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What is the difference between anaesthesia and analgesia?

Analgesia is only loss of pain perception

Anaesthesia is the loss of perception of pain, touch, pressure and temperature and abolition of motor function
-you can't move anything


What are the methods of pain control and anxiety and what are the types of sedation?

-Surface Anaesthesia
• Refrigeration
• Topical anaesthetics
-Local Anaesthesia
• Oral (valium, semi sedated, night before or morning)
• Transmucosal

• Intranasal (in kids, hurts a lot, its like a shot)

• Inhalational (ex: nitrous oxide, only up to 70%, no leaking gas from it - it leaves the room, needs a specific room, used for kids with fillings, done by anesthetist)

• Intravenous (BEST WAY, propofol - short acting, sleep w/in 15sec, lasts from 5-10min)

-General Anaesthesia
• Inhalation
• Intravenous
-Out patient drugs

• hypnosis
• phasic sensory inputs
-acupuncture (controls pre-dental anxiety and fear, pain and anxiety management during procedure, alleviation of gagging reflex)
-transcutaneous electronic nerve stimulation (TENS)
•patient management techniques


What is a Local Anaesthesic?

=drug used to prevent the transmission of nerve impulses in the area where it is applied, without affecting consciousness
/ =chemical that reversibly blocks action potentials in all excitable membranes

-stops nerve conduction
-is a weak base



How are Local Anaesthetic Drugs classified as?

according to their chemical structure:

Amides – e.g. Lidocaine, Prilociane, Mepivicaine, Articaine, Bupivicaine

Esters – e.g. Procaine, Benzocaine, Amethocaine, Cocaine (only one that causes vasocontsriction)

-Local anaesthetic usually causes vasodilatation


What are the three main components of local anaesthetics?

• lipophilic/hydrophobic aromatic compound
• intermediate chain (ester or amide)
• hydrophilic amine



What properties the ideal anaesthetic should have?

 A specific and reversible action
 Good shelf life
 Non-irritant
 Produces no permanent damage
 No systemic toxicity
 High therapeutic ratio
 Active topically and by injection
 Rapid onset
 Suitable duration of action
 Chemically stable and sterilizable
 Combinable with other agents
 Non-allergenic
 Non- addictive



What do local anaesthetic cartridges contain?

 Local anaesthetic
 Vasoconstrictor (+/-) – adrenaline or octapressin !!!!
 Reducing agent (used to stabilize the vasoconstrictor so it doesn’t get oxidized – SODIUM METABISULPHITE) !!!!
 Preservatives
 ?Fungicide
 Vehicle - Ringer’s solution (Isotonic solution) - Sodium Chloride
 Methylparaben – bacteriostatic agent and antioxidant
• only found in multi-dose drugs, ointments , creams
• bacteriostatic, fungistatic and antioxidant
• removed due to single use and paraben allergies



How does Local Anaesthetic work?

 Inhibits sodium influx through sodium- specific channels in nerve cell membrane
 LA binds to Na+ channels when channel is open
 Works by inhibiting passage of Na+ into the cell in 2 ways:
• Non specific expansion of nerve cell membrane
• LA binds to receptors in Na+ channel and maintains cell in the REFRACTORY PERIOD

 Binding site for Na+ is intracellular
 To cross membrane LA molecule must be uncharged/lipophilic
 To bind to Na+ channel LA molecule must be charged
 The quicker LA crosses cell membrane the more effective it is
 LA with high proportion of uncharged molecules most effective


Absorption of Local Anaesthetics depends upon:

 Dose
 The drug used (is it a vasodilator?)
 Presence of vasoconstrictors
 Site of deposition



How is ester metabolized?

-in plasma by pseudocholinesterase !!!!
-hydrolysis in liver
-excreted in urine



How is amide metabolized?

hydrolysis in liver apart from prilocaine and articaine

-Lidocaine in liver
-Prilocaine partly in lung
-Articaine undergoes hydrolysis in plasma by pseudocholinesterase
-excretion in urine


Benefit of Vasoconstrictor in LA?

 More profound anaesthesia
 More prolonged anaesthesia
 Reduced operative haemorrhage
 Produce vasoconstrictor of blood vessels and control tissue perfusion by:
• Decreasing blood flow to the site of drug administration
• Absorption of LA into CVS is slowed so decreased toxicity
• More LA enters the nerve and remains for longer periods thus increasing duration of action
• Decrease bleeding at the site


Routes of administration/Uptake Local Anaesthetic Drugs

 Oral
• Poorly absorbed by tissues except cocaine
• Undergo significant hepatic first- pass metabolism

 Topical
• Absorbed at different rates after application to mucous membranes

 Injection
• Absorption related to vascularity of injection site and vasoactivity of drug
• IV (parenteral) provides most rapid elevation of blood levels – used clinically in the primary management of ventricular dysrhythmias


How is anesthesia distributed in the body?

 Absorbed in the blood and distributed throughout the body to all tissues

 Plasma conc of LA influenced by:
• Rate of absorption into CVS
• Rate of distribution of drug from vascular compartments to the tissues
• Elimination of the drug through metabolic or excretory pathways

 Elimination half- life !!!
• The time necessary for a 50% reduction in the blood level
1st: 50%
2nd: 75%

 All LA cross the blood-brain barrier and placenta (enter circulatory system of the developing fetus)



Which local anaesthetic can be used for pregnant women?

Which local anaesthetic cannot be used for pregnant women?





Biotransformation products of Amides:

• methemoglobin responsible for methemoglobinemia – Prilocaine

• Monoethylglycinexylidide and glycine xylidide produce Sedation - Lidocaine




 Gold standard !!
 2% concentration with 1:80 000 adrenaline/epinephrine (used with adrenaline in dentistry)
 Pulpal anaesthesia lasts 45 min
 Soft tissue anaesthesia lasts longer
 < 3% excretion
 rarely has contraindications
 if allergic to lidocaine (not adrenaline) better to use Mepivacaine than lidocaine plain - anything plain; so adrenaline is not good



 2% concentration with 1:100,000 adrenaline/epinephrine
 Has similar effect to lidocaine
 3% plain
 Better anaesthesia than 2% lidocaine vasoconstrictor – free solution
 1% excretion



 3% with vasoconstrictor felypressin/octapressin (synthetic analog of vasopressin)
 4% plain
 Produces less vasodilation than lidocaine
 Is one of the constituents of EMLA (eutectic mix of lidocaine and prilocaine)
 3% formulation useful alternative to 2% lidocaine with epinephrine if a vasoconstrictor-free solution is indicated
 Excreted in urine as o-toluidine




 4% concentration
 1:100,000 (surgical - more constricted) or 1:200,000 (restorative - more diluted) adrenaline
 Fast metabolism – low toxicity
 Half life 20 minutes
 Partly metabolized in the plasma
 Increased risk of nerve injury in IDB (higher risk than Lidocaine)
 Evidence of buccal infiltration of 4% articaine as effective as IDB with 2% lidocaine in anaesthesia of mandibular molar teeth




 Long acting LA !!!
 lasts for: 6hr plain, 8hr with adrenaline
 0.25 – 0.75%
 Reduced the number of analgesics required for post-operative pain when used as supplementary infiltration during general anaesthesia
 With/out epinephrine 1:200,000
 Ability to bind to proteins – 96% of it is protein bound


What are the systemic effects of LA on:
1. Central Nervous System
2. Cardiovascular System
3. Local Tissue Toxicity
4. Respiratory System
5. Drug Interactions

1. Central Nervous System:
• Depression
• Anticonvulsant properties
• Analgesia
• Mood elevation

2. Cardiovascular System: (action it has on the heart)
• Myocardial depression
• Therapeutic advantage in cardiac dysrhythmias
• Hypotension

3. Local Tissue Toxicity:
• Skeletal muscle more sensitive – produces skeletal muscle alterations – muscle regeneration within 2 weeks

4. Respiratory System:
• Dual effect on respiration
• At therapeutic levels – direct relaxant action on bronchial smooth muscle
• At overdose – may produce respiratory arrest (unable to breath)

5. Drug Interactions:
• Potentiate CNS- depressant effects of LA if used in combination with other CNS depressants e.g. opioids, antianxiety drugs
• Ester LA and use of muscle relaxant succinylcholine lead to prolong apnea as they share same metabolic pathway
• Drugs that induce production of hepatic microsomal enzymes e.g barbiturates can lead to increase rate of metabolism of amide LA


Which are Catecholamines?

=Catechols and if have an amine group (NH2)



Which are Noncatecholamines?

