Chap. 4 Inhaled Gases Flashcards
Blood:gas partition coefficient of all gases
Intermediate soluble
Halothane: 2.54
Enflurane : 1.90
Isoflurane : 1.46
Poorly soluble N2O : O.46 DES : O.42 SEVO : O.69 *Xenon : 0.115
Which volatile gas is most soluble in blood and which is the least soluble in blood?
Halothane is the most soluble
Desflurane is the least soluble in blood
Stability in Soda Lime (inhaled gases) at 40 C
All gases are stabile except Halothane and Sevoflurane
MAC of all gases (100% oxygen, middle aged healthy patient)
N2O 104
Halo 0.75
Enfl. 1.63
ISO 1.17
Des 6.6
Sevo 1.8
Odor of all inhaled gases
N2O sweet Halo organic Enfl. Ethereal ISO. Ethereal Des ethereal -very pungent causes airway irritation Sevo ethereal
MAC with 60-70% N2O added
N20 -same obviously Halo 0.29 Enfl 0.57 ISO 0.50 Des 2.83 Sevo 0.66
Decreases the cost of the anesthetic by you are diluting it with a cheaper gas and you can still achieve the same affect.
Boiling points in C
N2O- already a gas Halo 50.2 Enfl 56.2 ISO 48.5 Des 22.8- Des will boil at normal OR temps Sevo 58.5
Molecular weight of inhaled gases
N2O 44 Halo 197 Enfl 184 ISO 184 Des 168 Sevo 200 -you can try to remember sevo based on its MAC which is basically 2
Vapor pressure (mm Hg at 20 C)
N20 is already a gas so no vapor pressure Halo 244 Enfl 172 ISO 240 Des 669 Sevo 170
Preservative necessary for volatile inhaled anesthetic
Halothane is the only inhaled gas that requires a preservative.
Sevoflurane and desflurane have lower blood and tissue solubility, why is this significant?
More precise control over the induction of anesthesia and a more rapid recovery when the drug is discontinued.
Seizure activity among inhaled anesthetic
Enflurane decreases the threshold for seizures. Primarily used for procedures in which a low threshold for seizure generation is desirable such as ECT.
Inhaled anesthetic relationship to Cerebral Blood Flow (CBF)
Volatile anesthetic produce dose dependent increases in cerebral blood flow. (They are cerebral vasodilators, decreased cerebral vascular resistance (if you are dilating then you are decreasing resistance) and thus resulting in dose dependent increase in CBF.
Inhaled anesthetic and ICP
Traditional way to lower ICP?
Why is this a problem with Enflurane?
ICP increases in the same fashion that CSF increases, dose depending. Desflurane does not increase ICP at less than 0.8 MAC but at 1.1 MAC ICP is increased by 7 mm Hg.
Typically hyperventilation of the lungs decreases paco2 which leads to arterial vasoconstriction thus lowering CBF, cerebral blood volume and decreasing ICP.
Hyperventilation with enflurane increases the risk for seizure activity, which could lead to increased paco2 > increased CBF, which can then increase ICP.
Enflurane and CSF
Enflurane increases both the rate of production of CSF and resistance to reabsorption.
MAP and inhaled anesthetic
All inhaled anesthetics decrease MAP except for enflurane. Nitrous has no effect or slightly raises MAP, another reason to mix your gas with nitrous.
Halothane lowers MAP, how?
Decreased myocardial contractility and cardiac output.
How do isoflurane, desflurane, and sevoflurane decrease MAP?
Decrease in systemic vascular resistance.
HR and inhaled anesthetics
Halothane causes no change in HR
Isoflurane, desflurane, and sevoflurane increase HR
Sevoflurane and cardiac output
Sevo decreases CO at 1 and 1.5 MAC but when administered at 2 MAC CO recovers to nearly awake values.
Which inhaled does not increase right atrial pressure (central venous pressure) when administered to healthy human volunteers.
Sevoflurane
What happens after 5 hours or longer with administration of volatile anesthetics?
Recovery from the cardiovascular depressant effects of these drugs. Return of cardiac output towards prodrug levels, HR is also increased after 5 hours.
What does the recovery of the cardiovascular system after 5 hours of administration of volatile anesthetics show?
Resembles a Beta andrenergic agonist response. Pretreatment with propranolol prevents evidence of recovery with time from the circulatory effects of volatile anesthetics.
