Anesthesia Pharm Lecture 2

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cmatthews
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Anesthesia Pharm Lecture 2
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2013-06-02 18:20:34
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BC CRNA Anesthesia Pharm Lecture
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Summer 2013
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  1. Explain the 4 phases of Pharmacokinetics of inhaled anesthetics
    Absorption (Uptake): movement of the anesthetic from alveoli into the pulmonary capillary blood

    • Distribution: transport of the anesthetic to the
    • sites of action (CNS)

    Metabolism: often limited for inhaled agents

    Elimination: principally via the lungs
  2. Explain the route inhaled anesthetics take
    They go from the anesethesia machine, through the vaporizer, to the fresh gas flow, into the breathing circuit, to the fraction of inspired anesthetic, from there to lungs, FA (alveolar), and to the Fa (arterial).
  3. What drives the distribution of inhaled anesthetics?
    • partial pressure gradient
    • Pi ↔ PA↔Pa↔Pbr
  4. With volatile anesthetics, total equilibration likely never occurs, why ?!
    because of the differences in solubility of each of the groups, particularly the fat group.
  5. If the the Fa/Fi ratio proportional or inversely proportional to the solubility of the inhaled anesthetic agent
    inversely related to solubility (of the agent in blood) the more soluble the agent is, the more of the Fi (inspired gas) that’s dissolved so that the FA doesn’t build up as quickly
  6. ________ determines the relationship between partial pressure and volume % (Henry’s law)
    Solubility of the agent in tissue
  7. Name the determinants of Alveolar partial pressure. There are 8...
    • Inhaled partial pressure
    • Alveolar ventilation
    • Spontaneous vs mechanical ventilation
    • Cardiac output
    • Alveolar-to-venous partial pressure differences
    • Concentration effect
    • Second gas effect
    • Solubility
  8. What does the following equation help determine?

    Uptake = λ x Q x (Pa-Pv)                                                         
                                  P

    alveolar to venous partial pressure difference
    P = atmospheric pressure
    Q = flow
    λ = solubility
    How quickly FA will approximate Fi.
  9. What can we do to the inhaled partial pressure to increase the alveolar partial pressure.
    • Increased inspired concentration helps to off-set uptake speeding the rise in Palveolar
    • -want to offset uptake because if it gets taken up by blood it's not building partial pressure (which is what drives onset!)
    • this is called “Overpressurization"-like giving a bolus to get FA to approximate Fi more quickly
  10. How does improving alveolar ventilation help the FA/Fi ratio approximate more quickly?
    • Increased alveolar ventilation promotes input to off-set uptake. (If certain amount of agent is being taken up, (uptake) by the blood, but more isn’t being brought in to offset that, then we’re not able to get the alveolar concentration to build up that quickly)
    • This effect is less with an agent less soluble in blood.  (because if the agent isn’t that soluble then then uptake isn’t as big of an issue)
  11. Why do we care whether or not the patient is spontaneous or mechanically breathing during induction? (with regards to alveolar ventilation)
    Because the inhaled anesthetics will depress respiration. So unless we increase alveolar ventilation artificially, there is in essence a negative feedback. The patient slows their breathing, less anesthetic is taken up.  So hypoventilation (a natural side effect of the inhaled agents) is we don’t do anything else, will slow the rate of raise of FA over Fi.
  12. What happens if the patient is hyperventilating during induction?
    Hyperventilation, the  PCO2 goes down, decrease cerebral perfusion, so there could conceivably be less delivery of inhaled anesthetic to the brain. That could slow the clinical effect of the inhaled agent as well.
  13. What type of effect does cardiac output have on the alveolar partial pressure and uptake of inhaled agents
    • ↑ CO causes more rapid uptake and a decrease in rate of rise of P alveolar & slows induction
    • (equilibrium with vessel rich groups, like the brain, is slow)

    Most prominent with a soluble anesthetic
  14. What does the arterial venous partial pressure difference have to do with alveolar partial pressure and uptake
    Reflects tissue uptake of anesthetic

    • The fraction of anesthetic removed from blood as it passes through the tissues depends on
    •    a) Solubility of anesthetic in tissue
    •    b) Blood flow
    •    c) Partial pressure difference
    • Vessel-rich groups equilibrate rapidly with arterial partial pressure
    • After 3 times constants (5-15 minutes), uptake is decreased due to decreased inspired-to-alveolar partial pressure difference (saturation of vessel-rich groups)
  15. What are the two aspects of the concentration effect?
    Concentrating effect

