung also besides liver.
47. • PABA(para-aminobenzoic acide) is the
byproduct result from biotransformation of
ester type. PABA excreted unchanged in the
urine.
• The allergic reactions from ester group are not
related to the parent compound but rather to
PABA.
48. • Patients with low hepatic perfusion
(hypotension, congestive heart failure) or liver
dysfunction (cirrhosis) are unable to metabolize
amide local anesthetics at a normal rate and
represent a relative contraindication to the use
of amide local anesthetics.
49. • Succinylcholine is a short acting muscle relaxant
employed during the general anesthesia
produces respiratory arrest (Apnea) for 2-3
minutes.
• Plasma pseudocholinesterase enzyme hydrolyze
succinylcholine and stops its action so any
person has a familial history of difficulty during
G.A should be carefully evaluated because may
he has atypical enzyme therefore Ester type of
L.A is absolute contraindicated.
50. • One of the metabolites of prilocaine and articaine
is ortho-toluidine, which reduces hemoglobin to
methemoglobin, which, in turn, may lead to
methemoglobinemia if produced in excess.
• In methemoglobinemia there is increasing a level of
HB in ferric form that fails to release oxygen
resulting in cyanosis and respiratory distress so in
cases of respiratory diseases the patient must not
take prilocaine or articaine.
• Articaine is the only amid- type local anesthetic
that contains an ester group (thiophene group).
biotransformation of Articaine occurs in both the
plasma and liver and excreted via kidneys 5-10%
unchanged.
51. D. Excretion
• Mainly by kidney.
• Esters generally appear in only very small
percentage in urine because of the almost
complete hydrolysis in the plasma.
• Amides are usually present in the urine in a
greater percentage than are esters, primarily
because of their more complex process of
biotransformation.
54. A- Central nervous system
1- Anticonvulsant properties
• All L.A. in normal doses producing generalized CNS
depression, but overdose cause increase excitability
of CNS.
• Some L.A. such as procaine, lidocaine, mepivacaine
have anticonvulsant properties and can be used
intravenously to terminate or decrease duration of
grand mal and petit mal seizures.
2- Analgesia
- In past procaine was injected intravenously for
management of chronic pain and arthritis.
55. B- Cardiovascular system
1- Direct action on myocardium
• L.A. produce depression of myocardium related
to anesthetic level in blood. So it decrease rate
of conduction and force of contraction.
• Overdose of L.A. cause different signs and
symptoms :
1. Low to moderate overdose Elevated
blood pressure, heart rate, and respiratory
rate .
2. Moderate to high overdose levels
decreased blood pressure, heart rate , and
respiratory rate.
56. 2- Direct action on peripheral vasculature
• Cocaine is the only L.A. that produce vasoconstriction
at normal dosage.
• All other L.A. produce peripheral vasodilatation,
through relaxation of smooth muscle in wall of blood
vessels.
• At normal dose, L.A. slight increase or no change in
blood pressure
• At overdose levels profound hypotension.
• At lethal levels cardiovascular collapse is noted.
57. C- Local tissue toxicity
Skeletal muscles are more sensitive to local irritant
properties of local anesthesia than other tissues.
D- Respiratory system
- Normal dose have direct relaxant action on
bronchial smooth muscles.
- at overdose levels respiratory arrest as a
result of generalized CNS depression.
E- Drug interaction
- Administration of CNS depressants in conjunction
with L.A. CNS depression.
58. F- Neuromuscularblockade
• L.A. block neuromuscular transmission in
humans.
• This is a result of inhibition of sodium diffusion
through the sodium channels in the cell
membrane.
60. I- Absolute contraindications
Medical problem Avoid May use
Anesthetic allergy Same chemical
class
Different chemical
class
Bisulfite allergy Anesthetics with
vasoconstrictors
Plain anesthesia
Sulfur allergy Articaine Non-sulfur types
61. 2- Relative contraindications
Medical problem Avoid May use
Atypical cholinestrase esters Amides
Methemoglobinemia Prilocaine& articaine Others
Severe liver disease
&congestive heart
failure(ASA III-IV)
Amides Esters, or amides
(reduce the dose)
Severe kidney disease
(ASA III-IV)
Amides &esters Either(reduce the dose)
Severe cardiovascular
disease(ASA III-IV)
Excess vasoconstrictors Plain anesthesia, or with
vasoconstrictor(low dose)
Severe thyrotoxicosis
(ASA III-IV)
Excess vasoconstrictors Plain anesthesia, or with
vasoconstrictors(low
dose)
64. 1. Local anesthetic drug.