Which volatile inhaled anesthetic is best for undergoing ablative procedures?
Sevoflurane
Are volatile inhaled anesthetics cardiac protective?
Yes, even isoflurane
They all induce coronary vasodilation on vessels with diameters of 20 um to 50 um
Desflurane irritating?
Des irritates the lungs, and the larynx and above, it has been know to cause laryngospasm at concentrations greater than 6% inspired.
Calcium blockers and inhaled anesthetics
Calcium blockers decrease myocardial contractility and thus render the heart more vulnerable to direct depressant effects of an inhaled anesthetic
Voltage gated calcium channels and inhaled gas
Are only inhibited to a small extent by inhalation anesthetics
What is cardiac preconditioning?
Brief episodes of myocardial ischemia occurring before a subsequent longer period of myocardial ischemia providing protection against myocardial dysfunction and necrosis is termed ischemic preconditioning.
What causes the heart to do cardio protection?
Brief exposure to volatile anesthetic (isoflurane, desflurane, and sevoflurane) can activate K atp channels resulting in cardioprotection (anesthetic preconditioning) against subsequent prolonged ischemia and myocardial repercussion injury that is identical to IPC.
Sevo and thoracic surgery- pg 133
Sevo is useful during thoracic surgery as it is a potent bronchodilator, its low blood gs solubility permits rapid adjustment of the depth of anesthesia, and effects on hypoxic pulmonary vasoconstriction are small
If a patient has COPD which two gases are likely to produce bronchodilation in patients.
isoflurane and sevoflurance
Which gas is the best at bronchodilation if you had to pick one?
Sevoflurane
Name the two CO2 absorbents
baralyme, soda lime
Dalton’s law of partial pressures
The total pressures of a mixture of gases is the sum of the pressures each gas would exert if it were present alone.
What is the goal and goal organ (tissue) with inhaled anesthetics
The goal is to achieve a constant and optimal brain partial pressure of inhaled anesthetics
Partial pressure of inhaled gases follows what pattern when inhaled and what pattern when the gas is turned off?
When inhaled the partial pressure of Aveoli is first then arterial then brain, thus Pbrain is a direct indicator of what the PA is showing you, it comes to equilibrium.
When the gas is stopped it follows the opposite direction, decreases from the brain first then in the arterial blood then it comes out of the PA last.
What is minute ventilation
Sum of all gas volume (inhaled and exhaled) in 1 minute. Minute ventilation=Tidal volume x breaths per min.
Ex. 5L/min
Alveolar ventilation:
Volume of inspired gases actually taking part in gas exchange in 1 min.
Alveolar ventilation = (tidal volume - dead space) x breaths per min
PCO2 indicates alveolar ventilation
What is dead space
Any volume of inspired breath which dose not enter the gas exchange areas of the lungs is dead space
Apparatus dead space
Only applies to patients attached to a ventilator
Physiologic dead space - 2 subdivisions
Airway (anatomical dead space) - portion of a breath which goes in the mouth, pharynx, and trachea bronchial tree, but does not enter the alveoli.
Alveolar- the portion of a breath that enters alveoli which are ventilated but not perfused (west zone 1)
Basically any gas that does not make it to the alveoli is some form of dead space
What determines PA
Input (delivery) of inhaled anesthetic into alveoli minus uptake (loss) of drug from alveoli into arterial blood.
Because you are subtracting uptake into the blood then the more soluble the gas the more you “lose” and the less that comes into contact with brain tissues.
Determinants of alveolar partial pressure PA (5 things)
ALVEOLAR VENTILATION ANESTHETIC BREATHING SYSTEM SOLUBILITY CARDIAC OUTPUT ALVEOLAR TO VENOUS PARTIAL PRESSURE DIFFERENCES
Tell me about PI in relation to the PA
The higher the PI the more rapidly PA approaches PI
If you turn you sevo up to 8 during induction then the PA and ultimately the Pbrain will reach equilibrium quicker, this is common in children but in adults you must watch the blood pressure by it can dump quickly.
Anesthetics follow its concentration gradient what is that gradient ?
Machine to alveoli to blood to brain
Remember the machine is a variable in how much gas goes into the alveoli
Concentration effect basically states what?
The higher the inspired concentration of anesthetic agent, the more rapid the relative rise in alveolar concentration of the agent.
