Local anesthetics work by reversibly blocking sodium channels in nerve cell membranes, preventing the generation and conduction of nerve impulses. Early local anesthetics included cocaine and procaine. Current local anesthetics are classified as esters or amides and differ in their metabolism and duration of action. The potency of local anesthetics depends on their lipid solubility, pKa, and ability to penetrate nerve sheaths. Co-administration with vasoconstrictors or opioids can prolong the duration and intensity of nerve blockade from local anesthetics.

1. Local Anesthesia
PRESENTED BY: DR.MADHANMOHAN

2. Early history of local anesthesia
 Koller and Gartner report local
anesthesia (1884)
Carl Koller
1857 -1944

3. Early history of local anesthesia
 1884 Halsted injects cocaine
directly into mandibular nerve
and brachial plexus
William S. Halsted

4. Early history of local anesthesia
 1904 Einhorn discovers
procaine (Novocaine)
 1943 Lofgren discovers
lidocaine (Xylocaine)

5. Cocaine Niemann 1860 Ester
Benzocaine Salkowski 1895 Ester
Procaine Einhorn 1904 Ester
Tetracaine Eisler 1928 Ester
Lidocaine Lofgren 1943 Amide
Chloroprocaine Marks, Rubin 1949 Ester
Mepivacaine Ekenstam 1956 Amide
Bupivacaine Ekenstam 1957 Amide
Ropivacaine Sandberg 1989 Amide
Levobupivacaine - 1998 Amide
Chronology of local anesthetics

6. Local Anesthetics
DEFINITION
• Drugs which
– produce a REVERSIBLE anesthesia and analgesia…
– in a localized part of the body…..
– when applied directly onto nerve tissues or mucous membranes
– Without causing damage to nerves

7. Local Anesthetics
DESIRABLE CHARACTERISTICS
Rapid onset of action
Brief, reversible block of nerve conduction
Low degree of systemic toxicity***
Soluble in water and stable in solution
Effective on all parts of the nervous system, all types of
nerve fibers
• NONE totally meets these optimally yet!!

8. C
LAs are Weak Bases
C O
O
R N
R
R
NH
O
R N
R
R
Aromatic portion Amine portion
Intermediate chain
ESTER
AMIDE
LIPOPHILIC HYDROPHILIC

9. Two types of linkages
give rise to 2 chemical classes of local anesthetics.
ESTER LINKAGE AMIDE LINKAGE (2 i’s!!)
PROCAINE
procaine (Novocaine)
chloroprocain
tetracaine (Pontocaine)
benzocaine
cocaine
LIDOCAINE
lidocaine (Xylocaine)
mepivacaine (Carbocaine)
bupivacaine (Marcaine)
etidocaine (Duranest)
ropivacaine (Naropin)
Prilocaine

10. Local Anesthetics
Clinical Significance of chemical classification
• Biotransformation
– ESTERS are rapidly metabolized in the plasma by a
cholinesterase
– AMIDES are more slowly destroyed by liver microsomal P450
enzymes.

11. Local Anesthetics
MECHANISM OF ACTION
(specific & non-specific)
• Specific (No effect on RMP)
– bind to specific receptors at the INTRACELLULAR end of
the voltage gated sodium channel
• prevent the transmission of nerve impulses (conduction blockade) by inhibiting the
passage of sodium ions through ion-selective sodium channels in nerve membranes.
• sodium ion channel permeability fails to increase-

12. Mechanism of action of LA
1. Impulse conduction slow
2. The rate of rise and magnitude of the action potential declines, and
3. The threshold for excitation increase
4. The ability to generate an action potential is abolished or cancelled..
• LA bind more readily to open sodium channels while they have greatest
affinity for sodium channel in inactivated state and slows its
reversion to the resting state.

14. + +
- -
+ +
--
- -
+ + + +
- -
Na+
+ ++ +
- - - -
Resting
(Closed**)
Open
(brief)
inactivated
Very slow repolarization
in presence of LA
LA receptor
LA have highest affinity
for the inactivated form
Refractory period
**Closed state may exist in various forms as it moves from resting to open. LA have a high
affinity for the different closed forms and may prevent them from opening.

