Vasoconstrictors

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
Epinephrine
Norepinephrine
Dopamine
 Noncatecholamines
Amphetamine
Methamphetamine
Phenylephrine

 Direct acting
Epinephrine
Norepinephrine
Dopamine
Phenylephrine
 Indirect acting
Tyramine
Amphetamine
Methamphetamine
 Mixed acting
Metaraminol
ephedrine

 Receptors β1, β2, β3, alpha receptors
Alpha receptors:- blood vessels
β 1:- heart and intestine
β 2:- bronchi, vascular bed, uterus
β3:- brown and white adipose tissue

 Alpha receptors
Activation 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 ---- 1ml
0.2mg----1/0.125x 0.2 = 16ml
 1:80,000 = 16 ml in healthy patients
0.0125mg ---- 1ml
0.04mg------1/0.125x0.04 = 3.2ml
 1:80,000 = 3.2 ml in cardiac patients

Dilution of vasoconstrictors
 1:1000
 1 gm/1000ml
1000mg/1000ml
1mg/ml
 1:10,000
1000mg/10000ml
0.1mg/ml
 1:80,000
0.0125mg/ml
 1:200,000mg/ml
0.005mg/ml
 1:100,000
0.01mg/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 Stimulates both α and β
β receptors receptors, but α effect
With higher doses α effects predominates
predominates, whereas
lower doses primarily
produce β receptor activity

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

Central Nervous System Greater effect of stimulation Does not stimulate central
of central nervous system in nervous system in
large doses 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 Increase in HR is of lesser
degree 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 Medically compromised
individuals individuals
(0.2 mg/appointment) (0.04 mg/appointment)
(ml) (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?
Methylparaben
Sodium metabisulfite
Sulfa drugs(Articaine)
latex

 What type of LA have greater allergic potential?
Esters
 How are LA metabolized?
Esters:- plasma by pseudocholinesterase
Amide:-in liver by microsomal enzymes
 Why is LA often ineffective when injected in
area on infection
area 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 as
Unresponsiveness
unconsciousness
Stupor
coma



 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 anxiety
Emotional stress
Pain of sudden and unexpected nature
Sight of blood
 Non psychogenic :-
Hunger or starvation
Poor physical condition
Overcrowded 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

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Vasoconstrictors