Local Anaesthesia and Vasoconstrictors Dr. Hassan Abdin Division of Oral & Maxillofacial Surgery.

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Local Anaesthesia Local Anaesthesia and and Vasoconstrictors Vasoconstrictors Dr. Hassan Abdin Dr. Hassan Abdin Division of Oral & Division of Oral & Maxillofacial Surgery Maxillofacial Surgery

Transcript of Local Anaesthesia and Vasoconstrictors Dr. Hassan Abdin Division of Oral & Maxillofacial Surgery.

Local Anaesthesia and Local Anaesthesia and VasoconstrictorsVasoconstrictors

Dr. Hassan AbdinDr. Hassan Abdin

Division of Oral & Maxillofacial Division of Oral & Maxillofacial SurgerySurgery

Local anaesthesiaLocal anaesthesia

Anaesthesia is the loss of Anaesthesia is the loss of consciousness and all form of consciousness and all form of sensation. sensation.

Local Anaesthesia is the local loss of Local Anaesthesia is the local loss of pain, temperature, touch, pressure and pain, temperature, touch, pressure and all other sensation.all other sensation.

In dentistry, Only loss of pain sensation In dentistry, Only loss of pain sensation is desirableis desirable. . Local Analgesia.Local Analgesia.

Local anaesthetic agents:Local anaesthetic agents:

Are drugs that block nerve Are drugs that block nerve conduction when applied locally conduction when applied locally to nerve tissues in appropriate to nerve tissues in appropriate concentrations, acts on any part concentrations, acts on any part of the nervous system, of the nervous system, peripheral or central and any peripheral or central and any type of nerve fibres, sensory or type of nerve fibres, sensory or motor.motor.

Local anaesthesiaLocal anaesthesia

Methods:Methods: Reducing temperatureReducing temperature..

Is used only to produce surface anaesthesia e.g. Is used only to produce surface anaesthesia e.g. ethyl chloride spray.ethyl chloride spray.

PhysicalPhysical damage to nerve trunk e.g. nerve damage to nerve trunk e.g. nerve sectioning.sectioning.

Unsafe for therapeutic uses, only in Trigeminal Unsafe for therapeutic uses, only in Trigeminal Neuralgia.Neuralgia.

ChemicalChemical damage to nerve trunk e.g. damage to nerve trunk e.g. neurolytic agents.neurolytic agents.

Silver nitrate, Phenol - Unsafe for therapeutic use.Silver nitrate, Phenol - Unsafe for therapeutic use.

Local anaesthesiaLocal anaesthesia Methods:Methods: ContCont

Anoxia or hypoxiaAnoxia or hypoxia resulting in lack of resulting in lack of oxygen to nerve.oxygen to nerve.

Unsafe as well.Unsafe as well. Stimulation of large nerve fibresStimulation of large nerve fibres, blocking , blocking

the perception of smaller diameter fibres.the perception of smaller diameter fibres. includes Acupuncture and TENS includes Acupuncture and TENS

(Transcutaneous Electronic Nerve Stimulation) (Transcutaneous Electronic Nerve Stimulation) DrugsDrugs that block transmission at sensory that block transmission at sensory

nerve endings or along nerve fibres.nerve endings or along nerve fibres. There action is fully reversible and without There action is fully reversible and without

permanent damage to the tissues.permanent damage to the tissues.

Local anaesthesiaLocal anaesthesia

Properties of Ideal local Anaesthetic:Properties of Ideal local Anaesthetic: Possess a specific and reversible action.Possess a specific and reversible action.

They stabilize all excitable membrane including They stabilize all excitable membrane including motor neurones motor neurones

CNS is extremely sensitive to its action.CNS is extremely sensitive to its action. Non-irritant with no permanent damage Non-irritant with no permanent damage

to tissues.to tissues. No Systemic toxicityNo Systemic toxicity

High therapeutic ratio.High therapeutic ratio. Rapid onset and long durationRapid onset and long duration Active Topically or by injectionActive Topically or by injection

Local anaesthesiaLocal anaesthesia

Chemistry:Chemistry: They are weak bases, insoluble in waterThey are weak bases, insoluble in water

converted into soluble salts by adding Hcl for clinical use.converted into soluble salts by adding Hcl for clinical use. They are composed of three partsThey are composed of three parts::

AromaticAromatic (lipophilic) residue with acidic group R (lipophilic) residue with acidic group R11..

