Surgery and allied

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

8. Techniques
• History and physical examination
• Induction
• Maintenance
• Emergence

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

14. 14
Induction
intravenous
Faster onset
avoiding the
excitatory phase
of anaesthesia
inhalational
where IV access
is difficult
Anticipated
difficult
intubation.
patient
preference
(children)

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)

20. 20
Monitoring
• ECG
• Pulse oximetry (SpO2)
• Blood Pressure Monitoring (NIBP or IBP)
• Agent concentration measurement
• Low oxygen alarm
• Carbon dioxide measurement (capnography)
• Temperature measurement
• Circuit disconnect alarm

21. Monitoring depth of GA
• concentration inhalational anaesthetics
• bispectral index (computerized EEG analysis)
• vegetative response (perspiration, pupils, blood
pressure, pulse rate)
• clinical status, esp. waning muscle tonus
(not available when muscle relaxants are used)

22. TOXICITY OF INHALATIONAL AGENTS
1. Hepatotoxic agent Isoflurane
2. Nephrotoxic agent Barbiturate
3. Cardiotoxic agent Enflurane
Halothane
4. Flammable agent Ether

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

30. Local anaesthesia
topic
infiltrative
cunduct
epidural
subarachnoid
scheme by J.Cendelín

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

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

47. Treatment of Toxicity

48. 48