Introduction of Low-Flow Anesthesia

(1)

Introduction of

low-flow anesthesia

麻醉科

_{R2 楊美惠}

2004/11/08

(2)

Definition of low-flow



The suggestion of Simionescu as:

Metabolic flow = 250ml/min

Minimal flow = 250-500 ml/min

Low flow = 500-1000 ml/min

Medium flow = 1-2 L/min

High flow = 2-4 L/min

Super-high flow = >4 L/min

(3)



Low-flow anesthesia can be defined as a

technique which, using a rebreathing

system, results in at least 50% of the

exhaled air being returned to the lungs

after CO

2

absorption.

<

Low-flow anaesthesia, Anaesthesia, 1995, Volume 50 (supplement), pages 37-44

>

(4)



Via the observation that anaesthetic vapours are

excreted unchanged with the expired air and

serial experiments, John Snow concluded In

1850 that: “ It follows as a necessary

consequence of this mode of excretion of a

vapour that, if its exhalation by the breath could

in any way be stopped, its narcotic effects ought

(5)

Basic concepts



The recognition of the functional residual

capacity as deadspace or extension of the

circuit.



The recognition of the alveolar membrane

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(7)

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The uptake of anaesthetics

(9)



Fick’s principle of alveolar membrane penetratio

n:

(DAk/x) (C

I

-C

B

)

D= diffusion constant

A= area of membrane (area is proportional to pul

monary capillary flow or cardiac output)

k= solubility coefficient

x= thickness of membrane

C

I

= inspired anaesthetic concentration at alveoli

(10)



The uptake can be simplified as:

Inspired concentration(%) ×

Fraction of uptake (1-F

_A

/F

_I

)×

(11)

(12)



Thus, the uptake of an inhalation

anaesthetic is concentration-dependent.

Respiration or alveolar ventilation per se

does not directly participate in the process

of uptake or play an indirect or supporting

role in uptake.

(13)

Is the concept of “MAC” wrong?

 The time required for the brain to equilibrate with the alv

eolar concentration (including wash in, uptake through al veolar membrane and uptake of brain) requires more tha n 15 minutes.

 For example, under 1.5-2% isoflurane in 2 L/min oxygen,

it took about 25 mins for mask ventilation to achieve a st ability of haemodynamics suitable for tracheal intubation. <Minimal low-flow isoflurane-based anesthesia benefits patients undergoing coronar y revascularization via preventing hyperglycemia and maintaining metabolic homeost asis, Chih-Cherng Lu, Acta Anaesthesiol Sin 41:165-172, 2003. >

(14)



In the very beginning, using MAC as a standard

measure of potency of anaesthetics and of the

depth of anaesthesia is one kind of misjudgment

because we use the partial pressure of an

anaesthetic in the alveoli instead of the partial

pressure in the brain as a measure

.

(15)



During induction of anaesthesia with inhal

ation anaesthetics, unstable haemodynami

c changes are often encountered because

of misunderstandings about uptake.

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Clinical performance

 After intubation, keep high flow (about 2-3L/min) for

three time constants to complete the wash in of FRC with anesthetics. Then turn to low flow with increased dial settings to keep constant anesthetic concentration for anesthesia maintenance.

 For example, if 6% of desflurane inspired concentration

is desired, 0.15×6/100×3000=27ml desflurane vapor/min would be uptaked. When the flow was reduced to

300ml/min, a vaporizer setting should become 27÷300=9%.

(17)



Despite the continuous uptake of inhalation

anesthetic and the increased anesthetic

concentration in the patient’s body, the

haemodynamic status usually is well maintained

throughout the course of closed-circuit

anesthesia. A high concentration of inhalation

anesthetics in the blood provides good muscle

relaxation without too much muscle relaxants.

(18)



As a result, nearing the end of surgery, when the

inhalation anesthetic’s concentration is highest,

we can reverse the muscle relaxant about 10-20

minutes before the end of surgery. At this time,

we can also shut off the vaporizer and reduce

the rate of ventilation in order to raise the CO

2

level in the blood. After the surgery ends, it only

requires 5~10 minutes of high-flow oxygen to

wake up the patient.

(19)

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Advantages of low flow anesthesia

1) Relatively stable haemodynamic conditions during the process of surgery.

With inhalation anesthetics, our response to a patient’s haemodynamic change is far from prompt because of the existence of the large circuit volume and FRC. The benefit of closed-circuit anesthesia is that, once a

certain anesthetic concentration is reached in the

brain, then, without surgical stimulation, the patient will be able to maintain reasonable haemodynamic

stability. With surgical stimulation, the patients is able instantly to increase the anesthetic uptake with the increase in cardiac output.

(21)

The beauty of closed circuit anesthesia is:

with fixed amounts of anesthetic supply

and a large circuit volume, the inspired

concentration does not change much, but,

after surgical stimulation, self-feed-back

control by the patient will take hold to a

certain extent, providing a prompt and

effective defense mechanism.

(22)

2) Reduced consumption of anaesthetic gases

and vapours

(23)

4) Reduced environmental pollution

5) Improved “climate” of anesthetic gases

The humidity of anesthetic gases is significantly higher in low-flow than in high-flow anesthesia, and although the specific heat of gas is low, significant reductions in

heat loss by the patient can be achieved by delivering

humidified gas. appropriate humidification and warming of anesthetic gases have a significant influence on the function and the morphological integrity of the ciliated epithelium of the respiratory tract.

(24)

Possible problems

1) Accumulation of CO₂

2) Carbon monoxide accumulation

CO production comes from the contact of anesthetics with dry soda lime and gradual accumulation is due to difficult elimination under low-flow

However, even in long-tem closed system anesthesia, generally, the increase in CO

concentration remains negligibly low and is of no risk to the patient.<Anaesthesist 1991; 40: 324-7>

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3) Accumulation of compound A

Compound A is derived from the contact

of sevoflurane with soda lime. However,

the highest value lies within the range

determined to cause histological renal

tubular damage in rats.<

Gonsowski CT, Toxicity

of compound A in rats: effect of increasing duration of administration. Anesthesiology 1994; 80:566-75