DENTALELLE TUTORING
Pharmacology -
Chapter 9
WHY IS EPI USED IN LOCAL ANESTHETICS?
MEANING. .THE LOCAL ANESTHETIC LASTS LONGER TO ENSURE PROPER FREEZING OF THE TOOTH AND TISSUES
PROLONG DURATION
WAS COCAINE USED AS AN ANESTHETIC?
. .BUT NOT ANYMORE! IT WAS QUICKLY RECOGNIZED FOR ITS ADDICTING PROPERTIES.
YES..
WHAT ARE SOME EXAMPLES OF LOCAL ANESTHETICS USED
TODAY?
• The amide lidocaine (Xylocaine) was released in 1952
• mepivacaine (Carbocaine) was released in 1960
• More recently, bupivacaine (Marcaine) has been made available for dental use
HISTORY
NO LOCAL ANESTHETIC IN USE TODAY MEETS ALL THE NECESSARY REQUIREMENTS
TRUE OR FALSE…
BUT…MANY ACCEPTABLE AGENTS ARE AVAILABLE
TRUE
potent local anaesthesia reversible local anaesthesia
should be followed by complete recovery without evidence of structural or functional nerve damage
absence of adverse systemic effects & allergic reactions
rapid onset & good duration should have moderate lipid solubility which
allows an anesthetic agent to diffuse across lipid membranes of all peripheral nerves (motor, sensory, autonomic)
adequate tissue penetration low cost long shelf life (stability in solution)ease of metabolism & excretion
IDEAL LOCAL ANESTHETIC PROPERTIES OF THE IDEAL
LOCAL ANESTHETIC
WHAT ARE THE TWO GROUPS OF LOCAL ANESTHETICS?
CROSS -HYPERSENSITIVITY BETWEEN AMIDES AND ESTERS IS UNLIKELY
AMIDES AND ESTERS
ACTION OF NERVE FIBERS• A resting nerve fiber has a large number
of positive ions on the outside and a large number of negative ions on the inside
• The nerve action potential results in the opening of sodium channels and an inward flux of sodium (Na+)
• This results in a change in potential• The outward flow of potassium (K+) ions
repolarizes the membrane and closes the sodium channels
MECHANISM OF ACTION
IN RELATION TO NERVE IMPULSES?
HOW DO LOCAL ANESTHETICS WORK?
AFTER COMBINING WITH THE RECEPTOR, LOCAL ANESTHETICS BLOCK CONDUCTION OF NERVE IMPULSES BY DECREASING THE PERMEABILITY OF THE NERVE CELL
MEMBRANE TO SODIUM IONS
DECREASING PERMEABILITY TO SODIUM IONS…
Local anesthetics slows or blocks depolarization by reducing Na+ permeability into the nerve cytoplasm, thus inhibiting the flow of K+ out of the cell.
↓interferes with the function of
the neurons↓
prevents the propagation of action potential (the reproduction of nerve transmission)
↓prevents the onset of nerve
conduction & blocks nerve impulse formation
MECHANISM OF ACTION
ACTION OF NERVE
FIBERS
SUMMARIZED
The mechanism of local anesthetics involves action
on Axons and Sodium channels
MECHANISM OF ACTION
ACTION OF NERVE
FIBERS
Local anesthetics bind to sodium channels found in the axons of nerves. They stop the propagation
of the electrical impulse along the axon.
ARE LOCAL ANESTHETIC AGENTS WEAK OR STRONG BASES?
WHEN THE ACIDITY OF THE TISSUE ↑, (AS IN INSTANCES OF INFECTION) , THE EFFECT OF A LOCAL ANESTHETIC ↓ THEREFORE, THE LOCAL ANESTHETIC IS A WEAK BASES.
WEAK BASES
Absorption & L.A.
infection
tooth • ↓ pH• ↑ ionization
• ↑ [H+]
localanaesthetic
(L.A.)L.A.
L.A.
L.A.
In the presence of infection, there may be a reduced clinical effect of L.A. due to the ↓’d pH level. The infection site is
more acidic and more ionized and less likely to absorb the L.A drug (weak base).
*Weak bases are better absorbed when the pH is greater than
the pKa
EG: Lidocaine’s pKa =7.9(Weak
base drug)
IF INFECTION IS PRESENT, HOW DOES THE LOCAL ANESTHETIC
REACT?
