1.
Inhalational Anesthetics
PGI Alm
eñana

2.
General vs regional anesthesia
RA – aim to block a certain part
of the body
- e.g Appendectomy
GA – brain is the target organ
- block CNS causing patient
to fall asleep

3.
Course of general anesthesia
1.Induction – giving medications prior to
intubation of patient (Sedative, Muscle
Relaxants)
2.Maintenance – Muscle Relaxants,
Gases (now running on ET tube)
3.Emergence – post op medications
given

4.
Stages
1.Amnesia
2.Delirum/Excitement/Uninh
ibited Response
3.Surgical Anesthesia
4.Impending
Death/Overdosage

5.
1. AMNESIA
• From beginning of induction to loss of
consciousness (loss of eyelid reflex)

6.
2. Delirum/Excitement/Uninhibited
Response
From loss of consciousness to onset of
automatic breathing
 Agitation, delirium, irregular respiration,
breath holding
 Dilated pupils and eyes are
divergent
 Vomiting, laryngospasm, hypertension

7.
2. Delirum/Excitement/Uninhibited Response
 DO NOT INTUBATE
Make sure you have given sedatives and
muscle relaxants
Propofol: onset of 1-2 minutes
Atravirium: onset of 2-3 minutesso do
intubation after 2-3 minutes (if done earlier,
patient may be at risk of having
bronchospasm episodes)

8.
3. Surgical Anesthesia
 From onset of automatic
respiration to respiratory
paralysis
 Central gaze
 Stage for INTUBATION

9.
4. Impending death/overdosage
 From onset of diaphragmatic
paralysis to apnea and death
 Dilated and non-reactive pupils,
hypotension
 Circulatory failure

10.
PHARMACOKINETICS

11.
“The higher the FGF rate, the
smaller the breathing circuit
volume, and the lower circuit
absorption, the closer the
inspired gas concentration
will be to the fresh gas
concentration.”

12.
Partition Coefficients
• The relative solubility of an
anesthetic in air, blood and
tissues.
• Insoluble agents are taken up by
the blood less avidly than soluble
agents. As a consequence,
alveolar concentration rises
faster and induction is faster.

13.
Different Tissue Groups based on Perfusion
Highly perfused
Brain, heart, liver, kidney and endocrine glands
Muscle group
Skin and muscle
Fat group
Minimal/vessel poor groups
Bones, ligaments, teeth, hair, cartilage

14.
pharmacodynamics

15.
General Anesthesia
• Reversible loss of consciousness
• Analgesia of the entire body (pain
reliever)
• Amnesia
• Muscle relaxation

16.
Brain Areas affected by Inhalational Anesthetics
• Reticulating Activating System (RAS)
• Cerebral cortex
• Cuneate nucleus
• Olfactory cortex
• Hippocampus
• Spinal cord –dorsal horn interneurons

17.
Inhalational Anesthesia
• Depress spontaneous and
evoked activity of neurons in
many regions of the brain
• GABA-receptor chloride
channel

18.
Pharmacology of
Inhaled Anesthetics

19.
Theories of Anesthetic Action
Agent-specific theory
Various agents produce anesthesia by different
methods
Unitary hypothesis
All inhalational agents share a common mechanism of
action at the molecular level
Meyer-Overton rule
The anesthetic potency of inhalational agents
correlates directly with their lipid solubility

20.
Depth of Anesthesia
Minimum Alveolar Concentration
(MAC)
The alveolar concentration of an inhaled
anesthetic that prevents movement in
50% of patients in response to standard
stimulus (surgical incision)

21.
Depth of Anesthesia
MAC-Beta-adrenergic response
(MAC-BAR: 1.5MAC)
Concentration of inhaled anesthetic
required to block the autonomic
responses to nociceptive stimuli
1.7 to 2 times the MAC

22.
Depth of Anesthesia
MAC-awake (0.5MAC)
The dose of inhaled anesthetics
necessary to produce
unconsciousness

23.
Depth of Anesthesia
MAC Amnesia (0.25MAC)
You can use this if you just
want to patient to not
remember to procedure.

24.
Factors that modify mac
Increase MAC
• Young age
• Hyperthermia
• CNS Hypo-osmolality
• Habituation to alcohol
• CNS Stimulus (Dextroamphetamine, Cocaine)
• Physostigmine

