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Top Drawer Drugs > 1 > Flashcards

1 Flashcards

1
Q

Sublimaze (Fentanyl) dose (induction, intraop, pediatric, epidural, infusion, post-op pain)

A 
Induction: 2 to 5 mcg/kg
Intraop: 2 to 20mcg/kg
Pediatric: 1 mcg/kg
Epidural: 50 to 100 mcg
Infusion: 25 to 50 mcg/hr
Post-op pain: 0.5 to 1.5 mcg/kg
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2
Q

Sublimaze (Fentanyl) MOA

A

Binds with Mu receptor; opens K+ channels inhibiting action potentials in pain pathways of CNS

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3
Q

Sublimaze (Fentanyl) onset

A

< 1 min

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4
Q

Sublimaze (Fentanyl) peak

A

5 to 15 min

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5
Q

Sublimaze (Fentanyl) DOA

A

30 to 60 min

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6
Q

Sublimaze (Fentanyl) Vd

A

4L/kg

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7
Q

Sublimaze (Fentanyl) halflife

A

219 min

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8
Q

Sublimaze (Fentanyl) metabolism

A

Hepatic; 75% cleared in urine as metabolites, 10% excreted unchanged

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9
Q

Sublimaze (Fentanyl) special considerations (4)

A

Greatest risk for respiratory depression during peak action (5 to 15 min);
high dose can cause chest wall rigidity;
highly lipid soluble;
75% first pass pulmonary uptake;

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10
Q

Midazolam (Versed) premedication dose

A

0.07 to 0.15 mg/kg

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11
Q

Midazolam (Versed) sedation dose

A

0.01 to 0.1 mg/kg

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12
Q

Midazolam (Versed) induction dose

A

0.1 to 0.4 mg/kg

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13
Q

Midazolam (Versed) MOA

A

Binds with GABA-A (alpha subunit); opens Cl- channels to hyperpolarize postsynaptic neurons in cerebral cortex, cerebellar cortex, and thalamus

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14
Q

Midazolam (Versed) onset

A

30 to 60 sec

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15
Q

Midazolam (Versed) peak

A

3 to 5 min

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16
Q

Midazolam (Versed) DOA

A

15 to 80 min

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17
Q

Midazolam (Versed) Vd

A

1 to 3 L/kg

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18
Q

Midazolam (Versed) halflife

A

1 to 4 hours

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19
Q

Midazolam (Versed) metabolism

A

Hepatic; active metabolites are rapidly conjugated; excreted in urine

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20
Q

Midazolam (Versed) special considerations (2)

A

pH dependent ring opening phenomenon (ring is open at pH <4 making it water soluble, ring is closed at pH >4 making it lipid soluble); cleft palate in neonates

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21
Q

Lidocaine dose

A

1 to 1.5 mg/kg; 4mg/kg (300mg); 7mg/kg (500mg)

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22
Q

Lidocaine MOA

A

Blocks Na+ channels from inside the cell membrane to inhibit rate of depolarization and pain transmission

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23
Q

Lidocaine onset

A

45 to 90 sec

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24
Q

Lidocaine peak

A

1 to 2 mins

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25
Q

Lidocaine DOA (IV, infiltration, spinal, epidural)

A

IV: 30 to 60 mins
Infiltration: 60 to 240 mins
Spinal: 30 to 60 mins
Epidural: 60 to 120 mins

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26
Q

Lidocaine metabolism

A

Hepatic

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27
Q

Lidocaine concentrations (IVRA, infiltration, spinal, epidural)

A

IVRA: 0.25 to 5%
Infiltration: 0.5 to 1%
Spinal: 1.5 to 5%
Epidural: 1.5 to 2%

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28
Q

Diprivan (Propofol) dose

A

1.5 to 2.0 mg/kg

100-300 mcg/kg/min

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29
Q

Diprivan (Propofol) MOA

A

GABA-A (beta subunit) agonist; opens Cl- channels to hyperpolarize postsynaptic neurons

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30
Q

Diprivan (Propofol) onset and LOC

A

onset < 15 sec, LOC in 30 sec

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31
Q

Diprivan (Propofol) peak

A

1 min

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32
Q

Diprivan (Propofol) DOA

A

5 to 10 min

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33
Q

Diprivan (Propofol) Vd

A

3.5 to 4.5 L/kg

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34
Q

Diprivan (Propofol) halflife

A

30 to 90 min

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35
Q

Diprivan (Propofol) metabolism

A

Hepatic with renal excretion

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36
Q

Diprivan (Propofol) special considerations (5)

