Everything you need to know about Local Anesthetics. Dose, mechanism of action, toxicity, management. How to use, where to use. It also contains receptors which are involved. Which factors prolongs and makes the drug work quicker.
“Local Anaesthetics”
These are agents which upon topical application or local injection cause reversible loss of pain sensation in a restricted area of the body. They act by blocking both sensory and motor nerve conduction to produce temporary loss of sensation without loss of consciousness.
Mechanism of action
These drugs reversibly prevent the generation and propagation of impulses in all excitable membranes including nerve fiber by stabilizing the membrane.
Local anesthetics block the nerve conduction by decreasing the entry of Na+ during action potential. They interact with a receptor situated within the voltage sensitive Na+ channel and raise the threshold of Na+ channel opening.
Therefore, Na+ can’t enter into the cell in response to an impulse which prevents depolarisation. Thus, action potential is not generated.
This action affecting the depolarization which leads to failure of conduction of impulse without affecting the resting membrane potential (RMP) is known as membrane stabilizing effect.
History- Cocaine is a naturally occurring compound indigenous to the Andes Mountains, West Indies, and Java.
It was the first anesthetic to be discovered and is the only naturally occurring local anesthetic; all others are synthetically derived.
Cocaine was introduced into Europe in the 1800s following its isolation from coca beans. Sigmund Freud, the noted Austrian psychoanalyst, used cocaine on his patients and became addicted through self-experimentation.
In the latter half of the 1800s, interest in the drug became widespread, and many of cocaine's pharmacologic actions and adverse effects were elucidated during this time. In the 1880s, Koller introduced cocaine to the field of ophthalmology, and Hall introduced it to dentistry
“Local Anaesthetics”
These are agents which upon topical application or local injection cause reversible loss of pain sensation in a restricted area of the body. They act by blocking both sensory and motor nerve conduction to produce temporary loss of sensation without loss of consciousness.
Mechanism of action
These drugs reversibly prevent the generation and propagation of impulses in all excitable membranes including nerve fiber by stabilizing the membrane.
Local anesthetics block the nerve conduction by decreasing the entry of Na+ during action potential. They interact with a receptor situated within the voltage sensitive Na+ channel and raise the threshold of Na+ channel opening.
Therefore, Na+ can’t enter into the cell in response to an impulse which prevents depolarisation. Thus, action potential is not generated.
This action affecting the depolarization which leads to failure of conduction of impulse without affecting the resting membrane potential (RMP) is known as membrane stabilizing effect.
History- Cocaine is a naturally occurring compound indigenous to the Andes Mountains, West Indies, and Java.
It was the first anesthetic to be discovered and is the only naturally occurring local anesthetic; all others are synthetically derived.
Cocaine was introduced into Europe in the 1800s following its isolation from coca beans. Sigmund Freud, the noted Austrian psychoanalyst, used cocaine on his patients and became addicted through self-experimentation.
In the latter half of the 1800s, interest in the drug became widespread, and many of cocaine's pharmacologic actions and adverse effects were elucidated during this time. In the 1880s, Koller introduced cocaine to the field of ophthalmology, and Hall introduced it to dentistry
In this presentation I tried to explain the classification of muscle relaxants. along with differences between these classes. there is also a brief discussion about NMT and how they work. furthermore it has dose, maintenance dose, adverse effects and how to manage toxicity about these drugs.
A short presentation covering most important anatomical differences along with physiological difference of pediatric population from adult. Also covers important aspects of anaesthesia consideration in pediatric patients.
I specifically made this presentation by using morgan and miller books.
More Related Content
Similar to Local Anaesthesia By Dr Sardar Saud Abbas
In this presentation I tried to explain the classification of muscle relaxants. along with differences between these classes. there is also a brief discussion about NMT and how they work. furthermore it has dose, maintenance dose, adverse effects and how to manage toxicity about these drugs.
A short presentation covering most important anatomical differences along with physiological difference of pediatric population from adult. Also covers important aspects of anaesthesia consideration in pediatric patients.
I specifically made this presentation by using morgan and miller books.