15. Structural characteristics
of Na+ channels
• 1 larger  subunit (260 kD) (has
ion conducting path)
• 1 or 2 smaller  subunits (30
kD)
• All subunits heavily
glycosylated

16. Structural characteristics
of Na+ channels
• 1 larger  subunit (260 kD) (has
ion conducting path)
• 1 or 2 smaller  subunits (30
kD)
• All subunits heavily
glycosylated

17. Local Anesthetics
MECHANISM OF ACTION
(specific)
• Action is voltage dependent
– This may be due to
• Voltage changes induce changes in form of Na+ channels
• LA have a higher affinity for Na+ channel in
–Some closed forms of the channel preventing them from opening
–higher affinity for channel in inactivated state slowing return to
resting form (prolonged refractory period)
• Increased entry into neuron through opened Na channel

18. Local Anesthetics
MECHANISM OF ACTION
(specific)
• LA are WEAK BASES and access to receptor site is dependent on:
– pKa
– lipid solubility
– molecular size and level of neuronal activity
• LA ACT IN CATIONIC FORM (charged)

19. Local Anesthetics
MECHANISM OF ACTION
(Non-specific)
• LA have some non-specific actions
– Appear to ‘dissolve’ in the membrane
– Distorting the membrane and altering function
• Benzocaine (pKa ~3 almost 100% in nonionized form)

20. Differential sensitivity of neurons to Local anesthetics
Fiber type Function Diameter (μM) Myelination Conduction velocity
(m/s)
Sensitivity to LA
block
Type A
Alpha proprioception, motor
12 – 20 Heavy 70 – 120 +
Beta touch, pressure 5 – 12 Heavy 30 – 70 ++
Gamma muscle tone 3 – 6 Heavy 15 – 30 ++
Delta pain, temperature 2 – 5 Heavy 12 – 30 +++
Type B preganglioniic
autonomic,(e.g. vasomotor)
<3 Light 3 – 15 ++++
Type C
Dorsal root pain, temperature 0.4 – 1.2 None 0.5 – 2.3 ++++
sympathetic postganglionic, (e.g.
vasomotor)
0.3 – 1.3 None 0.7 – 2.3 ++++

21. MINIMUM CONCENTRATION
Cm-The minimum conc. of LA necessary to produce the conduction blockade of
nerve impulses. (analogous to MAC)
 Cm of motor fibers ~twice that of sensory fibers.
 A minimal length of myelinated nerve fiber must be exposed to an adequate conc.
of LA for the conduction blockade.
 Preganglionic B fibers are more readily blocked than any fiber, even though these
fibers are thicker than C fibres.

22. Differential blockade
 The selective blockade of preganglionic sympathetic nervous system B
fibers in response to low conc. of LA.
 Slightly higher concentrations interrupt conduction in small C fibers and
small- and medium-sized A fibers, with loss of sensation for pain and
temperature.
 Touch, proprioception, and motor function are still present, so that the
patient will sense pressure but not pain with surgical stimulation.

23. FACTORS INFLUENCING LA ACTION
~ LIPID SOLUBILITY ~
• Potency and systemic toxicity directly correlate with Lipid Solubility
• Local duration positively correlated with Lipid Solubility and
inversely related to vasodilation

24. FACTORS INFLUENCING LA ACTION
Effect of pH
Charged (cationic) form binds to receptor site,efficacy of drug can be changed by
altering extracellular or intracellular pH

25. FACTORS INFLUENCING LA ACTION
~ Hydrogen ion concentration ~
• At pH 7.4 80 - 90% is ionized and can’t enter cells
– non-ionized (lipid-soluble) form needed for penetration
– cationic form required for binding to receptor
rate of ONSET is related to pKa (because it determines the % of LA in a LS form)
Alkalization hastens the onset of action

26. FACTORS INFLUENCING LA ACTION
~ Hydrogen ion concentration ~
• inflammation tends to produce lower pH in tissues therefore
• LA are more ionized
• don’t penetrate very well
• decreased ability of LA to produce effects
• RATE LIMITING FACTOR for LA onset is the time to penetrate nerve sheath
and permeate cell membrane

27. FACTORS INFLUENCING LA ACTION
• Central neuraxial coadministration of LA and opioids to prolong and
intensify analgesia and anesthesia
– LA act to decrease propagation of pain sensation
– Opioids act to diminish pain by decreasing NT from afferent neurons
• Alpha 2 agonists (e.g. clonidine) enhance intrathecal and epidural nerve
blocks by acting on alpha 2 receptors to decrease NT release

28. Local Anesthetics
~ PHARMACOKINETICS ~
• ABSORPTION
– LA generally have good absorption from mucous membranes and
intradermal injection sites. (into tissues)
Systemic absorption terminates local action (out of tissues). (Not local
metabolism!!!)