Ephedrine (nasal congestant)



Mode of action of vasoconstrictors:
Three categories of sympathomimetic amines:

• Direct-acting drugs:
epinephrine, norepinephrine, levonordefrin

• Indirect-acting drugs:
tyramine, amphetamine, hydroxyamphetamine

• Mixed-acting drugs:
ephedrine, metaraminol



Mode of action of vasoconstrictors:
Adrenergic receptors:

 α and β receptors based on inhibitory or excitatory actions of catecholamines on smooth muscle

 Activation of α receptors – contraction of smooth muscle – vasoconstriction
• α 1 – excitatory postsynaptic
• α 2 – inhibitory postsynaptic

 Activation of β receptors – smooth muscle relaxation
• β 1 – in the heart and small intestine causing cardiac stimulation and increased heart rate and lipolysis
• β 2 – brochi, vascular beds and uterus producing brochodilation and vasodilation


Systemic Actions of Epinephrine:

 Myocardium
• Stimulates β1 – positive inotropic (force of contraction) and positive chronotropic (rate of contraction) effect

 Pacemaker cells
• Stimulates β1 – increase irritability of pacemaker cells leading to increase incidence of dysrhythmias – e.g ventricular tachycardia and premature ventricular contractions

 Blood Pressure
• Increased systolic blood pressure, diastolic pressure is decreased
• Diastolic pressure is increased at larger doses due to α receptor stimulation

 Cardiovascular System
• Increased blood pressure, cardiac output, stroke volume, heart rate, strength of contraction, myocardial oxygen consumption (OPPOSITE EFFECT ON HR FROM NOREPINEPHRINE)

 Vasculature
• Constriction in the vessels – small arterioles supplying skin, mucous membranes and kidneys
• Small dose of epinephrine produces dilatation due to stimulation of β2 receptors, higher doses produce vasoconstriction due to stimulation of α receptors

 Haemostasis
• α receptor stimulation causing vasoconstriction at site
• As levels of epinephrine decrease action on blood vessels revert to vasodilation due to β2 receptors stimulation- therefore is common to notice bleeding at about 6hrs postoperative

 Respiratory system
• brochodilation due to β2 effect

 Central Nervous System
• No effect at therapeutic doses

 Termination of action
• Reuptake by adrenergic nerves
• If escaped reuptake is rapidly absorbed in the blood by the enzyme catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) both present in liver
• Only 1% unchanged in urine


Site effects and Overdose of Epinephrine:

• Increased fear, anxiety, tension, restlessness, trembling, throbbing headache, tremor, weakness, pallor, dizziness, palpitations, pallor, respiratory difficulty – CNS
• Cardiac dysrhythmias
• Dramatic increase in BP - Angina episodes in patients with coronary artery insufficiency


Systemic Actions of Norepinephrine:

 Mode of action
• Almost exclusively on α receptors (90%)
• Stimulates β actions in the heart(10%)
• ¼ as potent as epinephrine

 Myocardium
• +ve inotropic action through β1

 Pacemaker cells
• Stimulates β1 – increase irritability of pacemaker cells leading to increase incidence of dysrhythmias

 Coronary Arteries
• Increased coronary artery blood flow

 Heart rate
• Decrease in heart rate due to reflex actions on carotid and aortic baroreceptors and vagus nerve after a marked increased in blood pressure (OPPOSITE EFFECT ON HR FROM EPINEPHRINE)

 Blood Pressure
• Increased blood pressure – both systolic and diastolic due to α-stimulating actions

 Cardiovascular Dynamics
• Increase blood pressure
• Decrease heart rate (OPPOSITE TO EPI)
• Slight or no effect on cardiac output
• Increase stroke volume
• Increase total peripheral resistance

 Vasculature
• α-stimulating actions producing constriction and increased total peripheral resistance

 Respiratory system
• α-stimulating actions producing constriction of lung arterioles

 Central Nervous System
• No effect at therapeutic levels

 Metabolism
• Increase blood sugar level
• Increase tissue oxygen level consumption
• Increase basal metabolic rate

 Termination of Action and Elimination
• Reutake at adrenergic nerve terminals and its oxidation by MAO
• Exogenous norepinephrine is inactivated y COMT


Side effect and Overdose of Norepinephrine:

• Similar to epinephrine but less frequent and severe !!!
• Stimulation of CNS
• Marked increased in blood pressure – increasing risk of haemorrhagic stroke, angina episode in susceptible patients and cardiac dysrhythmias
• Extravascular injections into soft tissues can cause necrosis and sloughing – to be avoided for vasoconstrictive purposes in hard palate – some authorities grounded its use in LA


Felypressin (Octapressin):

• Synthetic analog of vasopressin
• A nonsympathomimetic amine
 Mode of action
• Direct stimulant of smooth muscle

 Myocardium – no direct effects noted
 Pacemaker cells
• Nondysrhythmogenic
 Coronary Arteries - No effect at therapeutic levels
 Vasculature – facial pallor in high doses
 Central Nervous System – no effect on adrenergic nerve transmission
 Uterus
• Antidiuretic and oxytocic actions, the latter CONTRAINDICATED IN PREGNANT patients !!!!!!!!!
Side Effects and Overdose
• Wide margin of safety
 3% Prilocaine and 0.03 IU/mL


What is ASA?

American Society of Anaesthesiologist


What ASA III means?

A patient with severe systemic disease

-poorly controlled DM, morbid obesity, active hepatitis, alcohol dependence, implanted pacemaker


What ASA I means?

A normal healthy patient

-non smoking, no or minimal alcohol use



What ASA II means?

A patient with mild systemic disease

-controlled DM, current smoker, social alcohol drinker, pregnancy, obesity, mild lung disease, asthma, epileptic, thyroid conditions, active allergies


What ASA IV means?

A patient with severe systemic disease that is a constant threat to life

-cardiac ishemia, severe valve dysfunction, sepsis


What ASA V means?

A moribund patient who is not expected to survive without the operation

-abdominal/thoracic aneurysm, massive trauma, intracranial bleed, ischemic bowel, cardiac pathology, multiple organ/system dysfunction


What ASA VI means?

A declared dead patient whose organs being removed for donor purposes


Trigeminal Nerve - Sensory innervations to:

• Dentition, mucosa of mouth
• Skin of face
• Nose and paranasal sinuses

• Except base of tongue and pharynx



Trigeminal Nerve - Motor innervations to:

• Muscles of mastication !!!
• Tensor ville palatini, Tensor tympany
• Anterior belly of digastric
• Mylohyoid


Origin of Trigeminal Nerve:

• EMERGES FROM the middle of the PONS
• Run to the front of petrous part of temporal bone
• Trigeminal ganglion (Semilunar or Gasserian ganglion)
• Trigeminal ganglion formed by aggregation of cell bodies of sensory neurons



three main branches which emerge from trigeminal ganglion:

What is the name of the foramen of each division that exits the skull?

V1 – superior orbital fissure

V2 – foramen rotundum

V3 – foramen ovale


Which are the motor and sensory nucleus within brainstem?

Mesenchephalic, Principal and Spinal Trigeminal nucleus


Ophthalmic V1 innervation:

Caries sensory information from the skin of the forehead, the upper eyelids, cornea and nose ridge, frontal sinus, parts of the meninges and nasal mucosa

• Supplies eyeballs, conjunctiva, lacrimal gland, mucosa of nose and paranasal sinus, skin of forehead eyelid and nose

 Smallest division
 Sensory only


Maxillary V2 innervation:

Innervates the skin of the middle facial area, the side of the nose, lower eyelids, maxillary dentition and associated gingival tissues, part of nasal mucosa (including the maxillary sinus), cheek, upper lip and the palate, ethmoid, sphenoid sinuses and part of meninges

 Pure Sensory
 Nasal and nasopalatine nerves – innervate back of nasal mucosa, anterior part of palatal mucosa, gingiva and maxillary incisors
 Greater palatine nerve – innervates hard palate and palatal gingiva of alveolar process
 Lesser palatine nerve – innervates soft palate



Mandibular V3 innervation:

Innervates skin of lower facial area, mandibular dentition and associated gingival tissues, mucosa of lower lip, cheeks, and floor of mouth, chin, jaw, tongue, parts of meninges and external ear

 Two main branches:
-Anterior trunk !!!!!
• Sensory- Buccal nerve
• Motor – lateral pterygoid, deep temporal and masseteric nerves
-Posterior trunk
• Sensory – auriculotemporal and lingual
• Mixed sensory and motor – inferior alveolar nerve


Course of Opthalmic Nerve:

1. Emerges from Trigeminal ganglion
2. Lateral wall cavernous sinus
3. 3 branches in anterior part of cavernous sinus Lacrimal, Nasocilliary, Frontal !!!
4. Superior orbital fissure
5. Orbit


Course of Maxillary Nerve:

1. Emerges from Trigeminal ganglion
2. Lateral wall cavernous sinus
3. Foramen rotundum
4. Pterygopalatine fossa
5. Through inferior orbital fissure reaches floor of the orbit as infraorbital nerve
6. Reaches the face through infraorbital foramen



Innervation of Tongue:

 Sensory - pain, touch, temperature - to anterior 2/3 is supplied by lingual nerve (branch of V3)

 Taste- to anterior 2/3 is supplied by chorda tympani (branch of VII) - sensory as well but not one of the mains

 Sensory to posterior 1/3 tongue is supplied by glossopharyngeal (IX)

 MOTOR innervation of tongue is supplied by hypoglossal (XII)


Ganglia Associated with Trigeminal Nerve:

 Cilliary Ganglion
 Pterygopalatine Ganglion
 Otic Ganglion
 Submandibular Gaglion


Injection Syringes must be:

-able to withstand repeated sterilization without damage
-capable of accepting a wide variety of cartridges and needles from different manufacturers and permit repeated use
-lightweight and simple to use with one hand
-provide aspiration so blood can be seen through the glass cartridge


Syringe Components:

needle adaptor
piston with harpoon
finger grip
syringe barrel
thumb ring


Advantages and Disadvantages of the Metallic, Breech-loading Aspirating Syringe:

Visible cartridge
Aspiration with one hand
Rust resistant
Long lasting with proper maintenance

Weight – heavier than plastic syringe
Syringe may be too big for small operators
Possibility of infection with improper care


Self- Aspirating Syringes:

 The syringe use the elasticity of the rubber diaphragm in the anaesthetic cartridge to obtain negative pressure
 The diaphragm rests on a metal projection inside the syringe that directs the needle into the cartridge
 Pressure acting directly on the cartridge through the thumb disk or indirectly through the plunger shaft distorts the rubber diaphragm producing positive pressure within the anaesthetic cartridge


Advantages and Disadvantages of Pressure Syringes (+their use):

for periodontal ligament injection

Measured dose
Overcomes tissue resistance
Nonthreatening (new devices)
Cartridges protected

Easy to inject too rapidly
Threatening (original device)


Jet injector – ‘needle-less syringe’:

 For topical anaesthesia
 Based on the principles that liquids forced through small openings called jets at very high pressures can penetrate intact skin and mucous membranes


Disposable Syringes:

 Plastic disposable syringes are available in a variety of sizes with assortment of needle gauges
 Commonly used for IM and IV injections but also can be use for intraoral injections
 No aspirating tip
 Cannot accept local cartridges


Safety Syringe:

 Aspiration is possible
 Some brands come with an autoclavable plunger and disposable self-contained injection unit
 Made to be single use items
 More expensive than reusable syringes
 Minimize the risk of needle injuries by having a sheath that ‘locks’ over the needle



Advantages of Larger-Gauge Needles Over Smaller-Gauge Needles:

Less deflection as needle advances through tissues
Greater accuracy in injection
Less chance of needle breakage
Easier aspiration
No perceptual difference in patient comfort


Rotational Insertion Technique:

 Bi-Rotational Insertion Technique –BRIT
• the operator rotates the needle in a back-and-forth rotational movement while advancing the needle through soft tissue



Components of the needle:

-Bevel: point or tip of the needle; long, medium and short
-Shaft: long portion of the needle (diameter of lumen)
-Hub: plastic/metal piece that attaches the needle to the syringe
-Cartridge penetrating end: perforates the diaphragm of cartridge
-Syringe adaptor


Components of the Cartridge:

 Latex rubber Diaphragm - through it the needle penetrates the cartridge
 Aluminum Cap - holds the diaphragm in position
 Neck
 Cylindrical glass tube
 Stopper (Plunger, Bang) -silicon rubber

Mylar plastic label surrounds glass with content information and colour coded band to identify anaesthetic


Care and Handling of Cartridges:

should not be permitted to soak in alcohol or other sterilizing solution because the diaphragm will allow diffusion


Maxillary Injection Techniques:

 Provide anaesthesia of teeth, soft and hard tissues
 Type of anaesthesia is determined by type of procedure

 Techniques include:
• Supraperiosteal (infiltration) !!!
• Periodontal ligament
• Intraseptal injection
• Intracrestal injection
• Intraosseous injection
• Superior Alveolar Nerve blocks
• Nasopalatine and Greater palatine Nerve blocks



Supraperiosteal Injection:

 Most frequently used technique to obtain PULPAL anaesthesia in MAXILLARY teeth

– also known as local infiltration !!!!

 Anaesthetises: pulp and root of tooth, buccal periosteum, CT and mucous membrane

 Indicated when treatment is limited to 1-2 maxillary teeth and for soft tissue anaesthesia when surgical procedure is in a circumscribed area

 Alternative supplemental techniques: PDL, intraosseous, regional blocks



Posterior Superior Alveolar Nerve Block:

Effective for maxillary third, second and first molar

Known as tuberosity or zygomatic block

Note: mesiobuccal root of maxillary first molar is not consistently innervated by PSA but also can be by MSA therefore a second local/subperiosteal infiltration is needed !!!!!!

 Area of insertion: height of mucobuccal fold above the maxillary second molar

 Landmarks: mucobuccal fold, maxillary tuberosity and zygomatic process of maxilla

temporary hematoma – if inserted too far posteriorly into pterygoid plexus of veins, also maxillary artery may be perforated



Middle Superior Alveolar Nerve Block:

 Present only in 28% of population

 Limited clinical usefulness however IF ASA BLOCK FAILS to provide pulpal anaesthesia distal to the maxillary canine then MSA block is indicated

 Anaesthetises: pulpal tissue of first and second premolars and mesiobuccal root of first molar

 No contact with bone

 Same as with PSA nerve

 Area of insertion: height of the mucobuccal fold above UPPER SECOND PREMOLAR



Anterior Superior Alveolar Nerve Block:

 known as Infraorbital Nerve Block incorrectly

 Profound pulpal and buccal soft tissue anaesthesia from maxillary central incisors through premolars in about 72% of patients

 Area of insertion: height of mucobuccal fold directly over the first premolar

 Landmarks: Mucobuccal fold, Infraorbital notch, Infraorbital foramen

Hematoma may develop across eyelid and the tissues between it
-This is rare as pressure is routinely applied to the injection site during and after administration
•Hematoma can get infected: prescribe antibiotics OR can go away by its own


Anterior Middle Superior Alveolar Nerve Block Technique:

Areas anesthetised:
• Pulpal anaesthesia of the maxillary incisors, canines and premolars
• Buccal attached gingiva of the same teeth
• Attached palatal tissues form midline to free gingival margin on associated teeth

 Palatal approach thus muscles of facial expression and upper lip are not anaesthetised

 Described as field block of the terminal branches of the ASA block

 Area of insertion: on hard palate halfway along an imaginary line connecting the midpalatal suture to the free gingiva margin ; the location between first and second premolars

 45-degree angle with bevel facing bone – insert until in contact with bone


2 approaches of Maxillary Nerve Block:

 Produces anaesthesia to hemimaxilla

 Two approaches:
-High Tuberosity Approach
• Area of insertion: height of the mucobuccal fold above the distal aspect of the maxillary second molar
• Landmarks: mucobuccal fold at the distal aspect of maxillary second molar, maxillary tuberosity, zygomatic process of maxilla

-Greater Palatine Approach Technique:
 Area of insertion: palatal soft tissue directly over greater palatine foramen
 Landmark: greater palatine foramen, junction of the maxillary alveolar process and palatine bone
 Same as greater palatine nerve block- once is complete proceed with very slow advancement into the greater palatine canal to a depth of 30 mm


Palatal Infiltration:

 Necessary when manipulation of palatal soft or hard tissues
 Topical anaesthesia at injection site – at least 2 minutes, using cotton roll/cotton applicator stick
 Pressure anaesthesia can be produced at the site of injection by applying considerable pressure using a firm object such as cotton applicator stick/ handle of the dental mirror
 This will produce ischemia (blanching) of normally pink tissues at the penetration site and a feeling of intense pressure (dull and tolerable, not sharp and painful)
Deposit anaesthetic solution slowly



Greater Palatine Nerve Block:

 Anaesthesia to the palatal soft tissues distal to the canine
 Profound hard and soft tissue anaesthesia
 Indicated when more than two maxillary teeth required periodontal/surgical treatment and sometimes for restorative treatment if subgingival restorations
 Minimizes patient discomfort as no need for multiple injections on the palate

 Insertion of needle slightly anterior to the greater palatine foramen
 Landmarks: greater palatine foramen and junction of the path of maxillary alveolar process and palatine bone
 Advance the syringe from the opposite side of the mouth at right angle to the target area – bevel of needle should face palatal soft tissues

Position for Right greater palatine nerve block – administrator should be at 7-8 o’clock position
Position for Left greater palatine nerve block – administrator should be at 11 o’ clock – positions apply for right-handed administrator

• Hematoma if maxillary artery is punctured
• Penetration of the orbit may occur if needle goes far
• Penetration of nasal cavity



Nasopalatine Nerve Block:

 Palatal anaesthesia achieved to anterior portion of the hard palate (soft and hard tissues) bilaterally from the mesial of the right first premolar to the mesial of the left first premolar
 Tissue penetration lateral to incisive papilla on the palatal aspect of the maxillary central incisors

 Insertion on palatal mucosa lateral to incisive papilla
 Target area the incisive foramen
 Needle at 45- degree towards incisive papilla
 Bevel of needle towards palatal mucosa
 Administrator position- sit at 9 or 10 o’clock position and ask patient to extend neck
Pressure anaesthesia at site of needle insertion
 Multiple Needle Penetrations


Palatal Approach- Anterior Superior Alveolar Nerve Block:

 Shares several common elements with the nasopalatine nerve block
 The P-ASA injection uses similar tissue point of entry (lateral aspect of incisive papilla) but differs in its final target – the needle is positioned within the incisive canal


Mandibular Injection Techniques:

 Inferior Alveolar Nerve block
 Mandibular Nerve Block:
• Gow-Gates Technique
• Vazirani-Akinosi Closed Mouth Technique
 Mental Nerve block
 Buccal Nerve block
 Incisive Nerve block



Inferior Alveolar Nerve Block Technique:

 Area of insertion: Mucous membrane on the medial side of the mandibular ramus

 Landmarks: Coronoid notch, Pterygomandibular raphe, occlusal plane of mandibular teeth

 Depth of penetration: 20-25 mm (2/3rd to 3/4th ) the length of a long needle until contact with bone

Height of injection: Imaginary line- place thumb of your left hand in the coronoid notch !!!!!

Anteroposterior site of injection: Needle penetration occurs at the intersection of two points !!!!
•Point 1- horizontal line form coronoid notch to deepest part of the pterygomandibular raphe
•Point 2 – vertical line through point 1 about 3/4ths of the distance from the anterior border of ramus

Insert the needle, when bone is contacted withdraw approximately 1 mm and aspirate

If negative aspiration deposit slowly 2/3rds of cartridge over 1 minute

Three parameters should be considered during penetration of Inferior Alveolar Nerve Block Technique: the height of injection, depth of penetration and anterior posterior placement of the needle



Buccal Nerve Block:

A branch of the anterior division of V3

Areas anesthetized: soft tissue and periosteum buccal to the mandibular molar teeth

•Area of insertion: through mucous membrane distal and buccal to the most distal molar (3rd molar)



Mandibular Nevre Block - The Gow-Gates Technique: (+nerves anaesthetised)

Nerves anaesthetised:
•Inferior alveolar nerve

Target area: Neck of condyle
•Extraoral- corner of mouth and Tragus
•Introral - Height of injection - needle tip just below the mesiopalatal cusp of the maxillary second molar



Mandibular Nerve Block - Vazirani-Akinosi Closed Mouth:

 Primary indication when mandibular anaesthesia is desired when limited mouth opening precludes the use of other mandibular injection

•Area of insertion: height of mucogingival junction adjacent to maxillary third molar
•Target area: medial border of ramus in the region of inferior alveolar, lingual, mylohyoid nerves



Mental Nerve Block:

Area of insertion: mucobuccal fold at or just anterior to the mental foramen
With your left index finger, pull lower lip and buccal soft tissues laterally
 Penetrate mucous membrane at the injection site between the 1st and 2nd premolars directing the needle to the mental foramen (towards apices of premolars) until in contact with bone
Aspirate and deliver slowly


Incisive Block:

Other common name: Mental nerve block- inappropriate
Technique similar to mental nerve block but instead the needle is directed at or just anterior to the mental foramen
-you also infiltrate until the mental foramen



3 Supplemental Injection Techniques:

Intraosseous Anaesthesia (IO)
Periodontal Ligament Injection and Intraseptal Injection are modification of traditional IO anaesthesia
Intrapulpal Injection



Medical Emergencies Identified in the Resuscitation Guidelines:

 Asthma
 Anaphylaxis
 Myocardial Infarction
 Epileptic Seizures
 Hypoglycaemia
 Syncope
 Chocking and Aspiration

 Asthma
 Anaphylaxis -> adrenalin injection (1:1000, 1mg/ml) !!!
 Myocardial Infarction -> aspirin dispersible 300 mg
 Epileptic Seizures
 Hypoglycaemia -> oral glucose solution/tablets/gel/powder
 Syncope
 Chocking and Aspiration



Needle Breakage:

what to do and how to reduce the risk:

 Extremely rare
 If visible, grasp the proximal end with a mosquito hemostatic clamp and remove from soft tissue
 If not refer to a specialist for evaluation and possible attempted retrieval

 Reduce the risk of breakage !!!
• Do not use short needles for IAN blocks
• Do not use 30-gauge needles (use larger gauge needles - 30 gauge needle has smaller diameter than 25 gauge needle)
• Do not bend needles
• Do not insert needle into its hub


Prolonged Anaesthesia or Paraesthesia:

Common causes:
side effects:

Paraesthesia = persistent anaesthesia, or altered sensation well beyond the expected duration of anaesthesia

-patients may experience hyperesthesia and/or dysesthesia which is both pain with numbness

 Common causes are during oral surgical procedures such as surgical removal of mandibular third molars (IAN and Lingual n.), placement of dental implants, block anaesthesia
 Local anaesthetic injections – ‘electric shock’ sensation throughout the distribution of the involved nerve

 Reassure
 Explain paresthesia is not uncommon after local anaesthetic administration
 Arrange a review
 Examine the patient and determine the degree and extent of paresthesia
 Reschedule a review appointment every 2 months until sensory deficit persists
 Refer to a specialist for a second opinion and surgical repair



Facial Nerve Paralysis:

how is it caused?

 Caused by introduction of local anaesthetic into the capsule of parotid gland – IAN or over inserting during Vazirani-Akinosi block !!!

 Duration of transient paralysis is equal to that of soft tissue anaesthesia

 Patient has unilateral paralysis and is unable to use these muscles and also unable to voluntarily close one eye

 Reassurance
 Contact lenses should be removed until muscular movement returns
 Eye patch should be applied to the affected eye until muscle tone returns
 Good practice next day phone call review




caused by?

managed by?

= prolonged tetanic spasm of the jaw muscles by which the normal opening of the mouth is restricted (locked jaw)

 Trauma to muscles or blood vessels in the infratemporal fossa is the most common causative factor

 Haemorrhage, infection and multiple missed Inferior alveolar nerve block

Managed by:
 Review appointment and advised heat therapy, jaw rest and analgesics and offer physiotherapy
 Consider antibiotics if trismus related to infection and refer to specialist


Soft Tissue Injury:

people more common to:
how is it managed?

 Self-inflicted trauma to the lips and tongue

 Young children and mentally or physically disabled children or adults and older patients

 Managed by analgesics for pain, lukewarm saline rinses, petroleum jelly to minimise irritation




how long it lasts?

managed by?

possible complications?

= effusion of blood into extravascular spaces can be caused by inadvertent nicking of a blood vessel during local anaesthetic

 Direct pressure should be applied to the site of bleeding for 2 minutes

 Possible complications of hematoma include trismus and pain

 Bruising subsides gradually over 7-14 days



Pain and Burning on Injection:

how is prevented?

Caused by?

 Pain on injection increases anxiety and may lead to sudden movement, increasing the risk of needle breakage, traumatic soft tissue injury to patient or needle stick injury to the administrator

 Prevented through careful adherence to the basic protocol of atraumatic injection technique

 Burning during injection: !!
caused due to pH of the solution (being deposited to soft tissues and rapidly disappears), rapid injection, contaminated solution, or overly warm solution !!!!!



how is it caused?

