This document discusses different types and techniques of anesthesia. It outlines general anesthesia which causes complete loss of consciousness and sensation, and describes its goals, induction, maintenance and monitoring. It also discusses local anesthesia techniques like infiltration, nerve blocks and various regional techniques. The document provides details on ideal properties, classifications, mechanisms and toxicity management for different anesthetic agents.
general anesthesia are the drug given before surgery which have reversible effect on consciousness. discussing ideal GA, stages of GA, mechanism of action of GA, classification of drugs parenteral or inhaled.
general anesthesia are the drug given before surgery which have reversible effect on consciousness. discussing ideal GA, stages of GA, mechanism of action of GA, classification of drugs parenteral or inhaled.
In this power point I have included information about the career of a Nurse Anesthetist. In it includes what their responsibilities are, job outlook, salary, level of education needed and many other specifics.
Post anesthesia care unit or , High Dependency unit is part of hospital for Post surgery/procedures recovery.Nursing, anesthesiologist, surgeons, hospital administration need to know about ideal conditions.
sedation in neuro icu requires frequent interruptions for serial neurological examination. incorporation of inhalational agents in icu improves sedation practices.
General Anesthetics
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Define sleep, amnesia, analgesia, general anesthesia
List different phases/planes of GA
Classify the agents used for general anesthesia
Describe the mechanism of action, pharmacokinetics, therapeutics and adverse effects and drug interactions of different anesthetic drugs
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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
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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anesth Lecture for 3rd year MBBS
1.
2. Types and modes of
anaesthesia
DR.NADIR MEHMOOD
Asst professor
Department ofSurgery, RMC
3. LEARNING OBJECTIVES
At end of this discussion, a student will be able to,
• Enumerate the types of anesthesia
• Describe techniques of G/A and L/A
• Enlist the advantages and indications of each type
of anesthesia
• Outline management plan in case of adverse effect
of technique or overdose of L/A, S/A, OR Bier’s A
• Technique and Video of spinal anesthesia
4. TYPES OF ANESTHESIA
• G/A- TIVA, I/M, RECTAL, INTRAPERIT,DISSO A,
INHALA A
• SPINAL, EPIDURAL, CAUDAL,
• REGIONAL A
• NERVE BLOCK A
• BIER’S A
• LA- SURFACE,INFILT, NERVE BLOCK,
COMBINATION
5. General Anaesthesia (GA)
• complete loss of perception & consciousness
• fundamental attributes of GA
– loss of consciousness – does not block autonomic reflexes to
painful stimuli (perspiration, arrhytmia, hypertension,
bronchoconstriction, bronchial hypersecretion)
– vegetative stabilisation
– analgesia – loss of pain sensation, suppression of autonomic
reactions
– muscle relaxation
• induction of all the GA attributes facilitated by mosaic assembly
of partial effects of many substances such as anaesthetics,
analgetics, tranquillizers, myorelaxants
6. Intravenous Anesthetic Agents
• First attempt at intravenous anesthesia by
Wren in 1656-- opium into his dog
• Use in anesthesia in 1934 with thiopental
• Many ways to meet requirements-- muscle
relaxants, opoids, nonopoids
• Appealing, pleasant experience
7. 7
Overview
• General anaesthesia is a complex procedure
involving :
– Pre-anaesthetic assessment
– Administration of general anaesthetic drugs
– Cardio-respiratory monitoring
– Analgesia
– Airway management
– Fluid management
– Postoperative pain relief
9. Types of GA according to the entry into organism
• inhalational
• intravenous
• intramuscular
• rectal – especially in children
• intraperitoneal – in animals
10. 10
Pre-anaesthetic evaluation
• medical history, current medications.
• previous anaesthetics.History
• age, weight, teeth condition.
• Airway assessment, neck flexibility and
head extension
Examination.
• Relevant to age and medical conditions.Investigations.
11. 11
Pre-anaesthetic evaluation
The plan
best combination ,
drugs and dosages and
the degree of how
much monitoring is
required .
fasting time
If airway management
is deemed difficult,
then alternative
placement methods
such as fiberoptic
intubation may be
used.
12. GA – premedication
Purpose of premedication
– satisfactory rest at night before operation
(premedication)
– calm down
– basal analgesia
– supression of readines to allergic reactions
– supression of vegetative reflexes (bradycardia,
hypersalivation, bronchial hypersecretion)
e.g: sedatives, hypnotics, anxiolytics, vagolytics (atropine),
atihistaminics
13. Ideal Characteristics of Inhalational
Anesthetics
• Rapid & pleasant induction & recovery
• Rapid changes in depth of anesthesia
• Adequate relaxation of smooth muscle
• Wide margin of safety
• Absence of toxic effect
15. 15
Maintenance
• In order to prolong anaesthesia for the
required duration (usually the duration of
surgery), patient has to breathe a carefully
controlled mixture of oxygen, nitrous oxide,
and a volatile anaesthetic agent. This is
transferred to the patient's brain via the lungs
and the bloodstream, and the patient remains
unconscious.
