This document discusses general anaesthetics. It begins by defining general anaesthetics as drugs that produce reversible loss of consciousness and sensation, including pain, reflexes, and mobility. It then covers various topics related to general anaesthetics, including historical uses, mechanisms of action, stages of anaesthesia, inhalational agents like ether, nitrous oxide, and halothane, and intravenous agents like thiopentone sodium. The ideal properties of anaesthetics are discussed. Inhalational agents have advantages like rapid induction but also risks like flammability, while intravenous agents allow rapid induction and recovery but are only suitable for short procedures.
General anaesthetics (GAs) are drugs which produce reversible loss of all sensation and consciousness.
The cardinal features of general anaesthesia are:
• Loss of all sensation, especially pain.
• Sleep (unconsciousness) and amnesia
• Immobility and muscle relaxation
• Abolition of somatic and autonomic reflexes.
GA was absent until the mid 1800’s
Original discoverer of GA
-Crawford long, physician from Gerogia(1842),
ETHER ANESTHESIA
. NITROUS OXIDE
- Horace wells(1844)
. GASEOUS ETHER by William T.G. Morton(1846)
. CHLOROFORM introduced by
- James simpson (1847)
METHODS OF ADMINISTRATION OF INHALATIONAL GENERAL ANAESTHETICS
OPEN METHOD: This is a simple method of administering a volatile anaesthetic.
A simple mask covered with six to ten layers of gauze, which does not fit the contour of the face is held on the face and an anaesthetic like ether, or ethyl chloride is poured on it in drops. The anaesthetic vapour, diluted with air, is inhaled through the gap between the mask and the face.
SEMI-OPEN METHOD: This method is similar to open method but the dilution with air is prevented by using either a well-fitting mask like Ogston’s mask or layers of gauze between face and the mask. A small carbon dioxide build-up occurs with this method.
SEMI-CLOSED METHOD: This method allows some rebreathing of the anaesthetic drug with the help of a reservoir but in addition, part of the volume of each succeeding inspiration is a new portion from an anaesthetic mixture. This method involves accumulation and rebreathing of carbon dioxide.
• CLOSED METHOD: This method employs the chemical agent soda lime to absorb the carbon dioxide present in the expired air. It requires the use of a special apparatus but is particularly useful when the anaesthetic agent is potentially explosive
STAGES OF ANAESTHESIA
Guedel, in 1920 outlined the four stages of general anaesthesia :
• Stage I: Stage of analgesia
• Stage II: Stage of delirium
• Stage III: Stage of surgical anaesthesia
• Stage IV: Stage of respiratory paralysis
Inadequate anaesthesia is indicated by:
Signs of ANS overactivity, such as tachycardia, rise of BP, sweating and lacrimation.
Grimacing;
Other muscle activity.
Surgical anaesthesia is indicated by:
Loss of eyelash (lid) reflex
Development of rhythmic respiration.
Deep anaesthesia is suggested by :
Depression of respiration.
Hypotension
Asystole
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
General anaesthetics (GAs) are drugs which produce reversible loss of all sensation and consciousness.
The cardinal features of general anaesthesia are:
• Loss of all sensation, especially pain.
• Sleep (unconsciousness) and amnesia
• Immobility and muscle relaxation
• Abolition of somatic and autonomic reflexes.
GA was absent until the mid 1800’s
Original discoverer of GA
-Crawford long, physician from Gerogia(1842),
ETHER ANESTHESIA
. NITROUS OXIDE
- Horace wells(1844)
. GASEOUS ETHER by William T.G. Morton(1846)
. CHLOROFORM introduced by
- James simpson (1847)
METHODS OF ADMINISTRATION OF INHALATIONAL GENERAL ANAESTHETICS
OPEN METHOD: This is a simple method of administering a volatile anaesthetic.
A simple mask covered with six to ten layers of gauze, which does not fit the contour of the face is held on the face and an anaesthetic like ether, or ethyl chloride is poured on it in drops. The anaesthetic vapour, diluted with air, is inhaled through the gap between the mask and the face.
SEMI-OPEN METHOD: This method is similar to open method but the dilution with air is prevented by using either a well-fitting mask like Ogston’s mask or layers of gauze between face and the mask. A small carbon dioxide build-up occurs with this method.
