1 Flashcards
(97 cards)
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
2
Q
Sublimaze (Fentanyl) MOA
A
Binds with Mu receptor; opens K+ channels inhibiting action potentials in pain pathways of CNS
3
Q
Sublimaze (Fentanyl) onset
A
< 1 min
4
Q
Sublimaze (Fentanyl) peak
A
5 to 15 min
5
Q
Sublimaze (Fentanyl) DOA
A
30 to 60 min
6
Q
Sublimaze (Fentanyl) Vd
A
4L/kg
7
Q
Sublimaze (Fentanyl) halflife
A
219 min
8
Q
Sublimaze (Fentanyl) metabolism
A
Hepatic; 75% cleared in urine as metabolites, 10% excreted unchanged
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;
10
Q
Midazolam (Versed) premedication dose
A
0.07 to 0.15 mg/kg
11
Q
Midazolam (Versed) sedation dose
A
0.01 to 0.1 mg/kg
12
Q
Midazolam (Versed) induction dose
A
0.1 to 0.4 mg/kg
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
14
Q
Midazolam (Versed) onset
A
30 to 60 sec
15
Q
Midazolam (Versed) peak
A
3 to 5 min
16
Q
Midazolam (Versed) DOA
A
15 to 80 min
17
Q
Midazolam (Versed) Vd
A
1 to 3 L/kg
18
Q
Midazolam (Versed) halflife
A
1 to 4 hours
19
Q
Midazolam (Versed) metabolism
A
Hepatic; active metabolites are rapidly conjugated; excreted in urine
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
21
Q
Lidocaine dose
A
1 to 1.5 mg/kg; 4mg/kg (300mg); 7mg/kg (500mg)
22
Q
Lidocaine MOA
A
Blocks Na+ channels from inside the cell membrane to inhibit rate of depolarization and pain transmission
23
Q
Lidocaine onset
A
45 to 90 sec
24
Q
Lidocaine peak
A
1 to 2 mins
25
Lidocaine DOA (IV, infiltration, spinal, epidural)
IV: 30 to 60 mins
Infiltration: 60 to 240 mins
Spinal: 30 to 60 mins
Epidural: 60 to 120 mins
26
Lidocaine metabolism
Hepatic
27
Lidocaine concentrations (IVRA, infiltration, spinal, epidural)
IVRA: 0.25 to 5%
Infiltration: 0.5 to 1%
Spinal: 1.5 to 5%
Epidural: 1.5 to 2%
28
Diprivan (Propofol) dose
1.5 to 2.0 mg/kg
| 100-300 mcg/kg/min
29
Diprivan (Propofol) MOA
GABA-A (beta subunit) agonist; opens Cl- channels to hyperpolarize postsynaptic neurons
30
Diprivan (Propofol) onset and LOC
onset < 15 sec, LOC in 30 sec
31
Diprivan (Propofol) peak
1 min
32
Diprivan (Propofol) DOA
5 to 10 min
33
Diprivan (Propofol) Vd
3.5 to 4.5 L/kg
34
Diprivan (Propofol) halflife
30 to 90 min
35
Diprivan (Propofol) metabolism
Hepatic with renal excretion
36
Diprivan (Propofol) special considerations (5)
```
High lipid solubility;
discard 6 hours after opening;
pain with injection;
caution in elderly and hypovolemic patients;
decreases ICP, CMRO2, and CBP
```
37
Succinylcholine (Anectine) dose (induction and spasm)
Induction: 1.0 to 1.5 mg/kg
Spasm: 0.25 to 1 mg/kg
38
Succinylcholine (Anectine) MOA
Induces depolarizing NMB by attaching to one or both alpha subunits of nACh receptors and mimics action of ACh (partial agonist); depolarizes postjunctional membrane
39
Succinylcholine (Anectine) onset
30 to 60 sec
40
Succinylcholine (Anectine) peak
60 sec
41
Succinylcholine (Anectine) DOA
3 to 5 min
42
Succinylcholine (Anectine) metabolism
Plasma cholinesterases
43
Succinylcholine (Anectine) special considerations (2)
Do not give if trauma is >24 hours;
| caution in renal failure due to increased K+
44
Rocuronium (Zemuron) dose
0.6 to 1.2 mg/kg
45
Rocuronium (Zemuron) dose (bolus and priming)
Bolus: 0.06 to 0.6 mg/kg
| Priming 10% ID 0.5 mg, give 3 to 5 mins prior
46
Rocuronium (Zemuron) MOA
NDMR quaternary aminosteroid, competitively inhibits cholinergic receptors at motor end plate
47
Rocuronium (Zemuron) onset
45 to 60 sec
48
Rocuronium (Zemuron) peak
1 to 3 min
49
Rocuronium (Zemuron) DOA
15-150 min
50
Rocuronium (Zemuron) metabolism
Hepatic, renal
51
Rocuronium (Zemuron) special considerations (2)
Onset decreased and DOA increased with increased dose;
| CV stable, good for infusion (mix 200 mg in 100 ml D5W for 2mg/ml)
52