Tell me what you know about 2nd gas effect (theory not so much clinical use)
Reflects the ability of a high volume uptake of one gas (the first gas) to accelerate the uptake (rate of increase of PA) of a concurrently administered 2nd gas.
Nitrous is always the first gas.
This effect is more applicable to agents with higher blood:gas solubility
Alveolar ventilation and inhaled gas…
Increased alveolar ventilation increases the rise of PA towards PI, resulting in induction.
Hyperventilation, what is the purpose?
Hyperventilation decreases PaCO2, resulting in decreased cerebral blood flow.
Neonates and alveolar ventilation
They have a greater metabolic rate, induction is quicker in neonates than in adults. Neonates is 5 to 1 and adults is 1.5 to 1, this is due to their metabolic rate.
Spontaneous breathing and gases
The rate and depth of Breathing will mimic how much gas the brain needs to be in equilibrium with the PA ultimately.
When concentration in the brain falls below a certain threshold breathing will increase to take up more anesthetic from the lungs. (Trying to reach equilibrium)
With spontaneous breathing is in use the brain will automatically breath less to decrease concentration in the brain and not be over anesthetized with gas compared to what is in the blood and ultimately the lungs.
When you mechanically ventilate all this is lost.
Stimulus and and the rate of spontaneous ventilation
When stimulated by incision the brain will tell the lungs to take in more anesthetic by breathing more and thus deliver more to the brain bc of the stimulus.
Poorly soluble anesthetics and rate of rise of PA
RAPID regardless of other factors, bc if it can not dissolve in the blood its going straight to the brain. Poorly soluble means quick indication and quicker to wake up.
Soluble anesthetic gas and PA (in regards to alveolar ventilation)
If the gas is more soluble then it is more affected by rate of rise of PA towards PI.
Mechanical ventilation increases the depth of anesthesia in soluble gas more.
Blood:gas most soluble to least soluble
Halothane is most at 2.54
Enflurane 1.90
Isoflurane 1.46
Sevo .69
Nitrous .46
Des .42
Anemic blood and induction?
More rapid induction in anemic blood due to decreased solubility (this applies more to gases that are more soluble such as halo, enf, iso)
Order of solubility, most soluble to least
Halo, enfl, iso, sevo, nitrous, des
Sevo and des solubility differences (in class discussion)
Sevo tends to hide in fat
Des does not tend to hide in fat thus if you have an obese patient you want to give des, most likely
Emergence is slower with fat loving gases (more soluble)
Tissue:gas ratios and what does it mean for emergence
The lower the tissue gas ratio the more rapid emergence
Stage one of anesthesia
Stage one begins with induction
ends with loss of consciousness (no eye-lid reflex)
Still can sense pain
Stage two of anesthesia
Excitation stage
Pupils dilated, divergent gaze
Potentially dangerous response to noxious stimuli - breath holding, muscular rigidity, vomiting, laryngospasm
(Any stimulation can cause a spasm, OR should be quite at this time, YOU CAN STILL FEEL PAIN and the response to that pain is worse in this stage than stage 1.)
Stage three (WHAT YOU WANT)
Surgical anesthesia can be performed
Centralized gaze with constriction of pupils
Regular resp.
Anesthetic depth is sufficient for noxious stimuli (as long as it does not cause increased sympathetic response )
Things are coming back to normal
Stage four of anesthesia
STAY AWAY FROM THIS STAGE, TOO DEEP
Apnea (will not breathe on their own)
Non reactive DILATED pupils (or unequal)
Hypotension resulting in complete CV collapse if not monitored closely.
CO (represented by pulmonary blood flow)
Influences uptake of PA by carrying away either more or less anesthetic from alveoli. (If the anesthetic can sit in the lungs it can get to the brain, but if it is removed by blood it will take longer thus the more soluble a gas is in blood the more affected by CO it is and the slower induction)
Increased CO more rapid uptake, slower induction
Decreased CO less uptake and quicker induction
MAC (what does it stand for)
MINIMAL ALVEOLAR CONCENTRATION
What specifically does MAC effect (body part)
MAC has effects on the spinal cord. This is what produces its immobility effects.
What procedure requires the highest MAC to suppress skeletal movement?
Tracheal Intubation (from the book pg 114)
Are MAC values additive?
Yes, .5 MAC of N20 and .5 MAC of sevo is the same as 1MAC of either alone.
