Dr.J.Edward Johnson M.D.(Anaes),D.C.H.
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Dr.J.Edward Johnson M.D.(Anaes),D.C.H. Asst. Professor, Dept. of Anaesthesiology, Kanyakumari Govt. Medical College Hospital. "Uptake and distribution of anesthetic gases. "Uptake and distribution of

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Uptake and distribution of anesthetic gases

Dr.J.Edward Johnson M.D.(Anaes),D.C.H.

Asst. Professor,

Dept. of Anaesthesiology,

Kanyakumari Govt. Medical College Hospital.

"Uptake and distribution of anesthetic gases


Uptake and distribution of anesthetic gases

"Uptake and distribution of

anesthetic gases is virtually incomprehensible"

wroteLawson: Gas Man Review, Anesthesia and Analgesia, August 1991


Uptake and distribution of anesthetic gases

"Uptake and distribution of anesthetic gases

Goal

To develop and maintain a satisfactory partial pressure or tension of anesthetic at the site of anesthetic action in brain.

Alveolar concentration of anaesthetic gas is indirectly reflects brain concentration.

Pa

PB


Path of anesthetic tension

Path of anesthetic tension

Vaporizer

Breathing Circuit

Alveoli (lungs)

Arterial Blood

Tissues (VRG [brain], MUS,FAT)

Venous blood (coming back to lungs)

Alveoli (lungs, again)

Breathing Circuit (to be rebreathed)


Alveolar tension is important

Alveolar Tension is important

Tension = Partial Pressure

Important

  • Tension equalizes when Concentration equilibrates

  • Concentration does not drive molecular motion

  • Tension drives molecular motion


If we know alveolar tension we know the hard part

If we know Alveolar Tension, we know the hard part

Inspired Tension drives Alveolar Tension

Alveolar Tension drives Arterial Tension

Arterial Tension drives Tissue Tensions

Brain is the important Tissue for Anesthesia

Brain Tension drives depth of anesthesia


Basics of uptake and distribution bird s eye view

Basics of Uptake and Distribution Bird’s eye view

1

2

FD

MAC

Fi

Ventilation

λB/G

λT/B

Fa

Equilibrates

CO

Tissue blood flow

Fa/Fi

PA - PV

[Parterial - PTissue]

VRG

Time constant

Brain Partial pressure drives depth of anesthesia

Time constant

Concentration and

second gas effects


I alveolar concentration factors raising the alveolar concentration f a f i

I. Alveolar concentration Factors raising the alveolar concentration (Fa/Fi )

  • The inspired concentration (Fi)Inspired concentration - Fa/Fi

  • The alveolar ventilation (Valveolar) - Minute alveolar ventilation - Fa/Fi - larger the FRC - slows raise of alveolar concentration

  • The time constant

  • Anesthetic uptake by the blood

  • The concentration and second gas effects


B the alveolar ventilation v alveolar

b)The alveolar ventilation (Valveolar)

Increase in

Minute alveolar ventilation

Increases Fa/Fi

The change is greatest for more soluble anesthetics

Halothane depress Valveolar

and limit the raise of alveolar concentration

Hyperventilation reduces cerebral blood flow soinduction time is function of solubility

Nitrous oxide and Halothane – slows induction

Ether – faster induction


C the time constant

c) The time constant


C the time constant example

c) The time constant - example

  • If 10 liter box is initially filled with oxygen and 5 l/min of nitrogen flow into box then,

  • TC is volume (capacity)/flow.

  • TC = 10 / 5 = 2 minutes ( 1 Time Constant)

  • So, the nitrogen concentration at end of 2 minutes is 63%. 

