Pharm Lecture 5 Opioids

  1. What is the definition of an opioid?
    all exogenous substances both natural & synthetic binding to opioid receptors producing “morphine-like” effects
  2. What is the EFFECT of opioids?
    Opioids produce analgesia without loss of touch (which make it different than local anesthetics), proprioception, or consciousness (except in large doses)

    *operate on different receptors than local anesthetics
  3. What are the 3 classifications of opioids?
    • Agonists
    • Agonist-antagonists
    • Antagonists
  4. What is a common antagonist of opioids?
    naloxone most used and most familiar with
  5. TRUE or FALSE. We give as much opioids as we want because we can reverse it.
    • FALSE! we don’t generally give an agonist
    • thinking we can reverse it w/antagonist
    • *Much more likely to reintubate if apnic in PACU than to give opioid antagonist.If we were to give it we’d dilute it down significantly.
  6. What are some hazards involved w/using an opioid antagnonist.
    can cause SNS stimulations as result of reversal of analgesia, get HTN, tachycardia, arrhythmias (VF) and pulmonary edema.
  7. What drug is the the Phenanthrene (T shaped) structural class of drugs?
  8. What drugs are in the Phenylpiperidines structural class of drugs
    Fentanyl and Meperidine
  9. What does Hemming's refer to Morphine's structure as?
  10. Semisynthetic opioids result from substitution of the morphine molecule (give an example)
    i.e. Codeine = methylmorphine
  11. TRUE or FALSE. Synthetic opioids are completely synthesized not just morphine modified
    TRUE! (ex: fentanyl family)
  12. What are the 4 classifications of opioid receptors?
    • Mu 1, Mu 2
    • Kappa
    • Delta
    • Sigma (probably not an opioid receptor)
  13. Where are the receptors that opioids act on?
    • CNS, mostly brainstem & spinal cord
    • (pre and post synaptic areas in CNS)
    • Periphery
  14. What are the endogenous ligands of the opioid receptors?
    • Enkephalins
    • Endorphins
    • Dynorphins
  15. How do we get the analgesic effect of the opioids?
    come from ability to directly inhibit the ascending transmission of info from spinal cord, interrupting the pain circuits

    Hemming's says they inhibit release of substance P from primary sensory neurons in the dorsal horn. This mitigates the transfer of painful sensations to the brain. Change the affective response to pain, they don’t complete block the pain but make the patient care less about the pain.
  16. How do opioids work once they attach to the receptor?
    • Part of the guanine (G) protein-coupled receptors (like muscarinic Ach, GABA, adrenergic, etc)
    • Inhibition via adenyl cyclase decreasing conductance of voltage-gated calcium channels or opening outward flowing potassium channels
    • Receptor activation causes:
    • --↓ neurotransmission 2° presynaptic inhibition of neurotransmitters including Ach,dopamine, norepi, substance P
    • --Postsynaptic inhibition of evoked activity
    • --↑ potassium conductance → hyperpolarization, calcium channel inactivation, or both → mediate ↓ in neurotransmitter release
  17. Which two receptors cause depression of ventilation? (This was highlighted in a chart on her slide)
    Mu2 and Delta
  18. What is the only receptor that does not cause supraspinal analgesia?
    • Mu2
    • *They all cause spinal analgesia
  19. Which receptors have low abuse potential?
    • Mu1
    • Kappa
  20. Which receptor causes sedation?
  21. Which receptor causes dysphoria and sedation?
  22. Which receptor causes Euphoria?
  23. Which two receptors cause miosis?
    • Mu1
    • Kappa
  24. Which receptors cause marked constipation?
    • Mu2
    • Delta
  25. Which two receptors cause physical dependence?
    • Mu2
    • Delta
  26. What receptor causes bradycardia and hypothermia?
  27. Which two receptors cause urinary retention?
    • Mu1
    • Delta
  28. Endorphins act as an agonist on what receptor (s)?
    Mu1 and Mu2
  29. Morphine acts as an agonist on what receptor(s)?
    Mu1 and Mu2
  30. Synthetic opioids act as an agonist on what receptor(s)?
    Muand Mu2
  31. The antagonists act on what receptor (s)
    • All of them!
    • Mu1
    • Mu2
    • Delta
    • Kappa
  32. What are the 4 clinical effects of the Mu receptor and the 4 agonist
    • Effects:
    • Supraspinal analgesia
    • Respiratory depression
    • Physical dependence
    • Muscle Rigidity

