1. Expired carbon dioxide:

1. Circle system: Components of the circle system which is what is used for the anesthesia machines are the following: inspiratory and expiratory limbs, unidirectional valves, and a reservoir bag. Circle systems are not really closed ones and they reuse oxygen and anesthetic agents but get rid of the CO2. Circle breathing allows you to use low flows – usually less than one liter. It is based on O2 consumption so that you provide just enough O2 to meet consumption. Normal consumption is 250cc. Advantages to this are that you can use low flows which decrease room pollution where the external scavenging units are out of the building, decrease cost, decrease heat and moisture loss, and you can supply a steadier amt of anesthetic gases. The true circle system has no outside extraction of gases. You must have CO2 or agent monitoring, should have no detectable leaks and is not common to use. Most now are the semi-closed or semi-open circle systems.
2. Methods of CO2 removal: there are 3 ways to remove it from the anesthetic loop. The most often used way is by chemical absorption. Second is by dilution with fresh gas and third is to use valves to separate inhaled vs exhaled – one way valves in each direction. These valves are plastic or metal pieces. The valve closing causes gas to change direction going in or out. Ie. An ambu- squeeze it and the valve opens gas goes in, release the pressure on the bag and the valve closes and gas goes out. The dilution with fresh gas method will depend on the type of circuit and what type of breathing is being done for the patient – controlled vs spontaneous. A general rule to remember is that you need 2 times the pts minute ventilation to clear the CO2. In the Bain circuit you should use 3 times the minute vent and also for use with the t-piece. These amts will assure you that the patient has cleared the CO2 and isn’t rebreathing. If you use a t-piece (avg min. vent. For 70kg pt is 8-12L) You would need to have fresh gas flow at 16-24L of flow. If the flow is 6-8L then they will rebreathe at a rate of 12. You could shorten the T on the t-piece to reduce the dead space and this will decrease the CO2 rebreathing. You may also want the pt to rebreathe more CO2 like COPD’ers so could add length to the t-piece. Usually there is rebreathing since we normally use flows of 6-8L/min
3. Components of baralyme and soda lime: CO2 is a gaseous nonmetal oxide that we produce. It forms carbonic acid in the presence of water. We use this principle in r/t getting rid of CO2 in anesthesia by a reaction with soda lime to produce a substance that has little effect of people. Soda lime and baralyme are the most common CO2 absorbers.

• Soda lime is composed of 4% Na Hydroxide, 1% K Hydroxide, 80%Ca Hydroxide, 0.2% silica, and 14-19% water.
• Baralyme is composed of 20% Barium Hydroxide and 80% Ca Hydroxide and occas. a small amt of K Hydroxide. Both have a dye indicator
• The difference btw the two is that soda lime has silica which is added to give it hardness which will decr the amt of dust so pts don’t breathe it in since it is very irritating to the airways. Baralyme is inherently hard and doesn’t need the silica. Baralyme also doesn’t contain any added water and so would work better in a dry, low humidity place like Arizona.

4. Reactions within absorbers: Soda lime reacts with the CO2 and water to make carbonic acid which reacts with NaOH and KOH which form carbonates, heat and water. Baralyme reacts with water, CO2, and Ba(OH)2 to form carbonates, heat and water. The inicators within the limes are ethylene violet. The pH change of becoming saturated with CO2 will activate the dye as the more acidic pH will turn the lime purple. The soda lime can also change back to white-gray if you allow enough time to pass. This dye indicates that the water content has been saturated and water is no longer available for the chemical reaction. The amt of CO2 absorbed is 26L/100 gm. Both soda and baralyme have dual chambers for safety so that you have a backup canister available. The dual chamber allows 2-3 times the tidal volume and allows for more surface area – not every breath has to do through the reactions. This gives you a reservoir. The size and shape of the granules make a difference. The smaller the granule size the more surface area but then this increases resistance. The standard size is 4 –8 mesh which is a combo of small and larger pieces and has less tendency to stick together. A thing called channeling can occur where the gas follows the path of least resistance and channels up through the lime. This can burn out that one area and the rest isn’t being used. Another fact to recall is that the hardness # is >75. When it is pulverized it takes this # to break up into an alkaline dust.
5. Exothermic reaction: All reactions occurring in the CO2 canister are producing heat.
6. Storage and handling: The canisters can be taken off the machines easily and disposed of in the biohazardous waste for the hospital. Care must be taken when installing a new canister since the metal rings surrounding each connection can cause a leak in the system.
7. Reactivity of components and anesthetics: Soda lime is neither intrinsically toxic nor toxic when exposed to common anesthetics. However when using an uncommon anesthetic, trichloroethylene, toxicity may result. In the presence of alkali and heat, trichlorothylene degrades into the neurotoxin dichloroacetylene. Phosgene, a potent pulmonary irritant, is also produced. These toxicities can cause cranial nerve lesions, encephalitis, and ARDS. Sevoflurane has been shown to produce degradation products on interaction with CO2 absorbents which are fluromethyl-2, 2-difluoro-1-vinyl ether, and Compound A which can be lessened by using low flow or closed circuit anesthesia techniques, use of baralyme instead of soda lime, higher concentrations of sevo in the anesthesia circuit, higher absorbent temps, and fresh absorbent.
8. Carbon monoxide poisoning: The carbon monoxide will bind with the hgb and not allow O2 to bind. For pulse oximetry the carboxyhemoglobin is interpreted by the pulse ox as a mixture of ~ 90%oxyhemoglobin and 10%deoxyhemoglobin. Thus at high levels of COHb, the pulse ox will overestimate true SaO2. A treatment for COHb could be treatment in a hyperbaric chamber. Here the partial pressure of O2 increases in blood while the saturation of hgb approaches 100%. Above this level all additional O2-carrying capacity of blood is from O2 dissolved in plasma. This allows for the preservation of aerobic metabolism in the face of severe anemia or hypoperfusion.