    Augmentation of tracheal inflow
  16. What is the concentration effect?
    Impact of inspired partial pressure on rate of rise of alveolar partial pressure

    Explained by Fick’s Law

    The higher the inspired partial pressure, the more rapidly the alveolar partial pressure approaches inspired.
  17. Explain the concentrating effect
    • Concentration of the inhaled anesthetic in a smaller lung volume due to uptake of all gases from the lung.
    • When you take up 50% (or any % of the gas) from the alveoli. If that was higher concentration of anesthetic, more is taken out, and less left of total volume in the alveolus, the anesthetic is concentrated in a smaller total volume. (the part that is left). Goes up  exponentially because of this.
  18. Explain the augmentation of tracheal inflow (part of the concentration effect)
    • Because of the uptake of gases from the alveoli, the absorbed gas must be replaced by an equal volume of the gas mixture to prevent alveolar collapse
    • This creates a negative pressure which pulls in more inspired gas
    • (50% of anesthetic was taken up but now because of negative pressure situation need to replace the amount (in ml) that was taken up w/inspired gas volume (Which is a concentration mixture). We’re essentially adding mls of high concentration anesthetic
  19. Simply put second gas effect is the concentration
    effect of one gas on another. Explain this to me
    Concentration effect is more significant w/N2O than with the volatiles as N2O can be given in much higher concentrations

    High nitrous concentration will augment its own uptake but also that of a concurrently administered volatile

    The volatile is the second gas

    *Second gas effect is weak & probably insignificant
  20. What is the max % of N2O we can give?
    70% not more because then we're taking away FiO2
  21. What is really the point of the second gas effect
    Initially if we turn on N2O, and we give in such a high amount, it gets taken up, you concentrate the volatile more quickly. And get induction (FA/Fi) ratio equilibrium faster.
  22. What are the partition coefficients of Methoxyflurane?
    • Blood Gas partition coefficient: 12
    • Brain Blood partition coefficient: 2
    • Muscle Blood partition coefficient: 1.3
    • Fat Blood partition coefficient: 48.8
    • Oil Gas partition coefficient: 970

    **Very soluble**
  23. What are the partition coefficients of Halothane?
    • Blood Gas partition coefficient: 2.54
    • Brain Blood partition coefficient: 1.9
    • Muscle Blood partition coefficient: 3.4
    • Fat Blood partition coefficient: 51.1
    • Oil Gas partition coefficient: 224
    • *Intermediately soluble*
  24. What are the partition coefficients of Enflurane?
    • Blood Gas partition coefficient: 1.9
    • Brain Blood partition coefficient: 1.5
    • Muscle Blood partition coefficient: 1.7 
    • Fat Blood partition coefficient: 36.2
    • Oil Gas partition coefficient: 98
    • *Intermediately soluble*
  25. What are the partition coefficients of Isoflurane?
    • Blood Gas partition coefficient: 1.46
    • Brain Blood partition coefficient: 1.6
    • Muscle Blood partition coefficient: 2.9
    • Fat Blood partition coefficient: 44.9
    • Oil Gas partition coefficient: 98
    • *Intermediately soluble*
  26. What are the partition coefficients of Nitrous Oxide?
    • Blood Gas partition coefficient: 0.46
    • Brain Blood partition coefficient: 1.1
    • Muscle Blood partition coefficient: 1.2
    • Fat Blood partition coefficient: 2.3
    • Oil Gas partition coefficient: 1.4
    • *Poorly soluble*
  27. What are the partition coefficients of Desflurane?
    • Blood Gas partition coefficient: 0.42
    • Brain Blood partition coefficient: 1.3
    • Muscle Blood partition coefficient: 2
    • Fat Blood partition coefficient: 27.2
    • Oil Gas partition coefficient: 18.7
    • *Poorly soluble*
  28. What are the partition coefficients of Sevoflurane?
    • Blood Gas partition coefficient: 0.69
    • Brain Blood partition coefficient: 1.7
    • Muscle Blood partition coefficient: 3.1
    • Fat Blood partition coefficient: 47.5
    • Oil Gas partition coefficient: 55
    • *Poorly soluble*

  29. when does the flattening of the curve happen?

