Vasoconstrictors Vasoconstrictors are the drugs that constricts the

blood vessels and thereby control tissue perfusion.

They are added to LA to oppose the vasodilatory action of local anesthetic agent.

Classification of Vasoconstrictors Catecholamines

EpinephrineNorepinephrineDopamine

Noncatecholamines AmphetamineMethamphetaminePhenylephrine

Direct actingEpinephrineNorepinephrineDopaminePhenylephrine

Indirect actingTyramineAmphetamineMethamphetamine

Mixed actingMetaraminolephedrine

Receptors β1, β2, β3, alpha receptorsAlpha receptors:- blood vesselsβ 1:- heart and intestineβ 2:- bronchi, vascular bed, uterusβ3:- brown and white adipose tissue

Alpha receptorsActivation results in vasoconstriction ( blood vessels)

Maximum recommended dose for adrenaline For healthy patients 0.2mg per appointment For cardiac patients 0.04mg per appointment

0.0125mg ---- 1ml0.2mg----1/0.125x 0.2 = 16ml

1:80,000 = 16 ml in healthy patients0.0125mg ---- 1ml0.04mg------1/0.125x0.04 = 3.2ml

1:80,000 = 3.2 ml in cardiac patients

Dilution of vasoconstrictors 1:1000

1 gm/1000ml1000mg/1000ml1mg/ml

1:10,0001000mg/10000ml0.1mg/ml

1:80,0000.0125mg/ml

1:200,000mg/ml0.005mg/ml

1:100,0000.01mg/ml

Felypressin (Citanest forte)

Available as a vasoconstrictor in combination with prilocaine

Acts by directly stimulating vascular smooth muscle

Has little effect on heart or on adrenergic nerve trasmission

Actions more pronounced on venous than arteriolar microcirculation

Epinephrine Norepinephrine

Receptor activity Powerful stimulant of α and β receptorsWith higher doses α effects predominates, whereas lower doses primarily produce β receptor activity

Stimulates both α and β receptors, but α effect predominates

Blood Pressure (BP) Lesser effect Greater increase in BP than epinephrine

Central Nervous System Greater effect of stimulation of central nervous system in large doses

Does not stimulate central nervous system in therapeutic doses

Cardiovascular system Greater effect of stimulation of CVS

Bronchi Dilatation Little or no effect

Heart Rate (HR) Increase in HR is of greater degree

Increase in HR is of lesser degree

Various dilutions available in India and MRD (in terms of m) for normal healthy adult individuals and medically compromised individuals

Dilutions Normal adult healthy individuals

(0.2 mg/appointment)(ml)

Medically compromised individuals

(0.04 mg/appointment)(ml)

1:80,000 16 3.2

1:1,00,000 20 4

1:2,00,000 40 8

What determines the potency of LA?Lipid solubility

What determines the duration of action of LA?Protein binding e.g. Bupivacaine

What determines the onset time of LA?pKa

To what components of LA are patients likely to be allergic?MethylparabenSodium metabisulfiteSulfa drugs(Articaine)latex

What type of LA have greater allergic potential?Esters

How are LA metabolized?Esters:- plasma by pseudocholinesteraseAmide:-in liver by microsomal enzymes

Why is LA often ineffective when injected in area on infectionarea of inflammation

After LA injection anesthetic effect will disappear and re-appear in a definite order. What are the sensation in increasing order of resistance to conduction?Pain < Cold < warm < touch < deep pressure

Toxicity The term toxicity, or toxic overdose, refers to the

symptoms manifested as the result of overdosage or excessive administration of a drug.

This complication depends on a sufficient concentration of the drug in the blood stream to adversely affect the central nervous system, the respiratory system, or the circulatory system.

The blood level necessary to produce a toxic effect may differ for the same drug from individual to individual and in the same individual from day to day.

Toxic effects on the central nervous system

Although local anesthetics used in dentistry have the ability to produce overt signs and symptoms of central nervous system stimulation, the effect is actually produced by depression of certain inhibitory centers.

Depression of inhibitory areas allows excitatory actions to occur unopposed, leading to overt manifestation of central nervous system stimulation.

In subtoxic doses(0.05-4 µg/ml of procaine and lidocaine), local anesthetics may be shown to produce anti-convulsant effects.

Epileptic patients exhibit hyper-excitable neurons at the cortical site from which their seizures originate.

Subtoxic doses of local anesthetics depress these hyper-excitable neurons, thereby producing an anticonvulsant effect.

Cortical stimulation

Medullary stimulation

Cortical depression

Medullary depression

Increasing blood levels of local anesthetics (in the range of 4.0 to 7.0 µg/ml) produce definite clinical signs and symptoms by stimulation of cortex. Signs of this degree of toxicity on cortical centers include

talkativeness, slurred speech, apprehension, localized muscular twitching tremor of the hands and feet. ringing in the ears (tinnitus), difficulty focusing the eyes disorientation

Medullary stimulation occurs at the dose of 7.5-10.0 µg/ml which causes generalised tonic clonic seizures by medullary stimulation.

In excessive medullary stimulation, cardiovascular and respiratory parameters increase.

Usually, respiratory function is totally ineffective during the seizure because of tonic and/or asynchronous contraction of the muscles of respiration.

Following the medullary stimulation, a period of cortical depression occurs.

This period is characterized by cortical depression followed by medullary depression.

Cortical depression is manifested asUnresponsivenessunconsciousnessStuporcoma

Medullary depression results in severe depression of cardiovascular function respiratory depression hypoxia with its subsequent effect on the cardiac

mechanism.

Syncope It refers to a sudden, transient loss of

consciousness usually secondary to cerebral ischemia due to peripheral pooling of blood and reduced cardiac output.

It can be due to;Fright and anxietyEmotional stressPain of sudden and unexpected natureSight of blood

Non psychogenic :-Hunger or starvationPoor physical conditionOvercrowded places

Syncope It is the most frequent complication of associated

with LA in dental office. It is a form of neurogenic shock and is caused by

cerebral ischemia secondary to the vasodilatation with a corresponding drop in blood pressure.

It is not always associated with loss of conciousness.

It should be treated as early as possible. It is characterised by change in patient’s

appearance, such as pallor.

Management of syncope

Any procedure that is going on should be stopped and the chair should be lowered and legs raised (Trendelburg position)

If the patient is conscious, ask for few deep breaths.

Keep a check on pulse, respiration, blood pressure

CPR Cardiopulmonary resuscitation (CPR) is an

emergency procedure for people in cardiac arrest or, in some circumstances, respiratory arrest. 

CPR is performed both in hospitals and in pre-hospital settings.

CPR involves physical interventions to create artificial circulation through rhythmic pressing on the patient's chest to manually pump blood through the heart, called chest compressions, and usually also involves the rescuer exhaling into the patient (or using a device to simulate this) to ventilate the lungs and pass oxygen in to the blood, called artificial respiration

Tilt the head back and listen for breathing.

If not breathing normally, pinch nose and cover the mouth with yours and blow until you see the chest rise.

Give 2 breaths.  Each breath should

take 1 second

If the victim is still not breathing normally, coughing or moving, begin chest compressions.  Push down on the chest 1½ to 2 inches 30 times.  Pump at the rate of 100/minute, faster than once per second.

CPR (when one person is doing):

Chest cpmpression : artificial respiration

4 : 1

CPR (when two persons are doing):

Chest cpmpression : artificial respiration

15 : 2