 Extremely rare occurrence subsequent to injection

 Major cause of post injection infection is contamination of the needle

 Injecting into an area of infection, local anaesthetic is less effective but if force applied during administration might transport bacteria into adjacent healthy tissue – spreading infection



caused by?

prevented by?

 Can be cause due to
• Trauma during injections
• Infection
• Allergy – Angioedema
• Hereditary angiodema
• Haemorrhage

 Prevention by adhering to atraumatic injection

 Life-threatening oedema of tongue, pharynx or larynx requires vigorous management



Sloughing of Tissues: (τραβίξεις)

 Epithelial desquamation and sterile abscess !!!!

 Causes of epithelial desquamation !!!!
• Prolonged application of topical anaesthetic
• Heightened sensitivity of tissues to topical or injectable local anaesthetic

 Causes of sterile abscess !!!!
• Secondary or prolonged ischemia due to local anaesthetic with vasoconstrictor
• Usually develops on palate

 No formal management is necessary – symptomatic management with analgesics




patient factors?

drug factors?

= those clinical signs and symptoms that result from an overly high blood level of a drug in various target organs and tissues

 Patient factors
• Age
• Weight
• Other medication – e.g. Phenytoin
• Sex
• Presence of disease
• Genetics
• Mental Attitude and Environment

 Drug Factors
• Vasoactivity
• Concentration
• Dose
• Route of administration
• Rate of injection
• Vascularity of the injection site
• Presence of vasoconstriction



CNS Toxicity:

At low dose:

At high dose:

Reduced by:

 At low dose excitatory

 At high dose inhibitory

 Generalized cortical sensitivity is noted – agitation, talkativeness and irritability

 Tonic clonic seizures occur at levels greater than 7.5 μg !!!!!!!

 Respiratory depression and arrest develop due to CNS depression at greater levels

 Direct action

 Indirect action via disinhibition of autonomic nerves

 Depressant action

 Minor ECG alterations, myocardial depression, decreased cardiac output and peripheral vasodilation ar 5-10μg/mL

 At levels above 10μg/mL – above effects intensified with possible cardiac arrest

Reduced by: !!!
 Limiting the dose
 Avoid intravascular injection
 Injecting slowly


Signs of adequate sedation:

•Awake + verbal contact
•Warm feeling
•Tingling hand and feet – Warn patients on this
•Reduced awareness to painful stimuli
•Vital signs and reflexes intact


Failure of sedation technique:

•Nasal obstruction
•Mouth breathing
•Inefficient seal on nasal hood
•Extreme anxiety
•Fault in machine



Conscious Sedation =

= a minimally depressed level of consciousness that retains patient’s ability to maintain an airway independently and respond appropriately to physical stimulation and verbal command

 Safe and effective for patients who need minor oral surgery or diagnostic procedures
 Patient easily aroused
 Reflexes are maintained
 Allows for quick recovery


 Kids under age 5 or 6 may require:

deep sedation

 Anatomical and physiological differences must be considered
 May be more vulnerable to respiratory depression and may pass into deeper sedation state that was intended


Action of Nitrous Oxide:

Start of treatment:
 Inhalation of N2O
 Raised partial pressure in lungs (high PP)
 Forces nitrous oxide to cross alveolar membrane
 Is then carried to brain
 Gaseous exchange with brain tissue

End of treatment:
 Nitrous oxide is stopped
 Partial pressure in alveoli falls (low PP)
 Nitrous oxide diffuses back into lungs and is exhaled


Mechanism of Action of Nitrous Oxide:

Analgesic effect:

Anxiolytic effect:

Analgesic effect:
Interaction with opioid receptors
Activates same receptors as heroin and morphine
50% N2O /O2 produces same analgesic effect of 5mg morphine

Anxiolytic effect:
Mediated by interaction with GABA-A receptors
GABA is an inhibitory neurotransmitter


Inhalation Sedation:

 Nitrous oxide is the only inhalation agent currently in use for conscious sedation in dental practice
 Colourless, faintly sweet smelling gas with a specific gravity of 1.53
 Has a low blood-gas partition coefficient of 0.47, so it is relatively insoluble and produces rapid induction of sedation
 When administration is discontinued, nitrous oxide dissolved in the blood is rapidly eliminated via the lungs

 Minimum alveolar concentration of anaesthetic that prevents a response to a standard surgical stimulus in 50% of a sample of patients – MAC
 MAC value Nitrous oxide 104 vs Sevofluorane 1.8
 The high MAC means that nitrous oxide is a weak anaesthetic which is readily titrated to produce sedation
 Has few side effects in therapeutic use - causes minor cardio- respiratory depression, and produces no useful amnesia
 During the first few minutes of this elimination, large volumes of nitrous oxide pour out of the blood and into the lungs. This can actually displace oxygen from the alveoli causing a condition known as diffusion hypoxia

 Maximum acceptable occupational exposure of personnel to nitrous oxide should not average more than 100 ppm over an 8-hour period under the current health and safety regulations
 Risks have been reduced considerably by the introduction of efficient scavenging and ventilation systems


Stage 1 Moderate Sedation:



5-25% Nitrous Oxide
Looks awake
Responds clearly
Retains open mouth
Gag reflex only slightly reduced

Feels relaxed
Tingling in fingers, toes, cheeks, tongue
Feeling of being well


Plane 2 – Dissociation:



20-55% Nitrous oxide
Dreamy faraway look
Slow response and slurred speech
Reduced gag reflex but retains open mouth
Analgesia marked

Feels light or heavy and warm
Marked paraesthesia
+/- giggling
Very suggestible


Plane 3 – Analgesia:



50-70% Nitrous oxide
Verbal contact difficult
Loss of open mouth sign
Glottic reflex depressed
Loss of co-operation

Feels disorientated
+/- nausea
Total analgesia
Feeling of doom and gloom
Loss of consciousness may occur

-We want stage I, plane III


Clinical Effects of Nitrous Oxide:

Nervous System:

Minimal effects
Cutaneous vasodilation
Myocardial depressant at high dose

Non irritant
Mild depression of alveolar ventilation
Diffusion hypoxia

Nervous System:
CNS depressant
Effects confined to cerebral cortex
Depression of senses (sight touch hearing)
Minimal effects on memory
Anaesthetic mechanism unclear


Effects of Nitrous Oxide:

Acute Adverse:
Chronic Adverse:
Hazards of Chronic Exposure:
Biochemical Effect of Chronic Nitrous Oxide Exposure:

Acute Adverse:
Patients > hypoxia
Methotrexate interaction
•Can increase anti-folate effect
•Liaise with rheumatologists
•Folate supplements?

Chronic Adverse:
Personnel – chronic exposure
Recreation use
Substance abuse

Hazards of Chronic Exposure:
hepatic disease, renal disease, malignancy, cytotoxicity, neurological problems

Biochemical Effect of Chronic Nitrous Oxide Exposure:
nitrous oxide causes oxidation of vit B12
reduced activity of methionine synthetase
impaired dna synthesis
impaired dna synthesis
pernicious anemia


Nitrous oxide:


Fast onset and recovery
Analgesic and hypnotic
Minimal effect on CVS and Respiratory system
No metabolites •Drug not metabolised
Extensively Documented, virtually no mortality
Easy to use
•Rapid peak action: 3-5 minutes
•Depth of sedation easily regulated
•Duration of sedation flexible
•Moderate analgesia
•No injection
•Few side effects
•No adverse effects on the liver, kidneys, brain, cardiovascular system or respiratory systems

Low potency (only for specific patients)
Pressure effects in gas filled cavities
Elaborate delivery system
Danger of hypoxia?
Recreational abuse
Cost of equipment
Space occupying equipment
Not a potent agent
A degree of co-operation is necessary
Possibility of chronic exposure
Technique of administration is operator sensitive


Contraindications of Nitrous Oxide:

Claustrophobic patients
Middle Ear/Sinus Infection
Certain types of ocular surgery
Behavioural problems which reduce cooperation
Upper respiratory tract infection
Inability to communicate
Severe COPD where reduced oxygen levels act as respiratory drive
Severe anxiety
Pregnancy (first trimester)
Patients on Methotrexate (N2O potentiates the anti-folate effect)
Myasthenia gravis

-indicated in epileptic patients, dental phobia


Intravenous Sedation:

Agents injected into bloodstream and carried in plasma to tissues
They diffuse down concentration gradient across lipid membrane to site of action in brain
All drugs exist free in the plasma or bound to plasma proteins
The un-ionised drug is also distributed into fat deposits and undergoes metabolism in the liver
The relative movement between ionised and un-ionised drug affects the pharmacokinetics of the IV agent

