A BRIEF INTRODUCTION AND CLASSIFICATION OF ANESTHESIA

2. If the best place for you in the world is
hospital, be a doctor; but; if your best place
in the hospital is operation theatre , be an
anesthesiologist.
PRESENTED BY; HIRAAROOJ
UCP

3. CONTENTS
 Introduction to anesthesia
 Definition
 Classification
 Stages of anesthesia
 General anesthesia
 Inhalational anesthesia
 Local anesthesia
 Conclusion

4. INTRODUCTION TO ANESTHESIA
anesthesia
‘An’
(without)
‘anesthesis
’
(sensation
s)

5.  ANESTHESIA refers to the practice of
administering medications either by injection or
inhalation that block the feeling of pain and
other sensations , or that produce a deep state
of unconsciousness that eliminates all sensations
that allows medical and surgical procedures to be
undertaken without causing undue distress or
discomfort.
ANESTHESIA
DEFINITION
In summary, anesthesia is a speciality in which an
extensive knowledge of phsiology and
pharmacology can be applied to the care of
patients in a unique one on one intensive care
setting.

6. General anesthesia
Local or regional
anesthesia
CLASSIFICATION OF
ANESTHESIA

7. PATIENT FACTOR IN SELECTING
ANESTHEISA
 STATUS OF ORGAN SYSTEM
• Cardiovascular system
• Respiratory system
• Liver and kidney
• Nervous system
• Pregnancy
o CONCOMITANT USE OF DRUGS
• Multiple adjunct drugs
• Concomitant use of other drugs

8.  State characterized by unconciousness ,
analgesia, amnesia, skeletal muscle relaxation and
loss ofconciousness.
PURPOSE
1. Analgesia
2. Amnesia
3. Immobility
4. Hypnosis
5. Paralysis

9. General
anesthetics
Inhaled
Gas Volatile liq
Intravenous
Barbiturates
Dissociative
Opioids

10.  Induction
 Maintenance
 Recovery
 Depth of anesthesia
 Stage 1___ analgesia
 Stage 2____ excitement
 Stage 3 ___ surgical anestheisa
 Stage 4 ___ Medullary paralysis

12. BIOCHEMICAL MECHANISM OF ACTION
 Biochemical mechanism of action of general
anesthetics is not well understood. To induce
unconciousness, anesthetics have myriad sites
of action and affect the central nervous system
at multiple levels.
 Common areas of central nervous system whose
functions are interrupted or changed during
general anesthetics include the:
 Cerebral cortex
 Thalamus
 Reticular activating system
 Spinal cord

13. BIOCHEMICAL MECHANISM OF ACTION
 Current theories on the anesthetized state
identify not only target site in the CNS but also
neural network and loops whose interaction is
linked with unconsciousness. Potential
pharmacologic targets of general anesthesia are:
 GABA
 Glutamate –activated ion channel
 NMDA receptor families
 Voltage gated ion channels
 Glycine and serotonin receptors

14. BIOLOGICAL MECHANISM OF ACTION
 These drugs usually increase the threshold for firing
of cns. Neurons. The potency of inhaled anesthetics
is roughly proportional to their lipid solubility.
 Mechanisms of action include effects of ion channels
with interaction of anesthetics, with membrane lipids
or proteins with subsequent effects on central NTR
mecahnisms
 Inhaled anesthetics, facilitate GABA mediated
inhibition at GABAA receptors
(these receptors are sensitive to clinically relevant
concentrations of the anesthetic agents and exhibit
the appropriate streospecific effects in case of
enantiomeric drugs)

16. RISKS OF GENERAL ANESTHESIA
 Obstructive sleep apnea
 Seizures
 High blood pressure
 Alcoholism
 Smoking
 History of reactions to anesthesia
 Drug allergies
 Diabetes

17. SIDE EFFECTS OF GENERAL ANESTHESIA
 Confusion and memory loss
 Dizziness
 Difficulty passing urine
 Bruising or soreness from IV drip
 Nausea and vomiting
 Shivering and feeling cold
 Sore throat

18.  Many inhalation anaesthetics that were once
widely used, such as ether, chloroform,
trichloroethylene, cyclopropane, methoxyflurane
and enflurane, have now been replaced in clinical
practice, particularly by isoflurane, sevoflurane
and desflurane which have improved
pharmacokinetic properties, fewer side effects
and are non-flammable. Of the older agents,
nitrous oxide is still used widely (especially in
obstetric practice), and halothane now only
occasionally. Inhalation anaesthetics are most
commonly used for the maintenance of
anaesthesia.

