Pain Control Final Flashcards
Pharmacology Structure: Explain the different parts
So theres going to be a lipophilic part and a hydrophilic part. The lipophilic part is the largest aromatic structure and this structure is responsible for action on the nerve
The hydrophllic part is an amino acid derivative and this is responsible for diffusion through the soft tissue
the lipophilic part and the hydrophilic part are connected by an intermediate chain which is either an ester or amide link
Describe the chemical characteristics using the terms water solubility and lipid solubility
These structures are WEAK BASES and have poor water solubility. They combine with weak acids to form soluble salts
-WATER SOLUBILITY: allows drug to be injected into the interstitial tissue
-LIPID SOLUBILITY: allows the drug to traverse the neuronal membrane
*note from lecture: structures are BOTH water soluble and lipid soluble depending on the phase
Local Anesthetic Action:
There is an equilibrium between a ______ and a ________. What is the proportion determined by?
Equilibrium exists as a quaternary salt (BH+) and a tertiary base (B)
The proportion is determined by the pKA and pH of the tissue.
*recall that the lipid soluble base (B) penetrates through the NEURONAL membrane and EPINEURIUM
What’s the mechanism of action?
Bascially the RNH+, hydrophilic positively charged quaternary salt wl bind to the sodium channel.
By binding to the sodium channel it prevents increase of permeability of nerve membrane to SODIUM (Na+)
As a result, action potential propagation is prevented
What are the two most important factors that affect the ONSET of ACTION of local anesthestics?
the pKa and pH of tissue
The lower the tissue pH the ______ rate of onset
The lower the tissue pH the SLOWER rate of onset
And, the HIGHER the pKa the SLOWER the onset of action
The more acidic the tissue youre injecting into, the _______ the onset of action
Slower
Bupivacaine has a ________(fast/slow) onset of action compared to other agents because of its _____________
Bupivacaine has a SLOW onset of action compared to other agents because of its GREATER degree of ionization at physiologic pH.
pKa of Bupivacaine is ______
percent base (RN) at pH 7.4 is _____
pKa of Bupivacaine is 8.1
perfect base at pH 7.4 is 17%
The higher the pKa the slower onset of action
Which of the three branches of the trigeminal nerve is both motor and sensory?
The mandibular division.
Fascicles are found in which layer of a nerve?
The perineurium
What are the four types of nerve fibers and respective conduction velocities?
- A-alpha (myelin) 70-120
- A-beta (myelin). 35-170
- A-delta (thin myelin) 2.5-3.5
- C (unmyelinated). 0.7-1.5
Match the following nerve fibers with the type of stimulus
- A-beta fibers
- A-delta fibers
- C fiber
a. Noxious mechanical stimulus
b. Non-noxious mechanical stimulus
c. Noxious heat and chemical stimuli
A-beta fiber = non-noxious mechanical stimulus
A-delta fiber = noxious mechanical stimulus
C fiber = noxious heat and chemical stimuli
What are the different types of nerve fascicular patterns? Trigeminal nerve possess what fascicular pattern?
Monofascicular (1 fascicle)
Oligofascicular (2-10)
Polyfascicular (more than 10 fasicles)
The trigeminal nerve is polyfascicular
What are the motor functions of V3? (there are 8 muscles you need to know)
Muscles of mastication: Masseter, temporalis, medial pterygoid, later pterygoid
Swallowing muscles: tensor veli palatini, tensor tympani, mylohyoid, anterior belly of digastric
memorize this
The trigeminal/gasserian/semilunar ganglion contains cell bodies of ONLY _____
Contains cell bodies of ONLY SENSORY trigeminal nerve fibers
The motor root cell bodies arise in the ___________
motor nucleus of the pons and medulla oblongata
The trigeminal/gasserian/semilunar ganglion is located where
Located in Meckel’s cave
State the specific exit points of the skull for each of the 3 branches of the sensory root trigeminal ganglion
- V1 opthalmic = superior orbital fissure
- V2 maxillary = foramen rotundum
- V3 mandibular = foramen ovale
What are the branches of V1
- nasociliary
- lacrimal
- frontal
Describe the motor and sensory functions of V3
Motor: motor to 8 muscles (muscles of mastication and muscles of swallowing)
Sensory: Taste is from chorda tympani branch of facial nerve and rubs with lingual nerve
Describe the structure of local anesthetics and which part of the structure is responsible for what action
- First, theres a hydrophilic part and a lipophilic part
- the hydrophilic part (amino derivative) is responsible for diffusion through soft tissue
- the lipophilic part is the largest part and is an aromatic structure. Its responsible for the actual action on the nerve
- There is an ester or amide link connecting the two
True or false: Local anesthetics are strong bases and have poor water solubility
false. They are weak bases and have poor water solubility
Explain the difference between water solubility and lipid solubility
Water solubility allows for drug to be injected into interstitial tissue
lipid solubility allows drug to traverse neuronal membrane
Describe local anesthetic action
Local anesthetics have two forms, a quaternary salt (BH+) and a tertiary base (B). The balance between these forms depends on the tissue’s pH and the drug’s pKa.
