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28 Cards in this Set

  • Front
  • Back
Short-acting NM blockers
Succinylcholine
Depolarizing NM blockers
Succinylcholine
Intermediate-acting NM blockers
Rocuronium
Vecuronium
Atracurium
Cis-atracurium
Long-acting NM blockers
Doxacurium
Pancuronium
d-Tubocurare (curare)
Succinylcholine
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
a. Two-linked acetylcholine molecules
b. n/a
c. < 1-1.5 min after 1-1.5 mg/kg intubating dose
d. 5-10 min after 1-1.5 mg/kg bolus
e. Plasma cholinesterases
Rocuronium
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
Intermediate-acting

a. Aminosteroid
b. 259-305 mug/kg
c. 90-110 sec after 570-850 mug/kg
d. 2-45 min after 570-850 mug/kg
e. No active metabolite
Most drug excreted in bile.
DOA not significantly changed in ESRF
DOA increased in hepatic disease
Vecuronium
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
Intermediate-acting

a. Aminosteroid
b. 50 mug/kg
c. 3-5 min after 0.06-0.10 mg/kg
d. 20-35 min after 0.06-0.10 mg/kg
e. Hepatic clearance accounts for 50%
Renal clearance accounts for 25%

NB: 3-desacetyl vecuronium in 70% as potent as vecuronium
Atracurium
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
Intermediate-acting

a. Benzylisoquinoline
b. 0.25 mg/kg
c. 3-5 min after 2x ED95
d. 35-45 min after 2x ED95
e. Hoffman elimination (minor route => nonspecific esterases)

NB: Laudanosine metabolite may accumulate in renal failure ?clinical relevance
Cis-atracurium
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
Intermediate-acting

a. Benzylisoquinoline
b. 0.05 mg/kg
c. 4.6-5.8 min after 2x ED95
d. 33-45 min after 2x ED95
e. Hoffman elimination 77%; renal 16%; other organs 7%
Doxacurium
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
Long-acting

a. Benzylisoquinoline
b. 25-30 mug/kg
c. 4.5 min after 40-60 mug/kg bolus
d. 75-100 min after 40-60 mug/kg bolus
e. Renal and hepatic
DOA doubled in renal disease
DOA mild increase in hepatic disease
Pancuronium
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
Long-acting

a. Steroidal
b. 0.06 mg/kg
c. 3-4 min after 0.07-0.1 mg/kg bolus
d. ~1.5 hrs after 0.07-0.1 mg/kg bolus
e. Some taken up by liver
5-10% deacetylated to form OH-metabolites
Mostly excreted unchanged in urine

Clearance reduced in hepatic, renal disease and in elderly
d-Tubocurare
a. Structure
b. ED 95
c. Onset of action
d. Duration of action
e. Metabolism and excretion
Long-acting

a. Naturally occurring
b. 0.5 mg/kg
c. 5 min after 0.5 mg/kg bolus
d. > 1.5 hrs after 0.5-0.6 mg/kg bolus
e. No active metabolites
Most eliminated unchanged in urine
12% in bile

DOA increased with renal failure and minimal increase with hepatic failure
Succinylcholine: Advantages/Disadvantages
Rapid onset
Elevated K+; increased w/
1. Sepsis
2. Recent burns
3. Trauma
4. UMN/LMN diseases
Muscle pain
Myoglobinuria
Bradycardia secondary to vagal activity
Hyperkalemia a/w succinylcholine increased with...
1. Sepsis
2. Recent burns
3. Trauma
4. UMN/LMN diseases
Rocuronium: Advantages/Disadvantages
Rapid onset of NMB
Hemodynamic stability
Vecuronium: Advantages/Disadvantages
Hemodynamic stability
Most frequently a/w prolonged NMB
Most frequently a/w prolonged NMB
Vecuronium
Atracurium: Advantages/Disadvantages
Histamine release w/rapid bolus of 2x ED95
Cis-atracurium: Advantages/Disadvantages
Hemodynamic stability
Little-to-no histamine release w/conventional doses
Doxacurium: Advantages/Disadvantages
Hemodynamic stability
Little-to-no histamine release w/conventional doses
Pancuronium: Advantages/Disadvantages
May cause tachycardia particularly w/bolus dose
d-Tubocurare (curare): Advantages/Disadvantages
Hypotension w/bolus dose secondary to ganglion blockade and histamine release
Lorazepam
a. Potency
b. Half-life
c. Solubility
d. Metabolism and excretion
e. Factors affecting pharmokinetics
Intermediate-acting

a. 5 times more potent than diazepam
b. 14 hours
c. Increased water-solubility => reduces volume of distribution & serum elimination half-life
d. Hepatic glucouronidation => inactive metabolites (75% excreted in urine as glucuronide)
1. Little effect by hepatic disease/CYP450 modulators
2. Prolonged half-life with renal disease
e. No significant alteration in elderly or critically ill
Midazolam
a. Potency
b. Half-life
c. Solubility
d. Metabolism and excretion
a. 3 times as potent as diazepam
b. 2-3 hours
c. At physiologic pH, ring closes => increased lipophilicity => rapid CNS penetration & redistribution
d. Hepatic oxidation to hydroxymidazolam
Clearance reduced by concurrent use of CCB, EES, triazole antifungal agents
Diazepam
a. Potency
b. Half-life
c. Solubility
d. Metabolism and excretion
a. N/A
b. 20-40 hours
c. Highly lipophilic
d. Hepatic metabolism to oxazepam and desmethyldiazepam
Half-life of desmethyldiazepam...
96 hours
Short-acting benzodiazepines w/no active metabolites
Oxazepam
Temazepam
Propofol
a. MOA
b. Distribution half-life
c. Elimination half-life
d. Solubility
e. Metabolism and excretion
f. Factors affecting clearance/elimination
a. Appears to be modulation GABA-A receptor
b. 2-8 hours
c. Up to 7 hours
d. Highly lipid-soluble
e. Mysterious
Sulfate & glucuronide conjugate or hydroxylated metabolited excreted in urine
Clearance exceeds hepatic blood flow (?extrahepatic metabolic route?)
f. Unchanged elimination a/w hepatic/renal disease
Decreased elimination a/w geriatrics