25.
Factors that modify mac
Decrease MAC
• Old age
• Hypothermia
• CNS hyperosmolality
• Acute effects of alcohol (occasional drinker)
• CNS depressants (Benzodiazepines, Barbiturates, Propofol)
• Tranquilizers (Chlorpromazine)
• CNS effects of local anesthetics
• Narcotics
• Pregnancy
• Alpha-2-adrenergic agonist (Clonidine, Dexmedetomidine)

26.
Agents Clinically Used in Anesthesiology
• Nitrous Oxide
• Methoxyflurane
• Enflurane
• Halothane
• Isoflurane
• Desflurane
• Sevoflurane

27.
1. Nitrous Oxide
• Laughing gas
• Only inorganic anesthetic gas
• Colorless and odourless
• Gas at room temperature and ambient
pressure; liquid under pressure
• Can cause bone marrow depression
(megalobalastic anemia) and even neurologic
deficiencies (peripheral neuropathy and
pernicious anemia) upon prolonged exposure

28.
1. Nitrous Oxide
• Has possible teratogenic effect hence
avoided in pregnant patients Tends to diffuse
into air containing cavities
• Nitrous oxide is 35X more soluble than
nitrogen so usually it goes inside the air
containing cavities

29.
1. Nitrous Oxide
Contraindicated if:
Pneumothorax
Air embolism
Acute intestinal obstruction
Intracranial air
Pulmonary air cyst
Intraocular air bubbles
Tympanic membrane grafting
Pulmonary hypertension

30.
2. Methoxyflurane
• Most potent of all (because it has the lowest
MAC, only .16)
• Sweet, fruity odor
• High solubility and low vapour pressure
• 50% is metabolized by cytP450 enzymes
• Associated with vasopressin-resistant high-
output renal failure
Due to free fluoride metabolites (inhibits tubular
function)

31.
3. Enuflurane
• Non-pungent, non-flammable
• Depresses myocardial contractility
and sensitizes the myocardium to
epinephrine
• Increases CSF and the resistance to
CSF flow
• Causes tonic-clonic seizures
• Don’t use this in patients with history
of seizures

32.
4. Halothane
• Halogenated alkane
• Carbon-fluoride bonds are responsible for its
non-flammable and non-explosive nature
• Least expensive volatile anesthetics
• Halothane hepatitis
Increased risk to patients exposed to multiple
halothane anesthetics, middle-aged obese women,
persons with familial predisposition to halothane
toxicity (centrilobular necrosis)

33.
4. Halothane
Contraindications
Liver dysfunction
Intracranial mass lesions
Because of possibility of intracranial
hypertension

34.
5. Isoflurane
• Non-flammable, pungent, ethereal odor
• Coronary steal syndrome
 Dilation of normal coronary arteries could divert blood away from
fixed stenotic lesions
 Causes regional myocardial ischemia during tachycardia or drops
of perfusion pressure
• Good bronchodilator like Halothane
• The difference between isoflurane and sevoflurane is
isoflurane is pungent; that’s why sevoflurane is
preferred but it is expensive

35.
6. Desflurane
Similar to Isoflurane
Substitution of Fluorine atom for Isoflurane’s chlorine
atom
High vapour pressure (681 vapor pressure)
Boils at room temperature at high altitude that’s why it
has special vaporizer
Low solubility in blood and body tissues
Causes rapid wash in and wash out meaning its blood
coefficient is very low, 0.4-1

36.
7. Sevoflurane
• Most commonly used because of its sweet odor
• Halogenated with fluorine
• Non-pungency and rapid increase in alveolar
concentration
 Excellent choice for pediatric and adult patients
• Low blood solubility
 Rapid emergence
• Compound A
 Fluoromethy-2,2-difluoro-1-vinyl ether)
 Nephrotoxic end product of soda lime + Sevoflurane
• Avoid Sevoflurane in patients with pre-existing renal
dysfunction

37.
FIN.