The lipid-soluble base (B) can pass through the outer covering of nerves (neuronal membrane) and the surrounding protective layer (epineurium).
Once inside the nerve, the ionized quaternary form (BH+) blocks the sodium channel, preventing nerve impulses and causing numbness.
So, the drug’s ability to go through the nerve’s protective layers and its effectiveness in blocking the sodium channel depend on its chemical forms and the pH of the surrounding tissue.
Describe the mechanism of action of local anesthetics
In simple and easy-to-remember terms:
The local anesthetic (L.A.) has a positively charged part (RNH+), which is attracted to the sodium channels on nerves.
When the L.A. binds to the sodium channels, it stops them from allowing sodium into the nerve cells.
Without the influx of sodium, the nerve cannot send signals, and this prevents the transmission of pain or sensation, leading to numbness in the area where the L.A. was applied.
The most important factors affecting onset of action are
pKa and pH of tissue
Describe the most important factors affecting onset of action of local anesthetics
When local anesthetics are used, their effectiveness depends on two main factors: the pKa of the drug and the pH of the tissue.
Local anesthetics exist in two forms: a lipophilic base (RN) and a hydrophilic positively charged cation (RNH+).
These two forms coexist together in a solution, and the proportion of each form depends on the pH of the environment.
To determine the balance between the two forms, we use the Henderson-Hasselbalch equation.
The lower the tissue pH (more acidic the environment), the slower the onset of the local anesthetic’s action.
Similarly, the higher the pKa of the drug, the slower the onset of its action.
In summary, the pH of the tissue and the pKa of the drug influence the local anesthetic’s effectiveness and how quickly it starts working.
rank the following agents from fastest to slowest onset of action
articaine, bupivacaine, procaine, prilocaine, lidocaine, mepivacaine, benzocaine
remember that higher pka means slower onset of action
- Benzocaine
- Mepivacaine
- Lidocaine
- Prilocaine
- Articaine
- Bupivacaine
- Procaine
Describe diffusion through soft tissue of a local anesthetic
The onset of action of a local anesthetic depends on its pKa and how easily it can diffuse through soft tissues.
If a local anesthetic has a high pKa (like procaine with a pKa of 9.1), there are very few free base molecules available to diffuse into the nerve cells. As a result, the onset of its action is slow.
On the other hand, if a local anesthetic has a lower pKa (less than 7.5), it has more lipophilic free base molecules available. This means it can more easily diffuse into the nerve cells, leading to a faster onset of action.
The pH of the fluid around the nerves (extracellular fluid) also plays a role. An acidic pH slows down the diffusion of the local anesthetic through the soft tissues. This can further affect the speed at which the anesthesia takes effect.
In summary, a local anesthetic with a low pKa and an environment with a neutral or slightly basic pH allows for better diffusion through soft tissues and leads to a quicker onset of action.
List all the factors affecting onset (hint there are 7)
-pH of tissue
-pKa of the anesthetic
-diffusion distance from needle to nerve
-nerve morphology, thin pain fibers
-concentration of drug
-volume injected
-lipid solubility
Describe local anesthetic action in local tissue beds (basically explain amides and esters in terms of their vasodilating qualities)
The effect of local anesthetics on blood vessels in the local tissue can be summarized as follows:
Amides: Most amide-type local anesthetics cause blood vessels to dilate to some extent. Among them, mepivacaine may be the least potent vasodilator.
Esters: Esters, on the other hand, are powerful vasodilators. Among them, procaine is so potent that it can even be used for intra-arterial injections, which means injecting it directly into an artery.
Cocaine: Cocaine is a unique exception among local anesthetics. It actually causes vasoconstriction, meaning it makes blood vessels narrow. This effect occurs because cocaine inhibits the uptake of catecholamines (such as norepinephrine) in the nerve endings, leading to an excess of free norepinephrine. This results in prolonged vasoconstriction, which can have specific medical uses.
So, to summarize, amides usually cause mild vasodilation, esters are potent vasodilators, and cocaine is a special case that produces vasoconstriction.
Describe pharmacokinetics absorption/uptake
How a local anesthetic is absorbed and taken up by the body depends on where it is injected:
Soft tissue injection: The rate of uptake (how quickly the drug is absorbed) depends on the blood supply (vascularity) and the drug’s effect on blood vessels (vasoactivity). More blood flow and vasoactivity lead to faster uptake.