2. Vasoconstrictor drug (may or may
not be found)
3. Vehicle to make the solution
isotonic
4. Preservative: found if vc is present.
67. Lidocaine
(Xylocaine)
Mepivicaine
(carbocaine)
Prilocaine
(Citanest)
Dental
concentration
2% - 3%
conc.
Both conc.
Can be used
with or
without V.C.
V.C. used is
epinephrin
1:50,000 or
1:100,000
3% without
V.C.
2% with V.C.
V.C. used are
Levonordephrin
(1:20,000) &
epinephrine
(1:100,000)
4% with or without
V.C.
V.C. used with it is
epinephrine
1:200,000
Maximum dose 300 mg without
V.C and 500 mg
with V.C or 4.4
mg/kg body
weight
400 mg or 4.4
mg/kg body
weight
6 mg/ kg body weight
or 400 mg
68. Lidocaine
(Xylocaine)
Mepivicaine
(carbocaine)
Prilocaine
(Citanest)
NOTES
For hemostasis,
2% lidocaine +
epinephrine
1:50,000 is
recommended.
For duration &
depth of pain
control, 2%
lidocaine with
1:100,000 or
1:50,000
epinephrine is
recommended.
It is the least
vasodilating L.A.
, so best for
short
procedures
It has the least
concentrated epinephrine
dilution 1:200,000.
Therefore cardiac or
hyperthyroid pt. may
receive up to 4 cartridges
in one appointment.
It’s relatively
contraindicated in pt. with
idiopathic or congenital
methmoglobinemia, sickel
cell anemia, cardiac or
respiratory failure because
methmoglobine level is
elevated.
71. Articaine
(Ultrcaine)
Bupivacaine
(Marcaine)
NOTES
It is the only anesthetic
agent of amide type
contain thiophene ring
as its lipophilic portion.
It cause
methmoglobinemia if
given in large doses.
Not recommended for younger
pt….. Why ?
indicated for :
1- lengthy dental procedures
for which deep anesthesia in
excess of 90 mint. is necessary.
2- management of
postoperative pain following
oral surgical procedure giving
pain free period up to 12
hours (long acting L.A.)
73. Procaine Baycaine Tetracaine Metycaine unacaine
Nature ester types L.A.
Metabolism in plasma by pseudocholinestrases enzymes
Excretion by kidneys
Why do we rarely use ester type LA in our practice?
1.Esters are absorbed rapidly into blood, and tend to have a very short
duration of action.
2.PABA (a known allergen) is the main metabolic product of esters.
Therefore they have high incidence of allergic reaction.
75. Action
• Vasoconstrictors are drugs that constrict blood
vessels and control tissue perfusion.
• They are added to local anesthetic solution to
oppose the vasodilatory actions of the local
anesthetics:
1. By constricting blood vessels thus decreasing
bleeding at site of injection.
2. Delayed absorption of L.A. into cardiovascular
system thus minimizing the risk of L.A. toxicity.
3. Decreases amount of local anesthetic solution
needs.
4. Increase potency and duration of anesthesia.
5. Lower rate at which the anesthetic drug is
destroyed in liver and excreted by kidney.
77. 1. Direct-acting drugs on adrenergic receptors
• Vasoconstrictors are act on specific receptors called
adrenergic receptors.
• These receptors are divided into alpha and beta
receptors.
• Alpha receptors are subdivided into alpha1 present
in smooth muscles of the blood vessels →
vasoconstriction and alpha2 (inhibitory) receptors.
• Beta receptors are subdivided into beta1 (as those
present in the heart → increased rate and force of
contraction) and beta2 (as those present in the
bronchi → bronchodilation.
78. • Norepinephrine excites mainly alpha receptors
and to a slight extent beta receptors.
• Epinephrine excites both receptors with slight
predominant effect on beta ones.
2. Indirect acting drugs: which act by releasing
nor-epinephrine from adrenergic nerve terminals.
3. Mixed acting drugs: with both direct and
indirect.
79. Contra-indications to the use of Vasoconstrictors
in local Anesthesia
• Diabetics: because it counteracts the action of
insulin.
• Hypertensive patients: because it raises the
blood pressure by constriction of the blood
vessels + acceleration of the heart rate.
• Extraction of teeth with chronic local sepsis
because it may lead to dry socket.
• Pregnancy: because it may cause uterine
convulsions.
80. • Hyperthyroidism absolute contraindication
of epinephrine.
• Cardiovascular disease (angina, myocardial
infarction and hypertension) decrease
amount of vasoconstrictor 1/5 permissible dose
or give felypressin.
• General anesthesia it sensitizes the
myocardium of the heart to adrenaline raise
in systolic blood pressure and ventricular
fibrillation may take place.
