Top Drawer Drugs Flashcards
(338 cards)
1
Q
Fentanyl mechanism of action
A
Stimulates / activates mu receptors
Opens potassium channels which then inhibit action potentials from firing in pain pathways thru the CNS
2
Q
Fentanyl Onset
A
3
Q
Fentanyl peak
A
5-15 minutes
4
Q
Fentanyl Duration of Action
A
30 min to 1 hr
Vd: 4L/ kg
T1/2: 219 minutes
5
Q
Fentanyl metabolism
A
Hepatic : 75% cleared in the urine as metabolites and 10% excreted unchanged.
6
Q
Fentanyl : special considerations
A
Greatest risk for respiratory depression is during the peak action
High doses can cause chest wall rigidity
Highly lipid soluble
75% first pass pulmonary uptake
7
Q
Midazolam (versed) dosing
A
Premedication: 0.07-1.5 mg/kg
Sedation: 0.01-0.1 mg/kg
Induction : 0.1-0.4 mg/kg
8
Q
Midazolam mechanism of action
A
Attaches and binds to alpha subunits on the GABA-A receptor.
Leaves the Cl- channel open, hyperpolarizing the cell post synaptically.
Works on GABA-A in the cerebral cortex , cerebellum cortex, and thalamus.
9
Q
Midazolam onset
A
30- 60 seconds
10
Q
Midazolam peak
A
3-5 minutes
11
Q
Midazlam duration of action
A
15-80 minutes
Vd : 1-3 L/kg
T1/2: 1-4 hr
12
Q
Midazolam metabolism
A
Hepatic
Active metabolites are rapidly conjugated and excreted in the urine
13
Q
Midazolam : special considerations
A
Ph dependent ring opening phenomenon in which the ring remains open for a pH of 4 making it highly lipid soluble.
Can cause cleft palate in neonates.
14
Q
Lidocaine dosing
A
1-1.5 mg/kg
4mg/ kg (300 mg)
7mg/kg (500mg)
15
Q
Lidocaine mechanism of action
A
Blocks sodium channels from inside the cell membrane
Occlusion of open sodium channel inhibits the permeability which slows the rate of depolarization
Causes interruption of pain signal transmission
16
Q
Lidocaine onset
A
45-90 seconds
17
Q
Lidocaine peak
A
1-2 minutes
18
Q
Lidocaine duration of action
A
IV : 30-60 minutes
Infiltration : 60-240 minutes
Spinal : 30-60 minutes
Epidural : 60-120 minutes
19
Q
Lidocaine metabolism
A
Hepatic
20
Q
Lidocaine : special considerations
A
Infiltration : 0.5-1%
IVRA: 0.25-5%
Epidural : 1.5-2%
Spinal 1.5-5%
21
Q
Propofol (diprovan) dosing
A
1.5-2.0 mg/kg
100-300mcg/kg/min
22
Q
Propofol mechanism of action
A
Induces GA by facilitating inhibitory neurotransmission by GABA-A receptors - binds to the beta subunit on GABA - A receptor.
Results in sedative/ hypnotic effects - GABA -A receptors activated, transmembrane chloride conductance increased = hyper polarization of post synaptic cell membrane and functional inhibition of post synaptic neuron.
23
Q
Propofol onset
A
24
Q
Propofol peak
A
1 minute
25
Propofol duration of action
5-10 minutes
Vd: 3.5-4.5 L/kg
T1/2 : 0.5-1.5 hr
26
Propofol metabolism
Hepatic
Renal excretion
27
Propofol: special considerations
High lipid solubility
Discard 6 hours after injecting.
Pain with injection
Caution in the elderly and hypovolemic patients : hypotension.
Decreases ICP, CRMO2, and CBP.
28
Succinylcholine (ancentine) Dosing
1.0-1.5 mg/kg
Spasm: 0.25-1mg/kg
29
Succinylcholine mechanism of action
Depolarizing NMB : attaches to one or both alpha subunits of the. Nicotinic acetylcholine receptor and mimics the action of acH. (Partial agonist)
Causes depolarization of the post junctional membrane.
30
Succinylcholine onset
30–60 seconds
31
Succinylcholine peak
60 seconds
32
Succinylcholine duration of action.
3-5 minutes
33
Succinylcholine metabolism
Plasma cholinesterases
34
Succinylcholine : special considerations
Dont give if trauma within last 24 hours
Caution in renal failure due to increased K+
35
Rocuronium (Zemuron) Dosing
0.6-1.2 mg/kg
Bolus:0.06-0.6 mg/kg
Priming 10% ID : 0.5 mg --> give 3-5 mg before intubation
36
Rocuronium MOA:
NMDR quaternary amniosteroid - competes for the cholinergic receptors at the motor endplate
37
Rocuronium onset :
45-60 seconds
38
Rocironium peak :
1-3 minutes
39
Rocuronium : DOA
15-150 minutes
40
Rocuronium metabolism
Hepatic
| Renal
41
Rocuronium: special considerations
Onset time is decreases and DOA prolonged with increasing doses
CV stable - good for infusions (mix 200 mg in 100 ml D5W for 2mg/ml)
42
Pancuronium (pavulon) dosing
0.04-0.1 mg/kg
Bolus: 0.01-0.05 mg/kg
Gtt: 1-15 mcg/kg/min
Priming 10% ID: 0.5-1.0 mg
43
Pancuromium MOA
Long lasting NDMR : bisquaternary amniosteroid competes for cholinergic receptors at the motor end plate
Increases HR and BP and CO can be secondary to vagilitic effects
44
Pancuromium onset
1-3 minutes
45
Pancuromium peak
3-5 minutes
46
Pan ironing DOA
40-65 minutes
47
Pancruonium metabolism
Hepatic
| Renal - heavily dependent on kidneys for excretion
48
Pancuromium : special considerations
Activation of SNS with decreases uptake of catcholimines - caution in CAD
Caution in renal failure due to kidney dependent excretion
Active metabolite accumulation with gtt infusing >16 hr.
