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Anesthesia Pharm Exam 1 > Intravenous Anesthetic Agents > Flashcards

Intravenous Anesthetic Agents Flashcards

1
Q

Drug distribution in the body: central

A
  • plasma and vessel-rich group of tissues
  • liver, brain, heart, and kidneys
  • elimination of intravenous medications occur through the central compartment. This is the area of action for the sedative and narcotics
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2
Q

Drug distribution in the body: peripheral

A

-this is considered to be the vessel-poor group which includes muscle, bone, skin, and fat

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3
Q 
Distribution of Cardiac Output:
VRG?
Muscle?
Fat?
VPG?
A 
VRG= 10% body mass but 75% CO
Muscle= 50% body mass but 19% CO
Fat= 30% body mass but 6% CO
VPG= bones and skeletal structures, 20% body mass but 0.5% CO
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4
Q

Factors affecting distribution: Drug binding

A
  1. Protein binding decreases available drug:
    - albumin binds acidic drugs (barbs)
    - A1AG bind basic drugs (local anesthetics)
  2. Protein availability:
    - —decreased albumin d/t liver, kidney, CHF, increased d/t
    - —-increased A1AG d/t trauma, infection, MI, chronic pain
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5
Q

What two factors affect distribution of drugs?

A
  1. Lipid solubility: good for anesthetic agents

2. Ionization: affects crossing cell membranes

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6
Q

Volume of Distribution:

A
  1. Vd quantifies the distribution of a medication between plasma and the rest of the body after dosing
  2. Theoretical volume in which the amount of drug would need to be uniformly distributed to produce the observed blood concentration
  3. The initial VD describes the distribution of a drug throughout the body after dosing and prior to reaching a steady state equilibrium
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7
Q

VD equation

A

total amount of drug in the body/ drug blood concentration

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8
Q

High Vd

A
  • highly lipid soluble drugs and therefore non-polar
  • low rate of ionization
  • low plasma binding
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9
Q

Vd blood, extracellular, and total body water

A 
<0.2= blood (confined to blood)
0.2-0.7= extracellular
.7= total body water (meaning it goes everywhere)
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10
Q

Propofol MOA

A
  1. presumed interaction with GABA
    - delays the dissociation of GABA from receptors
    - increasing GABA activated opening of chloride ion channels
    - also acts as a sodium channel blocker
    - hyper polarization of cell membranes (why patients go to sleep)
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11
Q

Propofol Pharmacokinetics

A

95-99% protein binding

  • elimination half life 4-7 hours
  • tissue uptake and redistribution are important factors in termination of action
  • metabolized via glucoronidation in the liver
  • clearance exceeds hepatic blood flow
  • renal excretion
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12
Q

Propofol therapeutic range

A
  • rapid upstroke of blood levels on induction
  • rapid decline over 5 minutes
  • below therapeutic window by 7 minutes
  • if no additional agent given, patient will wake up due to redistribution
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13
Q

Propofol CV, pulmonary and CNS effects

A
  1. CV: Decreased SBP, Decreased MAP, Decreasd SVP, HR same
  2. Pulmonary: RR depressed dose dependent
  3. CNS: CBF decreased, ICP decreased, CMRO2 decreased
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14
Q

Propofol induction dose and continuous infusion dose

A
  1. Supplied 10 mg/ml
  2. Induction: 1.5-2.5 mg/kg intravenous
    produces unconsciousness in 30-60 seconds
    decreased PONV
  3. Continuous infusion: sedation to general anesthesia. 25 to 100 mcg/kg/min= sedation, 100-300 mcg/kg/min= anesthesia TIVA
  4. Beware: allergic reactions, bacteria formulation in solution
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15
Q

Propofol infusion syndrome

A
  • Acute refractory bradycardia (kids)
  • RBBB is an early sign
  • May lead to systole if one or more:
  • metabolic acidosis
  • rhabdomyolisis
  • hyperlipidemia
  • enlarged or fatty liver
  • Associated with propofol infusions > 4mg/kg for long duration ( > 48 hours)
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16
Q

Propofol key points:

A
  1. Awaken due to redistribution
  2. CV depression slightly > than NaP
  3. Resp effects similar to NaP but good bronchodilator
  4. Does NOT cause PONV and PDNV
  5. Good hypnotic
  6. Burns upon rapid injection in small vein
  7. Contraindicated with egg allergy
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17
Q