81. Epinephrine Norepinephrin
Nature Most commonly used.
Acts directly on both α and
β adrenergic receptors and
β predominate
It is used for treatment of
acute allergy, acute
asthmatic attack, cardiac
arrest, for homeostasis and
to produce mydriasis
(dilate pupils).
Its effect is of shorter
duration than epinephrine
Systemic effect ↑ Bl. Pressure.
↑ Heart rate.
↑ Myocardial oxygen
consumption.
Branchial smooth muscle
dilation.
Mild effect on CNS.
↑ Bl. Pressure.
↓ Heart rate.
No effect in case of
bronchospasm.
Mild effect on CNS.
It is 1/8 as active as
epinephrine active in
raising the Bl. Sugar
82. Epinephrine Norepinephrin
Conc. & L.A
drugs
Conc used is
• 1:50.000 = 0.02 mg/ml
• 1:100.000 = 0.01 mg/ml
• 1:200.000 = 0.005
mg/ml
• 1:50,000 and 1:100,000
for pain control
• 1:50,000 for hemostasis
Conc. Used is 1:30.000
Maximum dose 0.2 mg in appointment 0.34 mg in appointment
83. Levonordefrin Phenylephrin Felypressin
Nature It is synthetic
V.C & similar in
action to
epinephrine.
Not suitable
with patient
taking tricyclic
drugs as
antidepressant.
It is synthetic
V.C.
It is the most
stable and the
weakest one.
It is synthetic
analogue of the
antidiuretic
hormone
vasopression.
It is non
sympathomimetic
amine so it has no
effect on
adrenergic nerve
transmission →
safe for
hyperthyroid pt.
Systemic
effect
It is 1/10 as active
as epinephrine
active in raising the
Bl. Sugar
• ↑ blood flow by
dilation of
coronary arteries
• ↑ both systolic
and diastolic
blood pressure
• It has minimum
effect on CNS
It has an oxytoxic
action so it is
contraindicated in
pregnant females
86. Type of V.C. Maximum dose in
normal patient
Maximum dose in
cardiac patient
Epinephrine
1:100.000
0.2 mg 0.04 mg
Norepinephrine
1: 30.000
0.34 mg 0.14 mg
Levonordefrine
1:20.000
1 mg 0.2 mg
Phenylephrin
1:2500
4 mg 1.6 mg
Felypressin
0.03 IU
1.35 IU 0.27 IU
89. • Physiologic salt solution (0.9 % Nacl) or ringer's
solution (Nacl 5%, Cacl2 0.04% and Kcl 0.02%)
Are proper vehicle to dissolve anesthetic drug.
• Diffuse of anesthetic solution, its efficiency and
its effect on the nerve fibers depend on physical
state of injected solution.
• If hypotonic:
Water will pass from injected anesthetic
solution to surrounding cell → rupture of cell
→ the diffusion power of the solution is
affected → decreased diffusion to nerve →
decreased effect.
90. • If hypertonic
Water will escape from cell (cell lose fluid)
→ cause dilution of anesthetic solution →
less profoundness of anesthesia → dilution
of L.A. → pain due to cell shrinkage →
decreased effect.
• If isotonic
Prevent escape of water from or to the
injected fluid with its subsequent effect on
the diffusion or concentration of the
anesthetic solution.
91. IV. PRESERVATIVE
Such as:
• Sodium meta bisulfite (0.5mg/ml) and
Methylparaben (1 mg/ml) are
antioxidants, prevent oxidation of
vasoconstrictors which cause
deterioration of solution.
92.
93. Advantages of local anaesthesia
• Non inflammable.
• Excellent muscle relaxant effect.
• During local anesthesia the patient remains
conscious.
• It requires less skilled nursing care as compared
to other anesthesia like general anesthesia.
• Maintains his own airway.
94. • Less pulmonary complications
• Less nausea and vomiting.
• Postoperative analgesia.
• There is reduction surgical stress.
• Earlier discharge for outpatients.
• Suitable for patients who recently ingested
food or fluids.
95. • Ideal for procedures in which it is desirable to
have the patient awake and cooperative.
• Less bleeding.
• Expenses are less.
96. Disadvantages of
local anaesthesia
• There are individual variations in response to
local anesthetic drugs.
• Rapid absorption of the drug into the
bloodstream can cause severe, potentially
fatal reactions.
• Apprehension may be increased by the
patient's ability to see and hear. Some
patients prefer to be unconscious and
unaware.
97. • Direct damage of nerve.
• Hypotension and bradycardia through
blockade of the sympathetic nervous system.
• Not suitable for extremes of ages.
• Multiple needle bricks may be needed.
