Local anaesthesia involves blocking nerve transmission through injection of local anaesthetic drugs near nerve endings or trunks. The document discusses various local anaesthetics including esters like cocaine and procaine, and amides like lidocaine, bupivacaine and prilocaine. It describes how local anaesthetics work by inhibiting sodium channels and preventing nerve impulse conduction. The ideal properties, structures, mechanisms of action, and uses of different local anaesthetics are summarized.

1. LOCAL ANAESTHESIA
BY- DR. AVIRAL VERMA
P.G. 1st year
Department Of Oral And Maxillofacial Surgery

2.  block transmission of impulses along
nerves
 short to medium duration of action (1-6
hrs)
 useful for pain control
 overdoses may cause convulsions

3. 
Applied in the vicinity of peripheral nerve ending or
major nerve trunks

inhibits action potential generation and propagation

Prevent conduction of electrical impulses from the
periphery to the CNS

Produce transient loss of sensory, motor, and autonomic
function in a discrete portion of the body without
producing unconsciousness

4. Structural Classification of local anaesthetics
•Examples of
amides include
lidocaine,
bupivacaine and
prilocaine.
Examples of
esters include
cocaine,
procaine and
amethocaine.

5. The structure of local anesthetics

6. Cocain
Articain
Procain
Bupivacain
Lidocain
Mepivacain

7. Ester
Amides

8. Esters vs Amides




The ester linkage is more easily broken so the ester drugs are
less stable in solution and cannot be stored for as long as
amides.
Amide anaesthetics are also heat-stable.
The metabolism of most esters results in the production of
para-aminobenzoate (PABA) which is associated with allergic
reaction.
Amides, in contrast, very rarely cause allergic phenomena.
For these reasons amides are now more commonly used than
esters.

10. Chemistry

esters vs amides
•

weak bases



of simple benzene derivatives
All carry at least one amine function
Administered as hydrochloride salts
the degree of ionization – pKa vs pH
–

pKa – pH = log proton/unprot
pKa of most local anesthetics is between 8.0 and 9.0

11. Properties of ideal LA











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

12. Fundamentals Of Impulse Generation And
Transmission




Concept behind action of local anaesthesia- prevent
conduction and generation of nerve impulse, set up chemical
roadblock between the source of impulse and the brain.
NEURON is the fundamental unit of nerve cell.
It transmits messages between CNS and all parts of the body.
It is of 2 types:

Sensory (afferent)
Motor (efferent)

13. Sensory Neuron

It transmits pain sensation with 3 major portions:


Peripheral process (dendritic zone) composed of an arborisation
of free nerve endings in the most distal segment of sensory
neuron.
Axon- Thin cable like structure, has free nerve endings that
respond to stimulation produced in the tissues in which they lie
provoking an impulse transmitted via axon.
Cell Body- located at a distance from axon, provide vital
metabolic support for the entire neuron.

14. Motor Neuron




They transmit nerve impulses from the CNS to the
periphery
Their cell body is interposed between axon and dendrites.
Axon branches with each branch ending as a bulbous
axon terminal (or button)
Axon terminals synapse with muscle cells.

16. Physiology Of Peripheral Nerves


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.
Action Potential- transient depolarization of membrane
which leads to brief increase in permeability of membrane
with delayed increase in permeability of potassium.

17. THE ELECTRICAL IMPULSE

18. Nerve impulses are conducted by a wave
of action potentials. When a stimulus is
great enough to reach the threshold
potential of -55mV, sodium ions flow into
the neurone. It does so via sodium gates
to produce depolarisation.
When depolarised, the membrane
potential is reversed to +40 mV.
At the same time, there is passive
outwards diffusion of potassium ions to
bring about repolarisation and the
membrane potential is again reversed to
-70mV

19. Electrophysiology Of Nerve Conduction


Nerve possesses a resting potential which is negative
electrical potential of -70mV because of differing in
concentration of ions on either side of membrane.
Internal to the membrane is negative in respect to the
outer part.