SEMI-CLOSED METHOD: This method allows some rebreathing of the anaesthetic drug with the help of a reservoir but in addition, part of the volume of each succeeding inspiration is a new portion from an anaesthetic mixture. This method involves accumulation and rebreathing of carbon dioxide.
• CLOSED METHOD: This method employs the chemical agent soda lime to absorb the carbon dioxide present in the expired air. It requires the use of a special apparatus but is particularly useful when the anaesthetic agent is potentially explosive
STAGES OF ANAESTHESIA
Guedel, in 1920 outlined the four stages of general anaesthesia :
• Stage I: Stage of analgesia
• Stage II: Stage of delirium
• Stage III: Stage of surgical anaesthesia
• Stage IV: Stage of respiratory paralysis
Inadequate anaesthesia is indicated by:
Signs of ANS overactivity, such as tachycardia, rise of BP, sweating and lacrimation.
Grimacing;
Other muscle activity.
Surgical anaesthesia is indicated by:
Loss of eyelash (lid) reflex
Development of rhythmic respiration.
Deep anaesthesia is suggested by :
Depression of respiration.
Hypotension
Asystole
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Nov 2008 - A presentation given during my lab animal rotation; reivews procedures, risks, and techniques for anesthetizing rats, focused on use in lab animal medicine
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THIS ppt explains in brief about general anesthesia for under graduates. It includes brief classification, mechanism of action, side effects of some important drugs. concepts like diffusion hypoxia, second gas effect, balanced anesthesia and pre- anaesthetic medication are discussed.
Lecture slides for Medical Undergraduate teaching in Pharmacology. Study material is based on Essentials of medical pharmacology by KD tripathi and Katzung. Figures are obtained from google image search and above mentioned textbooks.
Lecture slides for MBBS Undergraduate Medical students. Study material was taken from Essentials of pharmacology by KD Tripathi. Figures were searched from google.
Lecture slides for undergraduate MBBS class in Pharmacology on " Drugs for Diarrhoea" . It includes various treatment modalities which are used in the management of Diarrhoea. Basic source of information for preparing this slides is" Essentials of Pharmacology by KD tripathi, 7th Edition". Images are searched with the help of google images.
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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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3. General Anaesthetics
Drugs Which Produce Reversible Loss of
consciousness and all sensation
Loss of sensation – Pain
Unconsciousness and amnesia
Immobility and Muscle relaxation
Loss of reflexes
5. Some Strange Methods
Strangulation
Cerebral Concussion
Applying Cold or compression
Alcohol
Plants
6. Time Line
1799 – Davy
1818 – Michael Faraday
1844 – Horace wells
1846 – William TG Morton
1847 – John Snow and John Sympson
1956 – Charles Suckling
7. Mechanism of action
Main Sites of action are Cortex, Thalamus and
Hippocampus.
Can also act at Peripheral Sensory Nerves, Spinal
Cord, Brain Stem
9. Minimum Alveolar Concentration
(MAC)
Measure of Potency of inhalational General
anaesthetic agent
Lowest Concentration in alveoli
To produce immobility in 50 % subjects
In response to painful stimuli.
Correlation with oil/gas partition Coefficient
Reflect capacity of anaesthetic to enter into
CNS
10. MAC : Practically
Alveolar concentrations can be monitored
continuously by measuring end-tidal anesthetic
concentration using spectrometry
End point (immobilization) – can me measured.
Other end points – Verbal commands or
memory etc.
11. MAC
Premedication with CNS depressant lowers MAC
When combination is used MAC is additive
DRC of inhaled anesthetic is steep
Concentration exceeding 1.5 MAC are not used
2-3 MAC is lethal
Patient wakes up when concentration falls to 0.4 MAC
12. Guedel’s Stages of Anaesthesia
Guedel in 1920 described with ether
Descending depression of CNS.
Higher to lower areas of brain are involved.
Vital centers located in medulla are paralyzed last.
In spinal cord lower segments are affected earlier
than the higher segments.
13. Stage I – Analgesia
Starts with inhalation up to loss of consciousness
Can Hear, See and Dream like state
Reflexes and respiration normal
Minor Operations can be carried out
14. Stage II - Excitement
Delirium and combative behavior
Rise and irregularity in BP and Respiration
Chance of laryngospasm
Pupils dilated
No procedure is carried out in this stage
15. Stage III – Surgical Anaesthesia
Onset of regular respiration to cessation of
spontaneous breathing
Phase1: Roving eyeballs.
