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123 Cards in this Set
- Front
- Back
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MAC definition
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-the alveolar concentration of anesthetic at which 50% of patients move in response to surgical stimuli
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things that decrease MAC (increase anesthetic potency)
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1. hypoxia (PaO2 < 40 mmHg), hypotension (severe), hypothermia
2. anemia (Hb < 4), age, a-methyldopa 3. benzos, barbiturates, hypercarbia (PaCO2 > 90 mmHg) 4. cholinesterase inhibitors, chronic amphetamines, clonidine 5. narcotics, ketamine 6. pregnancy 7. reserpine, lithium |
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things that increase MAC (decrease anesthetic potency)
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Notice everything is too high!!
1. alcohol too high chronically (ie. chronic alcoholism) 2. hyperthermia, hypernatremia 3. drugs which increase catecholamines a. ephedrine b. acute cocaine c. acute amphetamines d. MAOIs |
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things that leave MAC unchanged
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1. duration of anesthesia
2. sex or species 3. hypocarbia or hypercarbia (PaCO2 < 90 mmHg) 4. alkalosis or acidosis 5. hypo or hyperthyroidism |
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what are 2 more important points to make about MAC?
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how it relates to thyroid disease and age
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MAC and thyroid disease
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-MAC is not altered by hyper or hypothyroidism, as shown by the figure
-even though CO is increased in hyperthyroidism, and this necessitates a higher concentration of volatile anesthetics (because the rate of rise of alveolar concentration is decreased), but the potency of the volatile agent, as reflected by MAC value, does not change |
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MAC and age
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-MAC is greater in neonates than adults, and rises further until about age 1, when it begins to fall for the rest of life
-the mechansim for this is unknown |
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summary of CV effects of volatile anesthetics
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MAP and volatile anesthetics
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-halothane, enflurane, and desflurane all decrease MAP in a dose dependent manner
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which volatile agent decreases MAP the least? most?
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-halothane decreases it least
-desflurane and isoflurane the most |
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CO and volatile anesthetics
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-halothane decreases CO, which parallels its effect on MAP
-isoflurane and desflurane have little effect on CO, because even though they profoundly decrease SVR, they both cause tachycardia |
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SVR and volatile anesthetics
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-isoflurane and desflurane decrease SVR
-halothane has little effect on it |
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HR and volatile anesthetics
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-isoflurane and desflurane increase it
-halothane has little effect |
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myocardial oxygen consumption and volatile anesthetics
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severe agents decrease myocardial oxygen consumption:
-halothane does it the most of modern volatile agents, which makes it advantageous in the settinng of CAD as it depresses the myocardium and decreases myocardial oxygen consumption |
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what else does halothane do to the myocardium though?
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-it sensitizes the heart to the effects of catecholamines, which can result in dysrhythmias
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what is the first new volatile anesthetic is 20yrs?
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desflurane
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how is desflurane produced?
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-by substituting a fluorine for the single chlorine in isoflurane
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desflurane speed in changes of anesthetic depth
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-changes in anesthetic depth are very rapid, due to the low blood-gas solubility coefficient (0.41), which is lower than all other volatile agents, and also slightly lower than nitrous
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what is the MAC of desflurane in middle aged adults?
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6%
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desflurane metabolism
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-it strongly resists biodegradation, and therefore only a small amount is metabolized in animals and humans
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cardiorespiratory effects of desflurane
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-similar to those for isoflurane
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cerebrovascular effects of desflurane
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similar to isoflurane, produces:
-dose related increases in CBF -dose related decreases in CMRO2 -dose related depression of the EEG -though it increases CBF, like isoflurane, this can be attenuated by prior hyperventilation, and its probably safe to use in all cases except severe intracranial hypertension |
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advantage to using desflurane in neurosurgery
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-rapid emergence at the end of prolonged surgery is advantageous
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desflurane and inhalational induction
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-its associated with a higher incidence of breath holding, coughing, excessive secretions, and laryngospasm (sevo is a better choice)
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why is the desflurane vaporizer heated?
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-the partial pressure (vapor pressure) of des is 660 mmHg, which is very close to atmospheric pressure (760 mmHg) at room temp, meaning small changes in liquid temperature or barometric pressure will greatly impact vaporizer output; the vaporizer is therefore heated to raise its partial pressure so the vapor can be metered more accurately
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physical properties of sevoflurane:
MAC B/G partition coefficient vapor pressure |
-MAC: 2.0
-B/G partition coefficient: 0.60-0.65 -vapor pressure: 200 |
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which is the most important of these properties and why?