  30. If Desflurane has a lower solubility than N2O, why does N2O equilibrate (FA/Fi) sooner?
    You can give N20 in higher concentrations so it can equilibrate in higher concentrations.
  31. What do tissue: blood coefficients determine?
    Determines uptake of anesthetic into tissues & time for equilibration with those tissues
  32. Time constant is an estimate of that time
    to equilibration of the anesthetic in the blood and tissues. How do we figure out the time constant?
    • Amount of inhaled anesthetic that can be
    • dissolved in the tissue divided by tissue blood flow

    • Capacity (ml)
    •  Flow(ml/min)

    Capacity means volume of tissue. Time constant is in minutes (the mls cancel out)
  33. When talking about time constants, The
    larger the capacity, the larger the volume of tissues, and the lower the flow and the _____ the time constant.
    • LONGER!
    • the longer it’s going to take for the anesthetic to equilibrate in that tissue. So again fat has a larger volume, of all the tissue group, and a lower flow. (why fat has a longer time constant!)
  34. Fat has an _____ capacity to hold anesthetic as well as a ____blood flow so the time to equilibration is long.
    large and low
  35. 1 time constant   = __% change
    2 time constants = __% change
    3 time constants = __% change
    4 time constants = __% change
    • 1 time constant   = 63% change 
    • 2 time constants = 86% change 
    • 3 time constants = 95% change 
    • 4 time constants = 98% change
  36. We can talk about time constants in terms of the anesthesia machine, if total volume of the circuit system has a capacity and we set the flows.
    If the capacity is 8L, and we set fresh gas flow at 4L/min, what is the time constant?
    •  8L    =     2min
    • 4L/min

    • So that means  as we change the vaporizer setting from the vaporizer to the circle system, it takes 2minutes to get to that point. (@ 2 min see 60% change, it takes 3 -4 time constants, so 6-8 min) unless we increase the flow. To
    • accelerate that we increase the flow. We can’t change the capacity but we can increase the flow to change the time constant.
  37. The factors that will increase the rate of rise of FA over Fi:
    • •Low blood solubility
    • •Low Cardiac output
    • •High alveolar ventilation
  38. To decrease the rate of rise:
    • •High blood solubility
    • •High cardiac output
    • •Low alveolar ventilation
  39. FOR THE VESSEL RICH GROUPS
    What is the body mass %?
    Liters/70kg?
    % of CO?
    Liters/min?
    • body mass % is 9
    • L/70kg is 6
    • % of CO is 75
    • L/min is 4
  40. FOR THE MUSCLE GROUP
    What is the body mass %?
    Liters/70kg?
    % of CO?
    Liters/min?
    • Body mass % is 50
    • L/70kg is 33
    • % of CO 18
    • L/min is 1
  41. FOR THE FAT GROUP,
    What is the body mass %?
    Liters/70kg?
    % of CO?
    Liters/min?
    • Body mass % is 19
    • L/70kg is 14
    • % of CO is 7
    • L/min is 0.4
  42. FOR THE VESSEL POOR GROUPS
    What is the body mass %?
    Liters/70kg?
    % of CO?
    Liters/min?
    • body mass % is 22
    • L/70kg is 12
    • % of CO is 0
    • L/min is 0
  43. In the recovery from anesthesia phase, what is the  difference from induction?
    • Can’t “underpressurize” to speed emergence
    • Can only turn off vaporizer and increase fresh gas flows
  44. What is the metabolism for inhaled agents?
    minimal
  45. What is the context sensitive 1/2 time of inhaled agents?
    • Time to 50% ↓ in anesthetic concentration independent of duration.
    • What takes longer, that 50% is less than 5min for the agents we use now, but if we’re looking to get lower than that (say 80%) so we want 0.4 inspired and expired 0.3. The 80% is going to take longer. The first 50% happens quickly,
    • it’s the last 20% takes more time.