49
Vecuronium dosing (norcuron)
0.08-1mg/kg
Bolus:0.01-0.05 mg/kg
Gtt: 1-2 mcg/kg/min
Priming 10% ID: 0.5-1.0 mg
50
Vecuronium MOA
Intermediate NDMR that competes with cholinergic receptors at the motor end plate
1/3 as potent as pancuronium
Vagotonic effects can occur when combined with opioids.
51
Vecuronium onset
52
Vecuronium peak
3-5 min
53
Vecuronium DOA
25-30 minutes.
54
Vecuronium metabolism
Hepatic. Small amount in kidneys.
55
Vecuronium : special considerations
Reconstitute with sterile water
Gtt 20 mg/ 100 ml for 0.2mg/ml
56
Atracurium dosing ( tracrium)
0.3-0.5 mg/kg
Bolus: 0.1-0.2 mg/kg
Gtt: 1-5 mcg/kg/min
Priming : 0.03-0.05 mg
57
Atracurium MOA
NDMR that competes at cholinergic receptors at the motor end plate.
58
Atracurium onset
59
Atracurium peak
3-5 minutes
60
Atracurium DOA
20-35 minutes
61
Atracurium elimination
Hoffmann elimination - independent of renal elimination.
62
Atracurium : special considerations.
Laudenosine is a metabolite of Atracurium that can cause seizures.
Also causes histamine release and vasodilation/ tachycardia / bronchoscope, / laryngoscopes
63
Cisatracurium (nimbex) dosing
0.15-0.2 mg/kg
Bolus: 0.02-0.1 mg/kg
Gtt: 1-5 mcg/kg/min
Priming 1-2 mg
64
Cisatracurium MOA:
Isomer of Atracurium. Competes for cholinergic receptors at the motor end plate
65
Cisatracurium onset
90-120 seconds
66
Cisatracurium peak
3-7 minutes
67
Cisatracurium DOA:
20-35 minutes
68
Cisatracurium elimination
Hoffmann elimination
69
Cisatracurium : special considerations
Laudenosine is a metabolite of that can cause seizures
Histamine release can cause tachycardia hypotension broncho and laryngospasm.
70
Neostigmine dosing
Reversal : 0.05 mg/ kg
MAX DOSE : 5 mg
With atropine : 0.015 mg/ kg
With glycopyrrolate : 0.01 mg/kg
Myasthenia gravis treatment : 15-375 mg PO QD.
71
Neostigmine MOA
Reversal of NDMRs / treatment of MG, post op illeus, and urinary retention.
Inhibits hydrolysis of acetylcholine by inhibiting acetylcholinesterase at the esteric site
72
Neostigmine onset
3-5 minutes
73
Neostigmine peak
3-14 minutes
74
Neostigmine DOA
40-60 minutes.
75
Neostigmine metabolism
Hepatic / plasma esterases
76
Neostigmine : special considerations
Cholinergic effects : SLUDBBM
Cholinergic crisis - n/v, sweating, Brady or tachy, excessive secretions,broncho spasm, weakness and paralysis
- treat with 10mcg/kg of atropine Q 3-10 minutes.
77
Pyridostigmine dosing
0.25 mg/kg
MAX DOSE 30 mg
Myasthenia Gravis tx : 60-1500 mg / day (avg 600 mg/day)
78
Pyridostigmine MOA
Reversal of anticholinergic CNS effects due to the OD of atropine/ scopolamine.
Topical tx of glaucoma
Tertiary amine anticholinesterase agent effectively increases the concentration of acH.
Reverses central cholinergic effects (anxiety, confusion, seizures) and peripheral effects ( hyperpyrexia, vasodilation, urinary retention)
DOES NOT REVERSE NMBs.
79
Pyridostigmine Onset
3-8 minutes
80
Pyridostigmine Peak
5-10 minutes
81
Pyridostigmine DOA
30 min- 5hr.
82
Pyridostigmine metabolism
Plasma esterases
83
Pyridostigmine : special considerations
Give to reverse atropine toxicity
Crosses BBB (tertiary amine! )
84
Scopolamine dosing
IV: 0.3-0.6 mg
Patch delivers 1.5 mg (1mg over 72 hr)
85
Scopolamine MOA
Tertiary amine
Management of N/V associated with ovoid anesthesia /GA or motion sickness
86
Scopolamine onset
IV: immediate
TD:30 min.