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-the low blood/gas partition coefficient, because it means it has a rapid onset and offset time (rapid uptake and elimination)
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despite its advantages, what is the one major disadvantage of sevoflurane?
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-it is significantly biotransformed, it can result in serum fluoride concentrations which exceed the threshold for renal toxicity
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CV effects of sevoflurane
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-produces systemic vasodilation similar to isoflurane
-cardiac effects also resemble iso, and it seems to have less myocardial depressant effects than older agents like enflurane |
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big advantage of sevo compared to other volatile agents
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-its the least irritant in terms of inhalation inductions, and it does not elicit a cough reflex
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besides metabolism inside the body, what is another disadvantage of sevoflurane?
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-its vulnerable to degradation by soda lime and baralyme, producing potentially toxic effects (desflurane strongly resists this biodegredation)
-sevo specifically reacts with carbon dioxide absorbents to form a vinyl ether, called compound A, which is shown to be nephrotoxic in rats; this is why sevo should be run at higher fresh gas flow rates, which limit rebreathing of compound A and reduce the likelihood of adverse effects |
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ABA-ASA lock and load:
1 ml of liquid isoflurane will generate how much isoflurane vapor? |
-1 mL of liquid isoflurane generates 200 mL of isoflurane vapor
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use of nitrous oxide
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-its a good amnestic which decreases the dose requirements of volatile anesthetics
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nitrous oxide and the heart
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-it causes dose-dependent myocardial depression, though nitrous plus halothane causes less myocardial depression than halothane alone
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what tends to mask the myocardial depression caused by nitrous?
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-nitrous also causes sympathetic stimulation, which maintains HR, CO, and MAP
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ranger lock and load:
myocardial depressant effects of nitrous |
-NITROUS HAS MYOCARDIAL DEPRESSANT PROPERTIES (2/3 of CA-3's missed this)
-from Barash: when given alone in 40% concentration, nitrous can decrease CO, and when given to patients with heart disease, especially in combination with opiates, it causes hypotension and a decrease in CO |
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cerebrovascular effects of nitrous
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-it increases cerebral blood flow in a dose-dependent manner
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nitrous and patients with severe COPD
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-in patients with severe emphysema it can greatly expand blebs and predispose to tension pneumothorax
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nitrous and the pulmonary vasculature
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-it can increase pulmonary artery pressure and lead to cor pulmonale in the presence of severe pulmonary hypertension
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settings in which nitrous oxide is contraindicated
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-air embolus (also in congenital heart disease due to risk of air embolus)
-bowel obstruction -COPD-emphysema, severe cor pulmonale -cardiac dysfunction (severe LV depression) -eye and ear surgery of certain types -pneumothorax or pneumocephalus -trauma in the presence of chest wall or head trauma |
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lock&load about nitrous's capacity to expand air bubbles
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-during N2O anesthesia and air bubble in the blood will expand rapidly relative to other locations of air in the body (this was not recognized by 1/3 of CA-3's)
-since nitrous oxide is 34x more soluble than nitrogen, it can enter air containing spaces more rapidly than air causing them to expand, and since it encounters less barriers to diffusion in the blood relative to other areas of the body where it has to cross membranes, and therefore will expand air in the blood faster than in other locations |
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related lock&load on nitrous oxide
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just memorize that:
NITROUS OXIDE EXPANDS AN AIR EMBOLUS FASTER THAN IT EXPANDS A PNEUMOTHORAX |
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volatile anesthetics and patients with aortic or mitral stenosis
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-you want to avoid increasing HR or decreasing SVR
-use halothane (isoflurane decreases SVR and increases HR) |
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volatile anesthetics and patients with aortic or mitral regurg
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-want an increase in HR and decrease in SVR, therefore use isoflurane
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volatile anesthetics and patients with CAD
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-halothane may reduce myocardial infarct size, and since it depresses the myocardium it will lead to a decrease in myocardial oxygen consumption
-isoflurane likely dilates the coronary circulation, and can lead to coronary steal, so it is therefore not indicated for use in these patients in concentrations high enough to cause steal, but fine below these concentrations |
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coronary steal
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-a diversion of blood flow from the coronary vasculature distal to a critical coronary stenosis, since the vessels distal to the stenosis are already maximally dilated, when other vessels dilate blood flow is stolen from them, and blood flow is increased to normally perfused areas, and away from the infarcting areas
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what concentrations of isoflurane are thought to be insignificant in terms of coronary steal?