    That may or may not be significant. When the patient is awake enough to open eyes and follow commands in a second…
  46. For agents that aren’t highly soluble, the impact of the duration of the anesthetic is ___
    less
  47. Explain diffusion hypoxia
    Nitrous will dilute out the oxygen. When nitrous is stopped abruptly there is a reversal of partial pressure gradient. Removal of CO2 which can remove stimulus to breathe, always given 100% oxygen after nitrous is discontinued
  48. MAC – minimum alveolar concentration
    DEFINE IT!
    • the alveolar partial pressure of a gas at which 50% of animals will not respond to a noxious stimulus
    • (clamp tails for rats, surgical incision for humans)
  49. Advantages to using MAC as a potency measure
    • Very reproducible
    • End-tidal concentration is an index (allows us to follow where the pt is at, at level of the brain)
  50. What are some limitations to using MAC for potency
    • Patient is either anesthetized or not
    • MAC represents a whole population (or 50%) not response of a single patient
    • Only applies to anesthetic gases
    • Difficult to measure plasma brain concentration of IV anesthetics
  51. How can we pretty much guarentee immbolity in all our patients (with regard to inhaled anesthetics)
    Even though we use MAC and 50% of patients won’t move (that’s a good thing)  it also means 50% of patients will move (that’s a bad thing) so anesthesia usually requires a concentration that exceeds MAC by 10-30%. If we go up by 10-30% than we can pretty much guarantee immobility in nearly all patients.
  52. What happens to the MAC of a volatile if we add N20 as a carrier gas?
    decreases the MAC of other volatile agents. . It’s useful to know because volatiles cause hypotension and vasodilation, and by using N2O with the carrier gas, you reduce the amount of volatile needed, decreasing the  hpotensive & vasodilating effect. (while still getting the CNS depression)
  53. Tell me what fluoride substitution does to anesthetic potency
    Substituting a halogen of low atomic weight (F,atomic weight of 19) for one of higher atomic weight (Cl,atomic weight of 35) decreases potency

    Isoflurane vs Desflurane (potency decreases and MAC increases)
  54. MACawake: the average concentration permitting voluntary response to a command

    Approximately ____of MAC for Isoflurane, Desflurane, Sevoflurane

    Approximately ___ of MAC for Halothane

    More than ___% of MAC for nitrous oxide
    Approximately 1/3 of MAC for Isoflurane (0.4%), Desflurane, Sevoflurane (0.67%)

    Approximately ½ of MAC for Halothane

    More than 60% of MAC for nitrous oxide
  55. TRUE OR FALSE. Agents with higher
    MACawake/MAC ratio are poorer providers of amnesia.
    TRUE. N2O
  56. Normal pharyngeal function requires the anesthetic concentration to be at levels of ___MAC or ___
    0.1 or less
  57. Tracheal stimulation (laryngoscopy) is another MAC indice. What is this?
    Prevents movement or coughing or bucking

    Equal to or greater than MAC
  58. What is MAC BAR
    • MAC- B(locks) A(utonomic) R(reflexes)
    • ---Prevents response (↑ BP & HR)  to surgical stimulation
    • ---Considerably in excess of MAC
  59. The surgeon is about to make an incision, what are you going to do w/your volatile?
    • Turn up the volatile anesthetic for a few
    • breaths and make sure the patient is well above MAC (at the end tidal reading) to verify it was at the brain (it was higher than MAC). You can say you want to be 10-30% above MAC until they make incision and then titrate it back down.
  60. What is the effect of temperature on MAC?
    Hypothermia = ↓ MAC

    Hyperthermia = ↓ MAC **unless >42°C then it ↑
  61. What effect does age have on MAC?
    Young ↑ MAC

    Elderly ↓ MAC

    “Excluding patients <1yr of age (where MAC can be lower) there is a linear model that describes a decrease in MAC of approx. 6% per decade of life.”--Barash 

    MAC decreases by 6% per decade after the age of 40.
  62. What effect does alcohol have on MAC?
    • Acute intoxication ↓
    • Chronic abuse ↑
  63. what effect dose anemia have on MAC
    Hct <10% ↓
  64. What effect does PaO2 have on MAC?
    PaO2 <40 ↓
  65. What effect does PaCO2 have on MAC?
    PaCO2 >95mmHg ↓ caused by <pH in CSF
  66. What effect does the thyroid levels have on MAC?
    Trick question. There is NO CHANGE! Hypothyroidism or Hyperthyroidism just change the CO not the actual MAC
  67. What effect does BP have on MAC?
    MAP <40mmHg ↓
  68. What effect does hypercalcemia have on MAC?
  69. How do Na+ levels have on MAC?
    Hyponatremia ↓