29. Local Anesthetics
~ PHARMACOKINETICS ~
• ABSORPTION
– Factors influencing peak PLASMA concentration:
• Site of injection (vascularity)
(IV > tracheal > intrathecal > intercostal > caudal > paracervical > epidural >
brachial plexus > sciatic > s.c.)
• Total dose
• Specific drug characteristics
– tendency to produce vasodilation
• Presence of vasoconstrictor (e.g., epinephrine, phenylephrine)

30. Local Anesthetics
~ PHARMACOKINETICS ~
• ABSORPTION
– Effects of vasoconstrictors
• Decrease rate of systemic absorption and decrease systemic toxicity
• Increase local drug concentration and increase neuronal uptake of LA
• Increase local duration of action (e.g. lidocaine’s duration may increase two fold
with epi)

31. Local Anesthetics
~ PHARMACOKINETICS ~
• ABSORPTION
– Potential adverse effects of vasoconstrictors
• May produce tissue necrosis
• DON’T use in areas of toes, fingers, ear lobes, penis (ischemia)
• May produce systemic toxicity (cardiovascular)

32. Local Anesthetics
~ PHARMACOKINETICS ~
• DISTRIBUTION
– LA can be widely distributed to all parts of the body including CNS
– Distribution is a means of terminating local drug action ........ not
metabolism!!

33. Local Anesthetics
~ PHARMACOKINETICS ~
• METABOLISM
– Ester type LA
• Hydrolysis by cholinesterase in plasma to PABA derivatives
– pseudo cholinesterase or butrylcholinesterase
• Generally, short acting and low systemic toxicity**
• Prolonged effects seen with genetically determined deficiency , altered
esterase, cholinesterase inhibitors

34. Local Anesthetics
~ PHARMACOKINETICS ~
• METABOLISM
– Amide type LA
• Hydrolyzed by liver microsomal enzymes (P450)
• Longer acting & more systemic toxicity than esters
• Caution with severely compromised hepatic function

35. Effects of medical conditions & drugs on LA dosing &
kinetics
 Renal failure: ↑Vd; ↑accumulation of metabolic products
 Hepatic failure: ↑amide Vd, ↓amide clearance
 Cardiac failure; β and H2 blockers: ↓hepatic blood flow and ↓amide clearance
 Cholinesterase deficiency or inhibition: ↓ester clearance
 Pregnancy: ↑hepatic blood flow; ↑amide clearance; ↓protein binding

37. Contd…

38. Local Anesthetics
Systemic Effects (toxicities)
• Extensions of pharmacological action
• Primarily related to blocking sodium channels
• Intensity is dependent on blood levels
• Toxic levels of LA in blood will not occur if absorption (into
systemic blood) is slow or metabolism is rapid

39. Local Anesthetics
Systemic Effects (toxicities)
• CNS (More sensitive than cardio)
– Dose-related spectrum of effects and All effects are due to depression of neurons
Premonitory signs include: ringing in ears, metalic taste, numbness around lips
• First an apparent CNS stimulation (convulsions most serious)
• Followed by CNS depression (death due to respiratory depression)
– Cocaine - euphoria (unique in its ability to stimulate CNS)
– Lidocaine - sedation even at non-toxic doses

40. Local Anesthetics
Systemic Effects (toxicities)
• Cardiovascular System
– HYPOTENSION: Arteriolar dilation is a result of:
• Direct effect (procaine and lidocaine have most effect)
• Block of postganglionic sympathetic fiber function
• CNS depression
• Avoid by adding vasoconstrictor to prep
• Note: cocaine is exception: produces vasoconstriction, blocks NE reuptake

41. Local Anesthetics
Systemic Effects (toxicities)
• Cardiovascular System
– ARRHYTHMIAS: direct effect (More resistant than CNS)
• Decrease cardioexcitability and contractility
• Decreased conduction rate
• Increased refractory rate (bupivacaine)
• Note: cocaine is exception......it stimulates heart
• ALL can cause arrhythmias if conc. is high enough