A 
High lipid solubility;
discard 6 hours after opening;
pain with injection;
caution in elderly and hypovolemic patients;
decreases ICP, CMRO2, and CBP
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37
Q

Succinylcholine (Anectine) dose (induction and spasm)

A

Induction: 1.0 to 1.5 mg/kg
Spasm: 0.25 to 1 mg/kg

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38
Q

Succinylcholine (Anectine) MOA

A

Induces depolarizing NMB by attaching to one or both alpha subunits of nACh receptors and mimics action of ACh (partial agonist); depolarizes postjunctional membrane

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39
Q

Succinylcholine (Anectine) onset

A

30 to 60 sec

40
Q

Succinylcholine (Anectine) peak

A

60 sec

41
Q

Succinylcholine (Anectine) DOA

A

3 to 5 min

42
Q

Succinylcholine (Anectine) metabolism

A

Plasma cholinesterases

43
Q

Succinylcholine (Anectine) special considerations (2)

A

Do not give if trauma is >24 hours;

caution in renal failure due to increased K+

44
Q

Rocuronium (Zemuron) dose

A

0.6 to 1.2 mg/kg

45
Q

Rocuronium (Zemuron) dose (bolus and priming)

A

Bolus: 0.06 to 0.6 mg/kg

Priming 10% ID 0.5 mg, give 3 to 5 mins prior

46
Q

Rocuronium (Zemuron) MOA

A

NDMR quaternary aminosteroid, competitively inhibits cholinergic receptors at motor end plate

47
Q

Rocuronium (Zemuron) onset

A

45 to 60 sec

48
Q

Rocuronium (Zemuron) peak

A

1 to 3 min

49
Q

Rocuronium (Zemuron) DOA

A

15-150 min

50
Q

Rocuronium (Zemuron) metabolism

A

Hepatic, renal

51
Q

Rocuronium (Zemuron) special considerations (2)

A

Onset decreased and DOA increased with increased dose;

CV stable, good for infusion (mix 200 mg in 100 ml D5W for 2mg/ml)

52
Q

Pancuronium (Pavulon) dose

A

0.04 to 0.1 mg/kg

53
Q

Pancuronium (Pavulon) dose (bolus, gtt, priming)

A

Bolus: 0.01 to 0.05 mg/kg
Gtt: 1 to 15 mcg/kg/min
Priming 10% ID 0.5 to 1.0 mg

54
Q

Pancuronium (Pavulon) MOA

A

Long acting NDMR bisquaternary aminosteroid, competitively inhibits cholinergic receptors at motor end plate; can increase HR, BP, CO (vagolytic effects)

55
Q

Pancuronium (Pavulon) onset

A

1 to 3 min

56
Q

Pancuronium (Pavulon) peak

A

3 to 5 min

57
Q

Pancuronium (Pavulon) DOA

A

40 to 65 min

58
Q

Pancuronium (Pavulon) metabolism

A

Hepatic; renal is heavily dependent on kidneys for excretion, use caution in ARF/CRF

59
Q

Pancuronium (Pavulon) special considerations (3)

A

SNS activation with decreased catecholamine uptake;
use caution with CAD;
active metabolite accumulation with infusion > 16 hours

60
Q

Vecuronium (Norcuron) dose

A

0.08 to 0.1 mg/kg

61
Q

Vecuronium (Norcuron) dose (bolus, gtt, priming)

A

Bolus: 0.01 to 0.05 mg/kg
Gtt: 1 to 2 mcg/kg/min
Priming 10% ID 0.5 to 1.0 mg

62
Q

Vecuronium (Norcuron) MOA

A

Intermediate NDMR, competitively inhibits cholinergic receptors at motor end plate; 1/3 as potent as pancuronium; vagotonic effects can occur when combined with opioids

63
Q

Vecuronium (Norcuron) onset

A

< 3 min

64
Q

Vecuronium (Norcuron) peak

A

3 to 5 min

65
Q

Vecuronium (Norcuron) DOA

A

25 to 30 min

66
Q

Vecuronium (Norcuron) metabolism

A

Hepatic; small amount in kidneys

67
Q

Vecuronium (Norcuron) special consideration (1)