20. STEP 1




Stimulation excites the nerve cells.
Initial phase of slow depolarization, the electrical potential in
the nerve becomes slightly less negative.
Falling electrical potential reaches a critical level. Extremely
rapid phase of depolarisation results reaches to a threshold
potential or firing potential where reversal of electrical
potential across nerve membrane occurs.
Internal to the membrane becomes positive in respect to the
outside (+40mV)

21. STEP 2




This is a phase of Repolarisation.
Electrical potential gradually becomes more negative in
respect to the outside until -70mv is achieved.
Step1- 0.3msec
Step2- 0.7msec

22. Mechanism of action
-
-
Inhibiting excitation of nerve endings or blocking
conduction in peripheral nerves. Binding to and inactivating
sodium channels.
Local Anaesthetics are alkaloid bases that are combined
with acids, usually hydrochloric, to form water soluble salts.
All anaesthetic salts are formed by a combination of weak
base and a strong acid. The salts are used because they
are stable and soluble in water; water solubility isnecessary
for their diffusion through interstitial fluids to the nerve
fibers.

23. Sodium influx through these channels is
necessary for the depolarization of
nerve
cell membranes and subsequent propagation of
impulses along the course of the nerve.
when a nerve loses depolarization and capacity
to propagate an impulse, the individual loses
sensation in the area supplied by the nerve

24. block nerve fiber conduction by acting on nerve
membranes
-
inhibit sodium ion activity
blocks depolarization--> blocks nerve
conduction

25. 
When the influx of sodium is interrupted, an action
potential cannot arise and signal conduction is inhibited.
LA drugs bind more readily to sodium channels in
activated state, thus onset of neuronal blockade is faster
in neurons that are rapidly firing. This is referred to as
state dependent blockade.

26. 
Fig.

27. Effect of PH

Local anesthetics are weak bases and are usually
formulated as the hydrochloride salt to render them
water-soluble. At the chemical's pKa the protonated
(ionized) and unprotonated (unionized) forms of the
molecule exist in an equilibrium but only the
unprotonated molecule diffuses readily across cell
membranes. Once inside the cell the local anesthetic will
be in equilibrium, with the formation of the protonated
(ionized form), which does not readily pass back out of
the cell. This is referred to as "ion-trapping".

28. Effect of PH



LA are weak bases and their activity increases by
increasing PH
This because if large amount of a drug is unpolar, it will
facilitate its penetration through the cell membrane
Once the drug has penetrated the lipid barrier and reach
its site of action it ionized and the ionized form is
responsible for LA activity

29. 
Acidosis such as caused by inflammation at a wound
partly reduces the action of local anesthetics. This is
partly because most of the anesthetic is ionized and
therefore unable to cross the cell membrane to reach its
cytoplasmic-facing site of action on the sodium channel.

30. 
Local anesthetics block conduction in the following order:
small myelinated axons (e.g. those carrying nociceptive
impulses), non-myelinated axons, then large myelinated
axons. Thus, a differential block can be achieved (i.e.
pain sensation is blocked more readily than other sensory
modalities).

31. 

Disruption of ion
channel function via
specific binding to
sodium channels,
holding them in an
inactive state.
Disruption of ion
channel function by
the incorporation of
local anaesthetic
molecules into the
cell membrane .

32. 
Small nerve fibres are more sensitive than large
nerve fibres

Myelinated fibres are blocked before nonmyelinated fibres of the same diameter.

Thus the loss of nerve function proceeds as loss of
pain, temperature, touch, proprioception, and then
skeletal muscle tone. This is why people may still
feel touch but not pain when using local
anaesthesia.

33. LA and pH

All local anaesthetic agents are weak bases, meaning that
they exist in two forms: unionised (B) and ionised (BH+).

The pKa of a weak base defines the pH at which both forms
exist in equal amounts.

As the pH of the tissues differs from the pKa of the specific
drug, more of the drug exists either in its charged or
uncharged form.

35. Physicochemical
characteristics of a local
anaesthetic affect its function


The aromatic ring structure and
hydrocarbon chain length determine the
lipid solubility of the drug.
The more lipid soluble drug penetrates the
cell membrane more easily to exert its
effect.

37. Binding of local anesthetic to
receptor



The affinity of the receptor site within the sodium channel for
the LA is a function of the state of the channel
drugs binds to open and inactivated channels, therefore for
those with higher activity/firing
use dependence - rapidly firing fibers are usually blocked
before slowly firing fibers.