1. Closed system anesthesia: This is a type of low flow anesthesia in which the fresh gas inflow is equivalent to the uptake of anesthetic gases and oxygen and the relief valve on the anesthesia circle is closed. This is the system where the amt of gas flowing in will equal consumption of O2 and anesthetic gases. You need an accurate flowmeter capable of registering flows as low as 100ml/min. Use of a reliable oxygen analyzer and CO2 monitor is essential. The system should be free of leaks. A vent with bellows that rise during expiration will detect leaks more readily than one with bellows that descend during expiration. Induction with low flow is difficult since the excretion of nitrogen will dilute the gases present in the system and maximal uptake of the volatile agent during this period makes dosage difficult to predict, and inadequate or excessive concentrations could frequently develop in the circle. To counteract these problems, denitrogenation and induction are first accomplished with high flows. Disadvantages to the closed system are that inspired concentrations cannot be quickly altered, danger of hypercarbia is greater when low flows are used, more attention is required to constantly adjust fresh gas flow, and accumulation of high concentrations of undesired gases and vapors in the system may occur. To use this system you must calculate the vapor pressures of the agents. Another point is that you can still spontaneously breathe with the APL valve closed but this is like a PEEP valve.
2. Mapleson and Bain circuits: The Mapleson D is the most often used system. It is comprised of a t-piece with an expiratory limb. The fresh gas inlet is located near the pt and expiratory valve is close to the reservoir bag. During the expiratory phase of spontaneous ventilation, fresh gas and alveolar gas flow down the expiratory limb. The exp valve opens as pressure increases in the circuit, and a portion of this mixture is expelled. The pt receives a combo of fresh gas and mixed gas from the tubing during the next inspiration. The content of this inspired mixture is determined by the rate of fresh gas flow, the pt’s tidal volume, and the duration of expiratory pause. A long expiratory pause allows the fresh gas to move down the tubing and flush the alveolar gas. A short pause provides inadequate time to flush the alveolar gas and allows rebreathing to occur. Mapleson determined that a fresh gas flow greater than two times the minute ventilation was enough to prevent rebreathing. During the inspiratory phase of controlled ventilation, alveolar gas and dead space gas, instead of fresh gas, are forced out of the expiratory valve. The Bain circuit also called the Jackson-Reis is a modification of the Mapleson D system. It is a coaxial circuit in which the fresh gas flows through a narrow inner tube within the corrugated outer tubing. The central tube originates near the reservoir bag, but the fresh gas actually enters the circuit at the pt end. Exhaled gases enter the corrugated tubing and are vented through the expiratory valve near the reservoir bag. This circuit can be used for both spont and controlled ventilation. Advantages are that it is lightwt, convenient, easily sterilized, and reusable. Scavenging of the gases from the expiratory valve is facilitated because the valve is located away from the pt. Exhaled gases in the outer reservoir tubing add warmth to inspired fresh gases. The hazards of the Bain circuit include unrecognized disconnection or kinking of the inner fresh gas hose.

1. Pulse oximetry: This is determined by the relative proportions of oxygenated and deoxygenated hgb. Deoxyhemoglobin absorbs more light in the red band with a wavelength of 660 while oxyhemoglobin absorbs more light in the infrared band with a wavelength of 910nm. The pulse ox emits lights in the two wavelengths. The machine picks up a pulsatile component- plethmography and a ratio of red to infrared is gathered and the machine estimates an O2 Sat. Pulse oxes are dependent on a pulsatile waveform so any conditions of low or absent pulse amplitude will fail to give a reading or give an inaccurate one. These situations could be cardiac arrest, bp cuff inflation, tourniquet application, hypovolemia, hypothermia, vasoconstriction, or cardiac bypass. The pulse ox is also very sensitive to movement artifact and electrocautery. Hematocrits less than 10% may adversely affect the accuracy by underestimating the sat. An injection of methylene blue can cause a transient drop in your sat as can indocyanine green and indigo carmine. In a few deeply pigmented people, the sat may not be able to detect the red light thus not give a reading.
2. Beer-Lambert Law: This r/t amt of light picked up by the SaO2 monitor. The amt of it absorbed by the oxyhemoglobin is proportional to the concentration of oxyhemoglobin and the length of the pathway it travels.
3. Oxyhemoglobin dissociation curve: You need to know that for a PaO2 value of 90% will give you a pO2 of 60. A PaO2 of 50% will give you a pO2 of 27. The curve can shift to the left or right and this will cause changes in the amt of O2 taken up by the tissues or offloaded in the lungs.