19. A. CLASSIFICATION AND
PHARMACOKINETICS
 Solubility
 Inspired gas partial pressure
 Ventilation rate
 Pulmonary blood flow
 Arteriovenous concentration gradient
B. ELIMINATION
C. MINIMUM ALVEOLAR ANESTHETIC
CONCENTRATION
D. EFFECTS OF INHALED ANESTHETICS

21.  Local anesthetics bind reversibly to a specific
receptor site within the pore of the Na+ channels in
nerves and block ion movement through this pore.
When applied locally to nerve tissue in appropriate
concentrations, local anesthetics can act on any part
of the nervous system and on every type of nerve
fiber, reversibly blocking the action potentials
responsible for nerve conduction. Thus, a local
anesthetic in contact with a nerve trunk can cause
both sensory and motor paralysis in the area
innervated. These effects of clinically relevant
concentrations of local anesthetics are reversible
with recovery of nerve function and no evidence of
damage to nerve fibers or cells in most clinical
applications.

22. MECHANISM OF ACTION
 Local anesthetics block voltage gated sodium
channels and reduce the influx of sodium ions,
thereby preventing depolarization of membrane and
blocking conduction of the action potential. Local
anesthetics gain access to their receptors from the
cytoplasm or the membrane. Because the drug
molecule cross the lipid membrane to reach the
cytoplasm, the more lipid soluble form reaches
effective intracellular conc than does the ionized
form. On the other hand once, inside the axon, the
ionized drug is the more effective blocking entity.
Thus both the unionized and the ionized forms of the
drug play important roles___ first in reaching the
receptor site and the second in causing the effect.

23.  The affinity of the receptor site within the
sodium channel for the local anesthetic is the
function of the state of the channel, whether it
is resting, open or inactivated and therefore
follows the same rules of use dependence and
voltage dependence for sodium channel blocking
antiarrhythmic drugs.
 In particular, if other factors are equal, rapidly
firing fibers are usually blocked before slowly
firing fibers.
 High conc. of extracellular k may enhance local
anesthetic activity, whereas elevated ca may
antagonize it.

25. • Local anaesthetics are either esters or amides. Esters are
rapidly hydrolysed by plasma and tissue esterases, and
amides are metabolised in the liver. Plasma half-lives are
generally short, about 1–2 h.
• Unwanted effects are due mainly to escape of local
anaesthetics into the systemic circulation.
• Main unwanted effects are: – central nervous system
effects, agitation, confusion, tremors progressing to
convulsions and respiratory depression – cardiovascular
effects, namely myocardial depression and vasodilatation,
leading to fall in blood pressure – occasional
hypersensitivity reactions.
• Local anaesthetics vary in the rapidity with which they
penetrate tissues, and in their duration of action.
Lidocaine (lignocaine) penetrates tissues readily and is
suitable for surface application; bupivacaine has a
particularly long duration of action.
UNWANTED EFFECTS AND PHARMACOKINETICS
OF LOCAL ANAESTHETICS

26. CLINICAL USES OF LOCAL ANAEHETICS
• Local anaesthetics may be injected into soft tissue
(e.g. of gums) or to block a nerve or nerve plexus.
• Co-administration of a vasoconstrictor (e.g.
adrenaline) prolongs the local effect.
• Lipid-soluble drugs (e.g. lidocaine) are absorbed from
mucous membranes and are used as surface
anaesthetics.
• Bupivacaine has a slow onset but long duration. It is
often used for epidural blockade (e.g. to provide
continuous epidural blockade during labour) and spinal
anaesthesia. Its isomer levobupivacaine is less
cardiotoxic if it is inadvertently administered into a
blood vessel.

28. REFERENCE
 GOODMAN AND GILLMAN PHARMACOLOGY
 KATZUNG AND TREVORS PHARMACOLOGY
 LIPPINCOT’S ILLUSTRATED REVIEWS OF
PHARMACOLOGY
 K.D TRIPATHI ESSENTIALS OF PHARMACLOGY