IN THE PRESENCE OF AN ACIDIC ENVIRONMENT, SUCH AS INFECTION OR INFLAMMATION, THE AMOUNT OF
FREE BASE IS REDUCED
IT IS HARDER TO FREEZE –LIKELY INFECTION MUST BE CLEARED BEFORE
FREEZING IS DONE.
WHAT DOES ADME STAND FOR?
ABSORPTIONDISTRIBUTIONMETABOLISMEXCRETION
VERY IMPORTANT!
WHAT IS ABORPTION?
ABSORPTION DEPENDS ON ITS ROUTEWHEN INJECTED INTO TISSUES THE RATE DEPENDS ON
THE VASCULARITY OF THE TISSUES
ROUTE
ABSORPTION
Reducing the rate of systemic absorption of a local anesthetic is
important when it is used in dentistry because the chance of
systemic toxicity is reduced.
–A vasoconstrictor is often added to the local anesthetic to reduce the rate of absorption.
PHARMACOKINETICS
WHAT CAN BE ADDED TO REDUCE THE RATE OF ABSORPTION?
A VASOCONSTRICTOR
ABSORPTION
• Addition of vasoconstrictor to local anesthetic: Reduces the blood supply to the
areaso as to ↓ rate of diffusion of anaesthetic into the blood vessels
this also prolongs the duration & effectiveness of the desired action
decreases bleeding in the areaLimits systemic absorptionReduces systemic toxicity
PHARMACOKINETICS
WHY IS REDUCING THE RATE OF ABSORPTION SO IMPORTANT?
REDUCES SYSTEMIC TOXICITY
WHAT IS DISTRUBUTION?
LOCAL ANESTHETICS CROSS THE PLACENTA AND BLOOD-BRAIN BARRIER
LOCAL ANESTHETIC DISTRUBUTED THROUGHOUT
METABOLISMLA agents are metabolized differently,
depending on whether they are amides or esters.
• AMIDES: are metabolized primarily by the liver
• In severe liver disease or with alcoholism, amides may accumulate and produce systemic toxicity
• ESTERS: are hydrolyzed by plasma pseudocholinesterases and liver esterases
PHARMACOKINETICS
WHAT IS EXCRETION?
METABOLITES AND SOME UNCHANGED DRUG OF BOTH ESTERS AND AMIDES ARE EXCRETED BY THE KIDNEYS
EXCRETED BY KIDNEYS
WHAT NERVE DOES LOCAL ANESTHETIC BLOCK?
THE MAIN CLINICAL EFFECT OF LOCAL ANESTHETIC IS REVERSIBLE BLOCKAGE OF PERIPHERAL NERVE
CONDUCTION
PERIPHERAL NERVE CONDUCTION
COMMON ORDER OF NERVE FUNCTION LOSS
1. Autonomic *is the most sensitive to inhibition by local anesthetic agents
2. Cold3. Warmth4. Pain5. Touch6. Pressure7. Vibration8. Proprioception9. Motor
PHARMACOLOGIC EFFECTS
PERIPHERAL NERVE
CONDUCTION (BLOCKER)
The order of nerve impulse return:
opposite (reverse)
The order of loss of nerve function
WHY ARE LOCAL ANESTHETICS SUCCESSFUL IN TREATING ARRHYTMIAS?
WHAT DO PLASMA LEVELS HAVE TO DO WITH LOCAL ANESTHETIC?
ADVERSE REACTIONS AND TOXICITY
ADVERSE REACTIONS
• Although toxicity to local anesthetics is rare in the doses normally used in dentistry, patients can still suffer from a classic toxic reaction.
ADVERSE REACTIONS
LOCAL ANESTHETIC TOXICITY causes stimulation of the CNS
including:restlessness, tremorsseizures followed by CNS depression and coma.
HOW MANY CARPS ARE MAX FOR LIDOCAINE?
8.5 CARPS
WHY WOULD A HEMATOMA BE PRODUCED?
POOR INJECTION TECHNIQUE OR EXCESSIVE VOLUME
WOULD COULD RESULT IN RIDIGITY OF MUSCLES?