IntermediateIntermediate aliphatic chain, which is either ester or aliphatic chain, which is either ester or amide link Ramide link R22..

Terminal Terminal aminoamino (hydrophilic) group R (hydrophilic) group R33 and R and R44..

RR33

RR11CO RCO R22 N N

RR44

Classification:Classification:

Classified according to their chemical structures Classified according to their chemical structures and the determining factor is the intermediate and the determining factor is the intermediate chain, into two groups:chain, into two groups:

Ester Ester AmideAmide

They differ in two important respect:They differ in two important respect: Their ability to induce hypersensitivity reaction.Their ability to induce hypersensitivity reaction. Their pharmacokinetics - fate and metabolism.Their pharmacokinetics - fate and metabolism.

Physiochemical properties:Physiochemical properties:

These are very important for local These are very important for local anaesthetic activity.anaesthetic activity.

Ionization:Ionization: They are weak base and exist partly in an They are weak base and exist partly in an

unionized and partly in an ionized form.unionized and partly in an ionized form. The proportion depend on:The proportion depend on:

the pKthe pKa a or dissociation constantor dissociation constant The pH of the surrounding medium.The pH of the surrounding medium.

Both ionizing and unionizing are important in Both ionizing and unionizing are important in producing local anaesthesia. producing local anaesthesia.

Physiochemical properties: Physiochemical properties: (cont.)(cont.)

pKpKa a is the pH at which the ionized and is the pH at which the ionized and

unionized form of an agent are present in unionized form of an agent are present in equal amounts.equal amounts. The lower the pKThe lower the pKa a , the more the unionized , the more the unionized

form, the greater the lipid solubility.form, the greater the lipid solubility. The higher the pKThe higher the pKa a , the more the ionized , the more the ionized

form and the slower the lipid solubility form and the slower the lipid solubility

Physiochemical properties: Physiochemical properties: (cont.)(cont.)

Cont:Cont: Unionized form is able to cross the Unionized form is able to cross the

bi-lipid nerve membrane.bi-lipid nerve membrane.

The ionized form then blocks The ionized form then blocks conduction.conduction.

Some of the unionized inside the cell Some of the unionized inside the cell will become ionized depending upon will become ionized depending upon the pKthe pKa a and the intracellular pH and the intracellular pH (lower than extracellular)(lower than extracellular)

Physiochemical properties: Physiochemical properties: (cont.)(cont.)

Cont:Cont:

In general the amide type have lower In general the amide type have lower pKpKaa, and greater proportion of the drug , and greater proportion of the drug is present in the lipid-soluble is present in the lipid-soluble (unionized) form at the physiological (unionized) form at the physiological pH pH

This produces faster onset of action. This produces faster onset of action. Lignocaine 1 – 2 minutes Lignocaine 1 – 2 minutes Procaine 2 – 5 minutes.Procaine 2 – 5 minutes.

The lower the The lower the pKpKaa the faster the onset. the faster the onset.

Physiochemical properties: Physiochemical properties: (cont.)(cont.)

Partition coefficient:Partition coefficient: This measures the relative solubility of This measures the relative solubility of

an agent in fat and water.an agent in fat and water. High numerical value means:High numerical value means:

High lipid-solubleHigh lipid-soluble less water-soluble.less water-soluble.

More fat solubility, means rapid crossing More fat solubility, means rapid crossing of the lipid barrier of the nerve sheath.of the lipid barrier of the nerve sheath.

The greater partition coefficient, The faster the The greater partition coefficient, The faster the onsetonset

Physiochemical properties: Physiochemical properties: (cont.) (cont.)