    Hypernatremia ↑

    *caused by altered CSF
  70. What effect does MAC have on Pregnancy?
    ↓ MAC decreases by 1/2 @ 8weeks gestation, normal by 72hrs postpartum
  71. TRUE or FALSe. Local anesthetics decrease MAC?
    TRUE (except cocaine!)
  72. Name a few drugs that decrease MAC?
    • Opioids
    • Ketamine
    • Barbituates
    • Benzos
    • Verapamil
    • Lithium
  73. Sympatholytics increase or decrease MAC?
    • DECREASE!
    • (Methyldopa, Reserpine, Clonidine, & Dexmedetomidine)
  74. Sympathomimetics (Amphetamine) increase or decrease MAC?
    Chronic ↓

    • Acute ↑
    •  
    • *opposite of alcohol
  75. Cocaine and Ephedrine increase or decrease MAC?
    INCREASE!!!
  76. If we give opioids, we _______ the amount of volatile needed
    decrease
  77. Name 4 things that DONT CHANGE MAC!
    • Duration of anesthesia
    • MAP greater than 50 mmHg
    • Gender
    • Size
  78. What is the MAC of Halothane?
    0.75
  79. What is the MAC of Enflurane?
    1.63
  80. What is the MAC of Isoflurane?
    1.17
  81. What is the MAC of Sevoflurane?
    1.8
  82. What is the MAC of Desflurane?
    6.6
  83. What is the MAC of N2O?
    104
  84. How do you calculate a MAC?
    150 divided by the oil:gas partition coefficient (not quite identical)
  85. What effect does N2O have on the CV system?
    no effect
  86. What effect does Halothane have on the CV system ?
    • ↓↓ BP
    • ↓ HR
    • None on SVR
    • ↓ CO
  87. How does Sevoflurane effect HR?
    no change!!
  88. How does Halothane effect the cerebral system?
    • Increases Blood flow
    • Increases ICP
  89. What is the metabolism of Halothane?
    15-20%
  90. What is the metabolism of Methyoxyflurane?
    50%
  91. What is normal cerebral blood flow?
    Normal = 50-55 ml/100 grams of brain tissue/minute = 750 ml/min = 15% resting C.O.

    Closely related to tissue metabolism
  92. What effect do the volatiles have on CBF?
    • ↑ CBF 2°
    •     ↑ PaCO2
    •     ↑ [H+]
    •     ↓ oxygen concentration (low PaO2)
  93. True or False. CBF is autoregulated between MAP 60-140 mmHg
    TRUE!
  94. In the presence of normocapnia, volatile anesthetics produce vasodilation → ↑CBF
    Greatest effect with ______
    Least effect with ______ & _______
    • GREATEST increase with Halothane
    • Least increase with Isoflurane and Desflurane
    • The increase in CBF occurs within minutes of start of volatile and independent of blood pressure  changes.
  95. What do volatile agents do to cerebral metabolic rate?
    All inhaled agents produce dose-dependent decreases in cerebral metabolic oxygen requirements (good thing)