MALIGNANT HYPOTHERMIA
MALIGNANT HYPERTHERMIA
• An autosomal dominant trait characterized by often fatal hyperthermia with rigidity of muscles occurring in affected people exposed to certain anaesthetic agents– particularly halothane & succinylcholine (G.A.’s)
• NOT related to amides!– In the past, the belief was that the amide local
anesthetics might precipitate malignant hyperthermia, but they are currently no longer implicated. Patients with a family history of malignant hyperthermia can be given amide local anesthetic agents.
ADVERSE REACTIONS
. .WHAT IS BEST?
IF A WOMAN IS PREGNANT AND ANESTHETIC MUST BE GIVEN…
LIDOCAINE
AMIDES OR ESTERS?
WHAT TYPE HAS A GREAT POTENTIAL FOR ALLERGY?
ESTERS
ALLERGYIF A PATIENT REPORTS A
HISTORY OF ALLERGIES TO ALL LOCAL ANESTHETIC
AGENTS
Can use antihistamine
diphenhydramine (Benadryl)
as a local anesthetic
• Antihistamines, because of their similarity in structure to local anesthetics, have some local anesthetic action– diphenhydramine (Benadryl) in a concentration
of 1% plus 1:100,000 epinephrine is recommended to be given by injection to produce a block
– No prepared product is available; this combination must be prepared from its constituents
ADVERSE REACTIONS
WHICH INGREDIANT REDUCES BLEEDING?
VASOCONSTRICTORS
IF A PATIENT HAS ASTHMA, HOW MUST YOU BE CAREFUL?
THE ANTIOXIDANT FOR THE VASOCONSTRICTOR MAY PRODUCE A HYPERSENSITIVITY REACTION THAT
EXHIBITS ITSELF AS AN ACUTE ASTHMATIC ATTACK
ANTIOXIDANT IN LOCAL
WHERE IS TOPICAL PLACED?
THE MUCOUS MEMBRANE OF THE SKIN
I. Amides (Only class of anaesthetics used parenterally)
i. Lidocaine (Xylocaine)ii. Mepivacaine (Carbocaine)iii. prilocaine (Citanest; Citanest Forte)iv. bupivacaine (bu·piv·a·caine)
I. Esters (No esters are currently available in a dental cartridge)
i. procaineii. propoxycaineiii. Tetracaine
LOCAL ANESTHETIC AGENTS
**Esters are not used in dentistry as local
anesthetics, but used topically.
eg. Benzocaine.
SOME COMMONLOCAL ANESTHETIC AGENTS
LA AGENT NOTES
• procaine • no longer used
• lidocaine (Xylocaine) • most common used• least painful• can only use 100,000epi
• mepivacaine (Carbocaine; Isocaine)
• shortest duration • when no epi is needed.
• bupivicaine (Marcaine) • Painful• longest duration 6-8
hours
• articaine (Septocaine) • the most potent
• prilocaine plain (Citanest)• Prilocaine epi (Citanest
Forte)
• similar to lidocaine• rapidly metabolized
SEE NOTE
WHAT IS THE MOST COMMON LA USED IN DENTISTRY?
LIDOCAINE 2% - (1:100 000 EPI)
mepivacaine(Carbocaine, Isocaine)
• similar effectiveness as lidocaine• BUT is NOT effective topically.• produces LESS vasodilation than lidocaine
therefore can be used as a 3% solution WITHOUT a vasoconstrictor.– BUT systemic toxicity more likely
• Is combined with levonordefrin (not epinephrine) as the vasoconstrictor – usual dosage in dentistry: 2% solution with
1:20,000 levonordefrin • It can be used for SHORT procedures when
a vasoconstrictor is contraindicated. – duration of action of about 30 minutes
LOCAL ANESTHETIC
AGENTS
AMIDES
prilocaine(Citanest, Citanest Forte)
Severeal cases of METHEMOGLOBINEMIA
(cyanosis of the lips & mucous membranes & occasionally respiratory & circulatory distress)
have been reported with use of prilocaine
– should not be administered to patients in which problems with oxygenation may be critical
LOCAL ANESTHETIC
AGENTS
AMIDES
WHICH ONE HAS THE LONGEST DURATION OF ACTION?
MARCAINE
buprivacaine(Marcaine)
• Has the longest duration of action.– major advantage greatly prolonged
duration of action. – indicated in lengthy dental procedures when
pulpal anesthesia of greater than 1.5 hours is needed or when postoperative pain is expected.