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-its likely insignificant <0.5%
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other drugs which cause coronary steal
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-isoproterenol, dipyridamole, and nitroprusside
-nitroglycerine is thought to cause less |
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volatile anesthetics and respiratory function
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-all are respiratory depressants, with most depression to least being enflurane, halothane, and isoflurane
-they all decrease tidal volume and increase RR, with an overall decrease in minute ventilation |
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volatile agents in COPD patients
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-in patients with COPD the ventilatory response to CO2 is depressed, so they rely on hypoxic ventilatory drive, and volatile agents even in very low concentrations depress hypoxic ventilatory drive, even low concentrations of volatile agent can be dangerous
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what is the effect of volatile agents on the CO2 response curve in normal patients?
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it is unaffected
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what are the arguements for controlled ventilation while using volatile anesthetics?
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-expose to volatile anesthetics results in ventilatory depression
-oxygen consumption and work of breathing are increased with spontaneous ventilation |
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volatile agent effect on the CNS
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-they increase CBF and decrease CMRO2, while causing an uncoupling of CBF and CMRO2
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volatile anesthetic effect on the EEG
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-at 2 MAC iso and 4 MAC halothane there is burst supression of the EEG
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volatile anesthetics and SSEPs
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-above 1%, they cause a decrease in amplitude and increase in latency of the SSEP waveform
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volatile anesthetics and CBF
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-above 0.5 MAC, there is a dose dependent increase in CBF
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volatile anesthetics and CMRO2
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-isoflurane decreases the CMRO2 more than halothane, but both cause uncoupling of CBF and CMRO2
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volatile anesthetics and CSF
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-isoflurane likely does not alter CSF production, but does decrease resistance to absorption of CSF (therefore increasing absorption), decreasing the total volume of CSF
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what is the big problem with halothane?
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-its a possible cause of post-op liver dysfunction
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halothane hepatitis
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-its a diagnosis of exclusion
-2 types: 1. self-limited post-op hepatotoxicity (more common & less severe) 2. life-threatening hepatic toxicity (less common & more severe) |
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what about the use of halothane is most associated with liver damage?
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-repeated exposure is associated with the liver damage, with 20% of patients repeatedly exposed to halothane will have elevated aminotransferases, therefore HALOTHANE SHOULD NOT BE USED IN THOSE REPEATEDLY EXPOSED TO IT, OR WHO HAVE PAST HEPATIC DAMAGE RELATED TO ITS USE
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severe, potentially fatal liver damage with halothane use
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-does happen, 1 in 22000-35000
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mechanism of halothane liver damage
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-unknown, but the eosinophilia, rash, fever, and arthralgia associated with it suggest an immune process
-the plasma of pts who've had severe halothane hepatitis have been shown to have antibodies to specific halothane induced liver antigens called neoantigens, which are thought to be formed by the reaction of the halothane metabolite (trifluoroacetyl halide) with hepatic proteins; it was previously thought the hepatic damage was due to reductive biotransformation of metabolites, but not anymore |
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which patients are most at risk for halothane hepatitis,? and which seem to be resistant to it?
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-middle-aged obese females seem to be most at risk
-pediatric patients seem to be resistant, even after repeated exposure |
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use of halothane in patients with preexisting liver disease
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-while theres no evidence that liver dysfunction due to halothane is more likely in these patients, you should still consider not using it as there are easy alternatives, and the magnitude of post-op liver dysfunction if it does occur will be more exaggerated
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what is the one known genetic effect of an inhaled agent?
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-nitrous oxide causes inhibition of methionine synthetase in the bone marrow, which is a B12 dependent enzyme
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what concentration of fluoride in the plasma is necessary to cause renal damage?