87
Scopolamine peak
IV: 50-80 min
TD: 3 hr
88
Scopolamine DOA
IV:2 hr
TD : 3 days
89
Scopolamine metabolism
Hepatic/ renal
90
Scopolamine : special considerations
Lipid solubility allows for transdermal rout as well as greater CNS effects than atropine
Can cause sedation and amnesia
Crosses BBB.
91
Glycopyrrolate (robinul) dosing
0.2 mg for each 1 mg of Neo or 5 mg of Pyridostigmine
92
Glycopyrrolate MOA
Quaternary ammonium anticholinergic.
Because of its polar nature, it does not cross the BBB. It antagonizes muscadine can symptoms induced by cholinergic drugs
Produces less tachycardia than atropine.
93
Glycopyrrolate Onset
94
Glycopyrrolate peak
5 minutes
95
Glycopyrrolate DOA
Vagal blockade : 2-3 hr.
Antisialogogue effect : 7 hr.
96
Glycopyrrolate metabolism
85% excreted unchanged in the urine within 48 hours.
97
Glycopyrrolate : special considerations
Reduces LES tone - sphincter in the GIT are relaxed by NO that is released by parasympathetic fibers
Can increase IOP - caution In patients with glaucoma
Do not use in pt with BPH , MG, paralytic ileus, or UC.
Side effects : orthostasic hypotension, dry mouth, and urine retention.
98
Hydromorphone dosing
Analgesia: 0.01-0.04mg/kg
0.5-2mg q4-6 hr
2-4 mg PO q4-6 hr
Spinal : 0.1-0.2 mg (2-4 mcg/kg)
Epidural : 0.15-0.3 mg/ hr.
Epidural bonus :1-2 mg
Intrathecal : 0.1 mg
99
Hydromorphone MOA :
Opiate agonist that is a hydrogenated ketone Of morphine
7x more potent than morphine
Effects on CNS and organs containing smooth muscle.
100
Hydromorphone onset
IV:
101
Hydromorphone peak
IV: 5-20 minutes
Epidural : 30 minutes
102
Hydromorphone DOA
IV:2-4 hr
Epidural : 10-16 hr.
103
Hydromorphone metabolism
Hepatic
104
Hydromorphone : special considerations
Can cause drowsiness , euphoria, respiratory depression, interference with adrenocortical response to stress at high doses.
Releases histamine
Prolonged anesthesia by alpha agonists like clonidine
Reduce the dose in elderly, hypovolemic, or pt on other sedatives
Biliary smooth muscle spasm - not a heart attack!
105
Remifentanyl (ultiva) Dosing
Induction : 1mcg/kg over 30-60 sec.
Gtt: 0.5-4 mcg/kg/min
Bolus: 1mcg/kg
MAC: 0.5-1 mcg/kg over 30-60 seconds
MAC gtt : 0.025-0.1 mcg/kg/min
NOT RECOMMENDED AS A SOLE AGENT.
106
Remifentanyl MOA
Mu opioid agonist with rapid onset and peak effect
Short DOA d/t metabolism by nonspecific esterases in plasma and tissue esterases.
Recovery within 5-10 minutes if no other analgesia on board.
107
Remifentanyl onset
30seconds.
108
Remifentanyl peak
3-5 min
109
Remifentanyl DOA
5-10 minutes
110
Remifentanyl metabolism
Plasma / tissue esterases
111
Remifentanyl : special considerations
Decrease initial dose in elderly by 50%.
Can increase doses upward 20-100% and downward 25-50% every 2-5 minutes d/t rapid onset and short DOA.
CBF, ICP, and CRMO2 decreased. Not used for spinal or epidural or intrathecal. Contains glycine.
112
Morphine (duramorph) dosing
Premedication : 0.05-0.2 mg/kg
Pain intraop: 0.1-1 mg/kg.
Postop pain: 0.03-0.15 mg/kg
Epidural : 2-5 mg
Epidural infusion : 0.3-0.9 mg/hr.
113
Morphine MOA:
Prototypical opioid agent
Alkaloid of opiuk that exerts its effects on CNS and organs containing smooth muscle.
N/v secondary to CTZ Stimulation.
Histamine release
114
Morphine onset
IV:
115
Morphine peak
IV: 5-20 min
Epidural / spinal : 90 min.
116
Morphine DOA
IV:2-7 hr.
Epidural / spinal 6-24 hr.
117
Morphine ,metabolism
Hepatic / renal
118
Morphine : special considerations.
75-85% metabolized to morphine 3 glucuronide (inactive) but 5-10% metabolized to morphine-6 glucuronide (active that has analgesia and respiratory depression effects.
Caution in ARF/CRF secondary to accumulation of active metabolites and increased respiratory depression.
119
Sufentanyl citrate: (sufenta) dosing
Analgesia : 0.2-0.3 mcg/kg
Induction : 2-10 mcg/kg
Gtt: 0.1-0.5 mcg/kg/min
Epidural infusion : 0.2-0.7 mcg/kg
Epidural gtt : 0.1-0.6 mcg/kg/min
Spinal : 0.02-0.2 mcg/kg
120
Sufentanil citrate : MOA
Thienyl analogue of fentanyl with 5-7 x the analgesia potency.
