Local Anesthesia Lec#3 by Malik Al-issa

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Local Anesthesia Lec#3 by Malik Al-issa

Post by Sura on 26/10/2011, 1:03 am

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Pharmacology of Vasoconstrictors

Today we are going to talk about pharmacology of vasoconstrictors, vasoconstrictors are very important since it is the material

We are always worrying about this material or the addition of this material to the local anesthetic solution because it could lead to significant problems in the health of the patients.

For example; a patient with hypotension (especially stage II or III) we always restrict the use of epinephrine in those patients in order to avoid the sudden elevation of blood pressure.

Solution of local anesthetic consists of:

1. Local anesthetic drug itself.

2. The vasopressor.

3. Sodium bisulfate (conservative/preservative material) à prevent the oxidation of vasoconstrictor since it is unstable when it is exposed to the air.

4. Distilled water (all the previously mentioned components are dissolved in it).

Classification of anesthetic agents:

The main structure of the local anesthetic agent:

It is composed of the lipophilic part connected to the hydrophilic part by the intermediate chain (which determines the local anesthetic solution either an ester or amide).

We spoke in the summer course about the plain local anesthetic (without vasoconstrictor); it is mainly hydrochloride salt dissolved in distilled water.

In order to understand the pharmacology of vasoconstrictor; let us see the chemical effect of the local anesthetic solution itself; the pH of the local anesthetic solution without vasoconstrictor (plain local anesthetic) is a little bit close to the normal pH (5.5-7) so we expect a rapid onset (property of plain L.A) after administration of the local anesthetic solution because it does not need time to be modulated to reach the pH of the tissues.

And also this would not lead to a burning sensation during deposition because the pH is close to that of the tissues.

However; there are many properties which are unfavorable; for ex:

The plain local anesthetic (as well as ALL local anesthetics) is a vasodilator; this will lead to a kind of vasodilation, this vasodilation would increase the absorption of the local anesthetic solution into the blood stream which will lead to an increase risk of toxicity.

So in order to balance these unfavorable effects we add a vasoconstrictor, since the vasoconstrictor is unstable when exposed to the air we had to add a preservative which is an acidic material (adding this acidic material is usually referred to as acidification) à so the pH is expected to decrease from 3-4 so far from the pH of the tissue, so the deposition of this local anesthetic with vasoconstrictor would be painful for the patient (uncomfortable) this will also be due to vasoconstriction of blood vessels, which will lead to an increase in the depth of the anesthesia because it is preserved in the tissues as well as long duration.

Because the pH is 3-4 far from the normal pH of the tissues that means that the local anesthetic needs time in order to be modulated to reach the pH of the tissues so the onset of action is expected to be SLOW.

For ex; if u were in a hurry and u have let’s say 10 patients you need a plain local anesthetic; however it does not have a long duration of action.

Types of vasoconstrictors:

Let us start speaking about the chemical structure of the vasoconstrictors; in general we have 2 types of vasoconstrictors that are commonly used in our dental practice:

1. Sympathomimetic / adrenergic drugs (their effect is similar to sympathetic nerve stimulation) à so when u deposit the local anesthetic solution with vasoconstrictor this will lead to an effect similar to the sympathetic nerve stimulation or they act on adrenergic receptors α & β receptors.

These sypathomemtics are divided into 2 types: Catechol = OH, Amine = NH2

I. Catecholamines (this group contains the OH & NH2)

II. Non-catecholamines ( OH group is not present, but NH2 group is present)

2. Non-sympathomimetic drugs (felypressin, synthetic analogue, anti-diuretic hormone those were written in the slides)

They do not act on adrenergic receptors, they are usually indicated where sympathomimetic drugs are contraindicated (for ex; patient that is taking MonoAmine Oxidase Inhibitors MAOIs (patient with psychological problems, hyperthyroidism) we give him Non-sympathomimetic drugs à if u gave him epinephrine patient will suffer from tachycardia (which is a risk but it is a relative contraindication at the same time) so we prefer to use non-sympathomimetic drugs, however it is reported that these non-sympathomimetic drugs are not any safer than epinephrine à for ex; patient with angina cannot undergo any stressful procedure because stress and anxiety could lead to a constriction in the coronary artery and this will precipitate the angina: (some say we should not give the angina patient epinephrine since it can cause constriction in the coronary artery and they suggest we use non-sympathomimetic drugs (felypressin) but it will not provide adequate pain control (not potent); unlike epinephrine,

Note: in angina patients local anesthesia is safer than generalized anesthesia.

Dilutions of Vasoconstrictors:

This is very important, you will be asked in the theatre to combine/construct a solution of local anesthetic agent and epinephrine because there is no carpules, you should combine adequate concentration of each type of drug.

You should know the maximum recommended dose of epinephrine which is 0.2mg = 1/5th of the glass (the glass contains 1mg epinephrine).

The unit of the first figure is usually in gm (grams) so:

1:1000 means 1gm/1000ml solution à this means 1000mg / 1000ml à 1mg / 1ml

When we say 1000mg/1000ml = 1mg/1ml the concentration usually used for cardiac arrest patients (high concentration, S.C or I.M to avoid increased contraction of the heart).

1:10.000 = 1000mg/10.000ml = 0.1mg/1ml this is the most common concentration used in dentistry here in Jordan

1:80.000 = 1000mg/80.000ml =0.0125mg/ml this is the most common concentration used in Britain

1:100.000 = 0.01mg/ml à so 1:80.000 > 1:100.000

1:200.000 = 0.005mg/ml

PREVIOUSLY: if you give the patient local anesthesia with epinephrine it will have no effect on significance) the exogenous epinephrine will have no role.

