Vasoconstriction Flashcards
amides in general characteristic
vasodilation except cocaine - so they would have a short duration if no addition of vasoconstriction
big difference between LA drug and other drugs
LA - has to stay in area - other drugs go to different target areas
vasoconstrictor - general and what are its advantages
*agent that causes narrowing of the blood vessels
advantages:
1. decrease blood flow to the site of injection
2. prolong and increase the depth of anesthesia
3. reduce the toxic effect of the drug
4. render the area of injection with less bleeding
reduce the toxic effect of the drug?
a vasoconstrictor has this characteristic
same anesthetic max dosage with and without vasoconstriction
less toxic with vasoconstrictor
chemical structure of vasoconstrictor
chemically identical / quite similar to the sympathetic nervous system mediators epinephrine and norepinephrine
*resemble the response of adrenergic nerves to stimulation and are classified as sypathomimetic nerves or adrenergic
catecholamines
ones that we mainly use - epinephrine norepinephrine levonoproterenol isoproternol dopamine
noncatecholamines
still vasoconstrictors but not ones we clinically usually use amphetamine methamphetamine ephedrine phenylephrine
direct acting drugs
exert their action directly on adrenergic receptors IN THE POST SYNAPTIC
Indirect Acting drugs
drug enhances release of catecholamine norepinephrine from adrenergic nerve terminals
neurotransmitter release from the vesicles at the pre-synaptic area
*Tachyphylaxis could occur? or associated with this method of action
mixed acting drugs
act on the pre-synaptic area and enhance release from vesicle - from the adrenergic nerve terminals and also work directly on the post synaptic receptors
vasoconstrictors we use - epi and norepi function in what type of method/action
Direct acting – stimulate the receptors at the post synaptic area
Two types of adrenergic receptors
Alpha –> vasoconstrict
Beta –> vasodilate
activation of alpha receptor by sympathomimetic drug
+ alpha 1 vs alpha 2
stimulates contraction of smooth muscle in vessels = vasoconstrict
alpha 1 = EXCITATORY post-synaptic
alpha 2 = INHIBITORY
- so NE release and Ach release would decrease in release
Beta 1 activation causes
Vasodilate and bronchodilatation and cardiac stimulation
increase in contractility of the heart and lipolysis by small intestine
Beta 2 activation causes
Vascular beds - VESSELS - produces vasodilation
Bronchi - bronchiodilatation * = relaxation
potential contraindication of patient taking non-selective beta blockers and using vasoconstrictors?
*stimulation of B receptors is BLOCKED - so vasodilation or bronchodilatation does NOT occur
this will block the activation of dilation in the VESSELS of the smooth muscle/heart so could increase HR too much in these patients
- giving a vasoconstrictor and wont have the effect of dilation produced normally by the activation of these receptors
overview of administration of epinephrine
Stimulate alpha receptors and beta receptors
alpha – increase in contractility, gluconeogensis in liver and salviary gland secretion
beta - vasodilation of smooth muscle and bronchiodilation
epinephrine works mostly on?
alpha and beta receptors
norepinephrine works mostly on what receptors?
mainly alpha
levonordefrin works on what receptors?
contraindicated - see both occurring
specific characteristics of epinephrine + what is added to it and what are those implications?
as the acid salt it is highly soluble in water
*addition of sodium bisulfite is added to delay deterioration (if allergic rxn occurs it is usually due to this aspect of the drug)
synthetic + secreted from adrenal medulla
acts DIRECTLY on alpha and beta receptors
which receptors predominate with administration of epinephrine?
Beta predominates - which is vasodilation HOWEVER AT HIGH CONCENTRATIONS THE ALPHA predominate – which causes vasoconstriction and why we use it for this with administration of LA (high concentration in area we inject)
but at lower concentrations - beta receptors will dominate
marked increase in systolic pressure when?
epinephrine with alpha receptors
myocardial oxygen consumption?
increases when heart is working more
a systemic effect of epinephrine - increases cardiac output with HR and SV so more oxygen is needed to the heart
epinephrine effect on respiratory
is a potent dilator B2 effect of the smooth muscle of the bronchioles
termination of action of epinephrine
- reuptake by the adrenergic nerves
- inactivation in the blood by the enzyme catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO), both which are present in the liver
COMT and MAO
enzymes that are present in the LIVER - and these break down and elimate the action of epinephrine
max dosage of epinephrine in normal healthy pt.
.2mg per appointment
10 ml per 1:50,000 dilutoin - 5 cartridges
max dosage of epinephrine in ASA III or IV
0.04 mg per appointment
side effects and overdose of epinephrine
CNS stimulation - increases fear, anxiety, tension, resltessness, headache, tremor, weakness
cardiac dysrhythmias
increased systolic
angina
norepinephrine - specific +aka
AKA - levarterenol
relatively stable in acid solution, deteriorating on exposure to light and air
acetone-sodium bisulfite added to retard deterioration
natural and syntehtic forms
actions are 90% alpha and 10% beta
systemic effects of norepinephrine
DECREASED HR - because we increased systolic and diastolic pressures so maintain
*increased total peripheral resistance
most noteable are the increases in systolic (greatest variation) and diastolic and mean arterial pressure with compensatory effect of decreased HR
norepinephrine on respiratory system
does NOT relax bronchial smooth muscle as does epinephrine
termination of norepinephrine
reuptake and its oxidation by MOA
+ exogenous norepinphrine is inactivated by COMT
clinical applications of norepinephrine
in LA as vasoconstrictor + helps with management of hypotension because increases peripheral resistance
max dose of norepi in healthy patient
0.34 mg / appointment
max dose of norepi in ASA III or IV patient
0.14 mg / appointment
Levonodefrin
synthetic vasoconstrictor
direct alpha receptor - stimulation is 75% with some beta activity (25%)
systemic effects are similar to epinephrine but to a lesser degree
weakest vasoconstrictor used in dentistry?
Phenylephrine Hydrochloride
- soluble in water
- direct alpha receptor
- exerts little or no B action on the heart
Felypressin
Synthetic analogue of the antidiuretic hormone vassopressin
acts as a direct stimulant of vascular smooth muscle
*no direct effect on the myocardium - which could be of benefit
relative contraindications
patients with more significant cardiac disease
patients with certain noncardiovascular diseases (thyroid dysfunction, diabetes, sulfite sensativity)
patients receiving MAO inhibitors(drug would not be eliminated in normal fashion), tricyclic antidepresants and phenothiazines
