complete and detail study on the topic of general anesthetics by the collaboration of teacher and students for the student , teachers and other health care professionals to learn more on the topics

1. General anaesthetics
Ravish Yadav

2. CONTENT
1 . Definitions
2 . Principles of general anaesthesia
3 . Difference between general and local
anaesthetics
4 . Different stages of general anaesthesia
5 . Classification of general anaesthetics
6 . Mechanism of action general anaesthetics
7 . Comparative study of general anaesthetics
8 . Indications
9 . Drug interaction
10. Pre-anaesthetic medication

3. •Definition : Anesthesia (an =without, aisthesis =
sensation )
•Anesthesia is medication that attempts to eliminate
pain impulse from reaching the brain.
•In general anesthesia this is accomplished by putting
the patient asleep.
STREPTOKINASESTREPTOKINASEStreptokinaseANAESTHESIA

4. •A drug that brings about a reversible loss of all
sensation and consciousness.
•These drugs are generally administered by an
anesthesiologist in order to induce or maintain
general anesthesia to facilitate surgery and
unpleasant procedure.
•General anesthetics depress the central nervous
system.
•It causes immobility and muscle relaxant.
What Are General Anaesthetics?

5. Principle of General Anaesthesia
The practice of anesthesia is usually neither therapeutic
nor diagnostic.
The development of new anesthetic agent have
been driven by three general objectives –
 Sustaining physiologic homeostasis during surgical
procedure. That may involve – reperfusion of
ischemic tissue,major blood loss,fluid shift and
impaired coagulation.
 Minimize the potentiolly deleterous effects of
anesthetic agent and technique.
 Improving postoperative out comes.

6. Hemodynamic Effect of General
Anaesthetics
Decrease in arterial blood loss.
The causes include direct –
#. Vasodilation.
#. Myocardial depression.

7. Respiratory Effect of general anaesthetic
Decrease or eliminate both ventilatory drive and the reflexes that maintain air way
potency.

8. Hypothermia
 Temperature reduces less than 30 degree
during surgery.
 Metabolic rate and total body oxygen
consumption decreases with general
anesthetis by 30% , reduce heat generation.

9. Nausea And Vomitting
GENERAL ANAESTHETICS
post operative
period
Stimulate CTZ and brain stem
vomiting center
Nausea and vomiting

10. Stages of anaesthesia
• Stage I : Analgesia :
Start from beginning of anesthetic administration and
last upto loss of consciousness, feels a dream like state,
reflexes and respiration remain normal.
• Stage II : Stage of delirium :
From loss of consciousness to beginning of
irregular respiration.Apparent excitement is
seen. Muscle tone increases. Jaws are tightly
closed. Heart rate and blood pressure may rise.

11. Stage III : Surgical anesthesia :
Extends from onset of irregular respiration to
cessation of spontaneous breathing. This has
been devided into 4 planes-
Plane 1: This plane ends when eyes become
fixed.
Plane 2: Loss of corneal and laryngeal reflexes.
Plane 3: Pupil start dilating and no light reflexes.
Plane 4: Dilated pupil, decrease muscle tone ,BP falls.
Stage IV : Medullary paralysis :
Respiratory and vasomotor control ceases.

13. Lipid theory of General Anaesthetics
• Based on the fact the anesthetic action is correlated with the
oil/gas coefficients.
@. Higher the solubility of general
anesthetics in oil greater is the anesthetics action.

15. Minimum alveolar Concentration
(MAC)
MAC is the concentration necessary to prevent responding in
50% of population.
Blood gas partition coefficient
Lower the Blood : Gas partition coefficient the faster the
induction and recovery.

16. Other Theories included
Binding theory:
Anesthetics bind to hydrophobic portion
of the ion channel

17. Discription General Anesthetics Local Anesthetics
1. Site of action Central Nervous System Peripheral Nerves
2.Area of body involved Whole body Restricted area
3. Conciousness Lost Unaltered
4. Major surgery Preferred Can not be used
5. Minor surgery Can not be used Preferred
6. Poor health patient Risky Safer
7. Care of vital function Essential Usually not needed

18. 1. INHALATIONAL
a. Gas
* Nitrous oxide
b. Volatile liquids
* Halothane
* Enflurane
* Isoflurane
* Desflurane
* Sevoflurane
2. INTRAVENOUS
* Thiopentone sod.
* Etomidate
* Propofol
* Ketamine
* Methohexitone sod.

20. • Halothane
• Enflurane
• Isoflurane
• Desflurane
• Sevoflurane
Halogenated
compounds:
Contain
Fluorine
and/or
bromide
Simple, small
molecules

21. • Used in combinationwith Inhaled anesthetics to:
– Supplement general anesthesia
– Maintain general anesthesia
– Provide sedation
– Control blood pressure

22. DRUG BLOOD
: GAS
(PC)
OIL:
GAS
(PC)
MAC
%V/V
INDUCTI
ON/RECO
VERY
MAIN
ADVERS
EFFECT
NOTES
ETHER 12.0 65 1.9 slow Respiratory,
nausia&
vomiting
Now
obsolete
HALOTHANE 2.4 220 1.9 Medium Hepatotoxicity Significant
use
NITROUS
OXIDE
0.5 1.4 100 Fast Few adverse
effect
Sole
anesthetic
INFLURANE 1.9 98 0.7 Medium Risk of
convulsion
Less risk
of

23. ISOFLURANE 1.4 91 1.2 Medium Risk of
coronary
ischemia
Alternative
to
halothane
DESFLURANE 0.4 23 6.1 Fast RTI,
cough,
bronchospasm
Alternative
to nitrous
oxide
SEVOFLURANE 0.6 53 2.1 Fast Renal toxicity Recently
use similar
to
desflurane

24. • SITES OF ACTION
• In principle, general anesthetics could
interrupt nervous system function at myriad
levels, including peripheral sensory neurons,
the spinal cord, the brainstem, and the
cerebral cortex.