Mucosal injection: When the local anesthetic is injected into mucous membranes (like the trachea), it is rapidly absorbed because these tissues have a lot of blood vessels. However, absorption is slower in the pharynx and gastrointestinal (GI) tract, and a significant amount of the drug can be metabolized by the liver before it reaches the systemic circulation (hepatic first pass).
Skin: Local anesthetics are not absorbed well through intact skin. They need to be applied using specialized techniques or combined with other agents to enhance skin penetration.
In summary, the rate of uptake of a local anesthetic depends on the vascularity and vasoactivity of the injection site. Mucosal tissues absorb the drug quickly, while the intact skin is not an efficient route for absorption.
Explain the biotransformation of Esters
In simple and easy-to-remember terms:
Biotransformation of ester-type local anesthetics involves hydrolysis by pseudocholinesterases in the vascular system.
The rate of hydrolysis affects the potential toxicity of the drug.
For example, procaine gets broken down into a by-product called PABA, which is then excreted in the urine.
Allergic reactions to ester-type local anesthetics are often caused by PABA.
In some rare cases (1 in 2800 patients), individuals have atypical cholinesterase, which results in slowed hydrolysis and biotransformation of these drugs.
These patients may also have issues with succinylcholine, another drug used during anesthesia.
In summary, ester-type local anesthetics are broken down by pseudocholinesterases in the body, and the rate of this breakdown affects their potential side effects and toxicity. Allergic reactions are related to the by-products of this breakdown, and some individuals may have a genetic condition that affects the breakdown of these drugs.
Biotransformation of esters refers to the process by which ester-type local anesthetics are broken down or metabolized in the body. Esters are a specific type of chemical structure found in certain local anesthetic drugs.
When ester-type local anesthetics are administered, they undergo biotransformation, which involves enzymatic reactions that break down these drugs into simpler compounds. The primary enzyme responsible for this breakdown is called pseudocholinesterase, also known as plasma cholinesterase.
Pseudocholinesterase breaks ester-type local anesthetics into their individual components, which are then eliminated from the body through urine or other excretion pathways. One common by-product of this breakdown is para-aminobenzoic acid (PABA), which is produced when procaine (a type of ester) is metabolized.
The process of biotransformation is essential for the body to clear local anesthetics and prevent their accumulation, which could lead to toxicity or side effects. Biotransformation helps the body efficiently eliminate these drugs and restore normal physiological conditions after the anesthesia wears off.
Explain the biotransformation of Amides
In simple and easy-to-remember terms:
Biotransformation of amide-type local anesthetics occurs mainly in the liver.
The liver is responsible for breaking down amides like prilocaine and articane.
Prilocaine is primarily metabolized in the liver, with some also being metabolized in the lung.
Articane is mainly metabolized in the liver, but a small amount is metabolized in the blood by plasma cholinesterase because of its ester side chain.
Certain health conditions that affect liver function can slow down the biotransformation process:
Low hepatic blood flow (e.g., in hypotension, congestive heart failure) can reduce the rate of transformation.
Cirrhosis, a liver disease, can also slow down the transformation of amide-type local anesthetics.
When biotransformation is slower, the local anesthetic remains in the body for a longer time, which may increase the risk of potential toxicity.
In summary, amide-type local anesthetics are primarily broken down in the liver, and conditions that affect liver function can slow down this process, leading to a higher risk of toxicity if the drug accumulates in the body.
Name some ACTIVE biotransformation products
short answer: prilocaine=orthotoludine=methhemoglobinenemia
lidocaine=metabolites can produce sedation
When certain local anesthetics are broken down in the body, they produce active by-products that can have specific effects:
Prilocaine: The primary by-product of prilocaine is called orthotoluidine. This by-product can cause the formation of methemoglobin, which can be harmful in large quantities and lead to a condition called methemoglobinemia, affecting the oxygen-carrying capacity of blood.
Lidocaine: Lidocaine gets broken down into two active metabolites called monoethylglycinexylide and glycine. These metabolites can have a sedative effect, causing a feeling of drowsiness or relaxation.
So, the biotransformation of prilocaine can produce a by-product that affects blood oxygen levels, and the breakdown of lidocaine can result in active compounds that can induce sedation.
Explain the central nervous system effects
In simple and easy-to-remember terms:
When local anesthetics affect the Central Nervous System (CNS), they primarily cause depression, which means they slow down brain activity.
At therapeutic levels (the right dosage used for medical purposes), the CNS effects are generally not significant, and patients experience numbness and pain relief without severe side effects.
However, at toxic levels (when too much of the local anesthetic is present in the body), the CNS effects can become more severe and include tonic-clonic convulsions, which are intense and involuntary muscle contractions leading to seizures.
Other CNS effects of toxic levels may include slurred speech, shivering, numbness around the mouth and tongue, warm skin, twitching, dizziness, auditory disturbances, drowsiness, and disorientation.
So, it’s important to carefully administer the right dosage of local anesthetics to avoid toxic CNS effects and provide safe and effective pain relief.