Time Constant at Lungs

8 Mts

2 Mts

4 Mts

6 Mts

O2

N2

5 Lt/min

10 Lt

86%

95%

98%

63%


D anesthetic uptake by the blood

d) Anesthetic uptake by the blood

Uptake from the lung = Blood solubility x Cardiac Output x [PA-PV] / Barometric pressure

Factors that Increase or Decrease the Rate of Rise of FA/FI


E the concentration effect

e) The concentration effect

4Lt

3Lt

4Lt

2Lt

50%O2

Uptake of half

of the N2O

66%O2

2Lt

62%O2

2.5Lt

33%N2O

1Lt

1Lt of N2O

2Lt

50%N2O

38%N2O

1.5Lt

Ventilation Effect

Inspired Gas

1 Lt

50%O2 + 50%N2O


E the second gas effect

e) The second gas effect

4Lt

3Lt

4Lt

40ml

1% Isoflurane

1.3% Isoflurane

40ml

1.25% Isoflurane

50ml

61.25%O2

49%O2

Uptake of half

of the N2O

65.3%O2

1.960Lt

1.960Lt

2.450Lt

33.3%N2O

1Lt of N2O

1Lt

2Lt

50%N2O

37.5%N2O

1.5Lt

1Lt

Inspired Gas

1 Lt

50%O2 + 49%N2O + 1% Isoflurane

490ml 500ml 10ml


Concentration and second gas effect

Concentration and second gas effect

Concentration effect

65% nitrous oxide produces a more rapid rise in the Fa/Fi ratio of nitrous oxide than the administration of 5%

Second gas effect

Fa/Fi ratio for 4% desflurane rises more rapidly when given with 65% nitrous oxide than when given with 5%


I alveolar concentration

I. Alveolar concentration

We have Learned

Factors raising the alveolar concentration (Fa/Fi )

  • The inspired concentration (Fi)

  • The alveolar ventilation (Valveolar)

  • The time constant

  • Anesthetic uptake by the blood

  • The concentration and second gas effects


Ii uptake from lung

II. Uptake from lung

Factors determining uptake by blood

  • Solubility in blood

  • Cardiac Output

  • The mixed venous anesthetic concentration

    Tissue uptake of anesthetic

Uptake from the lung = Blood solubility x Cardiac Output x [PA-PV]

Barometric pressure


Solubility partition coefficient

Solubility / Partition Coefficient

  • Solubility is defined in terms of the partition coefficient

  • Partition coefficient is the ratio of the amount of substance present in one phase compared with another, the two phases being of equal volume and in equilibrium [λB/G = CB ] CG


Blood gas partition coefficient b g

Blood: gas partition coefficient λB/G

Partition Coefficient = Ratio of Concentration

Concentrations Equilibirates

CG =CB

Gas

Halothane

λB/G = CB =2.5 =2.5

CG 1

Equal volume

Blood

PG = PB

Partial pressure Equalize


Blood tissue partition coefficient b t

Blood: tissue partition coefficient λB/T

Concentrations Equilibirates

CG =CB = CT

Tissue

Gas

Equal volume

Blood

PG = PB = PT

Partial pressure Equalize


A solubility in blood

A.Solubility in blood

Poor solubility Rapid induction

0.47

The more soluble the anesthetic

The more drug will be taken up

by the blood

The slower the rise in alveolar concentration

0.65

1.4

15

High solubility Slow induction


B cardiac output

B.Cardiac Output

Greater the cardiac output

The more drug will be taken up

by the blood

The slower the rise in alveolar concentration

Cardiac output is lowered

cerebral circulation

less maintained (shock)

Induction Induction

slower rapid


C the alveolar to venous anesthetic gradient

C. The Alveolar-to-Venous Anesthetic Gradient

The difference between partial pressure in the alveoli and that in venous blood

Partial pressure in venous blood depends on tissue uptake of anesthetic

At equilibrium, (no tissue uptake)

The venous partial pressure = arterial partial pressure = alveolar partial pressure

PA – PV = 0

Rate of rise of the mixed venous concentration depends on the tissue uptake of the anesthetic


The alveolar to venous anesthetic gradient

The Alveolar-to-Venous Anesthetic Gradient

PA

Fa/Fi

VRG

4-8mts

No tissue uptake

AT EQUILIBRIUM

MG

PA= PV

2-6Hrs

PA – PV = 0

FAT

3-4 days

PV


D tissue uptake of anesthetic

D.Tissue uptake of anesthetic

The tissue uptake equals the uptake from the lungs

1. The tissue/blood partition coefficient (tissue solubility)

2. The tissue blood flow.

3. The tissue anesthetic concentration

Tissue Uptake = Tissue solubility x Tissue blood flow x [Parterial - PTissue]

Atmospheric pressure


Iii distribution to tissues

III. Distribution to tissues


Iii distribution to tissues contd

III. Distribution to tissues (Contd...)

Equilibration of the VRG complete in 4 to 8 minutes

After 8 minutes, the Muscle group (MG) determines most of uptake.

