1. SOURCES
Contemporary_Oral_and_Maxillofacial _ Surgery_4th_Ed_By_Peterson.
Peterson's Principles of Oral and Maxillofacial Surgery 2nd Ed 2004.
Oral Surgery.
Hand Book Local Anasthesia.

2. LOCAL ANEASTHESIA

3. Definition of local anesthesia
L.A. defined as a loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve ending or an inhibition of the conduction process in peripheral nerves.

4. Methods of inducing L.A.
In the “old days” the following were used for anesthesia.
Alcohol
Drugs
Ice for numbing
Blow to the head
Strangulation

5. Methods of inducing L.A. Mechanical trauma Low temperature Anoxia
Chemical irritation
Neurolytic agents like alcohol
Chemical agents such as L.A.

6. Properties of ideal L.A.
Onset of anesthesia should be short while duration and effect of anesthesia should be long and powerful
L.A should not irritate tissues
L.A should not cause permanent damage to nerves
L.A should be effective even with lower doses
L.A should has lower systemic adverse effects
L.A should not be allergic

7. Properties of ideal L.A L.A can be sterilized easily
L.A should be soluable within water
L.A should be cheap
L.A should be stabile
L.A should not get interaction with vasoconstrictors

8. Neurophysiology

9. Electrochemistry of nerve conduction
Resting state
Depolarization
Re polarization

11. Mode of action of L.A. Altering the basic resting potential
Altering the threshold potential(firing level)
Decreasing the rate of depolarization
Prolonging the rate of repolarization

12. What functions are lost with local anesthetics? Answer
Pain perception
Temperature
Touch sensation
Proprioception (reception of information about body position movements by the sensory systems )
Skeletal muscle tone

13. Factor affecting the local anesthetic action
1- PH value. Acidification of tissue decrease LA effectiveness Inadequate anesthesia result when local anesthetics are injected in to inflamed or infected areas since the inflammatory process produce acidic products.
2- Lipid solubility .↑ lipid solubility ↑ local anesthetic effect.
3- Protein binding . ↑ protein binding ↑LA duration .
4- Non nervous tissue diffusibility .
5-↑ Vasodilator activity ↓ LA solution activity.

14. Pharmacokinetic of local anesthetics
Administration.
Distribution.
Metabolism.
Excretion.

15. Induction of L.A. Recovery of L.A.
1-Diffusion
2-Blocking process
Recovery of L.A.
note all LA readily cross the blood brain barrier & also readily cross the placenta & enter the circulatory system of developing fetus.

16. Administration
Oral rout
Topical rout
Injection

17. Distribution The blood level of L.A. influenced by
Rate at which the drug is absorbed into CVS
Rate of distribution from vascular component into the tissue
Elimination by excretion

18. One half life =50% reduction Two half life=75% reduction
Continue
The rate at which the drug is removed from the blood mentioned as half life
One half life =50% reduction
Two half life=75% reduction
Three half life=87.5 reduction
Four half life=94% reduction
Five half life=97% reduction
Six half life= 98% reduction

19. Metabolism
Metabolism of L.A is important because the overall toxicity of the drug depend on the rate of absorption of the drug into the blood stream and its rate of metabolism and excretion.
Esters→ Hydrolysis in Plasma
Amides→ Liver

20. Excretion
Kidneys are the primary excretory organ for both local anesthetic drug and its metabolite.

21. Summary Clinical Pharmacology
The potency of Local Anesthetics, their onset and duration of action are primary determined by physicochemical properties of various agents and their inherent vasodilator activity of same local anesthetics.
Lipid solubility is the primary determinant of anaesthetic potency.
Protein binding influences the duration of action.
(acidity constant) of Local anaesthetics determines the onset of action.
The addition of vasoconstrictors, such as epinephrine or phenylephrine can prolong duration of action of local anaesthetics, decrease their absorption (and the peak plasma level) and enhance the blockade.

