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Stages of anaesthesia (Described by Guedel, Only for Ether Anesthesia)

Stage      Respiration Tidal Volume Pupils Eye Position Reflexes effected
(Stage of Analgesia)      
From analgesia to loss of consciousness
Irregular Small Constricted Divergent NIL
(Stage of Analgesia)    
From analgesia to loss of consciousness
Irregular Large Dilated (Reflex
dilatation due to
symp. +)
Divergent Eyelash
(Surgical Anaesthesia)
Regular Large Constricted
(Rolling eye balls)
Divergent    - Pharyngeal
- Skin
(Rhythmical resp. to cessation of eye movement)
        - Conjunctive
(cessation of eye
movement to start of
resp. paresis)
(excluding diaphr-
  Regular Medium 1/2 Dilated
Fixed centrally
PLANE 3 Regular Small 3/4 dilated Fixed Laryngeal
Jerky Small Fully dilated Fixed -  Carinal
- Anal sphincter
Medullary Paralysis
  1. General anaesthesia blocks the synaptic transmission effects mainly on unmyelinated fibres.
  2. Best estimate for the potency of inhalational anesthetics is MAC
  3. Minimum alveolar concentration (MAC) It is the alveolar concentration of an anaesthetic at one atmosphere that prevents movement in response to surgical stimulus in 50% of the patients
  4. Best measure of anaesthetic potency as it mirrors brain partial pressure.
  5. MAC 95 = 1.3 MAC
  6. MAC – BAR = MAC that blunts the adrenergic response to a noxious stimulus (1.5 MAC)
  7. MAC – Awake = MAC at which patients regain conciousness (0.1-0.4 MAC)

Various factors increase or decrease the MAC

  1. Factor increasing MAC
    1.  CNS metabolic activity
    2.  CNS neurotransmission
    3.  CNS neurotransmitter levels
    4. Up-regulation of CNS response
  2. Conditions:
    1. Young patient
    2. Chr. Alcohol Abuse
    3. Hypernatremia
    4. Acute Amphetamine
    5. Cocaine
    6. Ephedrine
  3. Factor decreasing MAC
    1.  CNS metabolic activity
    2.  CNS metabolic activity
    3.  CNS neurotransmission
    4.  CNS neurotransmitter levels
    5. Down-regulation of CNS response
  4. Conditions:
    1. Hypothermia and Hyperthermia
    2. L.A.
    3. Elderly patient
    4. Opioids
    5. Acute Alcohol intoxication
    6. I.V. Induction Agents
    7. Anemia
    8. Lithium
    9. Methyl dopa
    10. Reserpine
    11. MAP < 40m of Hg
    12. Clonidine
    13. Hypercalcemia
    14. Chronic Amphetamine
    15. Hypokalemia
    16. Hyponatremia
    17. Pregnancy
    18. Hypoxia (PaO2 < 40m of Hg) & Hypercarbia (PaCO2 > 90mg Hg)

Factors does not affect MAC

  1. Thyroid disease
  2. Gender (M/F)
Meyer overtons rule- anaesthetic potency of a inhalational agent is measured by its lipid solubility.

Must remember MAC

1. Chloroform 0.8%
2. Methoxyflurane 0.16%
3. Ether 1.92%
4. Halothane 0.74%
5. Isoflurane 1.15%
6. Sevoflurane 2%
7. Enflurane 1.68%
8. Nitrous oxide 104%
9. Xenon 73%


Extra Edge
Most potent anaesthetic: Methoxyflurane

Blood: gas partition coefficient

  1. Relative affinity of the anaesthetic for two phases at equilibrium.
  2. Equilibrium-When partial pressure is same on both sides.
  3. Lower the B/G solublity-
  4. Rapid rise in alveolar conc.
  5. Rapid induction and recovery
  6. Ready adjustment of depth of anaesthesia.
Must Remember Blood Gas Co-efficient
Xenon - 0.13
N2O - 0.47
Cyclopropane - 0.44
Enflurene - 1.8
Desflurane - 0.42
Sevoflurane - 0.69
Ether - 15
Methoxyflurane - 12
Trilene - 9
Isoflurane - 1.38
Halothane - 2.4
Chloroform - 8


  1. Potency of inhaled anaesthetic agents is estimated by the minimum alveolar concentration (MAC) that produces a lack of reflex response to skin incision in 50% individuals.
  2. Nitrous oxide has the highest MAC value of 104 among all inhalational anaesthetics. (MCQ)

MOA of inhaled anesthesia

  1. Agents incorporate in lipid membrane fluidization
  2. Mainly - Na+ Conductance is inhibited there by causes depolarization.
  3. Other minor mechanism - K+ & Cl- conductance is inhibited so causes depolarization (hyperpolarization)

Uptake of agent depends on (Directly proportional)

  1. Blood solubility
  2. Cardiac output
  3. Alveolar to venous partial pressure difference & inversely proportional to barometric pressure
Second Gas Effect
This is seen if N2O along with another potent anaesthetic is given. With the removal of N2O from lung, total volume of lung leading to conc. of remaining gas in the lung (concentration effect) with the next inspiration of same mixture, N2O & other agent concentration further increases; this is known as second gas effect.

Diffusion hypoxia (term given by FINK)

  1. At the end when N2O is discontinued, alveolar to venous gradient reverses causing to high conc. of N2O in alveoli displacing O2 this is called as diffusion hypoxia. 
  2. Diffusion hypoxia can occur whenever nitrous oxide (N2O) is used to supplement an anesthetic. N2O has a low blood: gas coefficient (i.e., low blood solubility) which means that, during induction, the blood and alveoli rapidly equilibrate. After N2O is discontinued, the diffusion gradient reverses, filling the alveoli with large amounts of N2O, thereby, displacing oxygen. Breathing room air during this time can cause alveolar hypoxia.
  3. The peak effect of this phenomenon occurs about 2-5 minutes after the cessation of N2O, and lasts approximately 5-10 minutes. The large influx of N2O also displaces alveolar carbon dioxide, thereby decreasing ventilatory drive, and potentially worsening the hypoxia.

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