How do opioids affect inhaled volatile aesthetics
They synergistically decrease anesthetic requirements for volatile anesthetics
Name some opioids
Oxycodone, hydrocodone, morphine, dilaudid or hydro morphine, fentanyl
If a volatile anesthetic in excessive dose decreases CO what can ultimately happen (think very bad)
Decreased CO due to excessive dose, increases PA, increases depth of anesthesia, which further decreases CO (cardiac depression) eventually cardiac collapse.
Concentration of anesthetic in tissues (brain) when the case is over is dependent on what two factors?
What kind of anesthetics does this effect more?
Duration of administration and the inhaled anesthetics solubility in tissues.
The more soluble the anesthetic the more this will come into play.
At emergence to wake up your patient, what two things do you need to remember to do, so that they actually wake up?
Turn the gas off
Turn your oxygen flow rate up
When you d/c nitrous it will diffuse rapidly out of the tissues and back into the blood and then back into the alveoli , what can you do to prevent the diffusion hypoxia that will then follow?
Bag the patient with 100% oxygen, you are then diluting the nitrogen that is coming out of the tissues and ultimately trying to get to the lungs.
CNS effects and MAC concentration below 0.4
Increased frequency and voltage similar for ALL volatile anesthetics
CNS effects at a MAC concentration of 0.4 or greater?
Shift of voltage activity from posterior to anterior portions of the brain
Also
Decreased cerebral 02 requirements.
Seizure activity, which gas makes the threshold less for seizure activity?
Enflurane
Evoked potentials
Volatile anesthetics cause a dose related decreased in evoked potentials…
What do inhaled anesthetics bind to in the cell to exert their action?
They either bind to proteins or dissolve in lipids, its not really definitive.
What specific advantage does des and sevo have over all other volatile anesthetics
Their lower blood and tissue solubility permit more precise control over the induction of anesthesia and a more rapid recovery sheen the drug is discontinued.
Cerebral blood flow and volatile anesthetics
All volatile anesthetics produce a dose dependent increase in cerebral blood flow (CBF)
Thus be careful with the use in ppl with head bleeds
At 1.1 MAC , cerebral blood flow from greatest to least
Halothane is greatest then enflurane and then isoflurane which is equal to desflurane
Nitrous also increases CBF
It occurs within minutes of administration of anesthetic
Which gas is best for cerebral protection, especially with a carotid endarterectomy ?
ISOFLURANE
Intracranial pressure
All gases increase ICP but nitrous does it the least.
What do all volatile anesthetics do to the BP?
They all dose depended decrease the BP.
True effect may not be reflected by BP due to artificial elevation due to sins activity (apprehension, etc. )
How does halothane decrease MAP?
Myocardial contractility is decreased
How does iso, des, and sevo decrease BP?
Decrease in SVR
What volatile anesthetics increase HR ?
ISO, des, and sevoflurane all increase HR. With sevo this only occurs at MAC greater than 1.5.
What can be given with volatile anesthetics to offset the increase in HR from iso, des, sevo?
Opioids such as morphine or fentanyl have prevented HR increases with ISO and assumed to help with the other two.
Des and increased HR…
The increase is transient, it will go away on its own (but if someone has an already high HR you will not want them to have it. )
Halothane and HR
No CHANGE
CO and anesthetic gas
Halothane decreases CO
ISO, DES- no real effect
Sevo- decreases CO under 2 MAC but once at 2 MAC it recovers.
Left SV and all anesthetics
Decreases
SVR and anesthetics
ISO des and sevo all decrease SVR
Halothane has no change
Halothane dilates only cerebral and cutaneous vessels, it will make you flush.
Pulmonary Vascular Resistance and gas anesthetics
All volatile gases have little to no effect
Nitrous increases PVR, exaggerated in pulmonary hypertension, neonates, congenital heart disease. Thus you do not want to use nitrous with these patients.
Nitrous is a no no - NO NITROUS WITH PULMONARY HTN
Cardiac dysrhythmias and anesthetics (Epinephrine)
Anesthetics decreases the dose of epinephrine required to produce ventricular dysrhythmias.
Effects greatest with Halothane, minimal with iso, des, sevo
Beta blockers and surgery
If someone is on a beta blocker you need to make sure they have taken it before surgery or that morning.