42. Lipid emulsion counteracts bupivacaine cardiac toxicity
• 20% Intralipid
• 1.5 mg/kg initial bolus
• 0.25 mg/kg/min infusion for 30-60 minutes
• Bolus may be repeated 1-2 times at 5 minutes interval for persistent
asystole
• May increase infusion rate up to 0.5 mg/kg/min if blood pressure
decreases

43. Local Anesthetics
Systemic Effects (toxicities)
• Methemoglobinemia
– Some LA metabolites have significant oxidizing properties
– This may cause a significant conversion of hemoglobin to methemoglobin
and compromise ability to carry oxygen
– May be a problem if cardiopulmonary reserve is limited
– Treat with oxygen and methylene blue (converts methemoglobin to
hemoglobin)
• prilocaine benzocaine have been implicated

44. Local Anesthetics
Systemic Effects (toxicities)
• ALLERGIC REACTIONS ... fairly rare
– Mostly with ester types; rarely amides (procaine)
• esters metabolized to PABA which has allergenic properties
– Cross-sensitivity within same chemical class of LA
– Anaphylactic reactions are rare ..... diphenhydramine can be used to control minor reactions.
– The preservative methyl paraban in multidose vials may be responsible for some allergic
phenomenon

45. Local Anesthetics
Systemic Effects (toxicities)
• NEUROTOXICITY
– LA can cause concentration-dependent nerve damage to central and
peripheral NS
– Mechanism(s) not clear
– Permanent neurological injury is rare
– May account for
• transient neurological symptoms after spinal anesthesia
• Cauda equina syndrome
• Ant.spinal artery syndrome

46. Local anesthetics
The esters

47. SELECTIVE PHARMACOLOGICAL PROPERTIES OF SOME ESTER - type LA
• Cocaine
• Natural alkaloid derived from leaves of erythroxylon coca
• Medical use limited to surface or topical anesthesia (corneal or
nasopharyngeal)
• Should never be injected, protoplasmic poison, can cause tissue necrosis
• Prominent CNS stimulation with marked effect on mood and behaviour
• Strong psychological but little physical dependence
• Stimulates vagal centre bradycardia

48. SELECTIVE PHARMACOLOGICAL PROPERTIES OF SOME ESTER - type LA
Contd..
•Stimulates vasomotor centre rise in BP
•Stimulates temperature regulatory centre pyrexia
•Avoid epinephrine because cocaine already has vasoconstrictor properties.
(EXCEPTION!!!)
•A toxic action on heart may induce rapid and lethal cardiac failure
.
•A marked pyrexia is associated with cocaine overdose

49. COCAINE TOXICITY
• Cocaine blocks the presynaptic uptake of NE and dopamine, thus increasing their
postsynaptic conc.
• Acute cocaine overdose
– Coronary vasospasm
– Myocardial ischemia and infarction
– Ventricular cardiac dysrhythmias (ventricular fibrillation)
– Hypertension and tachycardia (increased myocardial oxygen requirements)
– Dose dependent decreases in uterine blood flow (fetal hypoxemia)

50. Treatment of cocaine toxicity
• Nitroglycerin
• Nitroprusside
• α-Adrenergic blocking drugs
• Benzodiazepine (control seizures)

51. SELECTIVE PHARMACOLOGICAL PROPERTIES OF SOME ESTER - type LA
• Benzocaine (Americaine)
– pKa ~ 3, essentially all non-ionized.... mechanism may be non-specific
– for surface anesthesia (topical) only ... ointments, sprays, etc.
– Used to produce anesthesia of mucous membranes and to suppress gag
reflex during endoscopy
– methemoglobinemia

52. SELECTIVE PHARMACOLOGICAL PROPERTIES OF SOME ESTER - type LA
• Procaine (Novocaine)
– Topically ineffective
– Used for infiltration because of low potency and short duration but most
commonly used for spinal anesthesia
– Short local duration ......produces significant vasodilation. Epinephrine
used to prolong effect
– systemic toxicity negligible because rapidly destroyed in plasma