 After injection the drug passes through the venous system to right side of heart, through the pulmonary circulation to the left side of the heart
 Once in the arterial system reaches the brain and has its effect once it has crossed the blood-brain barrier (BBB)
 One arm-brain circulation time: 25 secs
 Final plasma concentration of drug depends on:
• Total dose of drug
• Rate of injection
• Cardiac output (=HRxSV)
• Circulating blood volume



 GABA (Gamma-aminobutyric acid) is an inhibitory chemical released from sensory nerve endings
 Once released it attached to GABA receptors on the post-synaptic membrane
 This causes the post-synaptic membrane to become permeable to chloride ions, which has the effect of stabilising the neurone and increasing the threshold for firing
 During this refractory period no further electrical stimuli can be transmitted across the synapse

 Benzodiazepines (BZDs) act throughout the CNS via the GABA network
 BZD receptors are located closed to GABA receptors
 All BZDs have a benzene ring structure on the same position of the diazepine part of each molecule
 It is this common core shape that allows them to attach to the BZD receptor
 A BZD present on the receptor prolongs the time it takes for repolarisation after a neurone has been depolarised by an electrical stimulus

 This further reduces excitatory stimuli reaching the higher centres
 Therefore, BZDs mimic GABA
 There are a range of BZDs
• Agonists (having the desired effect)
• Inverse agonist (having the opposite effect)
• Antagonists (binds to BZD receptor but is pharmacologically inactive)



Effects of BZDs:


 Induce conscious sedation with acute detachment for 20-30 mins and a state of relaxation for a further hour or so
 Amnesia !!!!
 Muscle relaxation !!!!
 Anticonvulsant action
 Minimal cardiovascular and respiratory depression if titrated correctly
 No clinically useful analgesia but sedation may alter patients response to pain

 Respiratory depression
 Synergistic effects between BZDs and other CNS depressants – required dose of BZD may be 25% less if taking opiates
 Rapid IV administration of BZDs may cause apnoea and can be avoided by slow incremental administration
 Some evidence that the laryngeal reflex may be momentarily obtunded immediately following injection of BZD – this is short lived and airway should always be well protected
 RCS Report 1993 says that due to risk of apnoea supplemental O2 should be used in all patients – not universally accepted. Should be considered in older or medically compromised
 BZDs cause minor CVS effects in healthy pts – decrease in vascular resistance causing a fall in BP. This is compensated for by an increase in heart rate and cardiac output so BP is minimally affected
 Elderly pts are particularly susceptible to effects of BZDs – total dose needed is smaller and increments should be smaller
 IV BZDs should be avoided in children – reactions are unpredictable and they can easily become oversedated
 Pts taking BZDs for anxiety or insomnia may be more tolerant of the effect of BZDs
 Pts may get sexual fantasy in IV BZD sedation – usually occurs only when higher than recommended doses are given



Dose Range:

ex: Vallium
Almost insoluble in H2O
Emulsified in soyabean oil
2ml ampoules (5mg/ml) or propylene glycol (valium)
2.5 & 10 mg tabs
Diazemuls best
Propylene glycol is organic solvent – can damage veins & cause pain, thrombophlebitis

Dose Range:
0.1-0.2 mg/kg

Metabolised in liver
Active metabolites:
(T½ = 72hrs) – risk of rebound sedation
Oxazepam (T½ = 6.3hrs)
Excreted via kidney



Dose Range:

ex: Versed
-benzodiazepine medication used for anesthesia, procedural sedation
-produce a calming effect on the brain and nerves
-work by increasing the effect of a certain natural chemical (GABA) in the brain
-eliminated via urine or feces
-effects last from 1 to 6 hours

Water soluble at pH<4.0
When injected becomes lipid soluble at physiological pH and can penetrate BBB
Ampoules of 5ml (1mg/ml)
Non-irritant to veins
2-3x more potent than diazepam
Recovery time faster
97% protein bound, 3% active
Decreased protein binding in elderly (>60yrs inject slowly)

Dose Range:
0.07-0.1 mg/kg

Rapidly metabolised in liver
Some extrahepatic metabolism
Active metabolites:
1-hydroymidazolam – has potency of 20-30% cf midazolam (T½ = 1.25hrs) – no rebound sedation
Oxazepam (T½ = 6.3hrs)
Excreted via kidney as glucuronide


Which LA is used in patients in whom a vasoconstrictor is not required?



General Anaesthesia:

- exerts its main effects on the central nervous system, in contrast to local anaesthetics
-Intra-operative and post-anaesthetic complications more likely to occur during general anaesthesia than during conscious sedation


The aim of anaesthesia during surgery is to induce:

triad of anaesthesia:
1. Unconsciousness
2. Analgesia
3. Muscle relaxation

 No single agent provides all these properties so several categories of drugs are used in combination during surgery


What Anaesthetics Do To The Body:

CNS systems
CVS systems
Respiratory systems

 Decrease CNS activity
• Reduce neuronal activity in the brain and spinal cord
(reduce excitatory and increase inhibitory activity,
especially in reticular activating system)
 Depress cardiovascular, respiratory and other systems


How do general anaesthetics work?

1. Physicochemical theories
2. Structural theories

 A wide variety of agents (ranging from single atoms such as xenon to complex hydrocarbons) can produce insensibility to pain and loss of awareness
 The molecular targets for these different agents do not appear to be the same
-Thus there is probably no single molecular mechanism of action for all anaesthetic agents

1. Physicochemical theories
Anaesthetic effect is exerted through physical / chemical perturbation of structures in the body
- Lipid solubility theory (anaesthetic effect is exerted through some perturbation of the lipid bilayer)

2. Structural theories
Anaesthetic effect is exerted through interactions with proteins
- Effects on ion channels
- Excitatory receptors are inhibited – e.g. Nicotinic acetylcholine
- Inhibitory receptors are potentiated – e.g. GABA A and glycine



Examples of General Anaesthetics:


 Inhalation:
• Isoflurane, Sevoflurane, Desflurane, Halothane
• Nitrous oxide

 Intravenous:
• Thiopental Sodium
-Very high lipid solubility – rapid transfer across blood-brain barrier but accumulation in body (‘hangover’)
- Short duration (due to redistribution)
• Propofol
-Rapid metabolism – rapid recovery – no ‘hangover’
- Can be used alone for induction and maintenance (total intravenous anaesthesia)
• Ketamine
- Dissociative anaesthesia
- Slower onset, longer duration of action
- Significantly different cardiovascular system and respiratory system effect


Inhalation Anaesthetics:

 Level of anaesthesia is correlated with the partial pressure of anaesthetic in brain tissue
 The forward movement of an inhalation agent is driven by a series of partial pressure gradients (agent moves from an area of high pressure to an area of low pressure)

-anesthesia breathed in -> goes in alveoli -> circulates in blood -> moves in brain and other tissues

 Gradients depend on the solubility of the anaesthetic in blood and body tissue
 The solubility of volatiles in different media can be expressed as partition coefficients
 The partition coefficient is a simple ratio of amounts: e.g. the blood/gas coefficient is the ratio of the amount of anaesthetic dissolved in blood to the amount in the same volume of gas in contact with that blood



Inhalation Anaesthetics:

High Solubility in Blood:
Low Solubility in Blood:

High Solubility in Lipid:
Low Solubility in Lipid:

High Solubility in Blood:
-slow induction and recovery
-slow adjustment of anaesthesia depth

Low Solubility in Blood:
-rapid induction and recovery
-rapid adjustment of anaesthesia depth
-the anaesthetic passes quicker in brain b/c of small resevoir

High Solubility in Lipid:
-high oil/gas partition coefficient
-more potent GA

Low Solubility in Lipid:
-low oil/gas partition coefficient
-less potent GA


Intravenous Anaesthetic Agents:

 Enable rapid induction because the blood concentration can be raised quickly
 As non-volatile compounds, intravenous agents cannot be removed from the body by ventilation
 Recovery occurs rapidly as the drug is redistributed around the body
 Metabolism and/or excretion then slowly decreases overall body levels


Intravenous Anaesthetics - Redistribution:

 The drug firstly moves into compartments of the body that are highly perfused and lipid soluble e.g. the brain, bringing on anaesthesia

 The drug then starts to distribute to other less well perfused tissues such as the muscle

 As it moves from the blood into the muscle the blood concentration will fall, so the anaesthetic will start to move back down its concentration gradient from brain into the blood resulting in recovery from anaesthesia



Intravenous anaesthetics Vs Inhalation anaesthetics:

Which anesthesia is responsible for a rapid induction and which is responsible for a maintenance?