Coronary blood flow
Volatile anesthetics cause coronary vasodilation preferentially in small vessels.
Even with the risk of coronary steel syndrome all volatile anesthetics are considered CARDIO PROTECTIVE.
If there is an abrupt increase in systemic blood pressure and or heart rate (as may occur with intensity of surgical manipulation) what gas is the best to treat that?
Desflurane presumably bc of its poor solubility. Des is far greater than ISO which can also help increase.
Which gas is unique for possessing mild beta adrenergic agonist properties?
ISOFLURANE
Blood pressure and SVR what you need to know
All volatiles produce dose dependent decreases in BP
ISOFLURANE PRODUCES THE MOST PROFOUND DECREASE IN SVR
ISO >DES>SEVO
Nitrous does NOT cause a decrease in BP
Who increases HR the most (pick two)
Des followed by ISO
Most potent of the volatile gases in clinical use and is a potent coronary vasodilator
Isoflurane
Which of the three vasodilating gases has the least effect?
Sevo
What is the dose limit on epinephrine for iso, des, sevo?
6mcg/kg
Possible cellular mechanism for ischemic preconditioning (IPC)
Release of adenosine to A1 and A2 receptors. Causing hyper polarization and inhibition of calcium entry decreasing the action potential of the SA node.
Basically the opening of the K channels is critical for beneficial cardio protective effects.
What can close or antagonize potassium channels?
Sulfonylureas and ketamine
^ glipizide
What does sliding scale insulin do for cardiac preconditioning?
Stimulates the sodium potassium pump, thus allowing potassium to enter the cell and decrease the likelihood of depolarization.
Who do you not give ketamine to?
People with High BP , ppl who may have an MI in the OR
Decreased minute ventilation and increased PaCO2 =
RESPIRATORY ACIDOSIS
Pattern of breathing and gas anesthetics
Dose dependent increases in breathing
except for isoflurane which has the same effect until the dose is over 1MAC, then no further increase in breathing.
If anything including gas anesthetics cause you to decrease your breathing then what is going to happen to your CO2 and PaCO2.
How is this fixed
Your CO2 and PaCO2 will both increase.
Most often the solution is mechanical ventilation.
Hepatic blood flow and the gas anesthetics
ISO @1.5% maintained hepatic artery blood flow while portal vein blood flow was increased. Confirming that isoflurane is hepatic vasodilator.
Des and sevo similar to ISO
Halothane constricts the hepatic circulation- bad. If you have a patient with liver issues you do not want to use halothane.
What does surgical stimulation do to LFTs
Increases all LFTs
HEPATIC metabolism that produces acetylated liver proteins.
Halothane > enflurane > isoflurane > desflurane
Des is the LEAST
SEVO AND HEPATIC EFFECTS
NOT metabolized to acetyl halide so cant stimulate antibody production to acetylated liver proteins.
Sevo and compound A
SEVO can be degraded by CO2 absorbent to produce compound A. Concentration in breathing circuit is below toxic level, only found to be an issues in animals.
JUST KEEP 2L of fresh gas flow running to decrease the risk of compound A.
Volatile anesthetics and renal blood flow
Dose dependent decreases in renal blood flow, GFR, urine output.
Probably as a result of BP and CO, preoperative hydration helps prevent.
If blood pressure starts to drop what is the first thing you are going to do?
Give fluids unless they have renal failure or CHF. Then you will probably start a pressor
Fluoride induced nephrotoxicity
Not seen with current volatile anesthetics because less metabolized, decreased solubility and most are exhaled by lungs so not available to be broken down into inorganic fluoride.
Which gas has greater intra-renal metabolism and which one has greater hepatic metabolism?
Enflurane is intra-renal
Sevoflurane is greater hepatic metabolism
Baralyme
No longer clinically available. Also had higher concentrations of compound A in its presence compared to soda lime.
Why the rule to run 2L of fresh gas flow with sevoflurane
To minimize the concentration of compound A that may accumulate in the anesthesia breathing circuit.
What is the absorber sucking up?
Compound A and vinyl ether
Skeletal muscle effects and NM blockers
Ether derived volatile anesthetics dose dependently increase skeletal muscle relaxation.
Dose dependent enhancement of NM blockers
N2O and halothane -skeletal muscle effects
N2O no relaxation, maybe rigidity
Halothane does nothing to cause skeletal muscle relaxation
MH and which gas anesthetic is the worst
All gas anesthetics can cause MH in genetically susceptible patients even in the absence of succinylcholine.
