Introduction of low-flow anesthesia 麻醉科R2楊美惠 2004/11/08
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 Definition of low-flow
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 CO2 absorption.<Low-flow anaesthesia, Anaesthesia, 1995, Volume 50 (supplement), pages 37-44>
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 to be much prolonged.
Basic concepts • The recognition of the functional residual capacity as deadspace or extension of the circuit. • The recognition of the alveolar membrane as a barrier of anesthetic uptake.
The uptake of anaesthetics Fraction of uptake = 1-FA/FI
Fick’s principle of alveolar membrane penetration: (DAk/x) (CI-CB)D= diffusion constantA= area of membrane (area is proportional to pulmonary capillary flow or cardiac output)k= solubility coefficientx= thickness of membraneCI= inspired anaesthetic concentration at alveoliCB= mixed venous anaesthetic concentration
The uptake can be simplified as:Inspired concentration(%) ×Fraction of uptake (1-FA/FI)× Alveolar ventilation (ml/min)
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.
Is the concept of “MAC” wrong? • The time required for the brain to equilibrate with the alveolar concentration (including wash in, uptake through alveolar membrane and uptake of brain) requires more than 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 stability of haemodynamics suitable for tracheal intubation.<Minimal low-flow isoflurane-based anesthesia benefits patients undergoing coronary revascularization via preventing hyperglycemia and maintaining metabolic homeostasis, Chih-Cherng Lu, Acta Anaesthesiol Sin 41:165-172, 2003. >
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 brainas a measure. <MAC presents the alveolar concentration of an anaesthetic at 1 atm which prevents a response to a painful stimulus in 50% of subjects.>
During induction of anaesthesia with inhalation anaesthetics, unstable haemodynamic changes are often encountered because of misunderstandings about uptake.
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%.
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.
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 CO2 level in the blood. After the surgery ends, it only requires 5~10 minutes of high-flow oxygen to wake up the patient.
Advantages of low flow anesthesia • 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.
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.
2) Reduced consumption of anaesthetic gases and vapours 3) Cost savings
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.
Possible problems • Accumulation of CO2 • Carbon monoxide accumulationCO production comes from the contact of anesthetics with dry soda lime and gradual accumulation is due to difficult elimination under low-flowHowever, 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>
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>
4) Difficulty in changing the inspired anesthetic concentration rapidly due to the limited dial settings.
Reference materials • CLOSED-CIRCUIT ANESTHESIA, Chung-Yuan Lin, M.D.May, 2000 • Uptake of Anaesthetic Gases and Vapours, C. Y. LIN, Anaesth Intens Care 1994; 22:363-373 • Low-flow anaesthesia, J.A. BAUM and A. R. AITKENHEAD, Anaesthesia, 1995, volume 50 (Supplement), pages 37-44