Phase2: Loss of corneal and laryngeal reflexes.
Phase 3: Pupil starts dilating and light reflex is lost.
Plane 4: Intercostal paralysis, shallow abdominal
respiration, dilated pupil.
Muscle tone decreases, BP falls, HR increases with
weak pulse, respiration decreases
16. Stage IV – Medullary Paralysis
Cessation of breathing to failure of circulation
Death.
Dilated Pupil, Flabby muscles
Thready or imperceptible Pulse
Low BP
17.
18. Observations
Eyelash reflex and swallowing movement present –
Stage I
Loss of response to painful stimuli – Stage III
Light Anaesthesia – Reflex increase in respiration, BP on
Incision,
Resistance to intubation, Coughing, Vomiting,
Laryngospasm
Deep Anaesthesia - Fall in BP, Cardiac and respiratory
depression
19. Phases of Anaesthesia
Induction: Beginning of administration of
anaesthesia to the development of surgical
anaesthesia
Maintenance: Sustaining the state of anaesthesia.
Recovery: At the end of surgical procedure
administration of anaesthetic is stopped and
consciousness regains
21. Pharmacokinetics
Depth of anaesthesia depends on Potency of
the agent (MAC) and Partial Pressure (PP)
attained in the brain.
Induction and recovery depends on rate of
change of PP in brain.
23. 1. PP of anaesthetic in the inspired
gas
Higher the inspired gas tension more anaesthetic
will be transferred to the blood.
Induction can be hastened by administering the
GA at high concentration in the beginning.
24. 2.Pulmonary Ventilation
Delivery of GA to alveoli depends on ventilation
Hyperventilation – More delivery per minute
Hypoventilation – Opposite effect
25. 3. Alveolar Exchange
The GAs diffuse freely across alveoli, but if
alveolar ventilation and perfusion are
mismatched the attainment of equilibrium
between alveoli and blood delayed
Induction and recovery both are slowed.
26. Solubility of anaesthetic in blood
Determined by Blood: Gas Partition coefficient
Lower the blood : gas co-efficient – faster the
induction and recovery – Nitrous oxide.
Higher the blood : gas co-efficient – slower
induction and recovery – Halothane.
27.
28. 5. Solubility of anaesthetic in tissues
It determines its concentration in that tissue
equilibrium.
Most of GAs are equally soluble in tissue as in
blood
Lipid soluble more rapidly enter and slowly leave
adipose tissue
29. 6. Cerebral blood flow
Highly perfuse so quick entry,
Hasten by CO2 inhalation (cerebral
vasodilatation)
CO2 causes hyperventilation
30. Elimination
Mostly through lungs in unchanged form.
Channel of absorption (lungs) become channel
of elimination
Enter and persists in adipose tissue for long
periods – high lipid solubility and low blood flow.
They are not metabolized except Halothane
31. Second gas effect
The ability of the large volume uptake of one
gas (first gas) to accelerate the rate of rise of the
alveolar partial pressure of a concurrently
administered companion gas (second gas) is
known as the second gas effect.
32. Diffusion Hypoxia
Diffusion hypoxia is a decrease in PO2 usually
observed as the patient is emerging from an
inhalational anesthetic where nitrous oxide (N2O)
was a component.
The rapid outpouring of insoluble N2O can
displace alveolar oxygen, resulting in hypoxia.
All patients should receive supplemental O2 at the
end of an anesthetic and during the immediate
recovery
34. Ideal For Patient
Pleasant, nonirritating, no nausea or vomiting.
Induction and recovery should be fast with no
after effects
35. Ideal for Surgeon
Adequate analgesia, immobility and muscle
relaxation.
Noninflammable and nonexplosive
36. Ideal for Anaesthetic
Easy, Controllable and Versatile
Wide margin of safety.
Potent so that low concentrations are needed.
Rapid adjustments in depth of anaesthesia should be
possible.
Cheap, stable and easily stored.
Not react with rubber tubing or soda lime.
40. Ether
Colorless, highly volatile liquid with a pungent odor.
Boiling point – 35ºC
Produces irritating vapors and are inflammable and
explosive.
85 to 90 percent is eliminated through lung and
remainder through skin, urine, milk and sweat.
Can cross the placental barrier.