HALOTHANE is the MOST POTENT trigger.
What is MH?
Life threatening acute disorder developing with GA.
Volatile anesthetics and or succinylcholine cause an increase in SR calcium concentration (from ryanodine receptors) in susceptible patient, resulting in persistent muscle contraction.
Hyper metabolic state, increased HR, unexplained increase in end tidal CO2 that does not go back to baseline.
Resp. And metabolic acidosis, rhabdomyolsis, arrhythmia, hyperkalemia, and sudden cardiac death.
A RISE IN TEMP IS A LATE SIGN
What are three possible causes of the end tidal CO2 to start increasing and not come back down to baseline?
CO2 absorber is full, water trap (is dry?) circulatory system could be the problem. And MH which is the least likely.
What will you most likely notice if MH takes place
Unexplained increase in end tidal CO2 (most sensitive indicator in OR)
Skeletal rigidity
Lactic acidosis
LATE SIGN IS HIGH FEVER
What microscopically causes MH
A constant leak of SR calcium through ryanodine receptors
Treatment for MH
- Notify the surgeon as soon as MH is suspected
- Stop triggering agents (gas)
- Hyperventilate with 100% o2 (tank)
- About procedure
- IV dantrolene
- Bicarbonate
- Cooling
- Insulin for hyperkalemia (d50)
- Monitor core temp
- Monitor urinary output and prevent shock to kidneys or ATN
Volatile anesthetics and OB
Dose dependent decrease in uterine smooth muscle contraction and blood flow
UTERINE ATONY
Relaxation is needed to expel the placenta or retained pieces but too much relaxation with no contraction ability can lead to blood loss and uterine atony.
Gas anesthetics and infections
Many normal functions of the immune system are decreased after anesthesia and surgery
Bacterialcidal and bacterialstatic in relation to gas anesthetics?
Liquid form of anesthetics may be bactericidal
Inhaled anesthetics do not have bacteriostatic effects at clinically used concentrations
Volatile anesthetics and measles/flu
Why might this occur?
All volatile anesthetics (dose as low as 0.2 MAC) produce dose dependent inhibition of measles virus replication and decreased mortality in mice receiving intranasal influenza virus
Metabolites of inhaled gases may be toxic to kidney, liver, reproductive organs, what does this mean for testing before anesthesia?
Pregnancy test on any female of child bearing age.
How to inhibit metabolism of N2O
Just make sure the 02 concentration is greater than 10%
Metabolism and halothane
10-15% metabolized by cytochrome p-450 enzymes (liver) Oxidative metabolism (which happens as long as you have plenty of 02 in your system) produces acetylated hepatic proteins resulting in formation of antibodies.
Enflurane metabolism
3% metabolized by P-450 enzymes
Isoflurane and metabolism
0.2% metabolized by cytochrome P-450
Desflurane and metabolism
0.02% metabolized by P-450 enzyme
Sevoflurane and metabolism
5% metabolized by P-450 enzyme
DOES NOT PRODUCE ACETYL HALIDES, NO POSSIBILITY OF HEPATIC PROTEIN AB COMPLEX LIKE ALL OTHER VOLATILE GASSES.
Degraded by c02 absorbent to potentially nephrotoxic compound A, but still not in levels that matter if fresh gas flow is 2L or greater. Compound A greater with baralyme than soda lime.
Carbon monoxide toxicity caused by CO2 absorbent
Desflurane > enflurane > isoflurane
Halothane and sevo can not produce CO
Why is it so hard to detect CO toxicity
The pulse ox can not distinguish between carboxyhemoglobin and oxyhemoglobin thus the pulse ox will cont. to read well.
What increases the magnitude of CO production
Dryness of CO2 absorbent (hydration prevents the dryness and thus CO2 productions)
High temperature of absorbent (they produce heat as they absorb CO2) occurs mostly during low flow fresh gas flow or increased metabolic production of CO2
Prolonged high fresh gas flows contributes to dryness of absorbent.
Baralyme is worse than soda lime
Carbon dioxide absorber fires
Most often associated with baralyme
Flammable metabolites can spontaneously combust at high temps. Sevo produces the most metabolites.