53. SELECTIVE PHARMACOLOGICAL PROPERTIES OF SOME ESTER - type LA
• Tetracaine (Pentocaine)
– topical, infiltration and spinal anesthesia
– Frequently used for topical ophthalomogical anesthesia
– Also for topical application to nose, throat and tracheobronchial tree
– slow onset and more prolonged effect than procaine d/t slow
metabolism(longest duration of the esters)
– ~10X more toxic and more potent than procaine

54. Local anesthetics
The AMIDES

55. SELECTIVE PHARMACOLOGICAL PROPERTIES OF SOME AMIDE - type LA
• LIDOCAINE (Xylocaine) Most widely used LA
– Effective by all routes.
– Faster onset, more intense, intermediate acting
– Good alternative for those allergic to ester type
– More sedative than others, early central effects are
drowsiness, mental clouding, altered taste and tinnitus

56. • Uses:
• surface application, infiltration, nerve block, epidural, spinal and IVRA
• Also as antiarrhythmic drug
• Produces intense analgesia when injected i.v., (continuous low dose
infusion of lidocaine to maintain plasma conc. Of 1-2 μg/ml decreases
severity of postop pain)
• Also has cough suppressant effect
• When inhaled, it attenuate histamine induced bronchospasm

57. • Mepivicaine (Carbocaine)
– Effective by all routes except topical
– Similar onset and duration as lidocaine
– More toxic to neonates so not used in obstetrical anesthesia

58. • Bupivacaine (Marcaine)
– No topical effect
– Slower onset and one of longer duration agents
– Unique property of sensory and motor dissociation can provide
sensory analgesia with minimal motor block
• has been popular drug for analgesia during labor
– More cardiotoxic than other LA

59. Bupivacaine contd.,
• Uses-infiltration, nerve block, epidural, spinal
• Due to cardiotoxicity , contraindicated for IVRA.

60. Levobupivacaine
• Newer amide LA
• S – enantiomer of bupivacaine.
• Almost similar pharmokinetics of bupivacaine
• Advantages : less cardio and neurotoxic than bupivac
• Disadvantage : less potent than bupivac.

61. • Ropivacaine
– Enantiomer of bupivacaine (S stereoisomer)
– No topical effectiveness
– Clinically ~ equivalent to bupivacaine
– Similar sensory versus motor selectivity as bupivacaine with
significantly less CV toxicity
– Continuous epidural ropivacaine is being used for relief of
postoperative and labour pain

62. • Prilocaine
– Similar clinical profile to that of lidocaine
– Does cause significantly less vasodilation than lidocaine
– Most popular clinical application is for topical anesthesia as in combo with
lidocaine in a eutectic mixture
– Because of rapid systemic metabolism considered least toxic of amide LA

63. Combination product
EMLA
• EMLA = Eutectic (easily melted) Mixture of Local Anesthetics
– Eutectic = two solid substances mixed together in equal quantities by
weight form a eutectic mixture
• EMLA =5% lidocaine and 5%prilocaine in 1:1 proportion becomes
an oily mixture

64. • Lidocaine/prilocaine combination is indicated for dermal anaesthesia
 prevents pain associated with intravenous catheter insertion,
 blood sampling,
 split-thickness skin-graft harvesting
 laser removal of portwine stains,
 lithotripsy
 circumcision
 topical anaesthesia of leg ulcers for cleansing or debridement
– it can also be used to numb the skin before tattooing.

65. EMLA
• Dermal analgesia sufficient for beginning an i.v.line requires a contact time of at least 1 h
under an occlusive dressing. Depth of penetration (usually 3–5 mm), duration of action
(usually 1–2 h), and amount of drug absorbed depend on application time, dermal blood
flow, keratin thickness, and total dose administered.
• Typically, 1–2 g of cream is applied per 10-cm2 area of skin, with a maximum application
area of 2000 cm2 in an adult (100 cm2 in children weighing less than 10 kg.)