Protein binding:Protein binding: Local anaesthetic agents bind with:Local anaesthetic agents bind with:

αα11-acid glycoprotein, which possess high affinity -acid glycoprotein, which possess high affinity but low capacity.but low capacity.

Albumin, with low affinity but high capacityAlbumin, with low affinity but high capacity The binding is simple, reversible and tend The binding is simple, reversible and tend

to increase in proportion to the side chain.to increase in proportion to the side chain. Lignocaine is 64% bound, Bupivacaine is Lignocaine is 64% bound, Bupivacaine is

96%96% The duration of action is related to the The duration of action is related to the

degree of binding. degree of binding. Lignocaine 15 – 45 minutes, Bupivacaine 6 Lignocaine 15 – 45 minutes, Bupivacaine 6

hourshours

Physiochemical properties: Physiochemical properties: (cont.) (cont.)

Vasodilatory ability:Vasodilatory ability: Most Local anaesthetics possess a Most Local anaesthetics possess a

vasodilatory action on blood vessels vasodilatory action on blood vessels except Cocaine.except Cocaine.

It influence the duration of action of the It influence the duration of action of the agent.agent.

Prilocaine is 50% bound to proteins but Prilocaine is 50% bound to proteins but has a longer duration than Lignocaine has a longer duration than Lignocaine (64%) since it possess no strong (64%) since it possess no strong vasodilatory effect.vasodilatory effect.

Affect the duration of action of the agentAffect the duration of action of the agent

Physiochemical properties: Physiochemical properties: (cont.)(cont.)

SummarySummary Rapid Onset:Rapid Onset:

Low Low pKpKaa value– more unionized – Amides value– more unionized – Amides Higher Partition coefficient – more lipid Higher Partition coefficient – more lipid

solublesoluble Long duration of action:Long duration of action:

High protein High protein binding.binding. Low vasodilating property.Low vasodilating property.

Physiochemical properties: Physiochemical properties: (cont.)(cont.)

AgentAgentpKpKaa

%base %base pH 7.4pH 7.4

P-CP-C P-BP-B tt0.50.5 (m)(m)

Max Max dose dose

mg/kgmg/kg

LignocaineLignocaine 7.97.9 2525 33 6464 9090 4.44.4

PrilocainePrilocaine 7.97.9 2525 11 5050 9090 6.06.0

MepivacaiMepivacainene

7.67.6 3333 11 7777 120120 4.44.4

BupivacaiBupivacainene

8.18.1 1717 2828 9696 160160 1.31.3

EtidocaineEtidocaine 7.97.9 2525 141411

9494 160160 8.08.0

ProcaineProcaine 9.09.0 22 0.60.6 66 66 6.06.0

Pharmacodynamics:Pharmacodynamics:Pharmacological actions:Pharmacological actions:

Reversible block of conduction in nerve. Reversible block of conduction in nerve. Direct relaxation of smooth muscle & Direct relaxation of smooth muscle &

inhibition of neuro-muscular inhibition of neuro-muscular transmission in skeletal muscle producing transmission in skeletal muscle producing vasodilatation.vasodilatation.

Intra-arterial procaine reverse Intra-arterial procaine reverse arteriospasm during I.V. Sedationarteriospasm during I.V. Sedation

Class I antidysrhythmic-like action on the Class I antidysrhythmic-like action on the heart.heart.

Stimulation and/or depression of the CNS.Stimulation and/or depression of the CNS.

PharmacodynamicsPharmacodynamics:: Mechanism of Action:Mechanism of Action: (cont.)(cont.)

The site of action is the nerve cell The site of action is the nerve cell membranemembrane

TheoriesTheories:: The membrane expansion theory.The membrane expansion theory. The specific binding theory.The specific binding theory.

Pharmacodynamics:Pharmacodynamics: Mechanism of Action:Mechanism of Action: (cont.)(cont.)