    • Greater with Isoflurane than Halothane
    • The greater decrease with Isoflurane may explain why CBF isn’t predictably increased by Isoflurane at low concentrations
    • ↓cerebral metabolism → ↓ carbon dioxide produced (TCA & oxidative phosphorylation)
    • This creates opposition to vasodilation
  96. Cerebral metabolic rate begins to ↓ at ___ MAC probably due to the transition from wakefulness to loss of consciousness
    • ↓ at 0.4 MAC 
    • Amnesia also likely occurs at this dose
  97. With volatiles, when is an increase in cerebral blood flow (from vasodilation causing increased ICP) a problem and what can we do to fix it or prevent it?
    • Problematic in setting of space occupying lesions
    • Hyperventilation to off-set
  98. TRUE or FALSE. Anesthetic induced ↓ in cerebral metabolic oxygen requirements offers cerebral protection during periods of ischemia from hypotension
    TRUE
  99. EEG: frequency decreases and maximum voltage occurs at ___ MAC
    1 MAC. Get burst suppression (straight line) at 2MAC
  100. All volatiles decrease MAP. Which decrease CO and which decrease SVR
    • Halothane decreases CO
    • All the others decrease SVR
  101. Which volatiles increase HR?
    Which decrease HR?
    • INCREASE = ISO/DES/SEVO
    • DECREASE = Halothane
  102. How is N2O helpful with regards to the CV system?
    Nitrous produces no change or slight increase in BP, so for pt that can’t tolerate a full MAC of volatile, we can add a little nitrous oxide (additive anesthesia) without the same amount of vasodilation
  103. Body temp increases or decreases with vasodilation caused by volatiles?
    DECREASES. Use the vasodilation to our advantage and get IVs
  104. What effect do inhaled anesthetics have on CO?
    • ↓ (Halothane)
    • No change (others volatiles)
    • Slight ↑ (nitrous oxide)
  105. All inhaled anesthetics decrease SVR except ______
    Halothane
  106. Which inhaled anesthetic may increase PVR and cauase a problem if the patient has pulmonary HTN
    N2O
  107. Why is someone more at risk for arrhythmias if they are  given an inhaled anesthetic?
    • sensitizing myocardium to EPI, (endogenous or exogenous). More of an issue w/Halothane and less of an issue w/Isoflurane/Desflurane/Sevoflurane
    • (exogenous limit for Iso/Des/Sevo is at 6mcg/kg of EPI)
  108. Explain the idea of coronary steal from volatile anesthetics
    Volatile agents (Isoflurane) can cause coronary vasodilation, dilating the small resistance  vessels. It’s called steal because it redirects blood from ischemic to non ischemic areas. The negative effect of Isoflurane in causing steal is offset by fact that it has negative inotropic effect as well, so it’s thought that only in patients w/steal prone anatomy are likely to be prone to coronary steal from Isoflurane.
  109. Explain what steal prone anatomy is
    • Steal prone anatomy
    • Total occlusion of major coronary artery
    • 90% stenosis by collateral distal to the occlusion
    • ~12 % of patients (are at risk for Isoflurane) (risk but low incidence. The reason for that is as long as adequate HD are maintained, then Isoflurane doesn’t increase the risk of  myocardial ischemia, more of potential than real phenomenon. Isoflurane, Desflurane, and Sevoflurane in concentration up to 1.5 MAC don’t cause steal
  110. Explain how volatiles provide cardio protection.


    Cardio protection: Des > Iso > Sevo
    Preconditioning: refers to patient that has brief periods of occlusion and ischemia from some sort of CAD, those areas of ischemia will begin cellular processes that are protective and it’s believed that the volatiles mimic this  preconditioning. There are a couple of things related to that we should know. The  sulfonylurea oral hypoglycemics and hyperglycemia, prevent this cardio protection. So if the patient were at high risk for ischemia, you may want to d/c the sulfonylurea oral hypoglycemics 24-48hrs pre-op cardiac surgery.
  111. How do the volatiles change the pattern of breathing?
    • ↑ respiratory rate
    • ↓ tidal volume
    • ↓ minute volume
    • ↑ PaCO2
  112. Is the ventilatory response to carbon dioxide dose dependent?
    • YES, there is a decrease in responsiveness to CO2.
    • Apnea at 1.5-2 MAC

    **Ventilatory response to hypoxemia also decreases
  113. How do the volatiles decrease airway resistance?
    relaxation of bronchial smooth muscle.
  114. All volatiles cause respiratory irritation, which one is the worst?
    Desflurane. At 2MAC Desflurane is more of an irritant and at 1MAC they are all considered to be the same.
  115. What two sources does the liver receive blood from?
    70% from portal vein, poorly oxygenated but nutrient rich (because it’s coming from GI tract)  30% is hepatic artery (Well oxygenated because it’s coming from the Aorta).
  116. Halothane produces 2 types of hepatotoxicity. Tell me about them.
    • 1. 20% of adults develop mild self-limited postop liver toxicity following halothane
    •    -Lethargy, fever, nausea, minor ↑ liver enzymes
    • 2. Halothane hepatitis
    •    - Immune-mediated response
    •    - 1 in 10,000 - 1 in 30, 000 adults following halothane
    •    - Massive hepatic necrosis & death possible
    •    - Children are less susceptible (why we still use it in pediatrics)
  117. What are some risk factors for Halothane Hepatitis?
    • female
    • middle age
    • obesity
    • multiple exposures to halothane