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-more than 50-80 uM/L
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fluoride nephropathy
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-when concentrations exceed 50-80 uM/L there is direct damage to the renal tubules, resulting in polyuria and a decreased ability to concentrate the urine
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isolfurane and fluoride nephropathy
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-the metabolism of iso does result in the formation of fluoride ions, but in very small quantities, and renal dysfunction is extremely rare
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factors affecting anesthetic gas delivery
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-FI: fraction inspired
-VA: alveolar ventilation -the greater the fraction of inspired gas and the greater the alveolar ventilation to deliver it, the faster the rate of rise of alveolar concentration, and the faster the effect of the agent |
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factors that affect anesthetic gas uptake
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-CO, solubility, and change in the alveolar to venous blood concentration
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CO effect on anesthetic gases
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-the greater the CO the slower the rate of rise of alveolar concentration, whereas the slower the CO the faster the rate of rise of alveolar concentration
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solubility and anesthetic gases
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-the greater the solubility of the gas, the slower the rate of rise of the alveolar concentration (I think of it as more of the gas is being dissolved away by the blood, pulling more of it out of the alveoli, similar to the way the CO being higher causes a slower rise)
-in contrast, the lower the solubility of the gas, the faster the rise in alveolar concentration |
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FA/FI for common agents
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***************figure***********
-the rate of rise of the alveolar (FA) anesthetic concentration toward the inspired (FI) concentration is most rapid with least soluble anesthetics such as nitrous and des, and slowest with the most soluble, diethyl ether |
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what does cold do to volatile anesthetic induction?
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-it increases the solubility of agents, and therefore slows induction
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affect of right mainstem intubation on anesthetic gas induction
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-for very soluble agents, induction will not be delayed (think it is so slow anyway it wont be affected), but for insoluble agents, induction will be delayed
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affect of CO and vent changes on anesthetic gases
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-changes in CO and ventilation will have the greatest affect on soluble agents
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second gas effect
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-the uptake of large volumes of a first gas accelerates the alveolar (arterial) rate of rise of a second gas
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inhaled agent induction in neonates and pregnant patients
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-both groups have an increased ratio of minute ventilation to FRC, and therefore induction will be ACCELERATED
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advantages of isoflurane
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-induction and elimination are relatively rapid due to a low blood/gas partition coefficient (solubility)
-low metabolism results in minimal toxicity -its associated with good muscle relaxation |
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metabolism of all the volatile agents
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-methoxyflurane: 40%
-halothane: 20% -sevoflurane: 5% -enflurane: 2% -isoflurane: 0.2% -desflurane: <0.2% |
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how are volatile anesthetics metabolized?
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-by cytochrome P450 enzymes in the endoplasmic reticulum in hepatocytes, which mediate both oxidative and reductive metabolism
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what do cirrhosis and CHF do to volatile agent metabolism?
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-might decrease the magnitude of overall metabolism of agents
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morbid obesity and volatile agent metabolism
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-is associated with increased defluorination of volatile agents
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what does enzyme induction in the liver do to volatile agent metabolism?
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-it is not associated with an increase in metabolism
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what is the overall hepatic metabolism of halothane?
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about 20%
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pathways of hepatic metabolism of halothane
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there are 2 pathways:
1. oxidative pathway: the pathway followed normally 2. reductive pathway: the pathway followed during hypoxia and sometimes in obesity |
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oxidative pathway of halothane metabolism
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-the normal pathway followed which produces trifluoroacetic acid, bromide, and chloride
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reductive pathway of halothane metabolism
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-seen in states of hepatic hypoxia and sometimes obesity
-produces fluoride, chlorodifluoroethylene, and chlorotrifluoroethane -serum fluoride concentrations can reach 10 uM/l, well below the toxic threshold of 50-80 uM/l |
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hepatic toxicity during halothane metabolism
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-its thought the reductive metabolites of halothane bind to intracellular components of the hepatocyte and cause its destruction, with the key seeming to be hepatic hypoxia
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isoflurane metabolism
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-overall metabolism is very small, 0.2%
-the major metabolites are difluoromethanol and trifluoroacetic acid -difluoromethanol is degraded to minute amounts of fluoride |
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sevoflurane metabolism
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-the rate of defluorination is about the same as for methoxyflurane, but there are far less F- on sevo
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what is the most slowly metabolized of the fluorinated agents?