Membrane expansion theory:Membrane expansion theory: A non-specific mechanism similar to the A non-specific mechanism similar to the

action of general anaesthetic agents.action of general anaesthetic agents. Relies upon the lipophilic moiety of local Relies upon the lipophilic moiety of local

anaesthetic agent.anaesthetic agent. The molecules of the agent are The molecules of the agent are

incorporated into the lipid cell membrane.incorporated into the lipid cell membrane.

The resultant swelling produces physical obstruction The resultant swelling produces physical obstruction of the sodium channels, preventing nerve of the sodium channels, preventing nerve depolarization.depolarization.

Pharmacodynamics:Pharmacodynamics: Mechanism of Action: Mechanism of Action: (cont.)(cont.)

Specific receptor theory:Specific receptor theory: Local anaesthetic drug binds to specific receptor within Local anaesthetic drug binds to specific receptor within

the sodium channel producing physical obstruction to the sodium channel producing physical obstruction to entry of sodium ions.entry of sodium ions.

The act of binding produces a conformational changes The act of binding produces a conformational changes within the channel.within the channel.

It bind to a closed gate and maintain it in the closed It bind to a closed gate and maintain it in the closed position.position.

It is, then, essential that the nerve fires, and the It is, then, essential that the nerve fires, and the gate assumes the closed position. (Use-dependant gate assumes the closed position. (Use-dependant phenomenon phenomenon

Fate & Metabolism:Fate & Metabolism:

Absorption:Absorption: Many factors influence entry of local Many factors influence entry of local

anaesthetic into the circulation:anaesthetic into the circulation: Vasodilating ability of the drug.Vasodilating ability of the drug. Volume and concentration.Volume and concentration. Vascularity of the tissues.Vascularity of the tissues. The route of administration.The route of administration. The presence of vasoconstrictorThe presence of vasoconstrictor..

Ester-type drugsEster-type drugs

CocaineCocaine:: The first and most potent local The first and most potent local

anaesthetic agent, rarely used because anaesthetic agent, rarely used because of the problems of misuse.of the problems of misuse.

It is unique in it is ability to produce It is unique in it is ability to produce intense vasoconstriction. Half life 30 intense vasoconstriction. Half life 30 minutes.minutes.

Dosage:Dosage: Used as topical 4 – 10% solutionUsed as topical 4 – 10% solution Maximum dose is 1.5 mg/kg – 100mg max.Maximum dose is 1.5 mg/kg – 100mg max. Used intranasally during apical surgery. Used intranasally during apical surgery.

Ester-type drugsEster-type drugs

Procaine:Procaine: The only indication for its use in dentistry The only indication for its use in dentistry

is in patients with proven allergy to the is in patients with proven allergy to the amide group.amide group.

Used intra-arterially, as part of the Used intra-arterially, as part of the recognized regimen, to treat the recognized regimen, to treat the arteriospasm which might occur during arteriospasm which might occur during intravenous sedation. intravenous sedation.

It has an excellent vasodilatory properties.It has an excellent vasodilatory properties.

Ester-type drugsEster-type drugs Procaine (cont)Procaine (cont)

Onset & duration of Action:Onset & duration of Action: Has a very shot duration (5 minutes) and a long Has a very shot duration (5 minutes) and a long

onset time of 10 minutesonset time of 10 minutes

Dosages:Dosages: The maximum dose is 6 mg/kg, 400 mg max.The maximum dose is 6 mg/kg, 400 mg max. Used as 2% with 1:80 000 epinephrine to Used as 2% with 1:80 000 epinephrine to

increase efficacy.increase efficacy.

Metabolism:Metabolism: Rapidly by plasma esterase.Rapidly by plasma esterase.

Ester-type drugsEster-type drugs

BenzocaineBenzocaine:: Used mainly as topical, due to its poor Used mainly as topical, due to its poor

water solubility, and because of its low water solubility, and because of its low toxicity, it is used in concentration up to toxicity, it is used in concentration up to 20%.20%.

Hydrolyzed rapidly by plasma esterase Hydrolyzed rapidly by plasma esterase to p-aminobenzoic acid accounting for to p-aminobenzoic acid accounting for its low toxicity. its low toxicity.