A

Reconstitute with sterile water;

20mg/100ml D5W for 0.2mg/ml gtt

68
Q

Atracurium (Tracrium) dose

A

0.3 to 0.5 mg/kg

69
Q

Atracurium (Tracrium) dose (bolus, gtt, priming)

A

Bolus: 0.1 to 0.2 mg/kg
Gtt: 2 to 15 mcg/kg/min
Priming: 0.03 to 0.05 mg

70
Q

Atracurium (Tracrium) MOA

A

NDMR that competitively inhibits cholinergic receptors at motor end plate

71
Q

Atracurium (Tracrium) onset

A

< 3 min

72
Q

Atracurium (Tracrium) peak

A

3 to 5 min

73
Q

Atracurium (Tracrium) DOA

A

20 to 35 min

74
Q

Atracurium (Tracrium) metabolism

A

Hoffman elimination independent of renal

75
Q

Atracurium (Tracrium) special considerations (2)

A

Laudenosine is a metabolite that can cause seizures;

histamine release can cause vasodilation, tachycardia, bronchospasm, laryngospasm

76
Q

Cisatracurium (Nimbex) dose

A

0.15 to 0.2 mg/kg

77
Q

Cisatracurium (Nimbex) dose (bolus, gtt, priming)

A

Bolus: 0.02 to 0.1 mg/kg
Gtt: 1 to 5 mcg/kg/min
Priming: 1 to 2 mg

78
Q

Cisatracurium (Nimbex) MOA

A

Isomer of atracurium, NDMR that competitively inhibits cholinergic receptors at motor end plate

79
Q

Cisatracurium (Nimbex) onset

A

90 to 120 sec

80
Q

Cisatracurium (Nimbex) peak

A

3 to 7 min

81
Q

Cisatracurium (Nimbex) DOA

A

20 to 35 min

82
Q

Cisatracurium (Nimbex) metabolism

A

Hoffman elimination

83
Q

Cisatracurium (Nimbex) special considerations (2)

A

Laudenosine is a metabolite that can cause seizures;

histamine release can cause vasodilation, tachycardia, bronchospasm, laryngospasm

84
Q

Neostigmine dose (reversal, max dose, with atropine, with glycopyrrolate, MG Tx)

A 
Reversal: 0.05 mg/kg
Max dose: 5 mg
With atropine: 0.015 mg/kg
With glycopyrrolate: 0.01 mg/kg
MG Tx: 15 to 375 mg PO daily
85
Q

Neostigmine MOA

A

Reversal of NDMRs; treatment of MG, post-op ileus, urinary retention; inhibits hydrolysis of acetylcholine by inhibiting acetylcholinesterase at the esteric site

86
Q

Neostigmine onset

A

3 to 5 min

87
Q

Neostigmine peak

A

3 to 14 min

88
Q

Neostigmine DOA

A

40 to 60 min

89
Q

Neostigmine metabolism

A

Hepatic, plasma esterases

90
Q

Neostigmine special consideration (1)

A

Cholinergic effects of OD (SLUDGE) include N/V, sweating, brady- or tachycardia, excessive salivation, bronchospasm, weakness, and paralysis; treat with 10 mcg/kg atropine every 3 to 10 min

91
Q

Pyridostigmine dose (reversal, max dose, MG Tx)

A

Reversal: 0.25 mg/kg
Max dose: 30 mg
MG Tx: 60 to 1500 mg/day (average is 600 mg/day)

92
Q

Pyridostigmine MOA

A

Reversal of NDMRs and treatment of MG; inhibits hydrolysis of acetylcholine by inhibiting acetylcholinesterase; slower onset and slower DOA compared to neostigmine

93
Q

Pyridostigmine onset

A

2 to 5 min

94
Q

Pyridostigmine peak

A

< 15 min

95
Q

Pyridostigmine DOA

A

90 min

96
Q

Pyridostigmine metabolism

A

Hepatic, renal

97
Q

Pyridostigmine special consideration (1)

A

Cholinergic effects of OD (SLUDGE) include N/V, sweating, brady- or tachycardia, excessive salivation, bronchospasm, weakness, and paralysis; treat with pralidoxime 15 mg/kg IV over 2 min or atropine 10 mcg/kg every 3 to 10 min

Top Drawer Drugs (1 decks)

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