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desflurane; what little metabolism there is is due to oxidation
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pneumonic for order of amount of defluorination of volatile agents, from most metabolized to least
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Me So Horn-E, I Declare
methoxyflurane, sevoflurane, halothane, enflurane, isoflurane, and desflurane |
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pneumonic for amount of metabolism of volatile agents, from most to least
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Me Have Sinned Enough, I Declare
methoxyflurane, halothane, sevoflurane, enflurane, isoflurane, and desflurane |
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halothane MAC, B/G solubility, and vapor pressure
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MAC: 0.75
B/G solubility: 2.3 vapor pressure: 240 |
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isoflurane MAC, B/G solubility, and vapor pressure
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MAC: 1.15
B/G solubility: 1.4 vapor pressure: 238 |
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nitrous oxide MAC, B/G solubility, and vapor pressure
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MAC: 105
B/G solubility: 0.47 vapor pressure: --- |
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desflurane MAC, B/G solubility, and vapor pressure
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MAC: 5.70
B/G solubility: 0.42 vapor pressure: 665 |
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sevoflurane MAC, B/G solubility, and vapor pressure
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MAC: 2.0
B/G solubility: 0.6-0.65 vapor pressure: 160-200 (its temp dependent, at 20C its 160, at 25C 197, and at 36C 317) |
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MAC
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-the alveolar concentration at which 50% of patients will not respond to surgical stimulus; its a measure of anesthetic potency, the lower the MAC, the greater the potency
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B/G partition coefficient
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-the LOWER the coefficient, the LESS SOLUBLE the gas is, and the faster the rate of rise of the alveolar anesthetic concentration will be, so the patient will go to sleep and wake up faster
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effect of vapor pressure on anesthetic gases
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-the % of an anesthetic agent delivered increases with increasing vapor pressure
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if a machine is calibrated at sea level then taken to a higher elevation, what happens to the VP/BP ratio?
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-since the vapor pressure stays the same, but the barometric pressure decreases, the ratio increases, and therefore the delivered concentration is higher than indicated on the dial
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oxygen E cyclinder litres, pressure, and critical temp
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litres: 625 l
pressure: 2200 psi critical temp: minus 120 |
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nitrous oxide E cylinder volume, pressure, and critical temp
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volume: 1590 l
pressure: 745 psi critical temp: 36 |
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converting psi, atm, and torr
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1 atm = 14.7 psi = 760 torr
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what is the critical temperature?
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-the temp above which a substance cannot be liquified regardless of the pressure placed upon it
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oxygen and its critical temp
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-the critical temp of oxygen is -120 C, therefore oxygen can only exist as a gas as it cannot be liquified above -120 C regardless of the pressure placed on it
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nitrous oxide and its critical temp
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-can exist as a liquid at room temp as its critical temp is 36 C, therefore the temp above which it cannot be a liquid regardless of the pressure placed on it is well above room temp
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what can be said about oxygen E cylinders?
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-pressure is proportional to volume
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what can be said for nitrous oxide E cylinders?
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-there is always an equilibrium between gas and liquid, and only when all of the liquid is vaporized will the pressure begin to fall, and about 75% of the volume has been exhausted, and about 215L remains
-to calculate how much nitrous is in a cylinder it has to be weighed, there are 44 g/mol and 22.4 L/mol |
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why does frost form on the outside of the cylinder?
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-expansion of fresh gas absorbs heat, forming frost on the cylinder
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2 physical properties about nitrous oxide
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-ammonium nitrate plus heat equals nitrous oxide plus water
-nitrous oxide supports combustion: at temps <450 C nitrous oxide breaks down into nitrogen and oxygen |
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lock&load: what is the proper way to deal with a tipped vaporizer?
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-the vaporizer should be set at low concentration and flushed at 10 L/min for 30 min (only 25% of CA-3's got it right)
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fflowmeters
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-vertical glass tubes with the smallest diameter at the bottom
-the bobbin floats at a point of equilibrium, where the downward force of gravity is equal to the upward force of the gas flow |
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what does the rate of gas flow through a flowmeter depend on?
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-the change in pressure across the flowmeter, the circumference around the indicator, and the physical properties of the gas
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what happens as gas flows around the bobbin?
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-a pressure drop occurs, and increasing flow does not increase the pressure drop
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low vs. high flows on flowmeters
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-at low flows, gas flow varies according to viscosity, and at high flows according to density
-flowmeters are calibrated at a specific gas density and viscosity, and they cannot be interchanged |
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things which cause inaccuracies in flowmeters
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-large temperature fluctuations
-barometric pressure decreases at high flows, and at very high flows the density of gas decreases and the delivered flow is actually greater than the flow meter is reporting -the greater the flow, the more error in the flow actually being delivered -floats must be properly aligned and the float must be straight up and down |
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does the length of the flowmeter tube make a difference in accuracy?
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no
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how can you test for an oxygen flowmeter leak, and which is most sensitive?
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-you can test the low pressure system with positive pressure, and use the negative pressure check
-the negative pressure check is most sensitive |
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MAC of isoflurane is likely increased with:
A: acute ethanol intoxication B: PCO2 of 50 torr C: chronic guanethidine therapy D: rectal temp of 41C E: increased length of anesthetia |
D: rectal temp of 41C
**memorize the list at the beginning of the chapter |