Intravenous anaesthetics are the most commonly used drugs for anaesthetic rapid induction in adults

Inhalation anaesthetics are primarily used for the maintenance of anaesthesia


Complications of General Anaesthesia:

During Anaesthesia:
After Anaesthesia:

During Anaesthesia:
- Respiratory depression
- Cardiac arrhythmias (you increase the risk of arrhythmia b/c the anesthetic will go straight to the blood)
- Fall in BP
- Aspiration
- Laryngospasm and asphyxia
- Delirium and convulsion
- Fire and explosion

After Anaesthesia:
- Nausea and vomiting
- Headache
- Persisting sedation
- Pneumonia
- Cognitive defects


Indications of general anaesthesia:

- Acute infection
- Children
- Mentally challenged patients
- Dental phobia
- Allergy to local anaesthetic
- Extensive dentistry, oral and maxillofacial surgery



Local anesthesia is associated with which effect?

a. Tissue irritation
b. Unconsciousness
c. Irreversible onset
d. Loss of sensation

d. Loss of sensation



Which local anesthetic is the strongest vasodilator?

a. Procaine.
b. Prilocaine.
c. Lidocaine.
d. Mepivacaine.

a. Procaine.



Each statement is correct, EXCEPT one. Which is the EXCEPTION?

a. Amide local anesthetics are hydrolyzed in the plasma.
b. Amide local anesthetics cross the blood–brain barrier easily.
c. Ester local anesthetics readily cross the placenta.
d. Ester local anesthetics are more toxic for those with atypical pseudocholinesterase.

a. Amide local anesthetics are hydrolyzed in the plasma.

-esters are hydrolyzed in plasma
-all la cross the placenta and the blood–brain barrier easily


The effect of local anesthesia is prolonged with the addition of a vasoconstrictor because:

a. the risk of local anesthetic toxicity is reduced.
b. bleeding is decreased at the site of administration.
c. the local anesthetic slowly enters the circulatory system.
d. more local anesthetic enters and inhabits the nerve for a longer duration.

d. Correct. The duration of anesthesia is increased with the addition of a vasoconstrictor because more local anesthetic enters the nerve, where it stays for a longer period of time.


Beta receptors produce each of the following EXCEPT one. Which is the EXCEPTION?

a. Vasodilation.
b. Vasoconstriction.
c. Increased heart rate.
d. Stronger cardiac contractions.

b. Vasoconstriction.


Epinephrine decreases which cardiovascular dynamic?

a. Heart rate.
b. Stroke volume.
c. Cardiac efficiency.
d. Systolic blood pressure

c. Cardiac efficiency.

and DBP


Which occurs when a vasoconstrictor is added to most local anesthetics?

a. The depth of hard tissue anesthesia is reduced.
b. The duration of pulpal anesthesia is prolonged.
c. The duration of soft tissue anesthesia is shortened.
d. The depth and duration of hard and soft tissue anesthesia are unaffected.

b. The duration of pulpal anesthesia is prolonged.


Which is an absolute contraindication for local anesthetic use?

a. Renal dysfunction.
b. Cardiovascular disease.
c. Local anesthetic allergy.
d. Atypical plasma cholinesterase.

c. Local anesthetic allergy.


Which action is advised when a relative contraindication for a local anesthetic is discovered?

a. Perform the procedure without anesthesia.
b. Reduce the dosage of the drug in question.
c. Use an alternative drug that is not contraindicated.
d. Proceed with use of the drug in question until complications arise.

c. Use an alternative drug that is not contraindicated.


The duration of anesthesia is decreased when less than the recommended dose of anesthetic is administered. However, excessive amounts will not increase the duration of anesthesia.

a. Both statements are true.
b. Both statements are false.
c. The first statement is true; the second is false.
d. The first statement is false; the second is true.

a. Both statements are true.


Which dose of local anesthetic should be administered to each patient?

a. Maximum recommended dose.
b. Largest clinically effective dose.
c. Smallest clinically effective dose.
d. Manufacturer’s recommended dose.

c. Smallest clinically effective dose.

-this enhances pt's safety


Which is the most likely cause of inadequate local anesthesia?

a. Hyperresponse.
b. Faulty technique.
c. Bad batch of local anesthetic.
d. Consecutive doses within a brief time frame

b. Faulty technique.


Which statement is true?

a. Procaine is an amide local anesthetic.
b. Procaine has a rapid anesthetic onset.
c. Procaine provides no pulpal anesthesia.
d. Procaine produces profound vasoconstriction.

c. Procaine provides no pulpal anesthesia.

-only soft tissue anaesthesia


Which local anesthetic is most likely to elicit a true allergic reaction?

a. Procaine.
b. Lidocaine.
c. Etidocaine.
d. Mepivacaine.

a. Procaine.

-esters cause allergies, not amides



Prilocaine undergoes biotransformation in each place, EXCEPT one. Which is the EXCEPTION?

a. Liver.
b. Lungs.
c. Plasma.
d. Kidneys.

c. Plasma.


The primary purpose of the jet injector is to provide:

a. regional block anesthesia.
b. localized anesthesia in periodontal pockets.
c. topical anesthesia before the insertion of a needle.
d. pulpal anesthesia of one isolated mandibular tooth.

c. topical anesthesia before the insertion of a needle.


The operator applies pressure to which syringe component to deliver anesthetic?

a. Finger grip.
b. Thumb ring.
c. Syringe barrel.
d. Needle adaptor

b. Thumb ring.



The ability to aspirate blood is largely influenced by the

a. gauge of the needle.
b. patient’s blood type.
c. weight of the syringe.
d. type of local anesthetic.

a. gauge of the needle.


Which creates the tip of the needle?

a. Hub.
b. Shaft.
c. Bevel.
d. Lumen.

c. Bevel.


Which is associated with a larger-gauged needle?

a. Less accuracy.
b. Easier aspiration.
c. Greater deflection.
d. Frequent needle breakage.

b. Easier aspiration.


Which statement is correct?

a. The smaller the gauge of the needle, the less exaggerated the deflection.
b. The longer the length of the needle, the greater the degree of deflection.
c. Rotating the needle during penetration and advancement increases deflection.
d. Pressure on a downward-facing bevel causes the needle to deflect downward

b. The longer the length of the needle, the greater the degree of deflection.



Needle breakage occurs at the weakest point, which is where?

a. Tip.
b. Hub.
c. Syringe adaptor.
d. Shaft mid-section.

b. Hub.


The needle penetrates the cartridge through the:

a. stopper.
b. diaphragm.
c. aluminum cap.
d. cylindrical tube.

b. diaphragm.


The dental cartridge should be sterilized before use. Local anesthetic drugs remain stable when autoclaved or boiled.

a. Both statements are true.
b. Both statements are false.
c. The first statement is true; the second is false.
d. The first statement is false; the second is true.

c. The first statement is true; the second is false.


Which amide is safe for oral topical administration?

a. Lidocaine.
b. Articaine.
c. Bupivacaine.
d. Mepivacaine.

a. Lidocaine.

-the only amide sade for oral topical administration


EMLA (eutectic mixture of local anesthetics) is a blend of which two anesthetics?

a. Lidocaine and prilocaine.
b. Benzocaine and lidocaine.
c. Prilocaine and mepivacaine.
d. Mepivacaine and benzocaine.

a. Lidocaine and prilocaine.



After removing the colored needle cap, a few drops of anesthetic are expelled to test for proper flow.

a. few drops of anesthetic are expelled to test for proper flow.
b. confirm adequate harpoon engagement.
c. wet the tip of the needle with anesthetic.
d. remove air bubbles from the cartridge and needle.

a. few drops of anesthetic are expelled to test for proper flow.


Which syringe component is examined, before discarding a needle?

a. Barrel.
b. Harpoon.
c. Thumb ring.
d. Needle adaptor

d. Needle adaptor



Which local anesthetic can induce methemoglobinemia?

a. Articaine.
b. Lidocaine.
c. Prilocaine.
d. Procaine.

c. Prilocaine.


Elective dental care is contraindicated for which ASA classification?

a. 1.
b. 2.
c. 3.
d. 4.

d. 4.


Aspiration is crucial at which point?

a. Before depositing the anesthetic solution at the target site.
b. After burying the bevel of the needle in the surface mucosa.
c. Before injecting several drops of anesthetic solution to advance the needle.
d. During needle advancement, preceding the release of any anesthetic solution.

a. Before depositing the anesthetic solution at the target site.