Fospropofol

A
  • prodrug multicompartment model needed
  • supplied 35 mg/ml
  • initial dose 6.5 mg/kg (between 60-90 kg)
  • additional 1.6 mg/kg as needed
  • <60 kg or >90 use 60 or 90 kg
  • reduce dose 25% for >65 years and ASA 3-4
  • perianal paresthesia in 74%
  • not currently in use at UIHC
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18
Q

Barbituartes MOA

A
  • interact with GABAA receptor (beta subunit)
  • directly activate Cl- ion channels, increase their duration of opening (increases the efficacy of GABA)
  • hyerpolarize post synaptic cell membranes
  • also block AMPA receptors
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19
Q

Barbs Pharmacokinetics

A
  1. NaP 83% protein bound (albumin)
  2. highly lipid soluble- rapidly into CNS
    - achieve CNS uptake in 30 seconds
    - prompt awakening after a single dose
    - hepatic metabolism (inactive) and eliminated by kidneys)
    - NEVER RUN INFUSION OF THIOPENTAL
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20
Q

Barbs: CV, Pulmonary, CNS, Renal, PH effects

A
  1. CV: decreased SBP, increased HR, decreased SVR
  2. Pulmonary: resp depression, apnea, return with slow reapers and low tidal volumes
  3. CNS: decreased CBF, decreased ICP, decreased CMRO2
  4. Renal: modest decrease in blood flow and GFR
  5. pH: metabolic acidosis increases the effect of barbs; metabolic alkalosis decrease the effect of barbs
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21
Q

Barbs- thiopental and methohexital solutions

A
  1. Thiopental supplied in 2.5% solution (25 mg/ml)

2. Methohexital 1% solution (10 mg/ml)

22
Q

Barbs induction of anesthesia

A

-induction dose: 3-5 mg/kg NaP
1-1.5 mg/kg methohexital
-rectal methohexital 20-30 mg/kg sedative (circulation directly into rectal vein- lose to 1st pass effect)

23
Q

Beware of Barbs

A
  1. extravasation causes tissue sloughing
  2. NaP + SUX= concrete in IV
  3. Intra arterial injection= severe vasoconstriction
  4. induce the p-450 system
  5. contraindicated in patients with Acute Intermittent Porphyria*
24
Q

Barbs Key Points

A
  • awakening due to redistribution
  • NaP causes dose dependent decrease in SBP, SVR, CO due to myocardial depression and increased venous capacitance
  • potent respiratory depressants
  • poor analgesics-may cause hyperalgesia
  • contraindicated in Acute Intermittent Porphyria
  • can cause histamine release
  • avoid SubQ and intra-arterial injection
25
Q

Etomidate MOA and pharmacokinetics

A
  • MOA: rapid onset of sleep= 30-60 seconds
  • assumed to enhance effects of GABAA (Gaba A receptors with B3 subunits)
  • rapid awakening

Pharmacokinetics:

  • 75% protein bound
  • hydrolyzed to inactive metabolites via ester hydrolysis
  • elimination half life is 3-5 hours
  • clearance is 5-6X pentothal; equivalent to propofol
  • excretion 85% renal, 15% biliary
26
Q

Etomidate CV, pulmonary, and CNS effects

A
  1. CV effects: SBP equal or decreased, HR equal or decreased, SVR equal or decreased
  2. Pulmonary: minimal respiratory depression, increased with opioids
  3. CNS: decreased CBF, decreased ICP, CMRO2 decreased
27
Q

Etomidate: induction dose

A
  • supplied 2 mg/ml vials
  • induction of anesthesia: 0.2-0.4 mg/kg, burns on injection
  • Beware: myoclonus, adrenal suppression (inhibits 11 Beta- hydroxylase and to a lesser extent 17 alpha hydroxylase), increases PONV than propofol
  • no analgesia
28
Q

Ketamine MOA

A

MOA: NMDA; opioid; monoamingeric; muscarinic receptors; and voltage gated Ca+ channels