66. • Side effects include skin blanching, erythema, and edema.
• EMLA cream should not be used on mucous membranes, broken
skin, patients with a predisposition to methemoglobinemia

67. Other drugs with LA activity
• A few drugs, not generally used for local anesthesia, have LA
effects
• May be substituted if patient is allergic to both esters and amide
types.
– TCA
– diphenhydramine
– chlorpromazine
– corticosteroids

68. Local anesthetics
THINGS TO REMEMBER
• Give smallest volume and dose
• Make injections slowly to avoid inadvertent IV injection
• Have drugs available to manage adverse effects
• Don’t take food or liquids < 60 minutes after oral topical
application .... gag, swallow, cough reflexes may be not working

69. CLINICAL APPLICATIONS
• Regional Anesthesia
– Regional anesthesia is classified according to the following six sites of
placement of the local anesthetic solution:
– topical or surface anesthesia,
– local infiltration,
– peripheral nerve block,
– intravenous regional anesthesia (Bier block),
– epidural anesthesia, and
– intrathecal anesthesia

70. CLINICAL APPLICATIONS
• SURFACE ANESTHESIA (Topical)
– by placement on the mucous membranes of the nose, mouth,
tracheobronchial tree,cornea, esophagus, or genitourinary tract.
– Nebulized lidocaine- used to produce surface anesthesia of the upper
and lower respiratory tract before fiberoptic laryngoscopy and/or
bronchoscopy.
– Lidocaine, tetracaine

71. Topical anesthesia
drug Conc. onset Duration( min) Recomm. max.dose
( mg )
LIGNOCAINE 4%, 10% FAST 30-60 300
TETRACAINE 2% FAST 30-60 20
BENZOCAINE UPTO 20% FAST 30-60 200
COCAINE 4-10% FAST 30-60 150

72. CLINICAL APPLICATIONS
• INFILTRATION ANESTHESIA
– extravascular placement of LA in the area to be anesthetized, to reach
nerve terminals and branches
– Lidocaine- LA most often selected for infiltration anesthesia.
– Epinephrine-containing drugs should not be injected intracutaneously or
into tissues supplied by endarteries.
– Used in minor surgery.
– Immediate onset with variable duration.
• Most LA’s used

73. INFILTRATION ANAESTHESIA
drug Conc. onset Duration
( min )
Recomm. Max.dose
(mg)
LIDOCAINE 0.5-2% FAST 60-240 300 or
500 with adr
MEPIVACAINE 0.5-1% FAST 60-240 400 or
500 with adr
ETIDOCAINE 0.5% FAST 120-480 300 or
400 with adr
PRILOCAINE 0.5-1% FAST 60-120 600
BUPIVACAINE 0.25% FAST 120-480 175 or
225 with adr
LEVOBUPIVACAINE 0.25% FAST 120-480 150
ROPIVACAINE 0.2-0.5% FAST 120-360 200
CHLOROPROCAINE 1% FAST 30-60 800 or
1000 with adr

74. CLINICAL APPLICATIONS
• NERVE BLOCK or FIELD BLOCK
– Interruption of nerve conduction upon injection into the region of nerve plexus or trunk.
– nerve fibers located in the mantle of the mixed nerve are anesthetized first. These mantle
fibers usually are distributed to more proximal anatomical structuresthe initial development
of anesthesia proximally, with subsequent distal spread as LA solution diffuses to reach more
central core nerve fibers.
– Used for surgery, dentistry, analgesia.
• Most LA’s used

75. Nerve block anaesthesia

76. Peripheral Nerve Blocks
Any peripheral nerve can be blocked by injecting LA in their
perivascular sheath or the closed compartment in which it travels
Ex.,
- Cervical, Brachial plexus block
- Transverse abdominis block
- Lumbar block
- Sciatic nerve, Popliteal nerve block
- Ankle block

77. Nerve block anaesthesia
drug Conc. onset Duration
(min)
Recomm. max. dose
(Mg)
LIDOCAINE 1-1.5% fast 60-180 300 or
500 with adr
MEPIVACAINE 1-1.5% fast 120-240 400 or
500 with adr
ETIDOCAINE 0.5-1% fast 180-270 300 or
400 with adr
PRILOCAINE 1.5-2% fast 90-180 600
BUPIVACAINE 0.25-0.5% slow 240-960 175 or
225 with adr
LEVOBUPIVACAINE 0.25-0.5% slow 840-1020 150
ROPIVACAINE 0.5-1% slow 300-480 250
CHLOROPROCAINE 2% fast 30-60 800 or
1000 with adr