• Related to lidocaine & mepivacaine• More potent but less toxic than the other
amides• Available in dental cartridges as a 0.5%
solution with 1:200,000 epinephrine
LOCAL ANESTHETIC
AGENTS
AMIDES
WHAT IS BOTH AN ESTER AND AN AMIDE?
ARTICAINE
OVERVIEW
The vasoconstrictors are members of the autonomic
nervous system drugs called the
ADRENERGIC AGONISTSor sympathomimetics.
VASOCONSTRICTORS
OVERVIEW
• NO vasoconstrictor means: –the anesthetic drug is more quickly removed from the injection site and distributed into systemic circulation than if the solution contained a vasoconstrictor
–more likely to be toxic than those given without a vasoconstrictor
VASOCONSTRICTORS
OVERVIEW
Plain anesthetics without vasoconstrictor will exhibit a
SHORTER duration of action and result in a MORE RAPID buildup
of a systemic blood level.
– Any advantage gained by eliminating the vasoconstrictor must be weighed against the potential for adverse effects from the epinephrine.
VASOCONSTRICTORS
IF A CLIENT HAS UNCONTROLLED BLOOD PRESSURE – CAN LA BE GIVEN IN A
CONTROLLED DOSE?
NO – IT IS BEST TO DELAY TREATMENT
OVERVIEW
A CARDIAC PATIENT can be given
2.0 CARTRIDGES of
1:100,000 epinephrine without
exceeding the cardiac dose.
VASOCONSTRICTORS
WHAT IS THE MAXIMAL SAFE DOSE FOR A HEALTHY CLIENT?
THE MAXIMAL SAFE DOSE OF EPINEPHRINE FOR THE HEALTHY PATIENT IS 0 .2 MG AND FOR THE CARDIAC
PATIENT IS 0 .04 MG
0.2 MG OF EPI
SOME COMMON TOPICAL ANESTHETICS
TOPICAL AGENT NOTES
• Cocaine • highly effective• Not in use now
• Benzocaine • The only use for the Ester
• The most common used before LA
• Lidocaine • commonly used before procedures
• Tetracaine) • –solution/ointment
WHAT IS ORAQIX?
SOMETHING THE RDH CAN USE TO FREEZE THE GUMS
lidocaine & prilocaine (Injection-Free Anesthesia)
(Oraqix)
• May be combined for injection-free local anesthesia.
– The combination of Oraqix applied into the periodontal pocket offers pain relief during scaling and root planing procedures
– Duration of action: approx. 20min. – The onset of action: approx. 30sec after
application.
TOPICAL ANESTHETICS
AMIDES
WHAT IS THE MOST COMMONLY USED TOPICAL?
BENZOCAINE
• Patients should be advised to tell you if they are feeling anxious, nervous, or if they are having heart palpitations.
• Most of these symptoms can be avoided by lowering the dose or switching to another LA
• Some LA may cause drowsiness• Patients should use caution if an opioid
analgesic or antianxiety drug is also Rx• Avoid driving or doing anything that
require thought or concentration• Have the patient avoid eating or drinking
very hot or cold food or drink. The local anesthetic may make it difficult to detect temperature changes.
INSTRUCTIONS FOR PATIENTS RECEIVING LOCAL ANESTHETICS
CHAPTER 10
CAN NITROUS OXIDE BE USED ALONE AS AN ANESTHETIC?
NO!
WHAT ARE THE STAGES/PLANES OF ANESTHESIA?
STAGE I – ANALGESIASTAGE I I – DELIRIUM OR EXCITEMENTSTAGE I I I – SURGICAL ANAESTHESIA
STAGE IV – RESPIRATORY OR MEDULLARY PARALYSIS
STAGES…
STAGES AND PLANES OF ANESTHESIA
STAGE I – ANALGESIA
↓ sensation of painpatient conscious and responsivenitrous oxide in dental office is an
exampleend of this stage marked by loss of
consciousness
MECHANISM OF ACTION
STAGES AND PLANES OF ANESTHESIA
STAGE I – ANALGESIA
MECHANISM OF ACTION
Nitrous oxide, as used in the dental office, maintains the
patient in STAGE I Is characterized by the development of analgesia or reduced sensation to pain.
The patient is conscious and can still respond to commands.