Explain anesthetic effects on the cardiovascular system
Local anesthetics can affect the Cardiovascular System and the electrical events in the heart.
The main effects on the heart are:
Myocardial depression: Local anesthetics can slow down the activity of the heart muscle, leading to decreased heart rate and a reduction in the force of contraction.
Decrease in electrical excitability: Local anesthetics decrease the electrical excitability of the heart muscle cells. This means that the cells are less responsive to electrical signals, leading to a decrease in the heart’s conduction rate, which can affect the heart’s rhythm.
In summary, local anesthetics can cause myocardial depression, slowing down the heart’s activity and reducing its electrical excitability, which can affect the heart’s rhythm and contractile force. These effects should be carefully monitored, especially when using local anesthetics in patients with pre-existing heart conditions.
Explain local tissue toxicity of anesthetics
Local anesthetics can sometimes cause irritation and temporary changes in the tissues they are injected into.
Skeletal muscle tissue is most susceptible to this local tissue toxicity.
Local tissue irritation is more common with longer-acting local anesthetics.
The good news is that these changes are usually reversible, and the affected tissues typically return to normal within two weeks.
In summary, local anesthetics may cause temporary irritation in the tissues they are injected into, especially in skeletal muscle tissue. However, these changes are not permanent and generally resolve within two weeks. It’s essential to choose the right type and dose of local anesthetic to minimize the risk of local tissue toxicity.
Describe the therapeutic use of local anesthetics
Local anesthetics like lidocaine and procainamide can have therapeutic effects on the cardiovascular system, specifically for managing certain heart rhythm problems.
Lidocaine:
Most widely used and studied local anesthetic for cardiac purposes.
Effective blood levels range from 1.8 to 6 micrograms/ml.
After administering two carpules, blood levels are around 0.5 to 2 micrograms/ml.
A typical dosage is 1 to 1.5 mg per kilogram of body weight.
Used to manage premature ventricular contractions (PVCs) and ventricular tachycardia (V.Tach).
Procainamide:
Similar to procaine but with an amide linkage, which makes it act differently.
Procainamide is transformed much more slowly in the body compared to procaine.
In summary, lidocaine is commonly used and studied to manage heart rhythm problems, and the effective blood levels are carefully monitored. Procainamide, which is related to procaine, acts differently and is metabolized more slowly in the body. These local anesthetics have specific therapeutic applications in treating certain cardiac conditions.
Explain Potency
Potency refers to a drug’s ability to stop nerve transmission effectively. It’s a way to compare the strength of one drug to another.
For example, if we say 5mg of oxycodone is equivalent to 60mg of codeine, it means oxycodone is 12 times more potent than codeine.
In the case of local anesthetics, their potency is determined by their lipid solubility. The more lipid-soluble a local anesthetic is, the lower concentration is needed to achieve the desired effect.
In summary, potency is about comparing the strength of different drugs, and lipid solubility determines how much of a local anesthetic is needed to be effective. A more lipid-soluble local anesthetic requires a lower concentration to do its job well.
Rank the following agents from most to least potent and define potency
mepivacaine
bupivacaine
lidocaine
prilocaine
articaine
Potency refers to how well a drug can stop nerve signals.
It’s a way to compare the strength of one drug to another.
For local anesthetics, their potency depends on their lipid solubility. The more lipid-soluble a local anesthetic is, the lower concentration is needed to be effective.
In summary, potency measures a drug’s ability to block nerve signals, and for local anesthetics, lipid solubility determines their strength—the more lipid-soluble, the more potent at lower concentrations.
Ranking from most to least
1. Bupivacaine
2. Lidocaine
3. Prilocaine = articaine
4. Mepivacaine
compare and contrast lidocaine base (5%) to lidocaine gel (2%) as a topical anesthetic
Lidocaine base has poor water solubility, indicated on ulcerated, abraded, or lacerated tissues
Lidocaine gel is water soluble, penetrates tissues better than the base but greater risk for toxicity
both are hypoallergenic
In simple and easy to remember terms:
Lidocaine is a topical anesthetic available in two forms:
Lidocaine Base (5%):
Poorly dissolves in water.
An amide-type local anesthetic.
Considered hypoallergenic, meaning it’s less likely to cause allergic reactions.
Suitable for use on ulcerated, abraded, or lacerated tissues.
Lidocaine Gel (2%):
Water-soluble formulation of lidocaine.
Also an amide-type local anesthetic.
Hypoallergenic like the lidocaine base.
It can penetrate tissues more effectively than the base, but this also means there’s a greater risk of toxicity if too much is used.
In summary, lidocaine comes in two forms: the base and the gel. The base is less soluble in water but is safe for use on damaged tissues. The gel is water-soluble and penetrates tissues better, but it requires more caution to avoid excessive use and potential toxicity. Both forms are considered hypoallergenic, meaning they are less likely to cause allergic reactions.