22. Chemistry Three structural domains 1) Aromatic or Lipophilic portion
-necessary for penetration lipid rich
nerve membranes
2) Amino end (hydrophilic end)
-confers water solubility
-ensures solubility of local in cartridge and prevent precipitation
3) Intermediate chain (-COO-) or (-NHCO-)
-provides spatial separation and divides local into esters or amides

23. Local Anesthesia Esters Short acting
Metabolized in the plasma and tissue fluids
Excreted in urine

24. Ester L.As are more allergic than amide L.As
Local Anesthesia
Amides
Longer acting
Metabolized by liver enzymes
Excreted in urine
Ester L.As are more allergic than amide L.As

25. Drug List Local Anesthesia Esters Cocaine. Benzocaine. Procaine.
Tetracaine.

26. Drug List Local Anesthesia Amides Bupivacaine. Articain.
Lidocaine (Xylocaine).
Mepivacaine.

27. Properties of Local Anaesthetic Agents
AMINOESTERS
AMINOAMIDES
Metabolism
rapid by plasma cholinesterase
slow, hepatic
Systemic toxicity
less likely
more likely
Allergic reaction
possible - PABA derivatives form
very rare
Stability in solution
breaks down in ampules (heat,sun)
very stable chemically
Onset of action
slow as a general rule
moderate to fast
pKa's
higher than PH = 7.4 ( )
close to PH = 7.4 ( )
Benzocaine
Chloroprocaine
Dyclonine
Procaine
tetracaine
bupivacaine (Marcaine)
levobupivacaine
Lidocaine (Xylocaine)
lidocaine-prilocaine (EMLA)
mepivacaine (Carbocaine

28. CNS→The primary action is depression
Systemic action of L.A.
CNS→The primary action is depression
Anticonvulsant properties
Analgesia
Mood elevation

29. Preconvulsive signs and symptoms of CNS toxicity
Signs Symptoms
Slurred speech Numbness of Tongue
and circumoral region
Shivering Warm flushed feeling of
skin
Tremor of muscle of face Pleasant dream like
and extremities state
Dizziness
Visual disturbance
Tinnitus
Drowsiness
Disorientation
Signs Symptoms
Slurred speech Numbness of Tongue
and circumoral region
Shivering Warm flushed feeling of
skin
Tremor of muscle of face Pleasant dream like
and extremities state
Dizziness
Visual disturbance
Tinnitus
Drowsiness
Disorientation

30. CVS Direct action of L.A. on myocardium:
It will cause myocardial depression
↓ electrical excitability
↓ Conduction rate
↓ force of contraction

31. Direct action on peripheral vasculature
Continue
Direct action on peripheral vasculature
Cocaine is the only local anesthetic drug that cause vasoconstriction all others produce vasodilatation.

32. Local tissue toxicity
Skeletal muscles are subjected to the action of local anesthetic drugs more than other tissues intraoral and intramuscular injection of lidocaine,atricaine, mepivicaine, prilocaine, bupivacaine and etidocaine will produce skeletal muscle alteration.

33. Respiratory system
At a non overdose Local anesthetic drugs have a direct relaxant action on bronchial smooth muscle
At overdose level they may produce respiratory arrest as a result of generalized CNS depression

34. for local anesthetic agents
Vasoconstrictors
for local anesthetic agents

35. Vasodilatation Local Anesthetics
Procain (highest vasodilatation effect)
Vasodilatation
Prilocain, mepivacain

36. Vasodilatator effect of local anesthetics…
Increases absorbtion of anesthetic solution leading rapid move away of solution from injection area
Decreases depth and duration of anesthesia
Increases the plasma level of L.A that may cause possible TOXICITY
Causes increased bleeding due to increased vasodilatation