Which statement is true?

a. The trigeminal nerve is the smallest of the 12 cranial nerves.
b. The motor root of the trigeminal nerve is larger than the sensory root.
c. The motor root of the trigeminal nerve innervates the muscles of mastication.
d. The sensory root of the trigeminal nerve supplies the pharynx and base of tongue.

c. The motor root of the trigeminal nerve innervates the muscles of mastication.


The motor root the trigeminal nerve exits the cranium through which foramen?

a. Ovale.
b. Cecum.
c. Lacerum.
d. Rotundum.

a. Ovale.



Each, EXCEPT one, is a division of the ophthalmic (V1) nerve. Which is the EXCEPTION?

a. Frontal.
b. Lacrimal.
c. Zygomatic.
d. Nasociliary.

c. Zygomatic.

-the other 3 are its branches


The maxillary division of the trigeminal nerve (V2) is:

a. purely motor.
b. purely sensory.
c. primarily sensory, but partially motor.
d. primarily motor, but partially sensory.

b. purely sensory


The maxillary (V2) nerve innervates the skin in which area?

a. Forehead.
b. Upper lip.
c. Upper eyelid.
d. Tip of the nose

b. Upper lip.



The maxillary nerve (V2) exits the cranium through which foramen?

a. Ovale.
b. Magnum.
c. Spinosum.
d. Rotundum.

d. Rotundum.


The nasopalatine injection blocks sensation to which tissues?

a. Bilateral palatal mucosa and bone from canine to canine.
b. Unilateral palatal mucosa and bone from canine to central incisor.
c. Bilateral palatal mucosa and bone from the canines to the border of the soft palate.
d. Unilateral palatal mucosa and bone from the canine to the border of the soft palate.

a. Bilateral palatal mucosa and bone from canine to canine.


The posterior superior alveolar nerve (PSA) usually has:

a. a single trunk.
b. two branches.
c. three branches.
d. four branches.

b. two branches.



Which nerve innervates the maxillary premolars, in a majority of individuals?

a. Middle superior alveolar (MSA).
b. Posterior superior alveolar (PSA).
c. Anterior superior alveolar (ASA).
d. Lesser (middle and posterior) palatine.

a. Middle superior alveolar (MSA).



Which nerve block will most likely anesthetize the buccal soft tissues and bone of the premolar area, when the MSA nerve is missing?

a. Greater (anterior) palatine.
b. Posterior superior alveolar (PSA).
c. Anterior superior alveolar (ASA).
d. Lesser (middle and posterior) palatine.

c. Anterior superior alveolar (ASA).



Which nerve innervates the maxillary lateral incisor?

a. Nasopalatine.
b. Greater (anterior) palatine.
c. Middle superior alveolar (MSA).
d. Anterior superior alveolar (ASA).

d. Anterior superior alveolar (ASA).


The motor root of the mandibular (V3) division innervates which?

a. Tensor veli palatini.
b. Skin of the lower lip.
c. Temporomandibular joint.
d. Mandibular teeth and periodontal tissues.

a. Tensor veli palatini.


The buccal nerve innervates which structure?

a. Lower lip.
b. Buccinator muscle.
c. Corner of the mouth.
d. Buccal gingiva of the mandibular molars.

d. Buccal gingiva of the mandibular molars.


Anesthesia of the inferior alveolar nerve is important for:

a. hard tissue manipulation of the mandibular molars.
b. hard tissue manipulation of the maxillary premolars.
c. soft tissue manipulation of the lingual gingiva of the mandible.
d. soft tissue manipulation of the buccal gingiva adjacent to the mandibular molars

a. hard tissue manipulation of the mandibular molars.


The mental nerve and incisive nerve are terminal branches of the:

a. inferior alveolar nerve (IA).
b. middle superior alveolar nerve (MSA).
c. anterior superior alveolar nerve (ASA).
d. posterior superior alveolar nerve (PSA).

a. inferior alveolar nerve (IA).


The incisive nerve innervates which?

a. Skin of the chin.
b. Mandibular second premolar, and molars.
c. Skin and mucous membrane of the lower lip.
d. Mandibular first premolar, canine, and incisors

d. Mandibular first premolar, canine, and incisors


Which injection technique provides anesthesia for more than one tooth?

a. Intracrestal.
b. Intraosseous.
c. Nasopalatine.
d. Supraperiosteal.

c. Nasopalatine.


Which technique is used most frequently for pulpal anesthesia in the maxilla?

a. Maxillary nerve block.
b. Supraperiosteal injection.
c. Periodontal ligament injection.
d. Posterior superior alveolar nerve block.

b. Supraperiosteal injection.



The posterior superior alveolar nerve does NOT consistently innervate which root?

a. Palatal root of the maxillary third molar.
b. Mesiobuccal root of the maxillary first molar.
c. Distobuccal root of the maxillary second molar.
d. Mesiobuccal root of the maxillary second molar.

b. Mesiobuccal root of the maxillary first molar.


Which penetration site correlates with the MSA nerve block?

a. Height of the mucobuccal fold over the maxillary first molar.
b. Height of the mucobuccal fold over the maxillary second molar.
c. Height of the mucobuccal fold above the maxillary first premolar.
d. Height of the mucobuccal fold above the maxillary second premolar.

d. Height of the mucobuccal fold above the maxillary second premolar.


13. The anterior superior alveolar (ASA) nerve block will NOT anesthetize which?

a. Upper lip.
b. Lower eyelid.
c. Anterior hard palate.
d. Lateral aspect of the nose.

c. Anterior hard palate.


The administrator of an ASA nerve block should:

a. feel the anesthetic solution as it is deposited.
b. feel the needle through the facial skin as it advances toward the target.
c. see 4 mm of the needle when the correct depth of penetration is reached.
d. see a visible swelling or ballooning of the tissues during anesthetic deposition

a. Correct. The administrator will feel the anesthetic through the finger over the infraorbital foramen, where the solution is being injected.


Which nerve block provides bilateral anesthesia?

a. Maxillary.
b. Greater palatine.
c. Anterior middle superior alveolar.
d. Palatal approach-anterior superior alveolar.

d. Palatal approach-anterior superior alveolar.


The greater palatine foramen is usually located:

a. mesial to the maxillary first molar.
b. distal to the maxillary second molar.
c. distal to the maxillary first premolar.
d. mesial to the maxillary second premolar.

b. distal to the maxillary second molar.


Which sequence of injections leads to an atraumatic nasopalatine nerve block?

a. Labial frenum, incisive papilla, interproximal papilla.
b. Interproximal papilla, labial frenum, incisive papilla.
c. Incisive papilla, labial frenum, interproximal papilla.
d. Labial frenum, interproximal papilla, incisive papilla.

d. Labial frenum, interproximal papilla, incisive papilla.


The penetration site of the buccal nerve block is:

a. distal and buccal to the last molar.
b. distal and lingual to the last molar.
c. mesial and buccal to the last molar.
d. mesial and lingual to the last molar.

a. distal and buccal to the last molar.


Bone is gently contacted in each injection, EXCEPT one. Which is the EXCEPTION?

a. Buccal nerve block.
b. Inferior alveolar nerve block.
c. Gow-Gates mandibular nerve block.
d. Vazirani-Akinosi mandibular nerve block.

d. Vazirani-Akinosi mandibular nerve block.



If we want to anesthetize a lower molar tooth which anaesthesia do we use?

inferior alveolar nerve block and lingual n and long buccal n



In what medical conditions is best to avoid the vasoconstrictors?

 Significant cardiovascular disease (ASA 3 &4)
 Thyroid dysfunction, Diabetes, Sulfite sensitivity
 MAO inhibitors, Tricyclic antidepressants, phenothiazides
 No elective dental treatment on patients with Malignant Hypertension, Myocardial infarction, unstable angina – Significant uncontrolled cardiovascular disease
 Contraindicated in patients with clinical evidence of hyperthyroid state
• Signs: exophthalmos, hyperhidrosis, tremor, irritability, increased heart rate and blood pressure



If we want to anesthetize an upper molar tooth which anaesthesia do we use?

posterior superior alveolar nerve block
middle superior alveolar nerve block
greater palatine nerve


Max epinephrine for ASA I patient =
Max epinephrine for cardiac patient =
Max lidocaine without vasoconstrictor =
Max lidocaine with vasoconstrictor =

Max epinephrine for ASA I patient = 0.2mg
Max epinephrine for cardiac patient = 0.04mg
Max lidocaine without vasoconstrictor = 4.4mg/kg
Max lidocaine with vasoconstrictor = 7mg/kg


Allergic response to LA includes: (side effects)

• Dermatitis,
• Bronchospasm
• anaphylaxis