Once MG equilibration is complete Fat group (FG) determines the uptake


Tissue time constant

Tissue Time Constant

Time Constant = Tissue solubility x Volume

Flow

λ Fat/Bld: N2O 2.3

Sevo 48

Metho 38

λ Brain/Bld: N2O 1.1

Sevo 1.7

Metho 1.4

3 TC 95%


The alveolar tension curve synthesis of factors governing the rise in f a f i ratio

The Alveolar Tension CurveSynthesis of Factors Governing the Rise in Fa/Fi Ratio

AB

Initial Rise - Alveolar Wash-In

BC

8

First knee – Solubility with blood

C

8

C

B

Second knee – Equilibration with VRG

8 mts

A

Third knee - Equilibration of the MG


Mapleson hydraulic model

Mapleson Hydraulic Model

Cylinders : represent the inspired reservoir (mouth), the alveolar gas, vessel rich group, the muscle group, and the fat group

VRG

Anesthetic Gas

75%

MG

18%

Ventilation

Blood Supply

FAT

MOUTH

LUNG

5.5%

Cross sectional : surface of each cylinder corresponds to its capacity (λB/T * volume)

Diameter of the pipes : correlates to the λB/G * CO to each group

Height of the column of fluid : in each cylinder corresponds to the partial pressure of the anesthetic in that cylinder


Mapleson hydraulic model lo w solubility anaesthetic

Mapleson Hydraulic Model Low solubility anaesthetic

  • All compartments are small

VRG

  • Pipes are represented as small because low solubility of anaesthetic is less carried by the given blood flow

75%

Anesthetic Gas

MG

18%

Ventilation

Blood Supply

FAT

MOUTH

LUNG

5.5%

  • To achieve equilibrium for low soluble anaesthetic small quantity of anaesthetic has to go in to the system


Mapleson hydraulic model high solubility anaesthetic

Mapleson Hydraulic Model High solubility anaesthetic

  • All compartments are large

  • Pipes are represented as larger because high solubility of anaesthetic is more carried by the given blood flow

VRG

Anesthetic Gas

75%

MG

18%

Ventilation

FAT

Blood Supply

MOUTH

LUNG

5.5%

  • To achieve equilibrium for high soluble anaesthetic large quantity of anaesthetic has to go in to the system


Basics of uptake and distribution

Basics of Uptake and Distribution

1

2

FD

MAC

Fi

Ventilation

λB/G

λT/B

Fa

Equilibrates

CO

Tissue blood flow

Fa/Fi

PA - PV

[Parterial - PTissue]

VRG

Time constant

Brain Partial pressure drives depth of anesthesia

Time constant

Concentration and

second gas effects


Recovery

RECOVERY

100%

60%

10%

Recovery

0%


Recovery from an inhalational anesthetic

Recovery from an inhalational anesthetic

1. Increased solubility slows recovery

2. Increasing ventilation may help the recovery from potent agents

3. Prolonged anaesthesia delays recovery

4. There is no concentration effect on emergence


Diffusion hypoxia

Diffusion Hypoxia

  • The large outpouring of nitrous oxide diluting the inspired oxygen at the conclusion of a case in the first 3-5 minutes after terminating the nitrous oxide

  • Managed with supplemental oxygen for a few minutes following termination of the nitrous.


Further references

Further References

  • Eger's The Pharmacology of Inhaled Anesthetics

  • Miller's Anesthesia, Seventh Edition

  • Barash : Handbook of Clinical Anesthesia (6th Ed. 2009)

  • http://www.anesthesia2000.com/

  • www.gasmanweb.com


Thank you

Thank you

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