38. There are two theories on the subject of how
sodium channels are blocked:
1. Non-specific membrane expansion theory
2. Specific receptor theory

39. Non-specific membrane expansion
theory:
The lipophilic part of the local
anaesthetic attaches to the cell
membrane to cause swelling. This
then reduces the size of the sodium
channel to obstruct the flow of sodium

40. Specific receptor theory:
The hydrophilic charged amino
terminal binds to specific
receptors of the sodium gates to
block the passage of sodium ions

41. The duration of action


The duration of action of the drug is also related to the
length of the intermediate chain joining the aromatic and
amine groups.
Protein binding , Procaine is only 6% protein bound and
has a very short duration of action, wherease bupivacaine
is 95% protein bound. bupivacaine have a longer
duration of action .

43. Absorption and distribution


Some of the drug will be absorbed into the systemic
circulation: how much will depend on the vascularity of the
area to which the drug has been applied.
The distribution of the drug is influenced by the degree of
tissue and plasma protein binding of the drug. the more
protein bound the agent, the longer the duration of action as
free drug is more slowly made available for metabolism.

44. Metabolism and excretion


Esters (except cocaine) are broken down rapidly by
plasma esterases to inactive compounds and
consequently have a short half life. Cocaine is hydrolysed
in the liver. Ester metabolite excretion is renal.
Amides are metabolised hepatically by amidases. This is a
slower process, hence their half-life is longer and they
can accumulate if given in repeated doses or by infusion.

45. Adverse Effects



CNS: excitation followed by depression
(drowsiness to unconsciousness and
death due to respiratory depression.
Cardiovascular System: bradycardia,
heart block, vasodilation (hypotension)
Allergic reactions: allergic dermatitis to
anaphylaxis (rare, but occur most often
by ester-type drugs).

46. Uses

Local anesthesia.

Ventricular arrhythmia.

Decrease haemodynamic response to
tracheal intubation also decrease cough.

Treatment of epileptic fits.

47. Six Placement Sites
Surface/topica
l anesthesia
Local
infiltration
Peripheral
nerve block
Bier block (IV
regional
anesthesia)
Epidural
anesthesia
Spinal
anesthesia

48. Topical/Surface anesthesia
For Application to mucous
membranes:
Nose- Mouth- EsophagusTracheobronchial treeGenitourinary tract.
Commonly used drugs:

Cocaine (4%-10%).
> 50% of rhinolaryngologic cases
(USA).
 Unique pharmacological property:
produces localized vasoconstriction


49. Cocaine substitution:

lidocaine (Xylocaine) oxymetazoline (Afrin)
combinations.

tetracaine (pontocaine)oxymetazoline (Afrin)
combinations.
 Tetracaine (pontocaine) (1%-2%).
 Lidocaine (Xylocaine) (2%-4%).
Ineffective agents:
 Procaine (Novocain) &
chloroprocaine (Nesacaine): poor
mucous membrane penetration.

50. 
Nebulized lidocaine
(Xylocaine)-- surface
anesthesia
•
•
•
•
Upper & lower respiratory
tract prior to bronchoscopy or
fiber-optic Laryngoscope.
Treatment for intractable
cough.
Normal subjects: No effect on
airflow resistance (they
produce some
bronchodilation).
Patients with asthma:
nebulized lidocaine
(Xylocaine) may increase
airflow resistance

51. 
Systemic concentration following
nebulized lidocaine (Xylocaine)


Following mucosal absorption: systemic.
concentration may be similar to IV injection.
Reasons:


Large surface area.
Significant vascularity of tracheobronchial region.

52. Skin Surface Application
Barrier: keratinized skin layer

Higher local
anesthetic
concentrations
required:
o
5% lidocaine
(Xylocaine)-prilocaine
(Citanest) cream {2.5%
lidocaine (Xylocaine) &
2.5% prilocaine
(Citanest)}
 no local irritation.
 even absorption.
 no systemic toxicity.

53. Combination of local anesthetic:
Definition: eutectic mixture of local anesthetics (EMLA) .
General definition: eutectic--said of a mixture which has the lowest
melting point which it is possible to obtain by the combination of
the given components.
Melting point of combined drug is lower then either lidocaine
(Xylocaine) or prilocaine (Citanest) alone.

54. Clinical uses of EMLA applications-- pain relief for:

Venipuncture

Lumbar puncture

Arterial cannulation

55. Local Infiltration

Definition: Extravascular placement of the local anesthetic in the region to be anesthetized.