25. CELLULAR MECHANISMS
General anesthetics produce two important
physiologic effects at the cellular level.
 First, inhalational anesthetics hyperpolarize
neurons, possibly an important effect on neurons
serving a pacemaker role and on pattern-generating
circuits and in synaptic communication, since
reduced excitability in a postsynaptic neuron
diminishes the likelihood that an action potential
will be initiated in response to neurotransmitter
release.

26. Second, at anesthetizing concentrations, both
inhalational and intravenous anesthetics have substantial
effects on synaptic transmission and much smaller effects
on action-potential generation or propagation.
Inhalational anesthetics inhibit excitatory synapses and
enhance inhibitory synapses via effects on pre- and
postsynaptic sites.

27. The inhalational anesthetic isoflurane clearly can inhibit
neurotransmitter release and produce a small reduction in
presynaptic action potential amplitude (3% reduction at MAC
concentration) that inhibits neurotransmitter release, a
significant effect because the reduced action potential is
amplifiedinto a larger reduction in presynaptic Ca2+ influx,
and thence into an even greater reduction intransmitter release.
Intravenous anesthetics produce a narrower range of
physiological effects. Most of the intravenous agents act
predominantly by enhancing inhibitory neurotransmission,
whereas ketamine predominantly inhibits excitatory
neurotransmission at glutamatergic synapses.

28. Molecular mechanism of the GA :
GABA –A : Potentiation by Halothane,
Propofol, Etomidate
NMDA receptors : inhibited by Ketamine

29. • Receptor sits in the membrane of
its neuron at the synapse
• GABA, endogenous compound,
causes GABA to open
• Receptor capable of binding 2
GABA molecules, between an
alpha and beta subunit
– Binding of GABA causes a
conformational change in
receptor
• Opens central pore
• Chloride ions pass down
electrochemical gradient
– Net inhibitory effect, reducing
activity of the neuron

31. Anesthetic
Suppression of
Physiological
Response to
Surgery

33. BLOOD GAS PARTITION
COEFFICIENT

36. • Volatile liquid at room temperature.
• Light sensitive
• Halothane + oxygen = inflammable,
norexplosive
• PHARMACOKINETICS
• slow induction & recovery.
• Eliminated unchange via lungs.
• Metabolised in liver by Cyt-P450.

37. Commonly used in children, where
preoperative placement if an iv catheter
can be difficult.
Anesthesia is produced at end –tidal
concentration of 0.7 -1%.
CVS : cardiac arrhythmia,depression of
myocardial contraction.
CLINICAL USES
SIDE EFFECTS

38. >Depression of respiration.
MUSCLES : Malignant hyperthermia.
KIDNEY: Decrease renal blood flow and g.f.r.
LIVER AND GIT: Cause-halothane induced
hepatitis & nausea and vomiting.
DRUG INTERACTION : Halothane +
adrenaline,theophylline => arrhythmia may be
precipitated.
RESPIRATORY SYSTEM

39. • CONTRAINDICATION: Hepatic dysfunction
and/or jaundice.
• OVER DOSE: On over dose patient move to
fresh airway or inserting an emergency airway.

40. THIOPENTAL
• Barbiturate with very high lipid solubility.
• Rapid action, short duration.
• Slowly metabolised in liver and liable to
accumulate in body fat.
• Risk of sever vasospasm if accidently
injected into artery.
Intravenous Anaesthetics

41. PROPOFOL
Rapidely metabolised.
Very rapid recovery.
Useful for day-case surgery.
Safe for use in pregnant women.
KETAMINE
Analogue of phencyclidine with similar properties.
Act on NMDA receptor.

42. Onset of action is relatively slow(2-5 minutes).
Produce dissociative anaesthesia, in which
patient remain conscious though sensitive to
pain.

43. • Nitrous oxide (50%) has been used with oxygen for
dental and obstetric analgesia.
• Isoflurane ,Desflurane is preferred for neurosurgery.
• Sevoflurane is suitable both outpatient as well as
inpatient.
• Thiopentone sod. Occasionally used for control of
convulsion.
• Propofol : injection and perfusion is frequently
used for total i.v. anaesthesia when supplemented
by fentanyl.

44. • Ketamine have been used for operations on
the head and neck.

45. • Kitamine is dangerous for hypertensives ,in
ischemic heart disease. And
• Halothane is not given in liver disease.
• Sevoflurane is not given to sever hepatic
dysfunction , jaundice, fever .
• Nitrous oxide Is contraindicated in first two
trimester of pregnency because its effect on
DNA production => undesirable out comes.

46. Atelectasis: partial collapse or
incomplete inflation of the lung.

48. It is the use of drugs prior to anesthesia to make it
more safe and pleasant.
• To relieve anxiety – benzodiazepines.
• To prevent allergic reactions – antihistaminics.
• To prevent nausea and vomiting – antiemetics.
• To provide analgesia – opioids.
• To prevent bradycardia and secretion – atropine.

49. Decrease secretions and vagal stimulation caused by
anaesthetics.
Decrease acidity and volume of gastric juice.
Antiemetic effect extending to the post operative period.

50. 1. Sedative-anti anxiety drug => diazepam(5mg),
lorazepam (2mg-0.05mg/kg).
2. Anticholinergic drugs => Atropine and hyoscine are
use to reduce salivary & bronchial secretions.
3. H2 Blockers => Famotidine , & ranitidine are use to
reduce the PH & gastric juice.
4. Proton pump inhibitors => Omeperazole,
5. Antiemitic => metoclopramide (10-20 mg)
6. 5HT blockers => ondensetron (4-8 mg iv)