Fate & Metabolism:Fate & Metabolism:

Metabolism of Ester drugs:Metabolism of Ester drugs: Metabolized in plasma by Metabolized in plasma by

peudocholinesterase enzyme, and some peudocholinesterase enzyme, and some in the liver.in the liver.

People, who lack the enzyme, are at risk People, who lack the enzyme, are at risk of an overdose by the ester type local of an overdose by the ester type local anaestheticanaesthetic

Para-aminobenzoic acid (PABA) is the Para-aminobenzoic acid (PABA) is the major metabolite of ester with no major metabolite of ester with no anaesthetic effect.anaesthetic effect.

It is the agent responsible for ester allergies. It is the agent responsible for ester allergies. Rapid metabolism procaine half-life is 2 Rapid metabolism procaine half-life is 2

minutes minutes

Amide-type drugs:Amide-type drugs:

Lignocaine (Lidocaine):Lignocaine (Lidocaine): Synthesized in 1943 and used in Synthesized in 1943 and used in

dentistry since 1948 and is also known dentistry since 1948 and is also known as Xylocaineas Xylocaine

It highly lipophilic (partition coefficient 3) It highly lipophilic (partition coefficient 3) , rapidly absorbed., rapidly absorbed.

Metabolized only in the liver and its Metabolized only in the liver and its metabolites are less toxic with no action. metabolites are less toxic with no action.

Has half-life (Has half-life (tt0.50.5) of 90 minutes ) of 90 minutes

Amide-typeAmide-type drugsdrugs Lignocaine (cont)Lignocaine (cont)

Dosage:Dosage: 4.4 mg/kg – 300 mg max4.4 mg/kg – 300 mg max

Used as 2% plain or with 1:80 000 epinephrineUsed as 2% plain or with 1:80 000 epinephrine 4 and 10% spray, 2% gel and 5% ointments.4 and 10% spray, 2% gel and 5% ointments.

Onset & duration of action:Onset & duration of action: Rapid onset 2 – 3 minutesRapid onset 2 – 3 minutes Plain- short duration (10 minutes)Plain- short duration (10 minutes) With epinephrine- intermediate duration (45 – 60 With epinephrine- intermediate duration (45 – 60

minutes)minutes)

Amide-type drugsAmide-type drugs

Prilocaine:Prilocaine: A very potent local anaesthetic and is less A very potent local anaesthetic and is less

toxic than Lignocaine.toxic than Lignocaine. It produces less vasodilatation than lignocaine It produces less vasodilatation than lignocaine Rate of clearance is higher than other amide-Rate of clearance is higher than other amide-

types, suggesting extra-hepatic metabolism types, suggesting extra-hepatic metabolism with relatively low blood concentration.with relatively low blood concentration.

It’s metabolite o-toluidine lead to methaemo-It’s metabolite o-toluidine lead to methaemo-globinaemia globinaemia (more than 600 mg in adults) (more than 600 mg in adults)

Amide-type drugsAmide-type drugsPrilocaine:Prilocaine:

Used either plain 4% or 3% combined with Used either plain 4% or 3% combined with 0.03IU/mL of Felypressin as vasoconstrictor.0.03IU/mL of Felypressin as vasoconstrictor.

Onset & Duration:Onset & Duration: Slower onset – 4 minutes.Slower onset – 4 minutes. It’s duration of action is similar to Lignocaine.It’s duration of action is similar to Lignocaine.

Dosage;Dosage; 6.0 mg/kg – max. 400 mg.6.0 mg/kg – max. 400 mg.

Combined with Lignocaine as a topical Combined with Lignocaine as a topical anaesthetic agent to be used prior to vene-anaesthetic agent to be used prior to vene-section and during dental sedation in section and during dental sedation in children.children.

Amide-type drugsAmide-type drugs

Mepivacaine:Mepivacaine: Possess the least vasodilating effect.Possess the least vasodilating effect. Metabolized in the liver and has Metabolized in the liver and has tt0.50.5 of 120 of 120

minutes.minutes. It’s main indication is when local It’s main indication is when local

anaesthetic without vasoconstrictor is anaesthetic without vasoconstrictor is needed. 3% plain is more effective than needed. 3% plain is more effective than lignocaine.lignocaine.

