Anesthesia’s Principle Of Operation
The most common breathing circuits of Anesthesia are "circulatory systems". Search for two unidirectional flaps to allow the gas to flow into the recycle loop that chemically absorbs carbon dioxide. In this system, the fresh gas from the anesthesia machine enters the respiratory circuit upstream of the carbon dioxide absorption tank and upstream of the inspiratory one-way valve. The incoming fresh gas is mixed with the original gas in the loop system and flows through the suction one-way valve and flows through the reusable or disposable corrugated pipe to the Y-tube. The patient exhaled the gas through the other part of the circulatory system (exhaled), through the breath one-way valve into the airbag. By pressing, a positive pressure is generated in the airbag to force the collected gas to pass through the carbon dioxide absorber. Since the fresh air flowing into the loop system is much more than the gas consumed by the patient and the absorbent, it is necessary to install such a safety valve between the expiratory one-way valve and the carbon dioxide absorption tank. The excess gas may escape when the pressure exceeds a prescribed threshold. The absorption tank is filled with sodium carbonate lime (a mixture of sodium, potassium and calcium hydroxide) or a mixture of barium hydroxide lime (barium hydroxide, octahydron hydrate and calcium hydroxide). These substances absorb carbon dioxide by chemical reactions while releasing heat and water (the released water can wet the air in the circulation system). When the absorptive capacity is exhausted, the indicator changes color. The design of the absorption tank must be easy to replace the absorbent. The APL valve used to drain excess gas is usually a spring-loaded valve. Spring tension is the control circuit pressure, if the patient spontaneous breathing, the safety valve is in the open position, breathing with minimal resistance to inhale and exhale airflow. If the patient is deep anesthesia and deep paralysis, the anesthesiologist can partially or completely close the safety valve to squeeze the airbag to fill the lungs, help and control the patient breathing. Exhaust gas from the safety valve should be guided through the exhaust pipe to the operating room, in order to avoid the amount of anesthetic gas on the operating room staff health hazards.
Two factors make obtaining a detailed description of how these agents act difficult. The first is that volatile anesthetics, unlike most of the drugs used in medicine, bind only very weakly to their site(s) of action. As a result, high concentrations, often more than 1,000 times greater than for typical receptor- or protein-targeting drugs, are needed to achieve an anesthetic state. This makes it tricky to obtain structural details of anesthetics bound in a specific manner to a protein. It also affects the function of many proteins in nerve cell membranes, making it challenging to ascertain which of them are the key mediators of anesthetic action. A second problem is that volatile anesthetics tend to partition into lipids and exert their primary effects on synaptic neurotransmission by interacting with proteins in a lipid environment. It is harder to gain detailed structural information for membrane proteins than it is for water-soluble proteins. Such structural data are essential for understanding how anesthetics interact with proteins and, more importantly, alter their function. Because of the lack of structural data for membrane proteins both in the presence and absence of anesthetics, it remains unclear whether anesthetics exert their primary effects by direct interaction with these proteins, or indirectly via interaction with the lipids surrounding them.
Despite these limitations, researchers are taking advantage of a variety of methods to better discern how anesthetic agents induce an anesthetic "state" at the molecular level. The term state is in quotes, because a wide variety of agents--ranging from single atoms such as xenon to polycyclic hydrocarbons--can produce insensibility to pain and loss of awareness. The molecular targets for these different agents do not appear to be the same. Thus the notion that there is a single molecular mechanism of action for all anesthetic agents is probably an oversimplification.
Thus the simple answer to the question "How does anesthesia work?" is that, although we know a great deal about the physiologic effects and macroscopic sites of action, we don't yet know the molecular mechanism(s) of action for general anesthetics. Many of the tools necessary to answer these questions now exist and we can look forward to new insights into how this great boon to humanity works at the molecular level.