Reflexes are present, and respiration remains regular.
Some amnesia may also be present.
STAGES AND PLANES OF ANESTHESIA
STAGE II – DELIRIUM OR EXCITEMENT
Begins with unconsciousness. Involuntary movement & excitement.Respiration becomes irregular, and
muscle tone increases.Sympathetic stimulation produces
tachycardia, mydriasis, and hypertension (↑ BP).
Emesis (vomiting) and incontinence (defecation) can occur.
MECHANISM OF ACTION
STAGES AND PLANES OF ANESTHESIA
STAGE III – SURGICAL ANAESTHESIA
This is the stage in which most major surgery is performed
The loss of respiratory control (i.e., diminished carbon dioxide response, paralysis of intercostal muscles) first occurs during stage III Paralysis of intercostal muscles begins in plane III
and is complete in plane IV of stage III anesthesia.
MECHANISM OF ACTION
STAGES AND PLANES OF ANESTHESIA
STAGE III – SURGICAL ANAESTHESIADivided into four planes differentiated by
eye movements, depth of respiration, muscle relaxation:
• Plane I & II– return of REGULAR respiration, muscle
relaxation and normal HR & pulse rate• Plane III
– ↓ skeletal muscle tone, dilated pupils, ↓ BP• Plane IV
– characterized by intercostal muscle paralysis (diaphragmatic breathing remains) & absence of all reflexes
MECHANISM OF ACTION
STAGES AND PLANES OF ANESTHESIA
STAGE IV – RESPIRATORY OR MEDULLARY PARALYSIS
Characterized by complete cessation of respiration and circulatory failure.
Pupils are maximally dilated, and blood pressure falls rapidly.
If this stage is not reversed immediately, the patient will die.
Respiration must be artificially maintained.
MECHANISM OF ACTION
STAGES AND PLANES OF ANESTHESIA
MECHANISM OF ACTION
Stage I – Induction PeriodNitrous oxide, as used in the dental office, maintains the patient in STAGE I
Analgesia AnalgesiaAmnesiaEuphoriaconsciousness
Stage II – Induction Period Excitement ExcitementDeliriumcombativeness
Stage IIIWhere most major surgery is performedDivided into four planes
Surgical Anesthesia
UnconsciousnessRegular respirationDecrease in eye movementloss of respiratory control
Stage IV Medullary Depression
Respiratory arrestCardiac depression and arrestNo eye movement
FOR GENERAL ANESTHETICS – WHAT ARE TWO TYPES?
INHALATION AND INTRAVENOUS (IV)
THE LESS SOLUBLE THE ANESTHETIC IS IN BODY TISSUES, THE MORE RAPID THE ONSET AND RECOVERY.
REMEMBER..
CLASSIFICATION OF ANESTHETIC AGENTS
Nitrous oxide (NO2) =
Rapid onset and low solubility in blood
These physical factors allows the anesthesiologist to adjust quickly the
desired level of anesthesia.
GENERAL ANESTHETICS
PHYSICAL FACTORS
WHAT IS MAC?
T H E T E R M M I N I M A L A LV E O L A R C O N C E N T R AT I O N ( M A C ) I S U S E D T O C O M PA R E P O T E N C Y O F G E N E R A L A N E S T H E T I C I N H A L AT I O N A G E N T S
M A C I S T H E D E F I N E D A S T H E M I N I M U M A LV E O L A R C O N C E N T R AT I O N O F A N E S T H E T I C AT 1 AT M O S P H E R E R E Q U I R E D T O
P R E V E N T 5 0 % O F PAT I E N T S F R O M R E S P O N D I N G T O A S U P R A M A X I M A L S U R G I C A L S T I M U LU S
MINIMAL ALVEOLAR CONCENTRATION
CLASSIFICATION OF ANESTHETIC AGENTS
Of the following general anesthetic agents NITROUS OXIDE has the largest MAC
value
MAC of: nitrous oxide > 100;
halothane 0.75, enflurane of 1.68. isoflurane is 1.15
GENERAL ANESTHETICS
PHYSICAL FACTORS
Lower MAC values indicate a more potent
anesthetic
WHAT IS NITROUS OXIDE?
ANTIANXIETY AGENT + ANALGESIC AGENT
COLORLESS AND ODOURLESS GAS
WHAT IS BALANCED ANESTHESIA?