29
Q

Ketamine Pharmacokinetics

A
  • extremely lipid soluble (5-10X NaP)
  • metabolized in liver to norketamine (1/3 to 1/5 potency of Ketamine)
  • norketamine is hydroxylated and conjugated to H2O soluble and excreted
  • elimination half life 2-4 hours; approx dexmed
  • excretion >90% renal
30
Q

Ketamine CV, Pulmonary, CNS effects

A
  1. CV: SBP, HR and SVR all increased
  2. Pulmonary: no respiratory depression, increased with opioids
  3. CNS: CBF increased, ICP increased, CMRO2 increased
31
Q

Ketamine induction dose

A
  1. Supplied 10 mg/ml; 50 mg/ml; 100 mg/ml vials
  2. Induction of anesthesia: 1-3 mg/kg IV or 4-8 mg/kg IM
    - adjunctive analgesic: 0.2-0.5 mg/kg can provide analgesia
32
Q

Ketamine Beware

A
  • Emergence delirium: visual, proprioceptive, and confusion

- premedicating with midaz seems to help

33
Q

Benzodiazepines

A
  • used for sedation, anxiolysis, anticonvulsants, spinal-cord mediated muscle relaxation, and anterograde amnesia, and at high doses unconsciousness and respiratory depression
  • NO analgesic properties
  • High Therapeutic Indexes high 100s
  • Benzo + narcotic= TI <10
34
Q

BZD site on GabaA Receptor

A
  1. GABA is primary inhibitory NTM
  2. BZD facilitates action of GABA at the alpha subunit (2 alpha and 2 beta sites)
    - enhanced opening of Cl- channels
    - hyper polarization of post synaptic membrane
    - post synaptic neurons resistant to excitation
35
Q

Diazepam

A
  • Very lipid soluble: rapid uptake by then brain, rapid redistribution
  • large VD: 1-1.5 L/kg
  • 0.2-0.5 ml/kg/min clearance rate
  • Long elimination half life: 20-50 hours in healthy volunteers
  • much longer in the elderly (closer to 80 hours)
  • duration of action is determined by metabolism and elimination
36
Q

Diazepam Metabolism

A
  • primarily metabolized in the liver via oxidative N-demethylation
  • 3 active metabolites: desmethyldiazepam, oxazepam, temazepam
  • Hepatic Clearance does not change as we age: body proportion of fatty tissues increases, increase VD for lipid soluble drugs and takes longer to metabolize
  • Cimetidine delays hepatic clearance: affects diazepam and desmethyldiazepam clearance
37
Q

Anesthetic effects of Diazepam

A
  • reduces the dose of induction agent
  • reduces MAC of inhalation agent
  • .2 mg/kg IV diazepam reduces MAC of Halothane from .75% to .48%
  • increasing the dose of diazepam does not further reduce the MAC
38
Q

Midazolam

A

-2-4 times as potent as diazepam
-imidazole ring (water soluble at pH <4), ring closes upon injection and becomes highly lipid soluble
-96-98% protein bound
-very lipid soluble (rapid intake by brain, redistribution and re-uptake)
-Large Volume of Distribution: 1-1.5 L/kg
-High rate of clearance: 6-8 ml/kg/min
Short elim half life: 1.7-2.6 hours in healthy adults

39
Q

Midaz Pharmacokinetics:

A
  • Oxidative hydroxylation in liver
  • Glucoronide conjugation in the kidneys
  • Excretion in the urine
  • Metabolites are minimally active
  • Metabolism not affected by H2 receptor antagonists
  • Cardiac responses minimal and similiar to NaP
  • Depressed ventilation with 0.15 mg/kg dose
  • Renal failure has minimal effects on T 1/2, Vd, and clearance
  • Dose related decrease in CBF and CMRO2
  • Crosses the U-P membrane
40
Q

Lorazepam (Ativan)

A
  • more potent than diazepam or midday
  • elimination t 1/2 is 10-20 hours
  • less lipid soluble than diazepam
  • reliable GI and IM absorption- dissolved in propylene or polyethylene glycol
  • clinical effects may outlast diazepam dissociates from the GabaA slower
  • metabolized to inactive metabolites via glucuronide conjugation in the liver
  • metabolism is not altered by age, liver dysfunction, or H2 receptor antagonists
41
Q