Example: subcutaneous local anesthetic injection in support of
intravascular cannula placement.
Preferred local anesthetics for local infiltration:


Most common: lidocaine (Xylocaine).
Other choices: 0.25% Ropivacaine (Naropin) or Bupivacaine
(Marcaine) (effective for pain management at inguinal
operative location),

56. 
Duration of action:


Duration extended by 2x using 1:200,000
epinephrine.
Caution: Epinephrine-containing local
anesthetic solution should not be injected
intracutaneously (intradermal) or into tissues
supplied by "end-arteries" such as ears, nose,
fingers because vasoconstriction may be

57. LOCAL ANAESTHESIA
VASOCONSTRICTORS
REGIONAL ANALGESIA
TOXICITY
DATE:09/12/13
Presented ByDr. Aviral Verma
P.G. 1st Year
Department Of Oral And Maxillofacial Surgery
SLIDES_68

58. DEFINITION
- Local Anaesthesia is defined as a transient reversible loss of sensation in a
circumscribed area of the body caused by a depression of excitation in nerve
endings or an inhibition of the conduction process in peripheral nerves.
- 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 pain sensation) and paralysis (loss of muscle power) can be
achieved.

59. CLASSIFICATION OF LOCAL
ANAESTHESIA
1. Esters (of benzoic acid)
-Butacaine
-Cocaine
-Benzocaine
-Hexylcaine
-Piperocaine
-Tetracaine
2. Esters (of paraaminobenzoic acid)
-Chloroprocaine
-Procaine
-Propoxycaine

60. 3. Amides
-Articaine
-Bupivacaine
-Dibocaine
-Etidocaine
-Lidocaine
-Mepivacaine
-Prilocaine
4. Quinoline
-Centbucridine

61. 3- Combinations
- Lidocaine/Prilocaine(emla)
4- Natural local anesthetics
- Saxitoxin and Tetrodotoxin
-Naturally occurring local anesthetics not derived from cocaine are usually neurotoxins, and have
the suffix -toxin in their names.
-Unlike cocaine produced local anesthetics which are intracellular in effect,
-Saxitoxin & Tetrodotoxin bind to the extracellular side of sodium channels.

62. Indications for local anesthesia
-Most frequent use: regional anesthesia.
- Analgesic espescially post operative pain.
- Lidocaine (xylocaine) also reduces blood pressure response to direct laryngoscopic tracheal
intubation, an effect probably secondary to generalized cardiovascular depression.
- Treatment of intractable cough.

63. Contraindications for local
anaesthesia
- Heart block, second or third degree (without pacemaker)
- Severe sinoatrial block (without pacemaker).
- Serious adverse drug reaction to lidocaine or amide local anaesthetics.
- Concurrent treatment with quinidine, flecainide, disopyramide, procainamide (class 1
antiarrhythmic agents).
- Prior use of amiodarone hydrochloride
- Hypotension not due to arrhythmia.
- Bradycardia.
- Accelerated Idioventricular Rhythm.

64. VASOCONSTRICTORS
- Vasoconstrictors are the drugs that constricts the blood vessels and
thereby control tissue perfusion.
- They are added to local anaesthesia to oppose the vasodilatory action of
local anesthetic agent.

65. What happens if you don’t use a vasoconstrictor?
*Plain local anesthetics are vasodilators by nature
1) Blood vessels in the area dilate
2) Increase absorption of the local anesthetic into the
cardiovascular system (redistribution)
3) Higher plasma levels  increased risk of toxicity
4) Decreased depth and duration of anesthesia  diffusion
from site
5) Increased bleeding due to increased blood perfusion to the
area

66. 1) Patient is not numb as long without
epinephrine
2) Patient is simply not as numb
3) More anesthetic goes into the circulation
4) Increased bleeding; more blood to area

67. Why You Need Vasoconstrictors
Vasoconstrictors resemble adrenergic drugs and are called
sympathomimetic, or adrenergic drugs
1) Constrict blood vessels  decrease blood flow to the surgical site
2) Cardiovascular absorption is slowed  lower anesthetic blood levels
3) Local anesthetic blood levels are lowered  lower risk of toxicity
4) Local anesthetic remains around the nerve for longer periods 
increased duration of anesthesia
5) Decreases bleeding

68. Vasoconstrictors should not be used in the following locations




Fingers
Toes
Nose
Ear lobes

69. CLASSIFICATION
Chemical Structure
Catecholamines
*Epinephrine
*Norepinephrine
*Levonordefrin
Isoproterenol
Dopamine
Noncatecholamines
Amphetamine
Methamphetamine
Ephedrine
Mephentermine
Hydroxyamphetamine
Metaraminol
Methoxamine
Phenylephrine
Felypressin  synthetic analogue of vasopressin (ADH); not in U.S.