Rapidly acting IV agent + N2O-O2 (nitrous oxide & oxygen) combination + volatile anaesthetic =
balanced anaesthesia
COMBINATION OF…
WHY IS NITROUS OXIDE NOT GOOD TO USE AS A GENERAL ANESTHETIC ALONE?
B E C A U S E O F I T S L O W P O T E N C Y ( M A C > 1 0 0 ) , I T I S U NS AT I S FA C T O RY A S A G E N E R A L A NE S T H E T I C W H E N U S E D A L O N E
I F, H O W E V E R , A N E S T H E S I A I S F I R S T I ND U C E D W I T H A R A P I D LY A C T I N G I V A G E N T A N D N 2 O / O 2 I S A D M I N I S T E R E D I N
C O M B I N AT I O N W I T H A VO L AT I L E A N E S T H E T I C , E XC E L L E NT B A L A N C E D A NE S T H E S I A I S P R O D U C E D
MAC > 100
NITROUS OXIDE
THEREFORE,
Nitrous oxide combined with a halogenated inhalational
anesthetic (N2O/O2)
DECREASES THE MAC
• N2O/O2 is given throughout most surgical procedures that necessitate the use of general anesthesia because it reduces the concentration of other agents needed to obtain the desired depth of anesthesia.
GENERAL ANESTHETICS
NITROUS OXIDE
The average percentage of nitrous oxide required for patient comfort is 35%.
• DELIVERY: 100% O2 (2-3 minutes) → N2O added in
5-10% increments → until patient response indicates level of sedation reached→ after termination of N2O, 100% O2 (at least 5 minutes)
GENERAL ANESTHETICS
WHY SHOULD THE CLIENT BE PLACED ON 100% OXYGEN
AFTERWARDS?
TO AVOID DIFFUSION HYPOXIA
NITROUS OXIDE
• Advantages of the N2O/O2 technique
rapid onset – less than 5 minuteseasy administration – inhalation (no
needles)close control – via flow meters rapid recovery – no need for
designated driveracceptability for children –
apprehensive childrenrelaxed dental team
GENERAL ANESTHETICS
NITROUS OXIDE
• The best indicator of the degree of sedation is the patient’s response to questions– The patient may exhibit slurred speech or a
slow response• The patient is relaxed and cooperative and
reports a feeling of euphoria• The patient is easily able to maintain an open-
mouth position in the desired plane• The patient’s eyes may be closed but can be
opened easily• The respiration, pulse, rate, and blood
pressure are within normal limits
GENERAL ANESTHETICS
PHARMACOLOGIC EFFECTS
WHAT COLOR IS THE NITROUS TANK?
* *REMEMBER THIS!
BLUE
NITROUS OXIDE
• Complications have been the result of misuse or faulty installation of equipment
GENERAL ANESTHETICS
ADVERSE REACTIONS
• NO2 tank → blue
• O2 tank → green
DON’T GET THESE MIXED UP!!
• Cylinders are “pin coded” to prevent mixing of cylinders and lines
• NO2 concentration should be automatically limited and have a fail-safe system that shuts off automatically if the O2 runs out
WHEN SHOULD NITROUS NOT BE USED?
USE OF NITROUS OXIDE IS CONTRAINDICATED IN PATIENTS WITH ANY TYPE OF
UPPER RESPIRATORY OR PULMONARY OBSTRUCTION
IF THEY HAVE TROUBLE BREATHING…
NITROUS OXIDE
• Safety of use in pregnant patients or administration by pregnant operators is in question– The incidence of spontaneous abortion or
miscarriages is higher in female operating personnel chronically exposed to anesthetic agents or in wives of male operators
GENERAL ANESTHETICS
CONTRAINDICATIONS AND DENTAL ISSUESPREGNANCY CONSIDERATIONS
OTHER GENERAL ANESTHETICS
CHARACTERISTICS OF PROPOFOLa. Rapid onset of actionb. Potent vasodilatorc. Undergoes phase II metabolism in the liverd. Intravenous anesthetice. An agent that is unrelated to any other general anesthetic
GENERAL ANESTHETICS
propofol(Diprivan)
INTRAVENOUS
WHAT ARE THE PROPERTIES OF GOOD GENERAL ANESTHETIC?
NO TOXIC EFFECTS…