    • Agonists:
    • Morphine
    • Fentanyl
    • Met-enkephalin (endogenous)
    • Beta-endorphin (endogenous)
  33. What are the 2 clinical effects of the Kappa receptor and the 5 agonists?
    • Effects:
    • sedation
    • spinal analgesia

    • Agonists:
    • Morphine
    • Nalbuphine
    • Butorphanol
    • Dynorphin (endogenous)
    • Oxycodone
  34. What are the 3 clinical effects of the Delta receptor and the 2 agonists?
    • Effects:
    • analgesia
    • behavioral
    • epiletogenic

    • Agonists:
    • Leu-enkephalin (endogenous)
    • Beta-endorphin (endogenous)
  35. Although Stoelting does not include the Sigma receptor is not a true opioid receptor, what are the clinical effects and agonists of the Sigma receptor?
    • Effects:
    • Dysphoria
    • Hallucinations
    • Respiratory stimulation

    • Agonists:
    • Pentazocine
    • Nalorphine
    • ?Ketamine
  36. List the following drugs in order of pKa (lowest to highest):
    Morphine, Meperidine, Fentanyl, Sufentanil, Alfentanil, Remifentanil
    • Alfentanil (6.5)
    • Remifentanil (7.1)
    • Morphine (7.9/9.4)
    • Sufentanil (8.0)
    • Fentanyl (8.4)
    • Meperidine (8.5)
  37. What are the ONLY TWO drugs with pka less than pH and what does this mean for the pharmokinetics?
    • Alfentanil (6.5)
    • Remifentanil (7.1)
    • --this means the % ionized is lower than the rest, (they are basic drugs) so these drugs have a quick onset!
  38. List the following drugs in order of % ionized (lowest to highest): Morphine, Meperidine,  Fentanyl, Sufentanil, Alfentanil, Remifentanil

    Hint: it's the same order as pKa!
    • Alfentanil (11)
    • Remifentanil (33)
    • Morphine (76)
    • Sufentanil (80)
    • Fentanyl (91)
    • Meperidine (93)
  39. All the opioids are acidic or basic?
    BASIC drugs!
  40. List the following drugs in order of partition coefficient (lowest to highest): Morphine, Meperidine, Fentanyl, Sufentanil, Alfentanil, Remifentanil
    • Morphine (1.4)
    • Remifentanil (17.9)
    • Meperidine (38.8)
    • Alfentanil (130)
    • Fentanyl (860)
    • Sufentanil (1778)
  41. What does the partition coefficient of opioids relate to?
    refers to lipid solubility
  42. List the following drugs in order of protein binding:  Morphine, Meperidine, Fentanyl, Sufentanil, Alfentanil, Remifentanil
    (++, +++, or ++++)
    • ++ Morphine
    • +++Meperidine, Fentanyl, Remifentanil
    • ++++Sufentanil & Alfentanil
  43. List the following drugs in order of the non-ionized fraction (+, ++, +++, ++++)
    • + Meperidine & Fentanyl
    • ++ Morphine & Sufentanil
    • +++ Remifentanil
    • ++++ Alfentanil
  44. Which drug is highly non-ionized?
  45. Alfentanil has a more rapid onset & shorter duration of action than Fentanyl even though it is less lipid-soluble because of….(what two things)
    • High non-ionized fraction at physiologic pH
    • Small Vd
  46. Significant amounts of lipid-soluble opioids can be retained by the lungs (first-pass uptake) & amount of uptake depends on… (what 3 things)

    *this is very true for fentanyl
    • Prior accumulation of another drug - ↓ uptake
    • History of tobacco use - ↑ uptake
    • Inhalation anesthesia -↓ uptake
  47. Image Upload 1
    Describe this picture
    See a delay in onset of action at effect site (Brain) w/regard to fentanyl as opposed to alfentanil.