Attenuates the hemodynamics response to DVL and surgical manipulation
121
Sufentanil citrate : onset
IV :1-3 min
Epidural / spinal :4-10 min
122
Sufentanil citrate : peak
IV :3-5 min
Epidural / spinal :
123
Sufentanil citrate : DOA
IV: 20-45 minutes
Epidural / spinal : 2-4 hr.
124
Sufentanil citrate : metabolism
Hepatic
125
Sufentanil citrate : special considerations
Can cause dose dependent bradycardia.
Highly lipophilic - crosses the placenta causing respiratory depression in the fetus.
Rapid redistribution terminates effects of small doses but accumulates with larger doses.
126
Meperidine (Demerol) : dosing
Analgesic : 25-100 mg
Post op shivering : 12.5-25 mg
127
Meperidine : MOA
Premedication , analgesia , and tx of post op shivering.
Synthetic opioid agonist 1/10th as potent as morphine.
Direct myocardial depressant at high doses.
128
Meperidine : onset
129
Meperidine : peak
5-20 minutes
130
Meperidine : DOA
2-4 hr
131
Meperidine : metabolism
Hepatic
132
Meperidine : special considerations.
Active metabolite - NORMEPERIDINE - can Cause seizures!!!
DO NOT GIVE TO A PATIENT TAKING AN MAOI.
133
Ketorlac (toradol) : dosing
15-30 mg QID
134
Ketorlac: MOA
Analgesia.
NSAID that has analgesia / anti inflammatory and antipyretic effects.
30 mg is equivalent to 9mg morphine.
Inhibits synthesis of prostaglandins
No sedative effects
Peripheral analgesic.
135
Ketorlac: onset
136
Ketorlac : peak
1-3 hours.
137
Ketorlac : DOA
3-7 hours.
138
Ketorlac : metabolism
Hepatic / renal
91% renal dependent.
139
Ketorlac: special considerations.
Caution in renal / hepatic insufficient pt.
Can cause Htn d/t loss of prostaglandins synthesis.
Do not use in preggo bc it inhibits uterine contraction and effects fetal circulation( promotes closure of PDA) and is excreted in breast milk.
Do not use If pt. is taking another nsaid history of GIB or PUD
140
Narcan (naloxone) : dosing
0. 5-1mcg/kg/ min Q3-5 min.
0. 04-0.4 mg
Gtt : 4-5 mcg/kg/hr
141
Narcan : MOA
Pure opioid antagonist - competes and displaces narcotics at receptor sites
Reverses all narcotic properties including analgesia
Can cause tachycardia , HTN, plum edema.
142
Narcan: onset
1-2 minutes
143
Narcan: peak
5-15 minutes.
144
Narcan : DOA
1-4 hours.
145
Narcan : metabolism
Hepatic
Conjugation with glucuronic acid to form naloxone 3 glucuronide
146
Narcan: special considerations.
May antagonize the anti hypertensive effects of clonidine
147
Flumazinil (romazicon) : dosing
0.2-1 mg
Give at rate of 0.2mg/min repeating every 20 minutes
Gtt: 30-60 mcg/ min
Kids : 0.01 mg/kg
Kids gtt : 0.5-1 mcg/min
148
Flumazinil : MOA
Reversal of benzos. Benzo receptoe antagonist that competitively inhibits the activity at the benzodiazepine recognition site on the GABA / benzos receptor complex in the CNS.
149
Flumazinil : onset
1-2 minutes
150
Flumazinil : peak
2-10 minutes.
151
Flumazinil : DOA
45-90 minutes.
152
Flumazinil : metabolism
Hepatic
153
Flumazinil : special considerations
Precipitates Benzo withdrawal
Increased risk of seizures in those with concurrent tricyclics OD. May provoke panic attack
154
Etomidate: dosing
0.1- 0.4mg/ kg
Gtt : 0.25-1.0 mg/min
155
Etomidate: MOA
Induction and supplementation of anesthesia. Non barbituate hypnotic.
No analgesic activity. Can elicit alterations in SSEPs.
Minimal effects on BP make it a good choice to maintain CPP.
156
Etomodate : onset
30-60 seconds.
157
Etomidate : peak
1 minute
158
Etomidate : DOA
3-10 minutes.
159
Etomidate : metabolism
Hepatic
160
Etomidate: special considerations.
Can cause adrenocortical suppression that CN last up to 4-6 hours and is due toe to is at induced inhibition of 11 beta- hydroxylase. 30-60% chance of myoclonus
161
Ketamine : dosing
Sedation/ analgesia : 0.5-1 mg/kg.
Induction: 1.0-2.5 mg/kg
Gtt: 15-80 mcg/kg/min
Epidural/caudal : 0.5 mg/kg
162
Ketamine : MOA
Dissociative anesthetic- induction and maintenance of anesthesia.
Useful in hypovolemic or high risk patients.
Ideal for short procedures
A phencyclidine derivative that produces rapid acting dissociative anesthesia characterized. By normal or enhanced skeletal muscle tone, respiratory stimulation and minimal respiratory depression
Antagonist effect on NMDA receptors. Long term excitatory effects of nocioceptic transmission
163
Ketamine : onset
164
Ketamine : peak
1 minute
165
Ketamine : DOA
5-15 minutes.
166
Ketamine metabolism
Hepatic
167
Ketamine : special considerations.
CBF, CMRO2 and ICP are increased.