    the 4 Fs Female, Forty, Fat, & Frequent
  118. All volatiles produce dose-dependent ↓ renal blood flow,↓ GFR, & ↓ urine output. What do we do to prevent this?
    Hydrate the patient :)
  119. Explain Fluoride induced nephrotoxicity. What are the two volatiles that cause it?
    Due to extensive metabolism of  Methyoxyflurane (& Enflurane) to a fluoride ion. Metabolized in liver but the effect is on the kidney. Clinical toxicity occurs when plasma fluoride concentration is > than 80mmols/L (Clinical toxicity level). A threshold of 50mmol/L is indicator that renal toxicity could occur.

    What seen is vasopressin resistant, high output renal failure.

    • Polyuria, hypernatremia, hyperosmolarity
    • Inability to concentrate urine so urine is hypo-osmolar (dilute)

    • Methyoxyflurane (after 2-3hrs)
    • Enflurane (after 10hr)
  120. Explain Vinyl halide nephrotoxicity
    • Compound A formed when sevoflurane
    • reacts with CO2 absorbents

    Dose-dependent nephrotoxin The amount of compound A that is produced is far less than what’s been found to cause nephrotoxicity, but because of possibility, the company recommends a 2L/min of fresh gas flow (oxygen, nitrous, air or any combo) when using Sevoflurane
  121. Explain the skeletal muscle effects of volatiles at the neuromuscular junction
    • Ether-derived volatiles produce twice the skeletal muscle relaxation of halothane
    • Enhance neuromuscular blockers (DON’T REPLACE, just enhance)
    • Nitrous doesn’t produce muscle relaxation
  122. Malignant Hyperthermia is triggered by any of the volatiles in genetically susceptible patients
    ________ is most potent trigger
    _______ is a weak trigger
    • Halothane
    • Nitrous
  123. What is the only inorganic anesthetic gas
    N2O
  124. Tell me a little about the chemisty of N2O
    • Colorless, odorless, non-explosive & non-flammable but will support combustion (careful around lasers)
    • A gas at room temp & pressure but stored as a liquid under pressure
  125. What effect does N2O have on organ systems?
    • Stimulates SNS
    • Depresses myocardial contractility

    These two kind of cancel each other out and BP, CO, HR unchanged or slightly increased
  126. When could the effect of nitrous on depressing myocardial contractility be unmasked and cause ischemia?
    in hypovolemia or coronary artery disease, could become ischemic.
  127. What are some uses of N2O
    • Limited due to high MAC
    • Adjunct to volatile, TIVA
  128. What is the major side effect of N2O?
    PONV
  129. Prolonged exposure to N2O can result in what?
    • in bone marrow depression (megaloblastic
    • anemia) & neurological deficiencies exhibited by:
    •   - Peripheral neuropathies
    •   - Pernicious anemia (vitamin B-12 deficiency)
    •         *Inhibits enzymes that are vitamin B-12 dependent including … 
    •        Methionine synthetase (necessary for myelin formation)
    •        Thymidylate synthetase (necessary for DNA synthesis)
  130. Which volatile may have teratogenic effects and should be avoided in pregnant patients?
    Nitrous
  131. What are some contraindications to N2O?
    • Air embolism, pneumothorax, intestinal obstruction, etc
    • Pulmonary hypertension (↑PVR)
  132. What are some pros on N2O?
    • low cost and non-pungent.
    • (helps w/pediatrics because no smell or airway irritation)
    • Low BG partition coefficient, and unlikely MH trigger
  133. What are some cons to N2O?
    low potency, MAC awake is close to MAC, need a lot for anesthesia.  Increases PONV.