Onset & duration:Onset & duration: Rapid onset but slightly shorter duration.Rapid onset but slightly shorter duration.

Amide-type drugsAmide-type drugs

BupivacaineBupivacaine:: A long-acting local anaesthetic agent, with a A long-acting local anaesthetic agent, with a

tt0.50.5 of 160 minutes due grater binding capacity of 160 minutes due grater binding capacity to plasma protein and tissue proteinsto plasma protein and tissue proteins

Metabolized in the liver.Metabolized in the liver. Used mainly in Oral surgical procedures for its Used mainly in Oral surgical procedures for its

long-lasting pain control.long-lasting pain control. Longer onset and longer duration Longer onset and longer duration (Regional 6 – 8 (Regional 6 – 8

hors)hors) Dosage:Dosage:

1.3 mg/kg – Max 90 mg1.3 mg/kg – Max 90 mg 0.25 – 0.75% with or without adrenaline 1:200 0000.25 – 0.75% with or without adrenaline 1:200 000

Amide-type drugsAmide-type drugs

EtidocaineEtidocaine:: A long-acting agent similar to A long-acting agent similar to

Bupivacaine but with faster onset.Bupivacaine but with faster onset. Metabolized in the liver. Metabolized in the liver. Dosage:Dosage:

8 mg/kg – Max 400 mg8 mg/kg – Max 400 mg 1.5% with 1:200 000 epinephrine.1.5% with 1:200 000 epinephrine.

Lignocaine is the most common used agent both Lignocaine is the most common used agent both topically and by injection as 2% with or without topically and by injection as 2% with or without adrenaline, with a maximum dose of 4.4 mg/kg.adrenaline, with a maximum dose of 4.4 mg/kg.

Fate & Metabolism:Fate & Metabolism:

Amide Drugs:Amide Drugs: metabolized in the liver, except metabolized in the liver, except

Prilocaine which undergo some Prilocaine which undergo some biotransformation in the kidney and biotransformation in the kidney and lungs.lungs.

Some of the metabolites possess local Some of the metabolites possess local anaesthetic and sedative properties. anaesthetic and sedative properties.

Normal local anaesthetic dose in patient with Normal local anaesthetic dose in patient with impaired liver function will result in relative impaired liver function will result in relative overdosage. overdosage.

Old age patient shows reduction in liver Old age patient shows reduction in liver function function

Reduce doseReduce dose

VasoconstrictorsVasoconstrictors

Originally added to reduce systemic Originally added to reduce systemic uptake in an attempt to limit toxicity.uptake in an attempt to limit toxicity.

Prolong the duration Prolong the duration Produces profound anaesthesia.Produces profound anaesthesia. Reduce operative bleeding.Reduce operative bleeding.

Two types:Two types: Sympathomimetic naturally occurring.Sympathomimetic naturally occurring. Synthetic polypeptides, FelypressinSynthetic polypeptides, Felypressin

VasoconstrictorsVasoconstrictors

EpinephrineEpinephrine: (Adrenaline): (Adrenaline) Uses in dentistry:Uses in dentistry:

Local anaesthetic solution.Local anaesthetic solution. Gingival retraction cords.Gingival retraction cords. In the ER as life-saving drug in anaphylaxis.In the ER as life-saving drug in anaphylaxis.

Mechanism of action:Mechanism of action: Interact with adrenergic receptors in the vesselsInteract with adrenergic receptors in the vessels

αα1 & 1 & αα2 2 producing vasoconstriction in skin & MMproducing vasoconstriction in skin & MM ββ2 2 stimulation causing vasodilatation in skeletal stimulation causing vasodilatation in skeletal

muscles.muscles.