This presentation explains change physiological changes occurs in obesity. Which pre op investigation should be done of those patient before scheduling them for surgery. What in the end anaesthesia consideration of obesity with post op care.
This brief presentation does not cover all of the ophthalmology surgeries, but will give you a brief review about what is what. It starts with eye anatomy, physiology, pharmacology and leads up to anaesthesia considerations.
Just a review on cardiopulmonary resuscitation.
I hope everyone finds it useful and resourceful.
major reference is American Heart Association Guidelines
if there is any mistake or somebody wants to make an edition please feel free to email me at sardar.saud@gmail.com
By Dr Sardar Saud Abbas
Brief description on how to assess airway and manage difficult intubation. There is alot of detail about airway management but this will get you through
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
2. CONTENTS
CLASSIFICATION
MECHANISM OF ACTION
CLASSIFICATION OF NERVE FIBRE
ONSET OF ACTION
DURATION OF ACTION
SYSTEMIC TOXICITY
COMMONLY USED L.A
SUMMARY
3. CLASSIFICATION
BASED ON CHEMICAL STRUCTURE:
ESTERS AMIDES
PROCAINE LIGNOCAINE
CHLOROPROCAINE MEPIVACAINE
TETRACAINE PRILOCAINE
BENZOCAINE BUPIVACAINE
COCAINE ROPIVACAINE
NOTE:
ESTERS ARE METABOLIZED BY
PSEUDOCHOLINESTERASE
(except cocaine which is metabolized in liver)
AMIDES re metabolism primarily in liver
4. MECHNISM OF ACTION
Local anesthetics are deposited all around the nerve.
Drug in undissociated (nonionized) form penetrates the axonal membrane.
Once inside it gets dissociated (ionized).
It is this dissociated(ionized, protonated, cationic or uncharged) form which binds to
sodium channel (alpha subunit) from inner side, blocking the channel, preventing
depolarization and action potential.
Although local anesthetics can block sodium channel in any state however activated
channels (positive resting H+ {local anesthetic Axonal in undissociated form)
Membrane Na+ Local anesthetic in dissociated form blocks sodium channel from inside
very rapidly.
5. BASED ON DURATION OF ACTION
SHORT DURATION (15-30 MIN)
1) Chloroprocaine: shortest acting local anesthetic
2) PROCAIEN
INTERMEDAIATE (3O-90 MIN)
Lignocaine
Mepivacaine
Prilocaine
Cocaine
6. Based on Duration of Action
Long duration (2-3 hours):
Bupivacaine.
Levobupivacaine
Ropivacaine.
Tetracaine (Amethocaine).
Etidocaine.
Dibucaine: Longest acting local anesthetic
7. OTHER DRUGS WITH LOCAL
ANESTHETIC
PROPERTIES
Opioids
anesthetics can be given pethidine in place of local anPethidine: Patients hypersensitive to
local
esthetics.
Buprenorphine: Because of its local anesthetic properties it is frequently used to
supplement the effect of local anesthetics For nerve blocks.
Tramadol: Although weak but tramadol do havelocal anesthetic properties.
Methoxyflurane: The droplets o f methoxyflurane has got local anesthetic properties.
9. ONSET OF ACTION AND FACTORS
EFFECTING IT.
Depends on number of factors like:
Dose and concentration: Higher dose or higher concentration facilitates onset
pKa: It is the pH at which a local anesthetic is 50% ionized and 50% non ionized.
Since local anesthetics are weak bases, agents with pKa closer to physiologic pH will
have more drugs in non ionized form which can diffuse through axonal membrane
enhancing the onset.
That is why lignocaine with lower pKa of 7.8 has fast onset as compared to bupivacaine
with higher pKa of 8.l.
10. Continued
Type of nerve fiber: A fibers are blocked earlier than B which are blocked earlier than C
Frequency of nerve stimulation: Since activated channels are blocked more easily, a
stimulated nerve will be blocked earlier as compared to non stimulated nerve.
11. DURATION OF ACTION FACTORS
EFFECTING IT.