Increased EEG activity
Increased salivary and tracheal secretions.
Emergence delirium - dis conjugate eyes, and SNS effects from indirect NE release - HTN.
decrease VAs.
168
Esmolol : dosing (BREVIBLOC)
Loading dose : 0.5 mg/ kg
Bolus: 0.2-0.5 mg/kg (5-10 mg)
Gtt: 50-200 mcg/kg/min
HTN: 0.5-2 mg/kg (may repeat Q5min)
HTN GTT: 50-300 mcg/kg/min
169
Esmolol : MOA
Treatment of SVT and HTN.
Cardio selective beta blocker with rapid onset and short DOA.
At high doses can affect beta 2 rcp.
170
Esmolol : onset
1-2 min
171
Esmolol : peak
5 min
172
Esmolol : DOA
10-20 minutes.
173
Esmolol : metabolism
Hydrolized BY RBC esterases
174
Esmolol Special considerations
None
175
Hydralazine : dosing (APRESOLINE)
0. 1-2 mg/kg
| 2. 5-40 mg.
176
Hydralazine MOA
Penthalzine derivative lowers BP and has a greater effect on resistance arterioles by interfering with guananyl Cyclase and calcium ion transport in the vascular smooth muscle.
This can result In reflex Tachycardia
Increases plasma Renin activity.
177
Hydralazine onset
5-20 min
178
Hydralazine peak
10-80 min
179
Hydralazine DOA
2-4 hours.
180
Hydralazine metabolisim
Hepatic acetylation
Higher doses requires in rapid acetylators.
181
Hydralazine special considerations
Not the drug of choice for a patient with tachycardia.
Administration in conjunction with a beta blocker can limit the reflex increases In sympathetic activity.
Second line drug in pregnancy
182
Labatelol (NORMODYNE TRANDATE) : dosing
2.5-20 mg over 2 min.
Gtt : 0.5-2 mg/min
Max cumulative dose 1-4 mg/kg.
183
Labatelol MOA
Non selective Adrenergic receptor blocking agent with mild alpha and predominant beta activity.
Alpha: Beta =1:7 IV
Alpha : Beta = 1:3 PO
decreases BP with minimal risk of reflex tachycardia - risk of broncho spasm
184
Labatelol : onset
2-5 minutes
185
Labatelol peak action
5-15 min
186
Labatelol DOA
2-4 hours
187
Labatelol metabolism
Hepatic
188
Labatelol : special considerations
Crosses placenta
189
Metoprolol : dosing (LOPRESSOR)
2.5-5 mg
MAX DOSE :15 mg
190
Metoprolol : MOA
Beta1 selective antagonist - cardioprotective
Anti hypertensive -treatment of SVT, and ventricular arrhythmia, and acute MI, thyroxic patients , adjunct to ETOH withdrawal
Can inhibit beta 2 at high doses
191
Metoprolol : onset
Immediate
192
Metoprolol : peak
20 min
193
Metoprolol DOA
5-8 hours
194
Metoprolol metabolism
Hepatic
195
Metoprolol special considerations
Broncho spasm at high doses. Abrupt withdrawal can lead to rebound HTN and tachycardia dt up regulation of rcp.
196
Methyl dopa (ALDOMET) : dosing
200-500 mg Q6h
MAX DOSE IS 4 mg in 4 DIVIDED DOSES.
peds: 5-10 mg/kg q6h
MAX IS 3mg IN 4 DIVIDED DOSES.
197
Methyl dopa : MOA
Anti hypertensive.
Acts in the CNS to lower BP. Once in the brain- the drug is converted to alpha-methyl norepinephrine which lowers BP thru activation of alpha 2 Adrenergic rcp And decreasing SNS outflow
198
Methyl dopa : onset
1-2 hr.
199
Methyl dopa : peak
4-6 hours
200
Methyl dopa : DOA
10-16 hours
201
Methyl dopa metabolism:
Hepatic
202
Methyl dopa : special considerations
Crosses BBB. Contraindicated in hepatic dz. first line therapy for PIH.
Reduces the MAC of VAs.
203
Phenylepherine : dosing
0.5-1 mcg/kg
50-100 mcg bolus
204
Phenylephrine MOA
Direct alpha 1 agonist produces intense vasoconstriction peripherally.
Increases SBP/ DBP
reflex bradycardia can result in decreased CO
Increased SVR can aid in reducing shunt in fallot patients.
205
Phenylephrine onset
206
Phenylephrine peak
207
Phenylephrine DOA
15-20 min
208
Phenylephrine metabolism
Hepatic
209
Phenylephrine special considerations
Tachyphylaxis may occur
210
Ephedrine : dosing
2.5- 10 mg
MAX : 150 mg / 24 hr.
211
Ephedrine MOA
Vasopressor bronchodilator- non catecholamine sympathomimetic with mixed direct and indirect actions.
Resistant to MAO/COMT resulting in longer DOA.
Increases CO,BP,and HR by alpha and beta Adrenergic stimulation.
Increases coronary and skeletal blood flow - broncho dilation by beta 2 rcp
Restores uterine blood flow when used to treat epidural/ spinal hypotension.
212
Ephedrine onset
Immediate
213
Ephedrine peak
2-5 minutes
214
Ephedrine DOA
10-60 min.
