Anesthetics in general medicine and eyecare

1. ANESTHETICS
Presented by GROUP 3

2. History - The Primitive techniques
• Club
• Strangulation
• Alcohol
• Mesmerism
• Plants

3. History – contd.
 General anesthesia was
absent until the mid-
1800’s
 Original discoverer of
general anesthetics
 Crawford Long, Physician
from Georgia: 1842,
ether anesthesia
 Chloroform introduced
 James Simpson: 1847
 Nitrous oxide
 Horace Wells in 1845
19th Century physician
administering Chloroform

4. History – contd.
 William T. G. Morton, a Boston
Dentist and medical student -
October 16, 1846 - Gaseous ether
 Public demonstration gained world-wide
attention
 Public demonstration consisted of an
operating room, “the ether dome,”
where Gilbert Abbot underwent surgery
for removal of a neck tumour in an
unconscious state at the Massachusetts
General Hospital
 But, no longer used in modern
practice, yet considered to be the

5. They did it for a better tomorrow!

6. Analgesics
Analgesics is sometimes confused
with anesthesia. Below is the difference
between them

7. Anesthetic
A medication that causes loss of
sensation. This is sometimes used to
alleviate pain or for loss of
consciousness for surgical procedures.
It relieves pain by numbing nerve
impulses. Its action is reversible when
right dose is administered

8. Anesthesia
Loss of consciousness
Analgesia (loss of pain sensation)
Adequate muscle relaxation
Analgesia
•Loss of sensation to pain

9. Types of anesthesia
General
Regional
Local

10. GENERAL ANESTHESIA
They induce unconsciousness and
eliminate pain by blocking the general
body innervation
usually administered by
 IV
 inhalation for the purpose of
In ophthalmology general anesthesia is rarely used but does have a place
in physically or emotionally traumatic surgeries and in non co-operative
children.
General anesthesia
need for
unconsciousness
‘Amnesia-hypnosis’
need for analgesia
‘Loss of sensory and
autonomic reflexes’
need for muscle
relaxation

11. REGIONAL ANESTHESIA
 Regional anesthesia is an injection of a local
anesthetics around nerves or into the trunk of a
nerve so that all the areas supplied by these
nerves will not send pain signals to the brain.
 They anesthetized area is usually larger than the
area affected by local anesthesia.
 Eg: retrobulbar injection to numb all eye movents by
targeting the oculomotor nerve

12. LOCAL ANAESTHESIA
 It is an anesthetic agent given to temporarily
stop the sense of pain in a particular area of
the body. The entire area supplied by a nerve
is not be anesthetized. Only a certain
branches does.
 Patient remains conscious during a local
anesthetic.
 Giving ametocaine to numb the cornea (only
axons of the ophthalmic division are severed)

13. Mechanism of action
GENERAL ANESTHESIA
 General anesthetics have two main routes:
Inhalation
 Most general anesthetics target GABAA
receptor channel
 Intravenous

14. General anesthesia
Inhalational
Gas
Nitrous oxide
Zenon
Volatile liquids
Ether
halothane
enflurane
isoflurane
desflurane
Sevoflurane
methoxyflurane
Intravenous
Slower acting
Dissociative
anesthesia
ketamine
opiod analgesia
fentanyl
Benzodiazepines
diazepam
lorazepam
midazolam
Inducing agents
Thiopentone sod.
methohexitone
sod.
propofol
Etomidate
droperidol

15. Inhaled anesthetics
 Two main drugs used are
 Gases eg Nitrous oxide, cyclopropane
 Halogenated anesthetics e.g. halothanes,
isoflurane, desflurane and influrane
 Inhaled anesthetics have varying potency in proportion to
their lipid solubility.
 Every inhaled anesthetic has a specific MAC value.

16. A MAC (minimal alveolar anesthetic
concentration)
 is defined as the concentration of inhaled
anesthetic as a % of inspired air, at which
50% of patients will be anesthetized.
 MAC is a measure of potency: ED50.