Lorazepam as PO pre-med

A
  1. Excellent PO pre-med: 0.5-2.0 mg at night and 0.5-2.0 mg PO at 06-0700
  2. 50 mcg/kg (max 4 mg) gives maximal anterograde amnesia for up to 6 hours
  3. Larger doses produce greater sedation without increased amnesia
  4. Elderly patients are sensitive to benzo
  5. Slow onset limits usefulness as IV pre med or intra op sedation
42
Q

Reversal of BZDs

A
  1. Flumazenil: specific and exclusive BZD competitive antagonist with a high affinity for BZD receptor
  2. Reverses all BZD effects
  3. Not an abrupt reversal of sedative/amnesic effects as nalaxone w/ opioid reversal
  4. Onset is 30 seconds to 2 minutes
  5. Redistribution T1/2 is 7-15 minutes (may need to redose)
43
Q

Flumazenil Dosing

A
  • 0.2 mg IV over 15 sec(wait 45 seconds, redone 0.2 mg increments over 15 seconds)
  • Do NOT exceed 3.0 mg per hour
  • If no response after 1 mg flumazenil consider other causes:
  • incomplete reversal of muscle relaxation
  • residual anesthetics agents
  • narcotic overdose
  • hypoxemia
  • hypercarbia
  • surgical complication
44
Q

Reversal of BZDs (other agents)

A
  1. Non specific, unpredictable, and inconsistent
  2. Recommended since Flumezenil
  3. Physostigmine: tertiary amine, cholinesterase inhibitor that causes build up of Ach in brain tissue
  4. Aminophylline: 1 mg/kg may antagonize the sedative effects of adenosine in the CNS
45
Q

Midaz: active drug vs pro drug

A
  1. Active Drug: lipophilic

2. Prodrug: hydrophilic

46
Q

Dexmedetomidine

A
  1. Alpha 2 adrenergic agonist:
    - sedation
    - anxiolysis
    - hypnosis
    - analgesia
    - sympatholysis
47
Q

Dexmedetomidine MOA

A
  • Nonselective alpha 2 agonist
  • alpha 2 adrenoreceptors are membrane spanning G proteins (inhibition of adenylate cyclase, modulation of ion channels)
  • sedation- receptors in locus ceruleus
  • analgesia- receptors in LC and spinal cord
48
Q

Dex CV, pulmonary, CNS effects

A
  1. CV: decreased HR, decreased SVR, indirectly decreased CO, SBP, and contractility
  2. Pulmonary: decrease minute ventilation but maintains CO2 response, similar to natural sleep
  3. CNS: not well defined, some neuroprotection?
49
Q

Dex Premedication

A
  • premedication: .33 to .67 mcg/kg 15 minutes before surgery
  • decrease induction agent dose
  • decrease MAC
  • MAC: 1 mcg/kg over 10 minutes (slower onset and offset than propofol)
  • .7 mcg/kg/min keeps BIS 70-80
  • Maintenance of GA: reduce MAC of inhaled agent, reduces post operative opioid requirements, note useful as solo general anesthetic
50
Q

Droperiodol MOA

A
  • MOA: acts centrally at sites where dopamine, norepi, and serotonin
  • alters normal CNS signal transmission
  • exerts antiemetic effect at red astrocytes in the chemo-receptor trigger zone
  • has moderate alpha-adrenergic blocking ability
  • may occupy GABA receptors on the post synaptic membrane causing build up of dopamine in inter synaptic cleft
  • neuroleptic anesthesia
51
Q

Droperidol CV, Resp, CNS effects

A
  1. CV: decreased SVR, Map, Equal CO, equal contractility (prolonged QT= delayed repolarization, torsades de pointes)
  2. Respiratory: minimal
  3. CNS: decreased CBF in dogs- no human data, may worsen extrapyramidal side effects
    Contraindicated in Parkinson’s Disease ****
52
Q

Droperiodol uses and pharmacokinetics

A

Uses:
1. antiemetic: 0.625-1.25 mg IM/IV in adults

Pharmacokinetics:

  1. onset 5-8 minutes
  2. Vd 2.0L/kg
  3. Duration of action: 3-6 hours
  4. Elimination half life: 1.7-2.2 hours
  5. Hepatic transformation: 2 metabolites
  6. Elimination liver and kidneys

Anesthesia Pharm Exam 1 (4 decks)

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