215
Ephedrine metabolism
Hepatic / renal
216
Ephedrine special considerations
Tachyphylaxis may occur once catcholemine stores are depleted.
217
Ondansetron dosing (ZOFRAN)
4 mg IV/ PO Q4-8h.
218
ZOFRAN MOA
Selective 5ht3 antagonist. Receptors are found peripherally on Vaal nerve terminals and centrally in the CTZ. prevention and treatment of chemo induced and post op N/V
219
ZOFRAN onset
220
ZOFRAN peak
Variable
221
ZOFRAN DOA
12-24 hours
222
ZOFRAN metabolism
Hepatic
223
ZOFRAN special considerations
Expensive.
224
Metroclopramide dosing (REGLAN)
10 mg IV
Peds; 0.1 mg/kg.
225
REGLAN MOA
Stimulates motility of the upper GIT and increases the LES tone by 10-20 cm.
GASTRIC ACID SECRETION IS NOT ALTERED.
stimulates gastric emptying- antiemetic tx of symptomatic Gerd and diabetic gastroparesis.
Decreases nausea by blocking DA rcp in the CTZ of the CNS.
226
REGLAN onset
1-3 min
227
REGLAN peak
228
REGLAN DOA
1-2 hours
229
REGLAN metabolism
Renal
230
REGLAN special considerations.
Effects are blocked by antimuscarinics.
Rapid injection can cause abd cramping and can result in hypotension and arrhythmia.
Avoid in pheochromocytoma , pt on MAOI, GI obstruction, Parkinson's
Caution in elderly
Can cause eps.
231
Diphenhydramine dosing (Benadryl)
10-50 mg IV
25-50 PO
Max dose is 400 mg.
232
Benadryl MOA
H1 receptor antagonist with anticholinergic, antiemetic, and sedative effects.
Antiemetic, anti vertigo, treatment of allergic reactions adjunct use in tx of anaphylaxis, symptomatic treatment of drug induced eps
233
Benadryl onset
234
Benadryl peak
1-3 hr
235
Benadryl DOA
4-6 hr
236
Benadryl metabolism
Hepatic
237
Benadryl special considerations
Sry mouth, pvc,photophobia, mydriasis, sedation.
Give slowly IV as you can see exhibitory CNS effects.
238
Famotadine dosing (PEPCID)
20mg IV q12 hr.
239
Pepcid MOA
Competitive inhibitor of h2 rcp. Suppresses acid concentration and volume of gastric secretion
PUD , pathological hyper secretory states , prophylaxis against aspiration Pna , stress ulcers, and allergic reactions.
240
Pepcid onset
241
Pepcid peak
30min - 3 hr.
242
Pepcid DOA
10-12 hr
243
Pepcid metabolism
Renal
244
Pepcid special considerations.
DOES NOT CHANGE THE PH OD GASTRIC CONTENTS PRESENT UPON TIME OF ADMINISTRATION.
very effective when used with an h1 antagonists
245
Promethazine hydrochloride dosing (PHENERGAN)
12.5-50 mg q4-6h
246
PHENERGAN MOA
Phenothiazine derivative does not possess neuroleptic or antipsychotic activity.
H1 rcp antagonist with sedative , antiemetic, anticholinergic,and anti motion sickness effects.
247
PHENERGAN onset.
2-5 minutes
248
PHENERGAN peak
249
PHENERGAN DOA
2-8 hr
250
PHENERGAN metabolism
Hepatic
251
PHENERGAN special considerations
Eps symptoms may occur
DO NOT USE EPINEPHERINE TO TX HYPOTENSION. PHENOTHIAXINES CAUSE A REVERSAL OF EPINEPHERINES VASOPRESSOR EFFECTS AND CAUSE FURTHER DECREASES IN BP. USE PHENYLEPHRINE OR NOREPINEPHRINE
252
Ranitidine dosing (ZANTAC)
50 mg q1-2hr. Give at HS and 2 hr prior to surgery.
150-300 mg PO.
253
Zantac MOA
H2 receptor antagonist - blocks histamine, pentagram grin, and acetylcholine- induced secretion of H ions by parietal cells.
Also can suppress histamine induced peripheral vasodilation and into tropic effects. Decreases gastric volume ph inhibits only future acid production
254
Zantac onset
255
Zantac peak
1-2 hr
256
Zantac DOA
6-8 hr
257
Zantac metabolism
Hepatic
258
Zantac special considerations
None
259
Dexamethasone dosing (DECADRON)
0.2 mg/kg
max 12 mg.
260
DECADRON MOA
Corticosteroid - potent anti inflammatory agent. Treatment of inflammatory diseases, cerebral edema, raised ICP, airway edema, aspiration pneumonitis, bronchial asthma, myofascial pain,allergic rxn, prevention of rejection in organ tx, replacement therapy for adrenocortical insufficiency.
261
DECADRON onset
1-2 minutes
262
DECADRON peak
12-24 hr
263
DECADRON DOA
36-54 hr
264
DECADRON metabolism
Hepatic
265
DECADRON special considerations
Does. It cause sodium or water rentention.
Caution in DM
HPA Axis suppression
266
Furosemide dosing (LASIX)
0.1-1 mg/kg
10-40 mg IV bolus
267
LASIX MOA
An anthranilic acid derivative - loop diuretic inhibits reabsorption of sodium and chloride ions in the medullary portion of the loop of henle.