17. Comparison between Nitrous Oxide
and the Halothanes

18. Facts about inhaled anesthetics
 Rates of onset and recovery depend on the blood-gas ratio:
a. The more soluble the anesthetic in the blood, the slower the
anesthesia.
b. Anesthetics with high blood-gas ratios are associated with slow
onset.
c. Anesthetics with high blood-gas ratios are associated with slow
recovery.
d. Anesthetics with low blood-gas ratios have fast onset and
recovery.

19. Intravenous anesthetics
 Their onset of action faster than the fastest of the
gaseous agents so they are used for induction of
anesthesia.

20. 1. Thiopental
 Barbiturate used for induction
 Highly lipid soluble; rapid onset; short-acting due
to redistribution
Disadvantage:
Severe vasospasm
Cardiovascular depression
Hypersensitivity reactions

21. Midazolam
 Benzodiazepine used for:
 Preoperative sedation
 Anterograde amnesia
 Induction
 Outpatient surgery
Depresses respiratory function

22. Propofol (Michael Jackson's Killer)
 Used for induction and maintenance of
anesthesia
 Antiemetic
CNS and cardiac depressant
 It can induce prolonged sedation.
 Similar to thiopentone, but more rapidly
metabolized (rapid induction and recovery) so it
is suitable for one day surgery.
 Lacks tendency to induce involuntary movement
and adrenocortical suppression.

23. Propofol (Michael Jackson's Killer)
Propofol. The onset of its
action begins after 30 s. After
a single dose patient recovers
after 5 min with a clear head
and no hangover.

24. Fentanyl
 Opiate used for induction and maintenance
of anesthesia
 Depresses respiratory function – be careful
of your asthma patient

25. Ketamine
 Dissociative anesthetic
 NMDA-receptor antagonist
 Induction of anesthesia
 Emergent delirium, hallucinations
 Cardiovascular stimulation
 increases intracranial pressure
 Disadvantages:
 Cerebral hemorrhage
 Dysphoria and hallucinations

30. Mechanism of action of general
anesthetics
Most injectable and inhaled anesthetic agents produce anesthesia by
enhancing GABA-mediated neuronal transmission, primarily at
GABAA receptors. GABA is an inhibitory neurotransmitter found
throughout the CNS. Some inhaled anesthesia may also act by
inhibiting such excitatory ion channels as neuronal nicotinic and
glutamate receptors.
Note: Ketamine does not affect GABAA it
antagonizes glutamic acid on NMDA receptor

31. 4 (Four) Stages and signs !!!
• Traditional Description of signs and
stages of GA - Also called Guedel`s sign
• Typically seen in case of Ether

32. Stages of GA
Stage I: Stage of Analgesia
 Starts from beginning of anaesthetic inhalation and lasts upto
the loss of consciousness
 Pain is progressively abolished during this stage
 Patient remains conscious, can hear and see, and feels a dream
like state
 Reflexes and respiration remain normal
 It is difficult to maintain - use is limited to short procedures
only

33. Stage II: Stage of Delirium and Excitement:
 From loss of consciousness to beginning of regular respiration
 Excitement - patient may shout, struggle and hold his breath
 Muscle tone increases, jaws are tightly closed.
 Breathing is jerky; vomiting, involuntary micturition or defecation
may occur.
 Heart rate and BP may rise and pupils dilate due to sympathetic
stimulation.
 No stimulus or operative procedure carried out during this stage.
 Breatholding are commonly seen. Potentially dangerous responses
can occur during this stage including vomiting, laryngospasm and
uncontrolled movement.
 This stage is not found with modern anaesthesia – preanaesthetic
medication, rapid induction etc.

34. Stage III: Stage of Surgical
anaesthesia
Extends from onset of regular respiration
to cessation of spontaneous breathing.
 This has been divided into 4 planes:
Plane 1: Roving eye balls. This plane ends when
eyes become fixed.
Plane 2: Loss of corneal and laryngeal reflexes.
Plane 3: Pupil starts dilating and light reflex is
lost.
Plane 4: Intercostal paralysis, shallow
abdominal respiration, dilated pupil.

