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Local Anesthesia for Dental Professionals - Pharmacology
1. Of
Local Anesthetics
Based on Text- Local Anesthesia for Dental Professionals
1st ed. Dr. StanleyMalamed 2nd ed. Bassett, DiMarco, Naughton
Local Anesthesia for Dental Professionals
3. Most injectable medications enter circulatory system
to attain therapeutic levels
LA – when redistributed by circulatory system - their action is terminated
4. All LA possess a degree
of vasoactivity
Most cause vasodilation
Some may produce
vasoconstriction
Drug action and effect is
concentration dependent
5. Potent vasodilation drugs
Procaine is the most potent
Is used to enhance
circulation
with compromised blood
flows
Enhances the
redistribution and limits
effect / duration
9. Cocaine is the only LA that is absorbed well by GI
Most LA (amides) enter the hepatic circulation
72% is biotransformed and inactivated
10. Topical Route
Absorbed from mucous
membranes at differing
rates
Trachea
– almost as rapid as IV
Pharyngeal
– slower
Oral
– slow to moderate
11. Injection
Rate of absorption
following parenteral
injection
Is related to
The Vascularity of area
Vasoactivity of the drug
12. IV administration of LA
provides rapid elevation of
blood levels
Used for ACLS treating
ventricular arrythmias
Rapid administration
Induces high LA blood
levels
Can induce serious toxic
reactions
Absorbed into CNS
13. Lidocaine should be used
with caution due to
negative cardiovascular
effects which include
hypotension,
bradycardia,
arrhythmias, and/or
cardiac arrest. Some of
these side effects may be
due to hypoxemia
secondary to respiratory
depression.
Lidocaine 2% @ 1.8 ml = 36 mg lido.
14. Distribution
CV system distributes
thru body
Highly perfused organs
Brain
Liver
Kidneys
Lungs
Spleen
Skeletal muscle
Largest mass of tissue in
body
Will contain the
greatest % of LA due to
mass
15. Plasma concentration of LA in each organ
bears significantly on toxicity of drug
Affected by
Rate of absorption
into CV system
Rate of distribution
from the vascular compartment to tissues
Rate of elimination of drug
thru metabolic or excretory pathways
16.
17. Elimination half – life
Rate at which a LA is removed from blood
Time necessary for 50% reduction in plasma
concentration
One half life 50%
Two half lives 75%
Three half-lives 87%
18.
19. ALL local anesthetics
Cross the blood brain
barrier
Readily cross the
placenta
Enter the circulation of
the developing fetus
21. Toxicity of drug
proportional to
Rate of absorption –
into CV
Rate of removal – from
CV
with tissue uptake and
metabolism
22. Metabolism
Esthers
Esther
are hydrolyzed in blood
plasma by enzyme
Pseudocholinesterase
Rate of hydrolysis
impacts toxicity
Some esters converted to
PABA
Some people have
Atypical form of
Pseudocholinesterase
Unable to hydrolyze
esthers
Increased toxicity
Hereditary trait
Influences GA
Succinylcholine isn’t
metabolized
23. Absolute contraindication
Under no circumstance
should the drug be
administered
Possibly toxic or lethal
reaction
Relative Contraindication
May be administered to
patient after careful
consideration of the risks and
benefits
The smallest clinically
effective dose should be
given
Due to potential for adverse
reaction
24.
25. Amide anesthetics
Primary site of
biotransformation is the
liver
Liver function and
perfusion influences rate
of metabolism
Both amide and esther
Metabolized in blood
and liver
Shorter half life due to
plasma cholinesterase
metabolizes it quickly
Articane - Hybrid LA
26.
27. Metabolic byproducts of LA can cause clinical activity
Lidocaine – metabolic byproduct
monoethylglycinexylidide
and glycine xylidide
Causes sedation effect
Prilocaine can cause methemoglobinemia when
administered in large doses
Orthotoluidine
primary metabolite that causes the condition
28. Kidneys are the primary route of excretion
For both the LA and its metabolites
Patients with significant renal disease may be unable
to eliminate the LA or metabolites
Results in high blood levels
Possible toxicity
Patient with dialysis and renal impairment
need a medical consult
29. LA reversibly block action potentials in
ALL excitable neural membranes
Central nervous system
Cardiovascular system
30.
31. LA readily cross the blood brain barrier and placenta
Action is to depress neural transmission
By suppressing the sodium pump
At low levels – no CNS effect
At high levels – generalized tonic-clonic convulsions
LA have been used as anticonvulsant at blood levels
below seizure thresholds
Used for tx of epilepsy
By raising the firing threshold (action potential)
Diminishing the excitability of neuronal activity
32. CNS is more susceptible to LA
Is the initial clinical indication of LA toxicity
Initially a mild sedation or drowsiness
Toxic levels increase and CO2 increases
As CO2 increases
the level of LA needed for seizures decreases
Seizures will occur and increase
Duration of seizures is proportional to blood level of
LA
33. Seizures cause increase in blood flow to CNS
This increases the concentration of LA in CNS
Cerebral metabolism increases with seizures
Acidosis increases (hypercarbia)
This lowers the threshold for seizures and level of LA
needed to cause seizures
Further increases in LA concentration causes
Cessation of seizures
Due to generalized CNS depression
Flat EEG
34. LA are thought to inhibit the “inhibitory pathways” of
the cerebral cortex
This allows the facilitory (excitatory) pathways to
dominate
The balance between inhibition and facilitation is lost
and seizures occur
35. LA cause generalized
analgesia
Decrease the pain
threshold
Suppressing the afferent
registration of pain
Relatively low safety
margin
between analgesia and
overdose
38. Direct action on myocardium – depression
Decrease in excitability of myocardium
Decrease in conduction rate and force of contraction
Diminished cardiac output
Conduction & rhythm may be modified
Antidysrythmic – used in ACLS
Related to blood level of LA
39. Peripheral vasculature
Cocaine – vasoconstriction
All other LA produce vasodilation
Relaxation of smooth muscle in BV walls
Increased blood flow
Increased drug absorption and distribution
Decreased depth & duration of LA
Increased bleeding
Increased LA blood levels
40. Primary effect on Blood Pressure
Hypotension
Procaine
may cause 50% of patients to be hypotensive
other LA 6%
At non-overdose levels no change in BP
Near overdose slight drop in BP due to dilation of BV
At overdose – profound hypotension
Caused by decreased
myocardial contractility & cardiac output
vasodilation with peripheral resistance
Lethal levels – CV collapse
41. Direct relaxation
on bronchial smooth muscle
OD levels – respiratory arrest
Due to CNS depression
At therapeutic (normal) levels
No effect on respiration
42. Due to block of transmission of impulse
Sodium pump
diffusion is blocked in the sodium channels
Can be additive to
succinylcholine and
muscle relaxants
OTHER PRESCRIPTIONS – DEPRESSANTS
Abnormal period of muscle inactivity or paralysis
43. LA potentiate
all CNS depressants and their actions
Common metabolic pathways
Drug concentrations are elevated due to prolonged
metabolism
Toxic levels can be reached with lower doses
Hepatic microsomal enzymes
May be induced by drugs and enhance the metabolism of LA
Shorten the half life and effectiveness - duration