Diuretic of choice in acute fluid overload - increases excretion of K+ chloride mag and calcium
268
LASIX onset
5-15 minutes
269
LASIX peak
20-60 minutes
270
LASIX DOA
2 hr
271
LASIX metabolism
Renal
272
LASIX special considerations
Increases nephrotoxicity of amino glycosides and cephalosporins, causes hypokalemia, hyponatremia, and hypocalcemia
Can cause deafness or ringing in ears that's irreversible
DO NOT GIVE TO PT WITH SULFA ALLERGY.
273
Doxapram dosing (DOXPRAM)
0.5-1.5mg/kg may repeat Q5 min
Max dose 2mg/kg
274
Doxapram MOA
Respiratory stimulant with action mediated thru peripheral carotid chemoreceptors.
Increasing doses increases the stimulation of the respiratory centers In the brain and spinal cord.
Manifested as increased TV with increased RR.
may increase BP and co due to catcholemine release.
275
Doxapram onset
20-40'seconds
276
Doxapram peak
1-2 min
277
Doxapram DOA
5-12 minutes
278
Doxapram metabolism
Hepatic
279
Doxapram special considerations
Low PaO2 so it may be useful in patients with copd who are dependent on hypoxia drive to breathe.
It should not replace standard supportive therapy (mech. Vent. )
Most common cause of postoperative ventilation failure (obstruction ) will not be alleviated making many people believe that it's usefulness is limited.
280
Mannitol dosing (OSMITROL)
0.25-1 g/kg
281
Mannitol MOA
Osmotic diuretic - tx of increase ICP and IOP as well as volume overload.
It raises the osmolarity of the renal tubular fluid and inhibits tubular reabsorption of water and electrolytes.
282
Mannitol onset
Dieresis :15-60 min
Decrease ICP :
283
Mannitol peak
Diuretic :1 hr
Decrease ICP --
Decrease IOP 1-2 hr.
284
Mannitol DOA
Diuretic 3-8 hr.
Decrease ICP :3-8 hr
Decrease IOP : 4-6 hr.
285
Mannitol metabolism
Renal
286
Mannitol special considerations
Can worse. Or Induce pulmonary edema, intracranial hemorrhage, hypertension or rebound increase in ICP.
287
Methylene blue dosing
1-2 mg/kg
288
Methylene blue MOA
Treatment of drug induced methomoglobinemia,dye effect to delineate body structure and fistula and confirm rupture of amniotic membranes. Urinary antiseptic.
289
Methylene blue onset
Immediate
290
Methylene blue peak
291
Methylene blue DOA
Varies
292
Methylene blue metabolism
Renal
293
Methylene blue special considerations
High concentrations it converts ferrous iron to ferric form thus forming methemoglobin.
At low doses capable of hastening the conversion of methemoglobin to hbg.
294
Indigo carmine dosing
40 mg
295
Indigo carmine MOA
Excreted largely by kidneys regaining its blue color as it passes thru the body.
Used to localize orifices during cystoscopy and urethral catheterization.
Commonly see. In gyn procedures to ensure the bladder has not been lacerated.
296
Fentanyl dosing
```
Induction : 2-5 mcg/kg
Intraop : 2-20 mcg/kg
Pediatric : 1mcg/kg
Epidural :50-100 mcg/kg
Infusion: 25-50 mcg/ hr
Post op pain : 0.5-1.5 mcg/kg
```
297
Indigo carmine metabolism
Appears in the urine within 10 minutes of injection
Biological t1/2 4-5 min.
298
Indigo carmine special considerations
The vital dyes- methylene blue, indocyanine green, flurescein,and indigo carmine can cause cause erroneously low pulse ox reading
Methylene blue has the greatest impact on this.
These effects are transient and resolve as the dyes are diluted and metabolized.
May cause a mild pressor effect.
299
Oxytocin dosing
0.5- 10 u/ min
10-40 u/1000 l
10 u/250 cc NS.
300
Oxytocin MOA
Indirectly stimulates contraction of uterine smooth muscle by increasing sodium permeability of uterine myofibrils.
Induce/ augment uterine contractions , maintain uterine contractions maintain uterine tone postpartum to control uterine bleeding.
301
Oxytocin onset
IV immediate
IM: 3-5 min.
302
Oxytocin DOA
IV : 1 hr
| IM : 2-3 hr.
303
Oxytocin metabolism
Hepatic / renal
304
Oxytocin. Special considerations
May cause HTN. Arrhythmia and transient hypotension and reflex tachycardia fetal distress and water retention.
305
Protamine sulfate dosing
1mg/ 100 units of heparin
306
Protamine MOA
Reversal of heparin/ anti coagulation OD. The positive charged alkaline protamine binds to the negative charge of heparin rendering it Inactive.
307
Nitrous Oxide : Dosing
MAC 10% (104)
| BG : 0.46
308
Nitrous Oxide MOA
Produces General anesthesia through interaction with CNS cellular membranes
inhalation agent - a strong analgesic and weak anesthetic that is usually used in combination with other anesthetics.
Very low solubility in the blood --> rapid uptake and induction of anesthesia.
the low tissue solubility allows for rapid elimination and awakening.