Pancuronium (Pavulon) dose
0.04 to 0.1 mg/kg
53
Pancuronium (Pavulon) dose (bolus, gtt, priming)
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
Pancuronium (Pavulon) MOA
Long acting NDMR bisquaternary aminosteroid, competitively inhibits cholinergic receptors at motor end plate; can increase HR, BP, CO (vagolytic effects)
55
Pancuronium (Pavulon) onset
1 to 3 min
56
Pancuronium (Pavulon) peak
3 to 5 min
57
Pancuronium (Pavulon) DOA
40 to 65 min
58
Pancuronium (Pavulon) metabolism
Hepatic; renal is heavily dependent on kidneys for excretion, use caution in ARF/CRF
59
Pancuronium (Pavulon) special considerations (3)
SNS activation with decreased catecholamine uptake;
use caution with CAD;
active metabolite accumulation with infusion > 16 hours
60
Vecuronium (Norcuron) dose
0.08 to 0.1 mg/kg
61
Vecuronium (Norcuron) dose (bolus, gtt, priming)
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
Vecuronium (Norcuron) MOA
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
Vecuronium (Norcuron) onset
< 3 min
64
Vecuronium (Norcuron) peak
3 to 5 min
65
Vecuronium (Norcuron) DOA
25 to 30 min
66
Vecuronium (Norcuron) metabolism
Hepatic; small amount in kidneys
67
Vecuronium (Norcuron) special consideration (1)
Reconstitute with sterile water;
| 20mg/100ml D5W for 0.2mg/ml gtt
68
Atracurium (Tracrium) dose
0.3 to 0.5 mg/kg
69
Atracurium (Tracrium) dose (bolus, gtt, priming)
Bolus: 0.1 to 0.2 mg/kg
Gtt: 2 to 15 mcg/kg/min
Priming: 0.03 to 0.05 mg
70
Atracurium (Tracrium) MOA
NDMR that competitively inhibits cholinergic receptors at motor end plate
71
Atracurium (Tracrium) onset
< 3 min
72
Atracurium (Tracrium) peak
3 to 5 min
73
Atracurium (Tracrium) DOA
20 to 35 min
74
Atracurium (Tracrium) metabolism
Hoffman elimination independent of renal
75
Atracurium (Tracrium) special considerations (2)
Laudenosine is a metabolite that can cause seizures;
| histamine release can cause vasodilation, tachycardia, bronchospasm, laryngospasm
76
Cisatracurium (Nimbex) dose
0.15 to 0.2 mg/kg
77
Cisatracurium (Nimbex) dose (bolus, gtt, priming)
Bolus: 0.02 to 0.1 mg/kg
Gtt: 1 to 5 mcg/kg/min
Priming: 1 to 2 mg
78
Cisatracurium (Nimbex) MOA
Isomer of atracurium, NDMR that competitively inhibits cholinergic receptors at motor end plate
79
Cisatracurium (Nimbex) onset
90 to 120 sec
80
Cisatracurium (Nimbex) peak
3 to 7 min
81
Cisatracurium (Nimbex) DOA
20 to 35 min
82
Cisatracurium (Nimbex) metabolism
Hoffman elimination
83
Cisatracurium (Nimbex) special considerations (2)
Laudenosine is a metabolite that can cause seizures;
| histamine release can cause vasodilation, tachycardia, bronchospasm, laryngospasm
84
Neostigmine dose (reversal, max dose, with atropine, with glycopyrrolate, MG Tx)
```
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
Neostigmine MOA
Reversal of NDMRs; treatment of MG, post-op ileus, urinary retention; inhibits hydrolysis of acetylcholine by inhibiting acetylcholinesterase at the esteric site
86
Neostigmine onset
3 to 5 min
87
Neostigmine peak
3 to 14 min
88
Neostigmine DOA
40 to 60 min
89
Neostigmine metabolism
Hepatic, plasma esterases
90
Neostigmine special consideration (1)
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
Pyridostigmine dose (reversal, max dose, MG Tx)
Reversal: 0.25 mg/kg
Max dose: 30 mg
MG Tx: 60 to 1500 mg/day (average is 600 mg/day)
92
Pyridostigmine MOA
Reversal of NDMRs and treatment of MG; inhibits hydrolysis of acetylcholine by inhibiting acetylcholinesterase; slower onset and slower DOA compared to neostigmine
93
Pyridostigmine onset
2 to 5 min
94
Pyridostigmine peak
< 15 min
95
Pyridostigmine DOA
90 min
96
Pyridostigmine metabolism
Hepatic, renal
97
Pyridostigmine special consideration (1)
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