Describe the purpose and effects of vasoconstrictors
In simple and easy-to-remember terms:
Vasoconstrictors are substances used in combination with local anesthetics for several purposes and effects:
Decrease blood flow to the injection site: Vasoconstrictors cause blood vessels to narrow, reducing blood flow. This is sometimes referred to as the “tourniquet effect.”
Slows absorption into circulation: By narrowing blood vessels, vasoconstrictors slow down the absorption of the local anesthetic into the bloodstream.
Lowers blood levels of the local anesthetic: Slower absorption means that the concentration of the local anesthetic in the blood remains lower, reducing the risk of toxicity.
Prolongs the duration of action: The combination of a vasoconstrictor with a local anesthetic can make the anesthetic effect last longer.
Decreases bleeding: Vasoconstrictors help reduce bleeding at the injection site, leading to better visualization and a drier surgical field.
In summary, vasoconstrictors are used alongside local anesthetics to decrease blood flow, slow down absorption, lower blood levels of the anesthetic, extend its effect, and minimize the risk of toxicity. They also help control bleeding during procedures.
Explain effective epinephrine concentrations
For effective use, the concentration of epinephrine in local anesthetics matters:
Vasoconstrictor Effect: A concentration of 1:200,000 (0.005mg/ml) of epinephrine provides comparable results to 1:100,000 epinephrine but with fewer systemic side effects. So, a lower concentration of epinephrine can achieve similar outcomes with less risk.
Available Local Anesthetics: Epinephrine at these concentrations is available in local anesthetics like articaine, prilocaine, lidocaine, and bupivacaine.
Plasma Epinephrine Levels: After a single injection of lidocaine with 1:100,000 epinephrine in the mouth, the resting plasma epinephrine levels double. This means that epinephrine from the injection can enter the bloodstream and have systemic effects.
Exercise-Like Levels: The plasma levels of epinephrine achieved after a dental injection with usual doses (1:100,000 epinephrine) can be equivalent to those seen during moderate to heavy exercise.
In summary, using a lower concentration of epinephrine (1:200,000) in local anesthetics can still achieve effective results with fewer side effects. Epinephrine can enter the bloodstream after dental injections and may reach levels comparable to those experienced during exercise.
Properties of Epinephrine
Epinephrine has certain properties related to its use and action:
Sodium Bisulfite: Epinephrine formulations may contain sodium bisulfite, which is added to delay oxidation. Oxidation can reduce the effectiveness of epinephrine, so this additive helps maintain its potency.
Termination of Action: The action of epinephrine is primarily ended by the reuptake of adrenergic nerves. After performing its function, epinephrine is taken back up by these nerves, and its effects gradually subside.
Inactivation in Blood: Any remaining epinephrine in the blood is inactivated by enzymes called Catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). These enzymes break down epinephrine, reducing its concentration in the bloodstream over time.
In summary, sodium bisulfite is added to epinephrine formulations to delay oxidation. The action of epinephrine is terminated by reuptake into adrenergic nerves, and any leftover epinephrine in the blood is broken down by enzymes, which gradually reduce its effects.
Describe levonordefrin as a vasoconstrictor
Levonordefrin (Neo-Cobefrin) is a vasoconstrictor used in combination with local anesthetics. Here are some important points about it:
Less Stimulation: Compared to epinephrine, Levonordefrin produces less stimulation of the heart and the Central Nervous System (CNS). This means it has milder effects on the cardiovascular system and is less likely to cause nervousness or anxiety.
Available Concentration: Levonordefrin is available in a concentration of 1:20,000 when combined with mepivacaine, a local anesthetic.
Effectiveness: Levonordefrin is about 15% as effective as epinephrine as a vasoconstrictor.
Maximum Dosage: The maximum recommended dosage of Levonordefrin is 1 milligram per appointment or 20 milliliters (equivalent to about 11 cartridges).
Clinical Activity: Levonordefrin has a similar effect on the clinical activity of local anesthetics as epinephrine at a concentration of 1:100,000.
In summary, Levonordefrin is a vasoconstrictor used with local anesthetics. It has milder cardiovascular and CNS effects compared to epinephrine, but it’s still effective as a vasoconstrictor when combined with local anesthetics for dental procedures.
What are some considerations when it comes to vasoconstrictors and health status?
When considering the use of vasoconstrictors with local anesthetics, it’s essential to weigh the risks versus the benefits, especially for individuals with specific health conditions:
Cardiovascular Patients: For patients with cardiovascular issues classified as ASA III or IV (American Society of Anesthesiologists classification), caution is necessary when using vasoconstrictors. The potential risks to the heart and blood vessels need to be balanced against the benefits of using vasoconstrictors for prolonged anesthesia.