What is MAC or 1 MAC
The % of anesthetic agent (gas) which ceases movement in response to noxious stimuli in 50% of patients
What is Monday morning phenomena
Moderately decreased pulse ox readings despite adequate arterial partial pressures of oxygen (especially during the first case of the day on Monday ).
Possibility of carbon monoxide exposure and the need to measure carboxyhemglobin.
(This is because of the CO2 absorber that has been left over the weekend and not changed)
How long can it take for the side effects of CO toxicity to show up
3-21 days
Things that will cause you to increase your MAC
Red heads- excess phenomelanin production
High blood sodium-
Hyperthermia
Cyclosporine
Drug induced increases in CNS cholamine levels
Decreases in MAC
Hypothermia Increased age Pregnancy Preoperative medications (opioids) Etc.
MAC OF 1.3 WILL?
Prevent movement in 95% of patients
MAC awake
Opposite of MAC. MAC awake is where 50% of patients will respond appropriately. (2 sides same coin)
How does nitrous decrease the MAC of volatile anesthetics
Roughly (very roughly) by 1/3
What fraction of MAC should produce MAC awake?
1/10 of your MAC should be your MAC awake amount.
MAC BAR stands for ?
MAC Blunt Autonomic Responses to noxious stimuli
N2O
Induction and recovery?
Potency?
Does it need to be combined for GA?
Quick induction and quick recovery based on low blood solubility but you can never use nitrous alone. Low Potency
Where do you want your CO2 for a young healthy, non smoking (ASA1) patient who is breathing on their own
30-33 ET CO2 bc you do not want them breathing over your Vent, the closer to 35 the more likely they are going to try and start breathing to blow off some CO2
N2O Analgesic effect, sedation? N&V? What procedures not to use N2O? B12?
Good quick analgesic but only lasts about 20 min, sedative effects last longer than analgesic.
Thought to make N&V worse post op
Do not use with ear, sinuses surgery or pneumothorax. (Closed cavity that does not need increased pressure)
Inactivates vit B12
Halothane
Most of halothane characteristics are bad, we don’t use it in the USA. Needs a preservative added.
Intermittent blood solubility 2.54
Possible hepatotoxic
Isoflurane (stability)
Extreme physical stability , after five years of storage no deterioration and no preservative required.
Isomer of enflurane
Intermediate blood solubility 1.46
Desflurane
Pungent odor that causes airway irritation when 6% is used in awake patients.
High vapor pressure, increased molecular stability, decreased potency.
Would boil at room temp, converted to a gas in vaporizer and mixed with diligent fresh gas flow (needs to be heated) thus machine needs electricity.
Potency is five fold less than isoflurane.
Desflurane and CO production
Highest producer of CO
Desflurane > enflurane and isoflurane
Halothane and sevo are trivial producers of carbon monoxide.
Sevoflurane
Vaporizer
Odor
Induction and recovery
Unseated vaporizer can be used
Non pungent minimal odor- least irritating to the airways, acceptable for inhalation induction.
Resembles des with prompt induction and recovery.
Sevoflurane
Acyl Halide
Airway irritation
Bronchodilation
Can not be metabolized to acyl halide
Causes the LEAST degree of airway irritation
Bronchodilation similar to isoflurane
Sevo and CO
LEAST likely to form carbon monoxide on exposure to carbon dioxide absorbent.
Xenon, tell me everything you know about it
High cost causes it not to be used yet.
Blood gas coefficient of 0.115
Does bubble expand like N2O
Non pungent, odorless
Inert gas
Mac 63-74%
MAC is gender dependent being less in females
Does not contribute to MH
Emergence is 2-3 times faster than nitrous or sevo
Potent hypnotic and analgesic resulting in suppression of hemodynamics and catecholamine responses in surgical stimulation.
Dantrlene Dose
2.5mg/kg
right to left shunts
a right to left cardiac shut causes deoxygenated blood to leave the right heart and bypass the lungs. This blood does not pick up oxygen or inhalation agent. results in reduction in the partial pressure of anesthetic in the arterial blood.
a right to left intracardiac shunt produces a faster IV induction (blood bypasses the lungs and travels towards the brain faster as a result) examples: Tetralogy of fallot foramen ovale eisenmengers syndrome tricuspid atresia ebstein's anomaly
left to right shunt
will not have meaningful effect on anesthetic uptake or induction time
produces a slower iv induction (iv agent is recirculated in the lungs)