    Hemming's: refers to this as latency to peak effect. (new terminology in that text).
  48. Image Upload 2
    Describe this picture
    • Time to equilibration between brain and effect site (which produces rise in effect site concentration)
    • Alfentanil, Fentanyl, and then Sufentanil is last.
  49. List the following drugs in order of clearance (ml/min): Morphine, meperidine, Fentanyl, Sufentanil, Alfentanil, & Remifentanil
    (lowest to highest)
    • Alfentanil (238)
    • Sufentanil (900)
    • Meperidine (1020)
    • Morphine (1050)
    • Fentanyl (1530)
    • Remifentanil (4000)
  50. List the following drugs in order of Vd (low to high): Morphine, Meperidine, Fentanyl, Sufentanil, Alfentanil, & Remifentanil
    • Alfentanil (27)
    • Remifentanil (30)
    • Sufentanil (123)
    • Morphine (224)
    • Meperidine (305)
    • Fentanyl (335)
  51. Describe the biotransformation of the opioids
    • Morphine conjugated with glucuronic acid to active metabolite
    • Meperidine is de-methylated to normeperidine (active metabolite)
    • Fentanyl, sufentanil, alfentanil, to inactive
    • Remifentanil by ester hydrolysis
  52. What are the drugs w/active metabolites
    • Morphine (glucoronic acid)
    • Meperidine (normeperidine)
  53. Clearance of most opioids is dependent on what?
    hepatic blood flow
  54. Why is there a short elimination 1/2 life of alfentanil?
    small Vd
  55. Morphine is principally metabolized by conjugation in the liver into what?
    • the resulting water-soluble glucuronides (morphine 3-glucuronide & morphine 6
    • glucuronide) which are excreted via the kidneys.

    Morphine 6 glucuronide is more potent and long lasting than Morphine itself.
  56. What happens if a patient has renal failure and received meperidine?
    If pt. as renal failure (normeperidine not eliminated) then can have seizure activity.
  57. List the following drugs in order of elimination 1/2 time (hours)---from lowest to highest:
    Morphine, Meperidine, Fentanyl, Sufentanil, Alfentanil, and Remifentanil
    • Remifentanil (0.17-0.33)
    • Alfentanil (1.4-1.5)
    • Morphine (1.7-3.3)
    • Sufentanil (2.2-4.6)
    • Fentanyl (3.1-6.6)
    • Meperidine (3-5)
  58. List the following drugs in order of context-sensitive 1/2 time (4 hr infusion) in minutes:  (Low to high)
    Fentanyl, Sufentanil, Alfentanil, Remifentanil
    • Remifentanil (4)
    • Sufentanil (30)
    • Alfentanil (60)
    • Fentanyl (260)
  59. List the effect site (blood/brain) equilibration in minutes for the following drugs (From low to high): Fentanyl, Sufentanil, Alfentanil, Remifentanil
    • Remifentanil (1.1)
    • Alfentanil (1.4)
    • Sufentanil (6.2)
    • Fentanyl (6.8)
  60. What is the advantage to Remifentanil?
    • Rapid biotransformation. (Esters)
    • Terminal elimination ½ life is less than 10min.
    • Remifentanil is great because you can titrate but need analgesia on board in PACU so it requires a bit of a plan. (give Morphine or Fentanyl towards end of case for adequate pain control post-op)
    • Remifentanil metabolized by ester hydrolysis.
    • Pseudocholinesterase deficiency does not effect its metabolism
  61. For Fentanyl and Morphine, the Vd is pretty much the same, what is very different?
    huge difference in protein binding and partition coefficient.

    • Protein binding (Fentanyl 84 & Morphine 35)
    • Partition coefficient (Fentanyl 955 & Morphine 1)
  62. What are the effects of opioids on the CV system?
    • generally stable
    • Morphine & meperidine cause histamine release so ↓BP & ↓ SVR
    • Fentanyl family associated with vagus mediated bradycardia (high doses)
  63. What are the effects of opioids on the respiratory system?
    • depression (rate)
    • ↓response to CO2
    • ↓ hypoxic drive
    • ** chest wall rigidity: centrally mediated hypertonus of striated muscle
    • (more depression of  RR than TV)
  64. What are the effects of opioids on the CNS?
    • ↓ CBF, ICP, CMRO2 but < barbs/benzos
    • Stimulate chemoreceptor trigger zone
  65. What are the effects of opioids on the Endocrine system?
    • block stress hormone release > volatiles
    • --Catecholamines
    • --Cortisol
    • --ADH
  66. Explain the chest wall rigidity caused by opioids
    • is a centrally mediated hypertonus of all striated muscle.
    • It can be severe enough to prevent ventilation
    • that you need neuromuscular blocker.
    • Most common w/highly lipid soluble opioids,
    • most assoc. w/fentanyl.
    • Dose related, more likely to occur the higher the dose (all at once)
    • It’s refered to as chest wall or truncal but involves all striated muscle (includes pharyngeal and laryngeal muscle—narrow)
  67. What effect do opioids have on bile duct pressure?
    they increase it
  68. What drug increases HR because it's related to Atropine?
  69. How do opioids compare to benzos and barbs for the cerebral effects (CBF, CMRO2ICP)?
    MUCH less of reduction
  70. What is the prototype and standard drug upon which all other drugs are measured?
  71. Name 2 kinetic key points regarding Morphine
    • 1. Low lipid solubility
    • 2. Metabolism to:
    •     a)  Morphine-3-glucuronide (75-85%) - inactive
    •     b)  Morphine-6-glucuronide (5-10%) – active with potency & duration greater than that of morphine