VasoconstrictorsVasoconstrictors EpinephrineEpinephrine

Metabolism:Metabolism: Appears very rapidly in the systemic Appears very rapidly in the systemic

circulation !!! circulation !!! Exogenously administered epinephrine Exogenously administered epinephrine

is metabolized extraneuronal and 1% is is metabolized extraneuronal and 1% is excreted in the urine unchanged.excreted in the urine unchanged.

Dosage:Dosage: 1:80,000 is the commonest dose used, 1:80,000 is the commonest dose used,

12.5 12.5 µg/mlµg/ml

VasoconstrictorsVasoconstrictors EpinephrineEpinephrine

Systemic effect:Systemic effect: Being a naturally occurring hormone, it Being a naturally occurring hormone, it

exert a number of physiological exert a number of physiological responses on the different systems.responses on the different systems.

The heart:The heart: Has direct and indirect action.Has direct and indirect action.

Direct action on Direct action on ββ11 receptors increases the rate receptors increases the rate and force of contraction raising cardiac output.and force of contraction raising cardiac output.

Indirect action, increase pulse and cardiac Indirect action, increase pulse and cardiac output, lead to rise in systolic blood pressure, output, lead to rise in systolic blood pressure, (not with dental dose)(not with dental dose)

VasoconstrictorsVasoconstrictors EpinephrineEpinephrine

Blood vessels:Blood vessels: Contain Contain αα11,, αα22 andand ββ2 2 adrenoreceptors adrenoreceptors

in the vessels of the skin, mucous in the vessels of the skin, mucous membrane and skeletal muscles.membrane and skeletal muscles.

αα11 receptors causes vasoconstriction receptors causes vasoconstriction

since they are susceptible to endogenous since they are susceptible to endogenous nor-epinephrine and exogenous nor-epinephrine and exogenous epinephrine. Reduce operative bleedingepinephrine. Reduce operative bleeding

VasoconstrictorsVasoconstrictors EpinephrineEpinephrine

αα22 receptors are only susceptible to receptors are only susceptible to circulating epinephrine.circulating epinephrine.

ββ2 2 found in the skeletal muscles, found in the skeletal muscles, and very uncommon in the skin and and very uncommon in the skin and mucous membrane. mucous membrane. ββ22 stimulation stimulation result in vasodilatation, lowering result in vasodilatation, lowering peripheral resistance and a fall in peripheral resistance and a fall in the diastolic blood pressure. (with the diastolic blood pressure. (with dental dose)dental dose)

VasoconstrictorsVasoconstrictors EpinephrineEpinephrine

Haemostasis:Haemostasis: The vasoconstricting effect.The vasoconstricting effect. Adrenaline promote platelets aggregation in the Adrenaline promote platelets aggregation in the

early stages.early stages. Fibrinolytic activity compromise clot stability. Fibrinolytic activity compromise clot stability.

Lungs:Lungs: Stimulation of Stimulation of ββ22 receptors in the lung lead to receptors in the lung lead to

bronchial muscle relaxation, life-saving in bronchial bronchial muscle relaxation, life-saving in bronchial (spasm) constriction during anaphylactic reaction.(spasm) constriction during anaphylactic reaction.

Wound healing:Wound healing: Reduced local tissue oxygen tension.Reduced local tissue oxygen tension. Epinephrine-induced fibrinolysis. Epinephrine-induced fibrinolysis.

VasoconstrictorsVasoconstrictors

Felypressin:Felypressin: It is an analogue of the naturally occurring It is an analogue of the naturally occurring

Vasopressin.Vasopressin. Bind to vasopressin VBind to vasopressin V11 receptor in the vascular receptor in the vascular

smooth muscle producing vaso-constriction and smooth muscle producing vaso-constriction and reduce local blood flow.reduce local blood flow.

Less potent than the catecholamines &poorer Less potent than the catecholamines &poorer control of bleeding during operative procedures.control of bleeding during operative procedures.

Acts on the venous side rather than the arterial Acts on the venous side rather than the arterial side.side.

Dose:Dose: 0.03 IU/ml (0.54 0.03 IU/ml (0.54 µg/ml)µg/ml)