41. Ether: Advantages
Can be used without complicated apparatus.
Potent anaesthetic and good analgesic.
Muscle relaxation.
Wide safety of margin.
Respiratory stimulation and Broncho dilatation.
Does not sensitize the heart to adrenaline
Can be used in delivery.
Less likely hepatic or nephrotoxicity.
44. Nitrous Oxide
Non inflammable, nonexplosive, colorless and
odorless gas
Weak and low efficacy anaesthetic
Produces Light anaesthesia
45. Nitrous Oxide: Advantages
Quick and pleasant induction and recovery
Strong analgesic action even at low concentration
Requirement of toxic anaesthetic agent can be
reduced
No Nausea and vomiting
Non toxic to liver kidney and brain
47. Nitrous Oxide: Use
As an adjuvant with other agents
Obstetrics and terminal illness – 50% + O2
Maintenance anaesthesia – 30 to 60%
48. Nitrous Oxide: Precautions
Should always be used with 30% Oxygen
Should be avoided in patient with collection of
air in pleural, pericardial or peritoneal space.
On Prolonged use – Bone marrow depression
Megaloblastic Anaemia
49. Halothane
Fluorinated volatile liquid with sweet odour, non-irritant non-
inflammable and supplied in amber coloured bottle.
Potent anaesthetic, 2-4% for induction and 0.5-1% for
maintenance.
Boiling point - 50ºC
60 to 80% eliminated unchanged. 20% retained in body for 24
hours and metabolized.
50. Halothane: Advantages
Quick and pleasant induction and recovery
Non Inflammable – Electro cautery safe
Non Irritant – No effect on secretion,
Bronchospasm, Nausea and vomiting
Potent bronchodilator – Preferred in asthmatics
Do not react with Soda lime
51. Halothane: Disadvantages
Costly, Special Apparatus required
Poor Analgesic and Poor muscle relaxant
Sensitize heart to CAs – arrhythmias
Cerebral vasodilator – Increase ICT
induces Microsomal enzymes in patients and
exposed persons
52. Halothane on Uterus
Relaxation of uterine smooth muscle
Useful for manipulation of position of foetus in
perinatal period
Helpful in delivery of placenta postnatally
Not useful as analgesic or anaesthetic during
labour
55. Enflurane
Causes Hypotension with minimal effect on heart
Does not sensitize to CAs
Significant Muscle relaxation
Respiratory depression is more
↑ ICT, ↓ O2 consumption of cerebrum, Produce
convulsions
Less chances of hepatotoxicity
Can produce malignant hyperthermia
Same effect on uterus
56. Isoflurane
Isomer of Enflurane and have similar properties
but slightly more potent.
Intermediate onset induction
57. Isoflurane: Advantages
Rapid induction and recovery
Good muscle relaxation
Good coronary vasodilatation
Less Myocardial depression No renal or hepatotoxicity
Low nausea and vomiting
No dilatation of pupil and no loss of light reflex in deep
anaesthesia
No seizure and preferred in neurosurgery
Uterine muscle relaxation
58. Isoflurane: Disadvantages
Pungent and respiratory irritant
Special apparatus required
Respiratory depression
Maintenance only, no induction
ß adrenergic receptor stimulation
Costly
59. Sevoflurane
Rapid induction and recovery
Non irritant and Pleasant – Children
Bronchodilator – Asthmatics
Hypotension without tachycardia- MI or IHD
patients
Weak muscle relaxant
67. Thiopentone: Use
For Induction and ET intubation with muscle
relaxant
Endoscopies with short acting muscle relaxant
ECT
Short Surgical procedures
Status epilepticus
68. Objective
Intravenous general Anaesthetics
Administration of drugs for anaesthesia
Preanaesthetic Medication
Complication of General anaesthesia
69. Etomidate
Wide safety margin
Preferred in patient with poor cardiac function
Duration of action – 5 to 10 minutes
Metabolized in liver , excreted through kidney
and bile
70. Etomidate: Advantages
Rapid induction
Does not sensitize myocardium to adrenaline
No nausea and vomiting
Non-explosive and non-irritant
Short operations (alone)
71. Etomidate: Disadvantages
Involuntary movements during induction
Post operative Nausea and Vomiting
On Prolonged use- Suppression of adrenal cortex,
Hypotension, electrolyte imbalance and oliguria
Not used in Status epilepticus – Proconvulsant
Poorly soluble in water- Solution prepared in Propylene
Glycol
72. Propofol
Rapid Induction and Rapid recovery
One Dose – 4 minutes, t1/2 45 minutes
Recovery after multiple dose is much faster
Extensively metabolized
88% of an administered dose appears in the
urine
Metabolized by hepatic conjugation of the
inactive glucuronide metabolites
73. Propofol: Advantages
Inducing agent, Maintenance Agent
Suppression of laryngeal reflex – Endotracheal
intubation
Antiemetic and anticonvulsant action
Safe in pregnancy, can cross placenta
Suitable for OPD Anaesthesia
75. Benzodiazepines
PAM, Induction, Maintenance and Supplementation
Conscious Sedation
Produce Sedation, Amnesia, and Unconsciousness
in 5 minutes
No Respi/ CVS Depression.