    Sue said the metabolites were IMPT :)
  72. TRUE or FALSE. Morphine is better at relieving continuous dull pain rather than sharp intermittent pain, works best if given preemptively.
  73. How long does Morphine take to peak in CNS? Why does only 1/10th reach the CNS at time of peak?
    • Takes about 15-30min to peak in CNS (After IV injection).
    • Probably only a 1/10th (0.1%) reaches CNS at time of peak, because of lipid solubility as well as high degree of ionization.
  74. What happens to morphine if we make the patient alkalotic by hyperventilating?
    • The non-ionized fraction will increase, and therefore passage of drug into CNS will be enhanced.
    • If resp acidosis (Flip side) then we would expect more ionized however w/resp acidosis what happens there will be increase CBF d/t hypercarbia, increase in CBF will deliver whatever non-ionized drug is there, better delivery to CNS. This is thought to be a more important factor (Inc. CBF) than the increase in ionization d/t hypercarbia.
  75. What are the side effects of Morphine?
    • Histamine release – minimize by slow injection, IV fluids (preload)
    • --Pruritus
    • --Urticaria
    • --Erythema 
    • Orthostatic hypotension → venous pooling
    • Respiratory depression
  76. What are the uses of Morphine?
    • Analgesia
    • Acute pulmonary edema
    • --↓ perception of SOB
    • --↓ preload & afterload (because of venous pooling)
  77. What is the dosing, onset, peak, and duration of Morphine?
    • Dosing:
    • --Analgesia: 1 -15 mg IV
    • --Induction: 1 mg/kg IV
    • Onset: less than 1 minute
    • Peak: 5-20 minutes
    • Duration: 2-7 hours
  78. Analogs of Meperidine include what family?
    the fentanyl family
  79. What is Meperidine derived from?
  80. TRUE or FALSE. Structurally similar to atropine & possesses a mild atropine-like anti-spasmodic effect
  81. How potent is Meperidine compared to Morphine?
    1/10th as potent as morphine so 75-100 mg = 10 mg morphine
  82. What are the kinetic key points for Meperidine?
    • Metabolism by demethylation & hydrolysis to:
    • --Normeperidine which has elimination ½ life of 15 hours, is ½ as active as meperidine as
    • analgesic, produces CNS stimulation with toxicity & can cause seizures & myoclonus
    • --Meperidinic acid
  83. What are the side effects of Meperidine?
    • ↑ HR – remember structurally similar to atropine (rarely bradycardia)
    • *↓ myocardial contractility in large doses (unique among opioids)*
    • Delirium & seizures (2° normeperidine-metabolite)
  84. What are the uses of Meperidine?
    • Suppressing postop shivering (kappa receptors)
    • Small doses 12.5mg will help w/that
  85. What is a major drug interaction associated w/meperidine?
    • Contraindicated in patients on MAOIs (serotonin syndrome)
    • Serotonin syndrome: excess availability of serotonin in CNS characterized by confusion, fever, shivering*, diaphoresis, ataxia, hyperpyrexia, myoclonus, & diarrhea. 