• Right Shift- O2 is offloaded easier to tissues but isn’t picked up well in the lungs. Causes are Acidosis, and increases in the following: temp, CO2, levels of 2-3 DPG
• Left Shift - O2 is harder to unload to the tissues since the hgb has a higher affinity for the O2 but is easily picked up by the lungs. Causes are alkalosis and a decrease in the following: temp, CO2, levels of 2-3 DPG. A left shift will need better pO2 in order to offload O2 to the tissues. Abnormal hgb can cause a left shift such as fetal hgb, carboxyhgb or carbon monoxide poisoning, and methemoglobinemia
• A Way to Remember this: Left has an "L" in it as does alkalotic as does HOLD as in hgb holds on to the O2. All the other arrows in left are going down. A right shift is opposite this!

4. Capnography: The measurement of respiratory CO2 has become a standard. It is used to confirm ETT placement, follow the adequacy of ventilation, and estimate the partial pressure of CO2. Capnography is the visual representation of the relative or absolute concentration of CO2 in the sample. It uses infrared absorption, mass spectrometry, which exposes the sample to a magnetic field and colorimetric detection. The collection device determines the amt% and can give you several different gases at the same time. In most cases the expired CO2 end tidal closely follows the PaCO2 with gradients less than 5mmHg. The CO2 waveforms are important for clinical. Phase 1 is the area near the baseline and means end inspiration. Phase 2 is the sharp upswing and means beginning of expiration. Phase 3 is the long plateau across the top and means expiration. Phase 4 is the sharp downswing and means the start of inspiration. Every breath on anesthesia machines should return to normal on general ETT pts unless you are using a nonrebreathing system. This will mean that the CO2 is totally absorbed and you begin with zero. See class notes for diagrams of the abnormal waveforms.
5. Sources of CO2 rebreathing: This has been discussed already but they do include: low fresh gas flow in systems without CO2 absorption, in a circle system if the valves are incompetent or absent or if a nonrebreathing valve allows significant back leak of exhaled gases or is assembled inappropriately. Low tidal volume, wasted ventilation due to distention of system components, compression of gases in the system, inappropriate adjustment of the pop-off valve, leaks in the anesthesia machine, and disconnections can all lead to hypoventilation and result in hypoxia and hypercarbia. It is important to therefore monitor vital signs, observe chest motion, and use a precordial or esophageal stethoscope to detect inadequate ventilation. End-tidal CO2 monitoring, measurement of exhaled volumes, and blood gas analysis are invaluable tools.
6. CO2 dissociation curve: CO2 is the end product of aerobic metabolism. This curve tells us the relationship btw the total CO2 content of blood and the partial pressure of CO2. CO2 elimination depends on pulmonary bloodflow and alveolar ventilation. CO2 is transported in the blood in 2 ways; in the plasma and on the RBC. In the plasma it comes in 3 forms which are 1. CO2 combines with AA group of plasma proteins to form a carbamino group, 2. Remains in solution – dissolves in small amt since it is slightly soluble. And 3. As carbonic acid where it combines with water. The majority of the CO2 is carried on the RBC. A large portion of that combines to form carb-amino hgb which facilitates the release of O2 from hgb. The largest % of CO2 is transported as hydrated as carbonic acid. Carbonic anhydrase is the enzyme that facilitates the reaction of bicarb and H and allows the reaction to occur 10.000 times faster. The CO2 can go onto the RBC and the enzyme will speed up the process of breakdown of CO2 to bicarb and H. 99.9% of carbonic acid dissociates into bicarb and H even without carbonic anhydrase. The Hamburg phenomenon is that bicarb has a negative charge and will diffuse out of the cell and into plasma while chloride will diffuse from plasma to the RBC. This chloride shift is the Hamburg Phenom done to maintain electrical neutrality. The major difference with the CO2 dissociation curve from the oxyhemoglobin one is that the CO2 curve is much more linear and has a steeper slope. For a given change in partial pressure significantly more CO2 can be carried in the blood compared with O2. A part pres change – small in CO2 will give a larger difference. Ie. A partial pres of 50 vs 55. 55 can hold a lot more CO2 so you would see a larger jump here than a change from 50 –55 on the O2 curve. The O2 curve will affect the CO2 curve. The lower the sat of hgb for O2, the larger the CO2 content for a given pCO2. Haldane effect is that the deoxygenated blood (mixed venous) has a greater capacity to carry CO2 than does oxygenated blood. The slope of the CO2 curve is 3 times steeper than the O2 one. Deoxygenated blood can carry more CO2 but also has a higher affinity for H ions. If you didn’t have the Haldane effect the tissue pCO2 would have to rise to 51mmHg to load the same CO2 found in mixed venous blood of 46mmHg. You can offload CO2 at the tissues since the deoxygenated blood allows CO2 to come out of the tissue easier and load up on the RBC’s. O2 gets onloaded in the lungs. There is an affinity for O2 so CO2 goes off and O2 goes on.