16. 16
Maintenance
• Inhaled agents are supplemented by intravenous
anaesthetics, such as opioids (usually fentanyl or
morphine).
• At the end of surgery the volatile anaesthetic is
discontinued.
• Recovery of consciousness occurs when the
concentration of anaesthetic in the brain drops
below a certain level (usually within 1 to 30
minutes depending upon the duration of
surgery).
17. 17
Maintenance
• Total Intra-Venous Anaesthesia (TIVA): this
involves using a computer controlled syringe
driver (pump) to infuse Propofol throughout
the duration of surgery, removing the need for
a volatile anaesthetic.
• Advantages: faster recovery from anaesthesia,
reduced incidence of post-operative nausea
and vomiting, and absence of a trigger for
malignant hyperthermia.
18. 18
Neuromuscular-blocking drugs
• Block neuromuscular transmission at the
neuromuscular junction.
• Used as an adjunct to anesthesia to induce
paralysis.
• Mechanical ventilation should be available to
maintain adequate respiration.
19. GA muscle relaxants
depolarising muscle relaxants
• cholinergic receptor -> depolarisation -> generation AP
• fasciculations
• antagonisation is not possible
• e.g.: Suxametonium (succinylcholine)
non-depolarising muscle relaxants
• competetive block of cholinergic receptors without
generation of AP
• so called curariform medicaments, e.g.: Pancuronium,
Atracurium
• antagonist: neostigmin (decurarization)
23. 23
Mortality rates
• Overall, about five deaths per million.
• Most commonly related to surgical/anesthesia factors or
pre-existing medical conditions ( haemorrhage, sepsis).
• Common causes of death directly related to anaesthesia
include:
1- aspiration of stomach contents
2- suffocation (due to inadequate airway management)
3- allergic reactions to anaesthesia
4- human error
5- equipment failure
24. Local Anesthetics
• Followed general anesthesia by 40 years
• Koller used cocaine for the eye surgery in 1884
• Halsted used cocaine as nerve block
• First synthetic local-- procaine in 1905
• Lidocaine synthesized in 1943
25. Local Anesthetics
• Mechanism of action is by reversibly blocking
sodium channels to prevent depolarization
• Anesthetic enters on axioplasmic side and attaches
to receptor in middle of channel
26. Mechanism of the effect of LA
• blockade of the inner oriffice of sodium channel -> influenced
depolarisation
• non-ionized form – penetration throuhg connective tissue, myelin sheet
and cell membrane, intracellularly ionization and attachment to the
sodium channel (competetive antagonism)
• ionizoed vs. non-ionized form ratio dependent on pH
– healthy tissue: slightly alkaline pH -> more non-ionized form ->
easy penetration of LA into cells -> quick effect onset
– inflammatory focus: acid pH -> less non-ionized form ->
-> poor penetration intracellularily -> weak LA effect
• Vasoconstrictive addition agents (adrenaline/epinephrine)
– reduction of absorbtion ->longer lasting effect, lowered toxicity,
less bleeding
27. Classified into
a. Short acting – cocaine, procaine
b. Intermediate acting – lidocaine,
mepivacaine, dibucaine, prilocaine
c. Long acting – tetracaine, bupivacaine,
etidocaine
28. Properties of a Desirable Local Anesthetic
•contrary to general anaesthesia, consciousness
is preserved sites of action
• should not be irritating to tissues
• should not cause permanent damage to
nerves
• have low systemic toxicity
• must be effective
• should have rapid onset but long duration of
action
29. ROUTES OF ADMINISTRATION:
1. Topical (skin, mucosal)
2. Local Infiltration
3. Nerve Block
4. Spinal or Intrathecal injection
5. Epidural
6. Caudal
LOCAL ANESTHETICS
31. Effects of LA on nerve fibers
1. block of sympathetic division (warming of skin)
2. loss of sensation of heat and pain
3. loss of sensation of touch and pressure
4. loss of motorics
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44. Local Anesthetic Toxicity
• Central nervous system
– initially-- lightheadedness, circumoral numbness,
dizziness, tinnitus, visual change
– later-- drowsiness, disorientation, slurred speech, loss
of consciousness, convulsions
– finally-- respiratory depression
45. Local Anesthetic Toxicity
• Cardiovascular
– myocardial depression and vasodilation--
hypotension and circulatory collapse
• Allergic reactions-- rare (less than 1%)
– preservatives or metabolites of esters
– rash, bronchospasm
46. Prevention and Treatment of Toxicity
• Primarily from intravascular injection or
excessive dose -- anticipation
– aspirate often with slow injection
– ask about CNS toxicity
– have monitoring available
– prepare with resuscitative equipment, CNS-
depressant drugs, cardiovascular drugs
– ABC’s