It depends on:
1. Dose: Increased dose increases the duration.
2. Pharmacokinetic profile of drug: It includes:Potency (lipid solubility): Potency,
which correlates with lipid solubility, is directly proportional to duration; more the
potency, longer is the duration with the exception of chloroprocaine which in spite of
having intermediate potency is shortest acting.
3. Plasma protein binding (a l acid glycoprotein): Agents with high protein binding like
bupivacaine have prolonged action.
12. SYSTEMIC TOXICITY
CNS
As central nervous system is the first system involved in local anesthetic toxicity.
Typical sequence is excitation followed by depression of cerebral tissue (inhibitory
neurons are more sensitive than excitatory neurons). The common signs and symptoms
a numbness, dizziness, tongue paresthesia, visual and auditory disturbances,
twitching, tremors, convulsions followed by coma and death. Convulsions as first
presentation are quite common in local anesthetic toxicity.
Treatment includes maintenance of adequate ventilation and oxygenation. Convulsion
can be controlled by diazepam/ midazolam or thiopentone.
13. Cardiovascular System
Electrophysiological effects of local anesthetics on cardiac tissue are decrease in rate
of depolarization (main effect), effective refractory period and duration of action
potential
All local anesthetics have negative inotropic action on myocardium, causes depression
of conduction system (prolonged PR interval and increased duration of QRS complex).
At very high doses they may block conduction of sinus node producing bradycardia or
even sinus arrest. In addirion the above effects bupivacaine (and to lesser effect
levobupivacaine and ropivacaine) can also produce ventricular arrhythmias. Therefore,
either the isolated or combined actions like bradycardia, decreased myocardial
contractility, ventricular arrhythmias, hypotension can produce cardiac arrest with local
anesthetics. Management of cardiac arrest is immediate CPR.
14. Respiratory symptoms, Immunology,
Lignocaine depresses hypoxic drive. Direct depression of medullary respiratory Centre
can occur at high dose
Immunologic: Allergic reactions are common with esters but rare with amides. The
reaction with amides is because of the preservative (methyl paraben) it contains. Cross
sensitivity does not exist between classes (i.e. esters and amides) but exist between
agents of same class.
15. Methemoglobinemia :
1. Usually seen with Prilocaine however benzocaine can also cause methemoglobinemia.
2. Treatment: IVmethylene blue.
Coagulation: Lignocaine can inhibit coagulation
16. COMMONLY USED L.A
Lignocoine (Xylocoine, Lidocoine)
Metabolism
Metabolized in liver, excreted by kidney.
t½: 1.6 hrs.
Duration of Effect
Without adrenaline 45-60 minutes.
With adrenaline 2-3 hours.
Maximum Safe Dose
Without adrenaline 4.5 mg/kg
(maximum 300 mg)
With adrenaline 7 mg/kg
( maximum 500 mg)
18. BUPIVACAINE
It is 4 times more potent than lignocaine.
Metabolized in liver, t ½: 3.5 hours.
MAXIMUM DOSE:
WITHOUT ADRENALINE: 2.5 MG/KG
(MAXIMUM DOSE 175MG)
WITH ADRENALINE 3 MG/KG
(MAXIMUM DOSE 225MG)
DURATION OF EFFECT
WITHOUT ADRENALINE 2-3 hours.
WITH ADRENALINE 3-5 hours.
Addition of adrenaline only prolongs the duration of sensory block.
19. Concentration Used
1. For nerve block 0.5%
2. Spinal 0.5% (heavy)
3. Epidural 0.125-0.5% (depending whether used for sensory block or motor block)
Cardiot0xicity of bupivacaine may manifest as bradyarrhythmias, conduction blocks,
ventricular arrhythmias or cardiac arrest. Its high tissue binding (slow reversal of
sodium channels} and high degree of protein binding makes resuscitation after cardiac
arrest prolonged and very difficult.
Management of cardiac arrest
includes CPR along with the rapid bolus of lntralipid 20%, 1.5 mL/kg followed by
infusion if required. Intralipid binds the active form of bupivacaine