RECENTLY: it is reported that there will be an increase in the cardiac output and the stroke volume after deposition of local anesthetic solution which includes a vasoconstrictor. This increase in the cardiac output and stroke volume equals that achieved by moderate exercise.

So you have to consider the amount of epinephrine that is present in the carpules.

Adrenergic receptors:

Let’s talk about the site of action; epinephrine can be a vasoconstrictor or a vasodilator depending on the receptors present at the site of deposition. The site of action was first recognized by Ahlquist in 1948 as α & β receptors on smooth muscles.

1. Alpha receptors: activation of these receptors will lead to contraction of blood vessels (some tissues have α receptors others don’t; for ex. Kidneys, mucous membranes, skin have α receptors) so for that reason epinephrine could be used as a vasoconstrictor to the oral cavity.

Some say epinephrine should not be used as a vasoconstrictor because later on there will be a vasodilation!

You have to expect vasodilation 6 hours after the deposition of the local anesthetic with epinephrine because in the oral mucosa there is α receptors and β2 receptors, so the activation initially and predominantly for α receptors (vasoconstriction) and later on there will be an effect on β receptors (vasodilation).

It could be used as an urgent treatment to control the bleeding and identify the site of bleeding, epinephrine does not interfere with the healing of the wound.

For ex; if you extracted a tooth after administration of local anesthetic (ID block), and the patient came back with a bleeding, what should you do?

The very first thing you should do is to assess the vital signs; because bleeding could lead to hypovolemia, tachycardia, bradicardia…

The best way to control bleeding is direct pressure with gauze and wait for 15 minutes if bleeding did not stop, you’d make a suture, if bleeding continues we do hematological investigations (he could be a hemophilic patient, platelet deficiency) à blood transfusion.

ANE: accident and emergency department

2. Beta receptors :

· β1 are found in the heart and small intestine, activation will lead to cardiac stimulation

· β2 are found in the bronchi, vascular bed of skeletal muscles and uterus in slides , activation will lead to bronchodilation à for that reason epinephrine is the drug of choice for an acute asthmatic attack, cardiac arrest patients and anaphylactic shock (for ex; a patient who’s allergic to penicillin’s will suffer from bronchoconstrcition.. why?? Because of laryngeal edema) so we give epinephrine for bronchodilation and corticosteroids for edema.


· Source: epinephrine is normally secreted from the adrenal medulla, the dominant amountof secretion is for epinephrine 80% (in normal situations), in cases of fear, stress and anxiety there will be an increase in the secretion of epinephrine.

Adrenal medulla is only affected by pheochromocytoma when there is an elevation in the secretion of the medulla (epinephrine toxicity).

· Systemic actions:

When we deposit the local anesthetic solution with epinephrine it reaches the blood stream, the tissues, the mucosa and submucosal tissues and its effect is more dominant on α more than β receptors in the skin or mucosa so it would aid in vasoconstriction.

When it reaches the bronchi (there is only β2 receptors) no α no β2 receptors so we can notice bronchodilation.

In the heart there will be a stimulation in the myocardium; increase in systolic blood pressure (systolic blood pressure depends on the activity of the myocardium and the electrical activity of the SA node and the atrioventricular nodes which regulate the electricity of the heart), BUT the diastolic blood pressure is dependent on the peripheral resistance of blood vessels found in the skeletal muscles so it aids in the dilation of the vascular beds there àonce it reaches the skeletal muscles it will exert its effect on β2 receptors causing vasodilation so there will be a fall in diastolic blood pressure but its very temporary and transient, followed by activation of α receptors so that diastolic blood pressure will elevate again.

The final effect of epinephrine will be a slight increase or elevation (not very marked like that of norepinephrine) of diastolic & systolic blood pressure, ↑cardiac output, ↑stroke volume, ↑heart rate, ↑O2 consumption … the overall effect on the heart is the increase in its efficacy.

so for that reason it is used for the treatment of asthmatic attack patients, cardiac arrest patients, or even in local anesthetic carpules.

· Elimination: after distribution it is eliminated in the liver by 2 enzymes called (COMT & MAO) they are present in the liver and used to eliminate epinephrine from the body, 1% of epinephrine is excreted unchanged.

Patients with chronic liver disease, liver failure cirrhosis are relatively contraindicated to epinephrine.

Some say a diabetic patient do not give him epinephrine; well there is a risk but this risk if we gave him 4 carpules consisting of 1:100.000, elevation in blood pressure occurs after administration of 4 carpules à it will lead to vasoconstriction of the hepatic vessels and liberation of glycogen into glucose which will lead to an increase in blood glucose level.

· Availability in dentistry:

Epinephrine is available in dentistry in different concentrations






· Maximum dose: the maximum recommended dose of epinephrine is that contained in 11 carpules for fit and healthy patient (ASA I)

For ex: patient who’s ASA II, ASA III, ASA IV, especially III & IV u can only give him 2 carpules

11 carpules = 0.2 = maximum dose

Note: American Society of Anesthesiologist (ASA) – classification of physical status:

ASA I: a normal, healthy patient.

ASA II: a patient with mild systemic disease or significant health risk factor.

ASA III: a patient with sever systemic disease that is not incapacitating.

ASA IV: a patient with severe systemic disease that is a constant threat to life.

ASA V: a moribund patient who is not expected to survive without the operation.

ASA VI: a declared brain-dead patient whose organs are being removed for donor purposes. Contemporary Oral and Maxillofacial Surgery, P9

Anesthesia sheet number 3

Date of lecture: 5/10/2011

Dr. Al-Shayyab

Malik M. Al-Issa

عدد المساهمات : 484
النشاط : 2
تاريخ التسجيل : 2010-09-29

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