    Morphine and Codeine ok, alfentanil and remifentanil are ok.
  86. What is the dosing, onset, peak, and duration of Meperidine?
    • Dosing:
    • --Analgesia: 12.5-100 mg (0.5-2 mg/kg)
    • Onset: less than 1 minute
    • Peak: less than 1 hour
    • Duration: 2-4 hours
  87. What is the chemical structure of Hydromorphone (Dilaudid)
    • Semisynthetic opioid
    • Phenathrene (hydrogenated ketone of morphine)
  88. What is the potency of Hydromorphone (Dilaudid) compared to morphine?
    5 - 6 times as potent as morphine

    • Less opioid-related side effects than with morphine
    • May cause chest wall rigidity
    • Caution in the elderly
  89. What are the kinetic key points of hydromorphone (dilaudid)
    • Vd: 4 L/kg
    • 8-20% protein bound
    • Biotransformed in the liver
    • Active metabolites are:
    •    a) Dihydromorphine
    •    b) Dihydroisomorphine
    • Inactive metabolite is hydromorphone-3-glucoronide
    • Has been the preferred opioid for patients with renal impairment BUT hydromorphone-3-glucuronide can accumulate in renal failure & cause neuroexcitation & cognitive impairment
    • (caution is advised)
  90. What does Hemming's say about Hydromorphone compared to Morphine?
    • Slightly more duration of action than morphine.
    • More sedation and less euphoria than morphine.
  91. What is the dosing, onset, peak, and duration of Hydromorphone?
    • Dosing
    • --Analgesia: 0.5-2 mg
    • Onset: 15 min
    • Peak: 30-60 minutes 
    • Duration: 4-5 hours
    • (0.2mg incremental doses in 5min for total of 1mg) Small doses, received a lot of drugs in OR, don’t want to leave in PACU w/resp compromise.
  92. What is the chemical structure of Fentanyl?
    Phenylpiperidine derivative synthetic opioid structurally related to meperidine (w/out nasty effects)
  93. What is the potency of Fentanyl compared to Morphine?
    75-100 times more potent than morphine
  94. What are the kinetic key points of Fentanyl?
    • Faster onset & shorter apparent duration than
    • morphine because it is more lipid soluble and larger Vd. Faster onset, lipid soluble can go across BBB fast

    Lungs act as large & inactive store w/estimated 75% of initial fentanyl dose undergoing first-pass pulmonary uptake which limits the amount of initial dose reaching systemic circulation

    Saturation of inactive tissue sites → ↑ duration of action & context-sensitive half time (Repeated boluses will stack and saturate fat stores. Similar to thiopental, not high clearance and very lipid soluble)
  95. What should we know about the metabolism of Fentanyl?
    • Fentanyl is extensively metabolized to norfentanyl by N-dimethylation.  Norfentanyl is structurally similar to normeperidine.  It is excreted by the kidneys and has less analgesic potency than fentanyl.
    • ** note longer elimination ½ time (3-6 hours) compared with morphine (1.7-3.3 hours) even with apparent shorter duration (short acting, but not d/t eliminatioin...highly lipid soluble)
  96. What are the advantages of Fentanyl?
    • Stable hemodynamics
    • --No myocardial depression
    • --No histamine release
    • Suppression of stress response
  97. What are the side effects of Fentanyl?
    • Carotid sinus reflex control of heart is depressed → ↓HR
    • Chest wall rigidity
    • ----Because it is so highly lipid soluble
  98. Why should we be cautious when giving Fentanyl to an Elderly patient?
    prolonged elimination. ½ time, decreased clearance could be r/t hepatic blood flow
  99. What is the dosing, onset, peak and duration of Fentanyl?
    • Dosing:
    • a) Premedication/analgesia:  25-100 mcg (1.5 – 5 mcg/kg) IV
    • b) Induction:
    • --With hypnotic: 1.5-5 mcg/kg
    • --With 70% nitrous oxide: 8 -23 mcg/kg
    • --High dose opioid: 50 mcg/kg
    • c) Intermittent bolus: 25 -100 mcg
    • d) infusion: 0.05-0.2 mcg/kg/min (anesthesia
    • supplement)