100. Factors affect onset of action
I. Onset of action of
local anesthesia
1- PH of tissue and Pka of the agent
• The higher the Pka of local anesthesia, the
slower its onset of action due to the fewer
lipophilic particles initially available to cross
the nerve sheath .
• The closer the Pka of anesthesia to
physiologic PH, the more rapid onset of
action.
101. • The low the PH of tissue and /or the local
anesthetic solution, the slower its onset
of action due to the fewer lipophilic
particles initially available to cross nerve
sheath.
102. 2- The site of anesthetic deposition
The away from the nerve the local anesthetic is
deposited, the longer it takes for onset of action.
Thus the onset of infiltration technique is quite
rapid.
103. 3- Nerve type and size
The C fibers are unmylinated and responsible
for carrying sensations of pain and
temperature. They are easily blocked by local
anesthetic.
Type A fibers are the largest and are
responsible for carrying pressure and motor
sensation. Local anesthesia are not as effective
at blocking these fibers.
104. 4- Concentration
The effective concentration of local anesthesia
depend partly on the agent and partly on the
nerve to be blocked.
5- Lipid solubility
The uptake of local anesthesia by nerve is
facilitated with the more lipid soluble agents
(lipophilic) this result in rapid onset of action.
105. II. Potency
Potency of local anesthesia is its ability to
provide complete analgesia under almost all
circumstances.
Factors affecting potency of local anesthesia:
1- Lipid solubility
Low lipid solubility Less potent.
2- Concentration
MLAC: is a term used to determine the relative
potency for local anesthesia
MLAC(minimum local anesthetic concentration),
determine the amount of drug at which 50% of
patients will have the desired effect.
106. 3- Vasodilator activity of anesthesia
Increased vasodilator activity, decrease the
potency.
107. III. Duration of action
Is the length of time the drug is within the nerve.
It depend primarily on the redistribution of the
drug away from the site of action.
This redistribution can be altered by several
factors:
1- Protein binding
The more highly protein bound the drug, the
longer duration of action.
108. 2- Status of tissue in the injection
site(vascularity & PH)
Increased vascularity in the injection site
results in more rapid absorption of local
anesthesia. This most notable in areas of
infection and inflammation.
3- Concentration
Doubling the dose increases duration by about
one half-life.
4- Individual variation in response to the drug
5- Anatomical variation
6- Type of injection technique
109. 7- Presence of vasoconstrictor
The presence of vasoconstrictor prolong
duration of action of L.A. because it decrease
rate of absorption of L.A.
8- Type of local anesthetic drug (short,
medium, or long acting drugs)
9- Accuracy of anesthetic deposition
10- Vasodilator activity of anesthesia
112. What is meaning of 2% xylocaine?
• 2% xylocaine = 20 mg / ml
• Content of 2% xylocaine in one carpule = 20 mg
x 1.8 ml = 36 mg/carpule.
20 mg / ml
1 carpule
1 ml
? 1.8 ml
113. What is meaning of 1:100.000
epinephrine?
• 1: 1000 = 1 mg / ml
• 1: 50.000 = 0.02 mg / ml
• 1: 100.000 = 0.01 mg / ml
• 1: 20.000 = 0.05 mg / ml
• Content of carpule contain 1: 100.000 epinephrine
• 1: 100.000 = 0.01 mg / ml
0.01mg x 1.8 ml
1 ml
= 0.018 mg / carpule.
114. How many carpules can be used
in normal and cardiac patient of
2% xylocaine with 1:100.000
epinephrine?
115. For Xylocaine:
• 2% xylocaine = 20 mg/ml = 36 mg/carpule
• We know that the maximum dose of xylocaine
is 500 mg.
500 mg
36 mg
= 13.8 carpules
• In cardiac pt. 1/5 dose = 2.6 carpule.
116. For Epinephrine
• 1: 100.000 epinephrine = 0.01 mg/ml = 0.018
mg/carpule.
• We know that the maximum dose of
epinephrine in normal pt. is 0.2 mg.
0.2 mg
0.018 mg
=11.1 carpules.
• In cardiac pt. 1/5 dose = 2 carpule.
117. How many carpules can be used in
normal patient of 2% xylocaine?
• 2% xylocaine = 20 mg / ml = 20 mg x 1.8 ml = 36
mg/carpule
• Maximum dose = 300 mg.
300 mg
36 mg
= 8.3carpules
118. How many carpules can be given in
70 kg pt. weight with 2% xylocaine?
• Amount of xylocaine 2% / carpule = 36 mg
• Maximum dose of xylocaine in 70 kg pt = 70 kg
x 4.4 mg = 308 mg
• Number of carpules in this pt:
308 mg
36 mg.
= 8.5 carpules