Thyroid Dysfunction: Patients with thyroid problems should be considered carefully when using vasoconstrictors. Epinephrine, a common vasoconstrictor, can affect thyroid hormone levels, so proper evaluation is required.
Sulfite Sensitivity: Some vasoconstrictors may contain sulfites, which can cause sensitivity or allergic reactions in some individuals. It’s important to check for sulfite allergies before using vasoconstrictors.
MAO Inhibitors: People taking MAO inhibitors (medications for depression) generally have less concern when using vasoconstrictors, but it’s always best to consult with a healthcare professional.
Tricyclic Antidepressants: Levonordefrin (Neo-Cobefrin) should be avoided in patients taking tricyclic antidepressants, as the combination can lead to adverse effects.
Phenothiazines: Patients taking phenothiazines (medications for various conditions, including mental health disorders) may have interactions with certain vasoconstrictors.
In summary, the use of vasoconstrictors in combination with local anesthetics should be carefully considered for individuals with specific health conditions, including cardiovascular issues, thyroid dysfunction, sulfite sensitivity, and certain medications they may be taking. Always consult with a healthcare professional to ensure the best course of action for each patient.
What is Ora Verse?
There is a new reversal agent for local anesthesia called OraVerse:
OraVerse contains phentolamine mesylate.
It is used to reverse the soft tissue anesthesia caused by local anesthetics that contain vasoconstrictors.
However, it should not be used in children under 6 years of age or those weighing less than 15 kg (around 33 lbs).
The technique for administering OraVerse is the same as that used for local anesthesia. It can be administered through infiltration or block methods, just like regular local anesthetics.
In summary, OraVerse is a phentolamine mesylate-based agent used to reverse soft tissue anesthesia from local anesthetics with vasoconstrictors. It is not recommended for use in young children or those with low body weight. The same techniques used for regular local anesthesia can be applied when using OraVerse.
OraVerse is supplied as 0.4 mg in a 1.7 ml syringe.
It works as an alpha-adrenergic blocking agent, causing vasodilation and reversing the vasoconstrictor effects of local anesthetics.
It is used in a 1:1 ratio with the local anesthetic that contains a vasoconstrictor.
The median time for recovery after using OraVerse is about 50% reduction in the mandible (lower jaw) and 43% in the maxilla (upper jaw).
Precautions when using OraVerse:
Some potential side effects include tachycardia (rapid heartbeat), bradycardia (slow heartbeat), injection site pain, and headaches.
In rare cases, when used in higher than recommended doses, serious adverse events have been reported, such as myocardial infarction (heart attack), cerebrovascular spasm (blood vessel constriction in the brain), arrhythmias (abnormal heart rhythms), and hypotension (low blood pressure).
Explain some complications and adverse reactions associated with local anesthetics
Complications and adverse reactions related to local anesthetics are relatively uncommon, and most of them are not true allergies. Here are some important points:
Most Common Complication: The most common complication is psychogenic in nature, meaning it’s related to psychological factors. Syncope, or fainting, is a typical example, often triggered by anxiety or fear during dental procedures.
True Allergy to Amides: True allergies to local anesthetics of the amide type (e.g., lidocaine, bupivacaine) are rare.
Allergy to One Amide: If a person has an allergy to one amide local anesthetic, it does not necessarily mean they will be allergic to other amide types. Allergies are specific to each drug.
Epinephrine Allergy: Allergy to epinephrine, which is commonly used with local anesthetics, is virtually impossible. Instead, allergic reactions are more likely to be related to the preservative called bisulfite, which is sometimes added to epinephrine-containing solutions.
Sulfite and Sulfonamide Allergies: There is no cross-allergenicity between sulfites (e.g., bisulfite preservative) and sulfonamide antibiotics. Having an allergy to one does not mean a person is allergic to the other.
In summary, complications and true allergies to local anesthetics are rare. Most adverse reactions are psychogenic, and true allergies to amide local anesthetics or epinephrine are highly unlikely. Allergic reactions are more likely related to preservatives or additives rather than the core components of the local anesthetic solution.
Describe methemoglobinemia
Methemoglobinemia is a condition where there’s an excess of methemoglobin in the blood, which reduces its ability to carry oxygen. It can be induced by certain local anesthetics, including Prilocaine, Articaine, and Benzocaine.
Important points about methemoglobinemia:
Prilocaine Metabolites: Methemoglobinemia is more likely to occur with Prilocaine when used in doses greater than 600 mg. Articaine and Benzocaine can also cause this condition but to a lesser extent.
Symptoms: Symptoms of methemoglobinemia include lethargy (extreme tiredness) and respiratory distress. Patients may also appear cyanotic (bluish skin color) even when given 100% oxygen.
Treatment: Methylene Blue is an intravenous treatment used to manage methemoglobinemia.