    • Onset: 30 sec
    • Peak: 5- 15 minutes
    • Duration 0.5-1 hour
  100. How can we prevent apnea when giving Fentanyl?
    • spontaneous breathing, give small dose of opioid, give 25mcg of fentanyl decrease
    • RR but 50mcg will make them apnic.
    • So give 25 and then another 25 a few min. later, achieve same analgesic effect without knocking out their RR.
  101. What is Innovar?
    • Fentanyl and droperidol
    • (Referred to as neurolept anesthesia) because of issues w/droperidol (prolonged QT) inobar is no longer used
  102. What is Sufentanil? What is it's potency compared to Fentanyl?
    Fentanyl derivative, 10 times as potent as fentanyl
  103. What are the key kinetic points about sufentanil?
    • Similar to fentanyl
    • Higher degree of ionization & protein binding than fentanyl so smaller Vd & shorter elimination ½ life
    • Metabolism by dealkylation & demethylation in the liver 
    • *More lipophilic than fentanyl, 93% protein bound, as apposed to 80% of fentanyl (makes Vd smaller than fentanyl)*
  104. What is the major side effect of Sufentanil?
    sympatholysis with vasodilation but hemodynamic stability prevails
  105. What is dosing, onset, peak and duration of Sufentanil?
    • Dosing
    • a) Induction:
    • --With hypnotic: 0.1 – 1 mcg/kg
    • --With 70% nitrous oxide 1.3 – 2.8 mcg/kg
    • --High dose opioid: 10 – 30 mcg/kg
    • b) Intermittent bolus: 5 -20 mcg
    • c) Infusion: 0.005 – 0.015 mcg/kg/min (anesthesia supplement)
    • Onset: 1-3 minutes
    • Peak: 3-5 minutes
    • Duration: 30 minutes – 1 hour
  106. What is the potency of Alfentanil compared to Fentanyl?
    • 1/5th as potent
    • (Derivative of fentanyl)
  107. What are the kinetic key points of Alfentanil?
    • Peak brain effect in less than 1 minute
    • pKa of 6.8 so almost 90% is non-ionized at
    • physiologic pH
    • Moderate lipid solubility but less than fentanyl so…
    • ---Vd  is smaller than fentanyl
    • ---Highly protein bound (92%)
    • Metabolized by dealkylation & demethylation to inactive metabolites
  108. What are the side effects of Alfentanil?
    • Chest wall rigidity in 90-100% of pts at dose of 150-175 mcg/kg (high dose)
    • ? More hypotension & bradycardia than fentanyl or sufentanil
    • ? More N/V
  109. What is the dosing, onset, peak and duration of Alfentanil?
    • Dosing
    • a) Induction: 
    • --With hypnotic: 10 - 50 mcg/kg
    • --High dose opioid: 120 mcg/kg
    • --Intermittent bolus: 250-500 mcg (5-10 mcg/kg)
    • b) Infusion: 0.5-1.5 mcg/kg/min (anesthesia
    • supplement)
    • Onset: less than 1 min
    • Peak: 1-2 min
    • Duration: 10-15 min
  110. When was Remifentanil approved? (it was on Sue's slide...)
    Ultra short acting approved for use in 1996
  111. What are the kinetic key points for Remifentanil?
    • Short duration of action due to metabolism (not redistribution)
    • Metabolism by blood & tissue esterases (not pseudocholinesterase)
    • Small Vd
    • Rapid recovery with return of spontaneous
    • ventilation in 2-5 minutes
    • No lingering analgesia (great for cases that need analgesia intraop but not a lot of pain post-op. Need to give another opioid prior to  discontinuing infusion. Want to stay ahead of pain.)
  112. What is the dosing of Remifentanil?
    • Induction: not suitable alone
    • Analgesia: intraop as continuous infusion 0.3-1 mcg/kg/min
  113. What are the 4 partial agonist & mixed agonist-antagonist?
    • Nalbuphine (Nubain)
    • Butorphanol (Stadol)
    • Buprenorphine (Buprenex)
    • Pentazocine (Talwin)
  114. What partial agonist (or mixed agonist/antagonist) works on the Mu receptor?
    • Nalbuphine (Nubain)
    • Butorphanol (Stadol)
    • Buprenorphine (Buprenex)
  115. What partial agonist (or mixed agonist/antagonist) works on the kappa receptor?
    • Nalbuphine (Nubain)
    • Butorphanol (Stadol)
    • Pentazocine (Talwin)
  116. What is the advantage of the partial agonist (or mixed agonist/antagonist)
    They don’t cause significant respiratory depression (ceiling effect) increasing dose doesn’t increase the response.

    Stoelting: should be reserved for pt. that can’t tolerate the opioid agonist.

    • Hemming's: most common use periop is to
    • reverse resp depression from other opioids while maintaining analgesia.

    ** not commonly used in practice
  117. How does the context sensitive half time of fentanyl compare to remifentanil?
    • fentanyl, as tissue stores get saturated, its different than remifentanil which is completely independent of infusion duration.
    • So the context sensitive 1/2 time of Fentanyl is very long (especially w/a long infusion) and Remifentanil, infusion time doesn't really matter
Card Set
Pharm Lecture 5 Opioids
Summer 2013