70. Modes of Action
3 Classes of Sympathomimetic Amines:
1)*Direct Acting  directly on adrenergic receptors
2) Indirect Acting  use norepinephrine release
3) Mixed Acting  both direct and indirect actions

71. The dilution of vasoconstrictors is commonly referred to as a
ratio i.e., 1:50,000; 1:100,000; 1:200,000 etc,…
A concentration of 1:1,000 means that there is 1 gram
(1000 mg) of solute (drug) contained in 1000 ml (1 L) of
solution, therefore, 1:1,000 dilution contains 1000 mg
in 1000 ml or 1.0 mg/ml of solution (1000 ug/ml)
The concentration of 1:1,000 is very concentrated
(strong); a much more dilute form is used in dentistry
for example, 1:50,000 > 1:100,000 > 1:200,000
(1:100,000 = 0.01 mg/1 ml of solution)

73. 1:50,000 epinephrine is used to stop bleeding in a
surgical area; this amount of epinephrine is not used
for block anesthesia

74. - Resting plasma epinephrine levels are doubled when one cartridge of 2% Lidocaine 1:100,000
epinephrine is injected
- Recent evidence suggests that epinephrine plasma levels equivalent to those achieved during
moderate to heavy exercise occur after intraoral injection
- Moderate increase in cardiac output and stroke volume occurs
- Blood pressure and heart rate are minimally affected
- IV administration of .015 mg of epinephrine with Lidocaine can increase heart rate 25 to 75
beats and increase systolic blood pressure 20 to 70 mmHg
“Epinephrine reaction” causes tachycardia, sweating, apprehension
and pounding in the chest (palpitations)

75. 2 Types of Adrenergic Receptors:
1) Alpha
-contraction of smooth muscle in blood vessels
-vasoconstriction
-Alpha 1  excitatory; post-synaptic
-Alpha 2  inhibitory; post-synaptic
2) Beta
-smooth muscle relaxation
-vasodilation/bronchodilation
-cardiac stimulation, i.e., increased
rate and strength of contraction

76. 2 Types of Beta Receptors:
1) Beta 1
-found in heart and small intestines
-produces cardiac stimulation and lipolysis
2) Beta 2
-found in bronchi of the lung, vascular beds
and uterus
-produces bronchodilation and vasodilation

77. NOREPINEPHRINE

Norepinephrine lacks Beta 2 actions (bronchodilation and
vasodilation) and produces intense peripheral vasoconstriction
with possible dramatic elevations in blood pressure

Norepinephrine’s side effect ratio is 9 times higher than
epinephrine

Norepinephrine’s use in dentistry is not recommended and its
use is diminishing around the world

Epinephrine remains the vasopressor of choice in dentistry
*Norepinephrine is not used because of its many side effects

78. Norepinephrine

79. Epinephrine












Sodium Bisulfite antioxidant added
18 months shelf life
Acts directly on Alpha and Beta receptors
Beta effects predominate
Increases force / rate of contraction
Increases stroke volume
Increases myocardial O2 use
Increases cardiac output / heart rate
Increases dysrhythmias and PVCs
Increases coronary artery perfusion
Increases systolic blood pressure
Decrease in cardiac efficiency

80. 
Alpha receptor stimulation leads to hemostasis initially

Beta 2 actions predominate leading to vasodilation 6 hours after
a surgical procedure

Potent bronchodilator (asthma)

Not a potent CNS stimulant

Increases oxygen consumption in all tissues of the body

Reuptake by adrenergic nerves terminates epinephrine action

Ventricular fibrillation is possible

81. Epinephrine

83. 1.8 ml Cartridge of 2% Lidocaine 1:100,000 epi
Maximum Epinephrine: 11 Cartridges
Maximum Anesthetic: 300 mg
1.8 ml Cartridge of 2% Lidocaine 1:200,000 epi
Maximum Epinephrine: 22 Cartridges
Maximum Anesthetic: 300 mg

84. The maximum amount of 2% Lidocaine 1:100,000 epinephrine that can
be used is 300 mg which is 8.3 cartridges regardless of the patient’s
weight; so the maximum epinephrine will only be achieved after you
have already surpassed the maximum amount of anesthetic allowable
8.3 cartridges