309
Nitrous oxide metabolism
Exhalation
310
Nitrous Oxide Special considerations:
Second gas effect - Administration of high concentrations of rapidly absorbed first gas will facilitate the rate of rise in alveolar concentration.
Diffusion hypoxia - Rapid / abrupt d/c prevents the body from recognizing and compensating for decreased PaO2.
Caution in pregnancy and those with B12 deficiency, inhibition of tetrahydrofolate (vitamin B dependent enzymes)
311
Desfulrane Dosing :
MAC : 6.6
BG: 0.42
VP 669
312
Desfulrane MOA :
produces general anesthesia through interaction with CNS mollecular membranes.
Volatile agent, non flammable fluoridated methyl ethyl ether.
contains a fluorine atom instead of a chlorine atom. (compared to Iso.)
Requires the use of electrically heated and pressurized vaporizers, low solubility in the blood allows for a rapid onset and its low tissue solubility allows for rapid emergence.
313
Desflurane Metabolism
exhalation
| 15-20% hepatic
314
Desflurane Special considerations:
may cause coughing, breath holding, salivation, and layrngospasm.
Avoid as an induction agent.
315
Sevoflurane Dosing:
MAC 2.0
BG 0.65
VP 170
316
Sevoflurane MOA
Produces general anesthesia through interactions with CNS molecular membranes
Volatile agent, nonflammable flouronated isopropyl ether.
Low solubility int he blood allows for a rapid onset, and its low tissue solubility allows for rapid emergence.
317
Sevoflurane Metabolism:
Exhalation
| 3 % hepatic
318
Sevoflurane Special considerations:
Choice inhalation agent for pediatrics, good choice for mask induction.
Excellent bronchodilator.
Can be used for reverse bronchospasm.
compound A production, keep FGF at 2L / min or more
319
Isoflurane Dosing:
MAC : 1.17
BG 1.4
VP 240
320
Isoflurane MOA
Produces general anesthesia through interactions with the CNS cellular membranes.
volatile agent, nonflammable halogenated methyl ethyl ether.
321
Isoflurane metabolism
Exhalation
| 0.2% hepatic
322
Isoflurane Special considerations
at 2 MAC, produces electrically silent EEG.
Choice agent for neuro-anesthesia .
Coronary steal syndrome
Depression of baroreceptor reflexes.
inhibits pulmonary hypoxic pulmonary vasoconstrictor response in a dose related fashion.
323
Nitrous Oxide : Dosing
MAC 10% (104)
| BG : 0.46
324
Nitrous Oxide MOA
Produces General anesthesia through interaction with CNS cellular membranes
inhalation agent - a strong analgesic and weak anesthetic that is usually used in combination with other anesthetics.
Very low solubility in the blood --> rapid uptake and induction of anesthesia.
the low tissue solubility allows for rapid elimination and awakening.
325
Nitrous oxide metabolism
Exhalation
326
Nitrous Oxide Special considerations:
Second gas effect - Administration of high concentrations of rapidly absorbed first gas will facilitate the rate of rise in alveolar concentration.
Diffusion hypoxia - Rapid / abrupt d/c prevents the body from recognizing and compensating for decreased PaO2.
Caution in pregnancy and those with B12 deficiency, inhibition of tetrahydrofolate (vitamin B dependent enzymes)
327
Desfulrane Dosing :
MAC : 6.6
BG: 0.42
VP 669
328
Desfulrane MOA :
produces general anesthesia through interaction with CNS mollecular membranes.
Volatile agent, non flammable fluoridated methyl ethyl ether.
contains a fluorine atom instead of a chlorine atom. (compared to Iso.)
Requires the use of electrically heated and pressurized vaporizers, low solubility in the blood allows for a rapid onset and its low tissue solubility allows for rapid emergence.
329
Desflurane Metabolism
exhalation
| 15-20% hepatic
330
Desflurane Special considerations:
may cause coughing, breath holding, salivation, and layrngospasm.
Avoid as an induction agent.
331
Sevoflurane Dosing:
MAC 2.0
BG 0.65
VP 170
332
Sevoflurane MOA
Produces general anesthesia through interactions with CNS molecular membranes
Volatile agent, nonflammable flouronated isopropyl ether.
Low solubility int he blood allows for a rapid onset, and its low tissue solubility allows for rapid emergence.
333
Sevoflurane Metabolism:
Exhalation
| 3 % hepatic
334
Sevoflurane Special considerations:
Choice inhalation agent for pediatrics, good choice for mask induction.
Excellent bronchodilator.
Can be used for reverse bronchospasm.
compound A production, keep FGF at 2L / min or more
335
Isoflurane Dosing:
MAC : 1.17
BG 1.4
VP 240
336
Isoflurane MOA
Produces general anesthesia through interactions with the CNS cellular membranes.
volatile agent, nonflammable halogenated methyl ethyl ether.
337
Isoflurane metabolism
Exhalation
| 0.2% hepatic
338
Isoflurane Special considerations
at 2 MAC, produces electrically silent EEG.
Choice agent for neuro-anesthesia .
Coronary steal syndrome
Depression of baroreceptor reflexes.
inhibits pulmonary hypoxic pulmonary vasoconstrictor response in a dose related fashion.