Preferred for Endoscopies, Cardiac Catheterization,
Angiographies, Local/ regional Anaesthesia,
Fracture Setting
Balanced Anaesthesia
76. Ketamine
Dissociative anaesthesia
Commonly used as IV, IM, Oral, Rectal can also be given
Induction, Maintenance
Large Volume of Distribution, rapid Clearance
Metabolized in liver and excreted through Kidney and
Bile
77. Ketamine: Advantages
Effect of single dose last for 15 minutes
No Vomiting, No Hypotension
Little impairment of pharyngeal and laryngeal reflex
Bronchodilator – Asthmatics
Suitable for patient who lost circulatory volume due to
dehydration, Hemorrhage or burns
Poor risk and geriatric patient, Poor GC
Children – IM, rectal
79. Ketamine and Pregnancy
Contraindicated in pregnancy
Oxytocic actionm
Dangerous in eclampsia and preeclampsia
Can be used for assisted vaginal delivery – Less
Foetal and neonatal depression
80. Fentanyl
Opioid analgesic, given at the start of painful
procedures
Supplements Anaesthetics in balanced anaesthesia
In combination with BZDs – Diagnostic, Angiography
and minor procedures in poor risk patients
81. Fentanyl: Advantages
Patient is conscious- Patient cooperation can be
asked
Smooth onset and rapid recovery
Suppression of vomiting and coughing
Less fall in BP and no sensitization to adrenaline
83. Administration of Drugs in
Anaesthesia
Minimize deleterious effects – Preanaesthetic
medication
Maintain Physiological homeostasis
Better Post anaesthetic outcome
84. Preanaesthetic Medication
To relieve patients anxiety and apprehension
To produce amnesia
To prevent and control nausea and vomiting
Supplement analgesic, Less anaesthetic required
Decrease secretions and Vagal Stimulation
Decrease acidity and volume of gastric juice
85. Selection of preanaesthetic drug
Patient’s mental makeup
Anaesthetic agent to be used
Type of surgery
Presence of preoperative problems
86. Antimuscarinics Drugs:
Atropine, Glycopyrollate, Hyoscine
Decrease salivary and bronchial secretions
Prevents laryngospasm, bronchospasm, Nausea and
Vomiting
Prevent Vasovagal attack, Prevent Bradycardia,
Hypotension, Cardiac arrhythmia and arrest
Hyoscine – Sedation, amnesia, Antiemetic
They ↑ body temperature
Produce Pupillary dilation – alter pupil sign
88. Opioid Analgesics:
Morphine, Pethidine, Fentanyl
√ Good perioperative analgesic
√ Sedation and Hypnotic effects
x Respi. Depression, Hypotension, Post op Nausea,
Vomiting
x Constipation, Urinary retention
x Asthma can be precipitated
x Pupil constricted – Pupillary sign altered
90. Antiemetics:
Metoclopramide, Domperidone
Prevent Gastric reflux and aspiration pneumonia
Antiemetic action in perioperative period
Metoclopramide – EP Side effects
Promethazine- Antiemetic+ Sedative+
Anticholinergic
Promethazine reverses EP Side effects
91. Antacids, H2 Blockers, Proton Pump
Inhibitors
Antacids neutralize gastric acidity, H2 Blockers and
Proton Pump Inhibitors decrease acid secretion
Useful for emergency surgeries, Prolonged surgeries,
CS, Obese Patients
Given night before and in the morning
Prevent stress ulcers
92. Induction and Maintenance
Induction: Thiopentone/ other IV agent
Maintenance: 1. N2O + O2+ Ether
2. N20 + O2 + Halothane + SM Relaxant
3. O2 + Halothane + SM relaxant + Analgesic
Prevent/ Treat undesired side effects:
Anticholinergics, Antiemetics, Analgesics
93. After Anaesthesia
Oxygen: Prevent Diffusion Hypoxia
Neostigmine: Reverse effect of SM relaxant
Analgesic: Pain relief postoperatively
Antiemetic: to Control vomiting
95. During Anaesthesia
Bradycardia, Cardiac
arrhythmia, Cardiac arrest
Hypotension
↑ Salivary and bronchial
secretion
Respiratory depression,
Hypercapnia
Aspiration pneumonia