Precautions: It’s essential to avoid using these local anesthetics in patients with known congenital methemoglobinemia, a rare genetic condition that makes them more susceptible to developing the condition.
In summary, methemoglobinemia is a condition caused by certain local anesthetics, leading to reduced oxygen-carrying capacity in the blood. It can be managed with appropriate treatment, and caution should be exercised when using these anesthetics in susceptible patients.
Explain the advantages of Articaine
A meta-analysis by Brandt et al. (published in the Journal of the American Dental Association in 2011) compared the efficacy of Articaine versus Lidocaine in various clinical trials.
The study found that Articaine has superior anesthetic efficacy for pulpal anesthesia, meaning it is more effective at numbing the nerves inside the tooth.
When used for infiltration (injecting near the tooth), Articaine also showed a higher rate of anesthetic success compared to Lidocaine.
However, when used for nerve blocks (injecting near a nerve bundle), there was no significant difference in anesthetic success between Articaine and Lidocaine.
In summary, Articaine has an advantage over Lidocaine when it comes to pulpal anesthesia and infiltration, as it provides better numbing inside the tooth and has a higher success rate for numbing the area around the tooth. However, for nerve blocks, the two anesthetics show similar effectiveness.
Describe the possible interactions between non-selective beta blockers with Epinephrine and levonordefrin
When non-selective beta-blockers (medications like Corgard, Tasicor, Visken, Inderal, Timoptic) are taken along with local anesthetics containing vasoconstrictors like epinephrine and levonordefrin, there may be interactions and certain effects:
Increased Blood Pressure: Non-selective beta-blockers can interact with vasoconstrictors, leading to an increase in blood pressure in some patients.
Reflex Bradycardia: In some cases, the combination of non-selective beta-blockers and vasoconstrictors may cause reflex bradycardia, which is a slowing down of the heart rate.
To manage potential interactions and adverse effects, it is essential to consider reducing the use of vasoconstrictors or adjusting the dosage of local anesthetics containing these vasoconstrictors in patients taking non-selective beta-blockers.
Describe the possible interactions between tricyclic antidepressants with Epinephrine and Levonordefrin
Tricyclic antidepressants, such as Elavil (amitriptyline), Tofranil (imipramine), Norpramin (desipramine), Pamelor (nortriptyline), Sinequan (doxepin), and Vivactil (protriptyline), can interact with epinephrine and levonordefrin (vasoconstrictors) used in local anesthetics, leading to certain effects:
Increased Blood Pressure: Tricyclic antidepressants can cause an increase in blood pressure.
Contraindication with Levonordefrin: The combination of tricyclic antidepressants and levonordefrin is contraindicated, meaning it is not recommended due to potential adverse effects.
Reduce Dose of Epinephrine: If epinephrine is needed in local anesthetic solutions for dental procedures, the dose of epinephrine may need to be reduced in patients taking tricyclic antidepressants to minimize the risk of adverse reactions.
Describe possible interactions with Cocaine and EPI and LEVO
Cocaine can interact with epinephrine and levonordefrin (both are catecholamines) in potentially dangerous ways:
Inhibition of Catecholamine Uptake: Cocaine interferes with the uptake of catecholamines like norepinephrine, leading to increased levels of norepinephrine in the body.
Increased Blood Pressure: The elevated norepinephrine levels caused by cocaine can result in high blood pressure (hypertension).
Cardiac Dysrhythmias: Cocaine use along with vasoconstrictors like epinephrine or levonordefrin can increase the risk of irregular heart rhythms (dysrhythmias) and other cardiac complications.
Death: The combination of cocaine and vasoconstrictors can have severe consequences, including the potential for life-threatening events or even death.
What factors contribute to toxic reaction (overdose)
A toxic reaction, or overdose, to a local anesthetic can occur even if the administered dose does not exceed the maximum recommended dosage. Several factors can contribute to this situation:
Individual Factors: Extreme age (very young or elderly), body weight, and the use of other medications can influence how the body reacts to the local anesthetic.
Organ Dysfunction: If a person has liver or kidney problems (hepatic or renal dysfunction), their body may not process the local anesthetic efficiently, leading to higher circulating blood levels and an increased risk of toxicity.
Injection Factors: Certain injection-related factors can also play a role. These include administering the dose intravascularly (directly into a blood vessel), using a higher concentration of the local anesthetic solution, or using a solution with or without a vasoconstrictor.
Rapid Administration: Administering the local anesthetic too rapidly can also increase the risk of toxicity.
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How do you manage toxic reactions?
Toxic reactions to local anesthetics can range from mild to severe. Here’s how they are managed:
Mild Reaction: For mild reactions, the symptoms are typically self-limiting. The healthcare provider will reassure the patient, provide oxygen if necessary, and monitor vital signs (V.S.). Supportive care will be given as needed to alleviate any discomfort or side effects.