85. American Heart Association says that the
typical concentrations of vasoconstrictors
in local anesthetics are not contraindicated
in patients with cardiovascular disease so
long as aspiration, slow injection and the
smallest effective dose is administered;
ASA III and ASA IV pose the largest risk

86. How much Epinephrine in CV patients?
Maximum Epinephrine
.04 mg
Two cartridges of 1:100,000 epinephrine

87. Clinical Applications of Epinephrine
1)
2)
3)
4)
5)
6)
7)
8)
Management of acute allergic reactions
Management of bronchospasm
Management of cardiac arrest
Vasoconstrictor for hemostasis
Vasoconstrictor to decrease absorption into CVS
Vasoconstrictor to increase depth of anesthesia
Vasoconstrictor to increase duration of anesthesia
To produce mydriasis (excessive pupil dilation)

88. Contraindications to Using
Vasoconstrictors
1) Blood pressure > 200/115 mm Hg
2) Severe cardiovascular disease ASA IV+
3) Acute myocardial infarction in the last 6 months
4) Anginal episodes at rest
5) Cardiac dysrhythmias that are refractory to drug treatment
6) Patient is in a hyperthyroid state of observable distress
7) Levonordefrin and Norepinephrine are absolutely
contraindicated in patients taking tricyclic antidepressants
(Elavil, Sinequan)

89. Epinephrine
Norepinephrine
Receptor activity
Powerful stimulant of α and
β receptors
With higher doses α effects
predominates, whereas
lower doses primarily
produce β receptor activity
Stimulates both α and β
receptors, but α effect
predominates
Blood Pressure (BP)
Lesser effect
Greater increase in BP than
epinephrine
Central Nervous System
Greater effect of stimulation Does not stimulate central
of central nervous system in nervous system in
large doses
therapeutic doses
Cardiovascular system
Greater effect of stimulation
of CVS
Bronchi
Dilatation
Little or no effect
Heart Rate (HR)
Increase in HR is of greater
degree
Increase in HR is of lesser
degree

90. Various dilutions available in India and MRD (in terms of m) for normal
healthy adult individuals and medically compromised individuals
Dilutions
Normal adult healthy
individuals
(0.2 mg/appointment)
(ml)
Medically compromised
individuals
(0.04 mg/appointment)
(ml)
1:80,000
16
3.2
1:1,00,000
20
4
1:2,00,000
40
8

91. REGIONAL
ANAESTHESIA

92. Regional anesthesia - Definition
Rendering a specific area of the body, e.g. foot, arm, lower extremities,
insensate to stimulus of surgery or other instrumentation

93. Regional anesthesia - Uses

Provide anesthesia for a surgical procedure

Provide analgesia post-operatively or during labor and delivery

Diagnosis or therapy for patients with chronic pain syndromes

94. Regional anesthesia - types

Topical

Local/Field

Intravenous block (“Bier” block)

Peripheral (named) nerve, e.g. radial n.

Plexus - brachial, lumbar

Central neuraxial - epidural, spinal

95. Topical Anesthesia


Application of local anesthetic to mucous membrane - cornea, nasal/oral
mucosa
Uses :


Advantages :



awake oral intubation, nasal intubation, superficial surgical procedure
technically easy
minimal equipment
Disadvantages :

potential for large doses leading to toxicity

98. Local/Field Anesthesia


Application of local anesthesia subcutaneously to anesthetize distal nerve
endings
Uses:


Advantages:


Suturing, minor superficial surgery, line placement, more extensive surgery with
sedation
minimal equipment, technically easy, rapid onset
Disadvantages:

potential for toxicity if large field

99. IV Block - “Bier” block

Injection of local anesthetic intravenously for anesthesia of an extremity

Uses
 any surgical procedure on an extremity

Advantages:
 technically simple, minimal equipment, rapid onset

Disadvantages:
 duration limited by tolerance of tourniquet pain and Toxicity.

101. Peripheral nerve block

Injecting local anesthetic near the course of a named nerve

Uses:


Advantages:


Surgical procedures in the distribution of the blocked nerve
relatively small dose of local anesthetic to cover large area; rapid onset
Disadvantages:

technical complexity, neuropathy

104. Plexus Blockade

Injection of local anesthetic adjacent to a plexus, e.g cervical, brachial or lumbar plexus

Uses :
 surgical anesthesia or post-operative analgesia in the distribution of the plexus

Advantages:
 large area of anesthesia with relatively small dose of agent

Disadvantages:
 technically complex, potential for toxicity and neuropathy.