Delirium, Convulsions
Hypoxia
Awareness and recall of
events
Fire and explosion
96. After Anaesthesia
Nausea and Vomiting
Delayed recovery, Persistent sedation
Atelectasis and pneumonia
Liver and Kidney damage
Delirium
Nerve palsy
97. Drug Interactions
Patient on antihypertensive: fall in BP
Neuroleptics, Opioids, Clonidine and MAO
Inhibitors potentiate Anaesthetics
Halothane sensitize heart to adrenaline
Insulin need of diabetic increased
98. Summary
Stages of Anaesthesia
Ether, Nitrous Oxide
Second Gas Effect, Diffusion Hypoxia
Enflurane, Sevoflurane, Desflurane
Thiopentone, Propofol, Ketamine
Preanaesthetic Medication
Editor's Notes
Davy - Ether relieved severe Head ache
Faraday – Narcotic effects of ether
Horace wells - observed a young man injure his leg without pain while under the influence of nitrous oxide.
Morton – First Public demonstration of ether anaesthesia
John snow – Popularised chloroform
Suckling – Introduced halothane
Bind With GABA-A receptor protein and facilitate GABAnergic neurotransmission
Glycine at spinal cord
NMDA – aKetamine, N2o and xenon
Influence of minute volume on rate of induction is greatest in the case of agents which have high blood solubility because their PP in blood takes a long time to approach the PP in alveoli.
ratio of the concentration of an anesthetic in the blood phase to the concentration of the anesthetic in the gas phase when the anesthetic is in equilibrium between the two phases.
Lower anesthetic solubility in blood results in the "blood" compartment becoming saturated with the drug following fewer gas molecules transferred from the lungs into the blood.
Once the "blood" compartment is saturated with anesthetic, additional anesthetic molecules are readily transferred to other compartments, the most important one of which is the brain.
N2O +halothane
- Significant in case of low cardiopulmonary reserve
Hepatitis on repeted exposure – occurs after few days- Fever, anorexia, NV, Jaundice and eosinophilia
Malignant Hyperthermia – Genetically linked, can also occur with Succinyl choline, Neuroleptics
Dandrolene – blocks release of ca++
Properties are like halothane.
Differences are ---
Ultrashort action – Rapid redistribution in tissues
Recovery prolonged on excess administration
Apnoea, Hypotension when injecting drug rapidly.
Crush injury – Hyperkalemia, Thiopentone toxicity
Properties similar to Thiopentone – Dose which produces respi and CVS depression is much higher than anaesthetic dose
Action terminates because of redistribution
Concious Sedation - a technique of administering sedatives or dissociative agents with or without analgesics to induce a state that allows the patient to tolerate unpleasant procedures while maintaining cardiorespiratory function
Balanced Anaesthesia - A technique of general anesthesia based on the concept that administration of a mixture of small amounts of several neuronaldepressants summates the advantages but not the disadvantages of the individual components of the mixture.
Patient feels dissociated from the surroundings as well as from own body. There is analgesia, Amnesia, Sedation and patient is immobile
15 minutes – Diagnostic and minor surgical procedures, Traumatic wounds, Debridement and dressing, Severe burns, Cardiac catheterization,Angiography
Stimulates Sympthetic system – so BP and HR maintained
Administration of Drugs before anaesthesia to make it more pleasant and safe is known as Preanaesthetic medication
Mental make up – if unusually anxious patient BZDs are must
Anaesthetic- if irritant – atropine
Surgery – if vagal nerve involvement might be there
Instead of halothane Isoflurane, Sevoflurane, Desflurane can be used