Severe Reaction: In severe cases, the same measures as in mild reactions are taken, including reassurance, oxygen, and monitoring. However, additional measures might be required, such as intravenous (I.V.) administration of medications, including anticonvulsants if needed. In cases of severe toxicity, Basic Life Support (BLS) and Advanced Cardiovascular Life Support (ACLS) protocols may be initiated to manage the situation. If necessary, emergency medical services (EMS) will be called for immediate assistance and transportation to a medical facility.
Explain broken needles prevention
To prevent broken needles during dental procedures, follow these guidelines:
Needle Size: Use needles that are at least 27 gauge in diameter. Smaller gauge needles are more prone to breakage.
Needle Length: Choose the appropriate needle length so that it doesn’t need to be inserted all the way to the hub (the plastic part where the needle attaches to the syringe). This helps prevent excessive bending and stress on the needle.
Avoid Bending: Never bend the needle during use or when removing it from the patient. Bending can weaken the needle and increase the risk of breakage.
Technique: Use the proper technique when inserting and removing the needle. Withdraw the needle almost completely before redirecting it to avoid putting excessive pressure on it.
Cause and management of Facial nerve paralysis
Facial nerve paralysis can occur due to the accidental deposition of local anesthetic into the capsule of the parotid gland during an inferior alveolar nerve block, a common dental injection.
Cause:
It happens when the local anesthetic spreads unintentionally to the nearby facial nerve, leading to temporary paralysis of the facial muscles on one side of the face.
Management:
Reassure the patient that the problem will resolve on its own in a few hours or within a day.
Prevention is the best approach, achieved by using proper injection technique and having a good understanding of the facial anatomy to avoid the accidental deposition of anesthetic near the facial nerve.
Describe soft-tissue injury
Soft-tissue injury can occur when patients inadvertently bite or chew on areas of their mouth that have been numbed by local anesthesia. This is more common in children and patients with no previous experience with local anesthesia.
Causes:
The patient may unknowingly bite or chew their lips, tongue, or buccal mucosa (inside of the cheeks) while they are still numb from the anesthesia.
Treatment:
The best way to manage soft-tissue injuries is through prevention. Dentists and healthcare professionals should instruct patients, especially children and those new to local anesthesia, to be careful and avoid chewing or biting the numbed areas.
If a soft-tissue injury does occur, the treatment may involve:
Antibiotics: If there is any sign of infection or risk of infection.
Petrolatum: Applying petroleum jelly or a similar protective ointment to soothe the injured area and prevent further irritation.
Analgesics: Pain-relieving medications may be prescribed or recommended to manage any discomfort
Describe a post-injection hematoma
Post-injection hematoma is the result of accidental puncture of a vein or artery during a dental injection, leading to bleeding into the surrounding tissues.
Causes:
This is most common after certain dental injections like the inferior alveolar and posterior superior alveolar injections.
Prevention:
Healthcare professionals can prevent post-injection hematomas by having a good understanding of the anatomy, using the fewest needle insertions possible, and aspirating before injecting to ensure the needle is not inside a blood vessel.
Treatment:
If a hematoma occurs, applying pressure to the area for about 5 minutes can help stop the bleeding.
Using ice on the first day may help reduce swelling and discomfort.
Antibiotics may be prescribed to prevent any secondary infection.
Usually, post-injection hematomas resolve on their own within about 14 days.
Which LA’s are pregnancy category B
Which are C
B is Prilocaine and Lidocaine
C is articaine, bupivacaine, mepivacaine, epinephrine, and benzocaine
Explain Local Anesthetics in Children
When using local anesthetics in children, there are some important considerations to ensure their safety:
Toxic Dose: Always be mindful of the child’s weight and calculate the maximum safe dose of the local anesthetic based on their weight. This helps avoid giving them too much anesthesia, which could be harmful.
Low Concentration: It’s generally safer to use low concentration solutions of local anesthetics in children. Lower concentrations reduce the risk of giving them excessive amounts of the drug.
Avoid Bupivacaine: Bupivacaine is a long-acting local anesthetic that can lead to prolonged soft tissue anesthesia in children. It’s best to avoid using bupivacaine in pediatric patients to prevent extended periods of numbness.
Explain duration of action, specifically protein binding
The duration of action of a local anesthetic depends on its protein binding properties. When a local anesthetic has a higher tendency to bind to proteins, it will stay in the tissues for a longer time, resulting in a more prolonged neural blockade (numbing effect).
Examples:
Bupivacaine has a high protein binding capacity, with 95% of the drug binding to proteins. As a result, it provides a longer-lasting numbing effect.
Mepivacaine, on the other hand, has a lower protein binding capacity, with 55% of the drug binding to proteins. This means that mepivacaine’s duration of action is not as long as bupivacaine.
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