107. Central Neuraxial Blockade - “Spinal”

Injection of local anesthetic into CSF

Uses:


Advantages:


profound anesthesia of lower abdomen and extremities
technically easy (LP technique), high success rate, rapid onset
Disadvantages:

“high spinal”, hypotension due to sympathetic block, post dural puncture headache.

108. Spinal Anesthesia
Definition

Anesthesia following local anesthetic injection into lumbar subarachnoid space
Site of action:


Primary: preganglionic fibers leading the spinal cord in the anterior rami
Secondary: superficial spinal cord layers

109. Spinal anesthesia

110. Central Neuraxial Blockade - “epidural”

Injection of local anesthetic in to the epidural space at any level of the spinal column

Uses:
 Anesthesia/analgesia of the thorax, abdomen, lower extremities

Advantages:
 Controlled onset of blockade, long duration when catheter is placed, post-operative
analgesia.

Disadvantages:
 Technically complex, toxicity, “spinal headache”

111. Epidural Anesthesia
Definition
Anesthesia caused by local anesthetic solutions injected into epidural space.
Mechanism
Direct action on nerve roots and spinal cord following local anesthetic diffusion
across the dura.

112. Epidural anesthesia

113. Toxicity of local anaesthesia
1- Causes
2- Factors reducing toxicity.
3- Signs and symptoms.
4- Treatment of toxicity.

114. CAUSES

Accidental rapid intravenous injection

Rapid absorption, such as from a very vascular site ie mucous membranes.

Overdose .

115. FACTORS REDUCING TOXICITY

Decide on the concentration of the local anaesthetic that is required for the block
to be performed. Calculation of the total volume of drug should be done.

Use the least toxic drug available

Use lower doses in frail patients or at the extremes of ages

Always inject the drug slowly (around 10ml /minute) and aspirate regularly
looking for blood to indicate an accidental intravenous injection

116. 
If Injection of a test dose of 2-3ml of local anaesthetic containing adrenaline is
accidentally given intravenously it will often (but not always) cause significant
tachycardia

Add adrenaline (epinephrine) to reduce the speed of absorption. The addition of
adrenaline will reduce the maximum blood concentration by about 50%. Usually
adrenaline is added in a concentration of 1:200,000, with a maximum dose of 200
micrograms.

Make sure that the patient is monitored closely by the anaesthetist or a trained
nurse during the administration of the local anaesthetic and following the surgery.

117. SIGNS AND SYMPTOMS OF LOCAL ANAESTHETIC
TOXICITY:
1-CNS toxicity :

Early or mild toxicity: light-headedness, dizziness, tinnitus, circumoral
numbness, abnormal taste, confusion and drowsiness.

Severe toxicity: tonic-clonic convulsion leading to progressive loss of
consciousness, coma, respiratory depression, and respiratory arrest.

118. 2-CVS toxicity:

Early or mild toxicity: tachycardia and rise in blood pressure. This will usually
only occur if there is adrenaline in the local anaesthetic. If no adrenaline is added
then bradycardia with hypotension will occur.

Severe toxicity: Usually about 4 - 7 times the convulsant dose needs to be
injected before cardiovascular collapse occurs. Collapse is due to the depressant
effect of the local anaesthetic acting directly on the myocardium.

120. ADVANTAGES OF LOCAL ANAESTHESIA

During local anesthesia the patient remains conscious

Maintains his own airway.

Excellent muscle relaxant effect.

It requires less skilled nursing care as compared to other anesthesia like general
anesthesia.

Non inflammable.

121. 
Less pulmonary complications

Aspiration of gastric contents unlikely.

Less nausea and vomiting.

Contracted bowel so helpful in abdominal and pelvic surgery.

Postoperative analgesia.

There is reduction surgical stress.

Earlier discharge for outpatients.

122. 

Suitable for patients who recently ingested food or fluids.
Local anesthesia is useful for ambulatory patients having minor procedures.

Ideal for procedures in which it is desirable to have the patient awake and
cooperative.

Less bleeding.

Expenses are less.

123. 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.

124. 
Direct damage of nerve.

Post-dural headache from CSF leak.

Hypotension and bradycardia through blockade of the sympathetic nervous
system.

Not suitable for extremes of ages.

Multiple needle pricks may be needed.

125. THANK YOU