78. CLINICAL APPLICATIONS
• INTRAVENOUS REGIONAL ANAESTHESIA (BIER’S BLOCK)
– I.V. injection of a LA solution into an extremity isolated from the rest of the systemic circulation by a
tourniquet
– produces a rapid onset of anesthesia and skeletal muscle relaxation.
– duration of anesthesia- independent of the specific LA and determined by how long the tourniquet is
kept inflated.
– Normal sensation and skeletal muscle tone return promptly on release of the tourniquet, which
allows blood flow to dilute the conc. of LA
– Bupivacaine is contraindicated for IVRA

79. Bier’s block

80. IVRA
drug Conc. onset Duration
(min)
Recomm. max. dose
(Mg)
LIDOCAINE 0.25-2.0% FAST 30-60 300
PRILOCAINE 0.25-0.5% FAST 30-60 600

81. CLINICAL APPLICATIONS
• SPINAL ANESTHESIA
– Injection into subarachnoid space below level of L2 vertebra.
– act on superficial layers of the spinal cord, but the principal site of action is the
preganglionic fibers as they leave the spinal cord in the anterior rami.
– Because preganglionic SNS fibres are blocked by conc. of LA that are insufficient to affect
sensory or motor fibres, the level of SNS denervation during spinal anesthesia extends
approximately two spinal segments cephalad to the level of sensory anesthesia.

82. – For the same reasons, the level of motor anesthesia averages two segments below
sensory anesthesia.
– Use hyperbaric or hypobaric solutions depending on area of blockade.
– Used for surgery to abdomen, pelvis or leg when can’t use general anesthesia.
• Lidocaine, tetracaine

83. Spinal Anesthesia
PROBLEMS
• Spinal headache due to increased leak of CSF
• Hypotension and bradycardia, respiratory depression

84. Spinal anesthesia
ADVANTAGES OVER EPIDURAL
• Easy procedure
• Greater predictability
• Faster onset
• Shorter duration

85. SPINAL ANAESTHESIA
drug Conc. onset Duration
(min)
Recomm. max. dose
(Mg)
LIDOCAINE 1.5-5% FAST 30-60 100
MEPIVACAINE 2-4% FAST 60-120 100
BUPIVACAINE 0.5-0.75% FAST 60-240 20
LEVOBUPIVACAINE 0.5-0.75% FAST 60-360 20
CHLOROPROCAINE 2-3% FAST 30-60 Preservative free
PROCAINE 10% FAST 30-60 1000
TETRACAINE 0.5% FAST 120-360 20

86. Clinical Applications
• EPIDURAL AND CAUDAL ANESTHESIA
– Injection into epidural space usually at lumbar or sacral levels.
– produce anesthesia by diffusion across the dura to act on nerve roots and passage into the
paravertebral area through the intervertebral foramina, thus producing multiple
paravertebral nerve blocks.
– In contrast to SAB, often a zone of differential sympathetic nervous system blockade does
not exist, and the zone of differential motor blockade may average up to four rather than
two segments below the sensory level.

87. Clinical applications
– larger dose required, leading to a substantial systemic absorption of the LA. addition of
1:200,000 epinephrine solution decreases the systemic absorption of LA by
approximately one-third.
– Used like spinal and also painless childbirth.
– Unwanted effects similar to that of spinal less likely because longitudinal spread is
reduced.
– Addition of opioids to local anesthetic solutions placed in the epidural space results in
synergistic analgesia.
• Lidocaine, bupivacaine, ropivacaine

88. Epidural anaesthesia
drug Conc. onset Duration
(min)
Recomm. max. dose
(Mg)
LIDOCAINE 1.5-2% FAST 60-120 300 or
500 with adr
MEPIVACAINE 1.5-2% FAST 60-180 400 or
500 with adr
ETIDOCAINE 1-1.5% FAST 120-480 300 or
400 with adr
PRILOCAINE 2-3% FAST 60-180 600
BUPIVACAINE 0.5-0.75% MODERATE 120-300 175 or
225 with adr
LEVOBUPIVACAINE 0.5-0.75% MODERATE 300-540 150
ROPIVACAINE 0.5-1% MODERATE 120-360 200
CHLOROPROCAINE 2-3% FAST 30-60 800 or
1000 with adr

89. Next class : CVS physiology part – I
To be presented by : Dr. Sneha