37. Vasoconstrictor (vasopressor)
agents acts opposite
to local anesthetics
by constricting vessels

38. Why adding vasoconstrictors to L.A. (Advantages of vasoconstrictors)
↓ blood flow to the site of administration
Absorption of L.A. to the CVS is slowed resulting in lower level of anesthetic drug in the blood
Minimize the risk of toxicity by lowering the blood level of L.A. drug
↑ duration of action
↓bleeding at side of administration

39. Classification of vasoconstrictors according to chemical structure
Catecholamine's Noncatecholamines Epinephrine Amphetamine Nor epinephrine Methamphetamine Levonordefrin Ephedrine Isoproterenol Mephentermine Dopamine Hydroxyamphetamine Metaraminol Methoxamine phenylephrine

40. Classification of vasoconstrictors according to mode of action
Direct acting Indirect acting Mixed acting Epinephrine Tyramine Metaraminol Norepinephrine Amphetamine Ephedrine Levonordefrin Methamphetamine Isoproterenol Hydroxyamphytamine Dopamine Methoxamine Phenylephrine

41. Dilutions of vasoconstrictors
The most common dilutions of vasoconstrictors used in dentistry are:
1:50000
1:80000
1:10000
1:100000
1:200000
1:300000
1:400000

42. Epinephrine
Norepinephrine

43. Pharmacology of vasoconstrictors
EPINEPHRINE:
Mode of action:
Act directly on α and β receptors but more predominate on β receptor
Systemic action:
1-Myocardium:
Adrenaline stimulate β1 receptors of the myocardium
↑ cardiac output and heart rate

44. ↑ incidence of dysarthmias 3-coronory arteries:
Continue
2-Pacemaker cells:
↑ incidence of dysarthmias
3-coronory arteries:
↑ coronary arteries blood flow
4- BP:
In small doses ↑ systolic BP, ↓ Diastolic BP
In larger doses ↑ diastolic BP

45. Continue
Cardiovascular dynamic: ↑ Systolic and diastolic pressure ↑ Cardiac output ↑ Heart rate ↑ strength of contraction

46. Continue
5- Vasculature: Adrenaline produce constriction of vasculatures which supplying skin, mucous membrane and kidneys While its effect on vessels supplying skeletal muscle in small doses it produce dilatation while in larger doses produce vasoconstriction 6-Hemostasis: Adrenaline is used frequently as vasoconstrictor during surgical procedures 7- Respiratory system: It’s a potent dilator of bronchiole smooth muscle

47. Continue 8- CNS: Side effects of overdose:
In normal therapeutic doses it have no effect on CNS while in an excessive dose it stimulate CNS
↑ fear, anxiety, restlessness, headache, tremor, weakness and dizziness.
Side effects of overdose:
Cardiac dysarthmia
Ventricular fibrillation
Dramatic increase in both systolic and diastolic BP
Angina episode

48. Clinical applications
Management of acute allergic reaction
Management of bronchospasm
Management of cardiac arrest
For haemostatic
Increase depth of anesthesia
Increase duration of anesthesia
To produce mydriasis

49. Availability in dentistry
Epinephrine dilution LA 1:50,000 Lidocaine 1:80,000 Lidocaine 1:100,000 Lidocaine Atricaine 1:200,000 Atricaine Bupivacaine Etidocaine Lidocaine Mepivacaine Prilocaine 1:300,000 Lidocaine

50. NOREPINEPHRINE (NORADRENALINE, LEVARTERENOL)
Released from similar source like epinephrine
Effectiveness is one fourth of epinephrine
It has intensive adrenargic stimulative effect which may cause possible tissue necrosis. (especially within palatinal region in the mouth)
Its use with L.A is controversial.

51. SYSTEMIC EFFECTS OF NOREPINEPHRINE
Cardiovascular system
Increases systolic and diastolic blood pressure
Decreases heart rate
Increases volume of heart
It has no bronchodilatator effect
Increases metabolism but less effective than epinephrine
It causes vasoconstriction

52. Selection of vasoconstrictors
1-length of dental procedure.
2-Requirement of haemostatic.
3-Medical status of patient.