35. Stage IV: Medullary /
respiratory paralysis
 Cessation of breathing failure of circulation
death
 Pupils: widely dilated
 Muscles are totally flabby
 Pulse is imperceptible
 BP is very low.

36. Local anesthetics
Drugs used to provide local anesthesia are also used
to achieve regional anesthesia. Regional anesthesia
is an injection of a local anesthetics around nerves
so that the area supplied by these nerves will not
send pain signals to the brain. They anesthetized
area is usually larger than the area affected by local
anesthesia.

37. Mechanism of action
 Mechanisms:
Nonionized form crosses axonal membrane
- From within, ionized form blocks the inactivated Na+ channel
- Slows recovery and prevents propagation of action potentials
When local anesthetics are applied to the area that they numb,
they need to get to the axon by crossing to the membrane. Only
non ionized forms R-NH2 can enter the axon through the
membrane. Upon entering the axon, only the ionized forms can
block the sodium channels which causes depolarization of the
sodium channel consequently numbing the area.
Ionized form RNH3+

39. Classification of Local Anesthetics
based on chemical group
 - Esters:
procaine, cocaine, benzocaine are metabolized
by plasma and tissue esterases
 - Amides:
lidocaine, bupivacaine, mepivacaine are
metabolized by liver amides

40. Esters
Two types
1. Esters of benzoic acid (BA)
2. Esters of para amino benzoic acid.( PABA)

41. Esters of benzoic acid
 Butacaine
 Cocaine
 Ethyl aminobenzoate (benzocaine)
 Hexylcaine
 Piperocaine
 Tertracaine

42. Esters of para-aminobenzoic
acid
Cloroprocaine
Procaine
propoxycaine

43. Amides
 Articaine
 Bupivacaine
 Dibucaine
 Etidocaine
 Lidocaine
 Mepivacaine
 Prilocaine
 Roppivacaine

44. May also be classified into
a. Short acting – cocaine, procaine
b. Intermediate acting – lidocaine,
mepivacaine, dibucaine, prilocaine
c. Long acting – tetracaine,
bupivacaine, etidocaine

45. Metabolism
Esters are metabolized by the
plasma by enzymes esterase
amides are metabolized by liver
by the enzyme hepatic amidases

46. Clinical note
 Don’t give amides to patients with poor
liver function. Eg. patient with any form of
hepatitis! WHY?
 the amides will pile up due inability of the
liver to metabolize. Hence elicit a
complete history in your patient. In cases
where patients have liver problem; your
local anesthesia should be an ester.

47. How do we know which cocaine
derivative is an amides or ester?
The trick: the letter i
 in almost all cases if an i precedes the
“caine” sound, the drug is an amide but if not,
it is an ester.

48. Amides Esthers
 Articaine
 Bupivacaine
 Dibucaine
 Etidocaine
 Lidocaine
 Mepivacaine
 Prilocaine
 Roppivacaine
 Butacaine
 Cocaine
 Ethyl aminobenzoate (benzocaine)
 Hexylcaine
 Tertracaine
 Cloroprocaine
 Procaine
 propoxycaine

49. Limiting local anesthetics
 All local anesthetics should be co-administered
with alpha-1 agonist. E.g. phenylephrine,
metoximine. WHY?
Reason;
The alpha-1 agonist will cause a powerful
vasoconstriction and limit the access of
surrounding tissues to the local anesthetics.

50. The Cocaine saga
I am the only local anesthetics that
does not need an alpha-1 agonist.
WHY?
ANS: I am a NEP re-uptake blocker.
NOTE: it causes NEP build up in the synapsis. From the
synapsis NEP binds to the alpha-1 receptors and causes
vasoconstriction in the surrounding tissues. Therefore you don’t
need an alpha-1 agonist after administration of cocaine.