    Environmental: destroys the ozone layer.
  134. Tell me about the chemistry of Halothane
    • Halogenated alkane, alkyl halide
    • Nonflammable, nonexplosive
    • Thymol preservative & amber colored bottle retards spontaneous oxidative decomposition
  135. What effect does Halothane have on the CV system?
    • Hypotension from myocardial depression
    • Bradycardia and/or junction rhythm from SA node slowing* *very common
    • Sensitizes the myocardium to catecholamines (Doses above 1.5mcg/kg of Epi should be avoided)
  136. What effect does Halothane on the respiratory system
    • Depression
    • Potent bronchodilator (best of all volatiles)
  137. What effect does Halothane have on the cerebral system?
    • ↑ CBF with blunted autoregulation
    • Halothane is worst choice for pt w/brain tumor and space occupying lesion. Want to hyperventilate pt before you give halothane to avoid increase ICP.
  138. What are some contraindications to using Halothane
    • Hepatic dysfunction
    • Epinephrine use
    • Pheochromocytoma (increased sensitivity to catecholamines)
    • Myocardial depression exacerbated by beta-blockers & calcium channel blockers
    • Dysrhythmias with concurrent aminophylline use
  139. Tell me about the chemistry of Methyoxyflurane
    • Halogenated methyl, ethyl ether
    • Light sensitive, stabilized with butylated  hydroxytoluene
    • Nonexplosive, nonflammable
    • Most potent
    • **has similar effects on other organ systems
  140. Tell me about the biotransformation of Methoxyflurane
    • Extensive metabolism by cytochrome P-450 system
    • Resultant fluoride ion levels of 50 micromoles/L occurs with 2.5-3 MAC hours causes vasopressin-resistant, high output renal failure (F inhibits tubular function)
  141. Tell me about the chemistry of Enflurane
    • Halogenated ethyl, methyl ether
    • Nonflammable, nonexplosive
  142. Enflurane has similar effects to other volatiles on the organ systems, however deep anesthesia with enflurane has a major risk, what is it?
    • Deep enflurane anesthesia associated with high voltage, high frequency EEG changes & tonic-clonic seizures
    • Exacerbated by high anesthetic concentrations & hypocapnia
    • *Avoid in patient w/seizure disorder.

    • Likelihood went up if PaCO2 was low  (hyperventialted) and Enflurane
    • concentration was high.
  143. Fluoride ion nephrotoxicity is possible with Enflurane but much less likely than with methoxyflurane After ___ MAC hours, F levels average less than 40 micromoles
    10
  144. Tell me about the chemistry of Isoflurane
    • Halogenated ethyl, methyl ether
    • Structural isomer of enflurane
    • Nonflammable, nonexplosive
  145. What are the effects of Isoflurane on the organ systems
    • Minimal cardiac depression because CO is maintained by ↑HR
    • Mild beta stimulation
    • Coronary steal 2° coronary artery dilation
  146. TRUE or FALSE. Isoflurane is metabolized to 0.1 the extent of enflurane so renal and hepatic dysfunction are not an issue
    TRUE
  147. Are there any specific contraindications to Isoflurane?
    NOPE....one less thing to memorize :)
  148. Tell me about the chemistry of Desflurane
    • Halogenated ethyl, methyl ether
    • F substitution on isoflurane
    • Physical properties
  149. What are the effects of Desflurane on the other organ systems?
    • Most similar to others
    • Transient ↑ HR, BP with rapid increasing dose
    • Respiratory irritant *esp at higher doses
  150. What is the biotransformation and toxicity of Desflurane?
    • Minimal metabolism
    • Is degraded by dessicated (dryed out) carbon dioxide absorbent into clinically significant carbon monoxide levels(need to turn off flows and machine so we don’t dry out the CO2 absorbent).
  151. Wake up time of Desflurane can be ___ that of Isoflurane
    Because of BG solubility, quicker wake up and tighter anesthetic control than the others.
  152. Tell me about the chemistry of Sevoflurane
    • Halogenated methyl isopropyl ether
    • Nonflammable, nonexplosive
  153. What is important to know about the Biotransformation and toxicity of Sevoflurane
    • Degrades by carbon dioxide absorbents to compound A
    • Most likely with dry absorbent, low gas flows, high sevo concentration, prolonged exposure (long case)

    **Recommend gas flow of at least 2 liters/minute
  154. Why do we like to use Sevoflurane for mask induction ?
    • because sweet smelling and provides a relatively nice mask induction.
    • Used Halothane before but has drawbacks (solubility and hepatitis).
  155. Degradation of anesthetics by carbon dioxide absorbents presents 2 issues. What are they?
    • Loss of anesthetic
    • Toxicity 
    • --Compound A (only Sevoflurane)
    • ---Carbon Monoxide (more likely w/Desflurane)
  156. How do we avoid drying out of absorbent?
    Low gas flow rates

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