51. Side effect
 Local anesthetics can cause allergies
especially the ester groups because they
form PABA. All PABA containing compounds
can always cause allergic reactions.
 Therefore check your creams that you
buy on the market.

52. OCULAR FOCUS
QUICK NOTES

53. Injection:
amide + longer acting ester
= longer-acting motor and
sensory anesthesia.

54. Targets of injectable agents
 muscle cone of the orbit-blocks all motor
and sensory nerves of eye
 directly into orbicularis muscles into CNVII
 stylomastoid foramen –these two cause a
complete loss of facial nerve on that side
of face

55. Topical anesthesia
 Any test requiring contact with the cornea is made
more comfortable if topical anesthetic is used first
Indeed, some of these tests would be nearly
impossible for the patient to endure if the cornea was
not numbed first.
 In addition to numbing the cornea and conjunctiva
for testing, topial anesthetic is required in
procedures such as removal of a foreign body or
scraping a corneal lesion

56. Tetracaine
is the most popular topical
anesthetic. Tetracaine is
unpreserved.

57. Proparacaine and benoxinate
 contain preservatives and are effective in
anesthetizing the corneal nerve endings
through topical application.
 These formulations are highly osmotic and
therefore sting and burn when applied.

58. Home use?
never prescribed for a patient
to use at home. Frequent use
interferes with the healing
process and can cause corneal
melting

59. Please don’t rub your eyes!
the cornea now lacks sensation,
the patient could conceivably
rub hard enough to cause a
corneal abrasion.

60. Toxicity Potential
 . All anesthetics have a potential to become toxic
in higher doses. Individuals may experience
lightheadedness, ringing in their ears, or blurred
vision.
 At even higher doses, respiratory arrest can
occur, as well as convulsions, coma and death.

61. punctual occlusion
When topical anesthetic is used,
punctual occlusion can reduce the
amount of drug that is absorbed into
the system

62. MUSCLE RELAXANTS
Used mainly in anesthesia protocols
(EMERGENCIES) or in the (Intensive Care Unit)
ICU to afford muscle relaxation and/or
immobility. Used to relieve symptoms such as
spasms ,pain and hyperreflexia
Muscle relaxants interact with nicotinic ACh
receptors at the neuromuscular junction.

63. MECHANISM
 NORMAL CHOLINERGIC TRANSMISSION
Normally, a nerve impulse arrives at the motor nerve terminal, initiating an
influx of calcium ions, which causes the exocytosis of synaptic vesicles
containing acetylcholine.
Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by
acetylcholine esterase (AchE) or bind to the nicotinic receptors located on
the motor end plate.
The binding of two acetylcholine molecules results in a conformational
change in the receptor that opens the sodium-potassium channel of the
nicotinic receptor. This allows Na + and Ca 2+ ions to enter the cell and K+
ions to leave the cell, causing a depolarization of the end plate, resulting
in muscle contraction.

64. Normal end plate function can be blocked by
two mechanisms.
1.Nondepolarizing agents (competetive),
such as tubocurarine,
block the agonist , acetylcholine, from
binding to nicotinic receptors and activating
them, thereby preventing depolarization.

65. Major Non-depolarizing MRs
Atracurium
 Rapid recovery
 Safe in hepatic or renal impairment
 Spontaneous inactivation to laudanosine
 ,Laudanosine can cause seizures
Mivacurium
 Very short duration
 Metabolized by plasma cholinesterases

66. 2.depolarizing agents, (noncompetitive)
 Alternatively, depolarizing agents such as
succinylcholine, are nicotinic receptor
agonists which mimic Ach, block muscle
contraction by depolarizing to such an
extent that it desensitizes the receptor
and it can no longer initiate an action
potential and cause muscle contraction

67. MRs
mainly in anesthesia
protocols (EMERGENCIES) or
in the (Intensive Care Unit)

68. Beware of
Anesthetics!

69. Thank you
Any question?