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Anesthesia > Top Drawer Drugs > Flashcards

Top Drawer Drugs Flashcards

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

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2
Q

Fentanyl Onset

A
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3
Q

Fentanyl peak

A

5-15 minutes

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4
Q

Fentanyl Duration of Action

A

30 min to 1 hr

Vd: 4L/ kg

T1/2: 219 minutes

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5
Q

Fentanyl metabolism

A

Hepatic : 75% cleared in the urine as metabolites and 10% excreted unchanged.

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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

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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

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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.

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9
Q

Midazolam onset

A

30- 60 seconds

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10
Q

Midazolam peak

A

3-5 minutes

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11
Q

Midazlam duration of action

A

15-80 minutes

Vd : 1-3 L/kg

T1/2: 1-4 hr

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12
Q

Midazolam metabolism

A

Hepatic

Active metabolites are rapidly conjugated and excreted in the urine

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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.

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14
Q

Lidocaine dosing

A

1-1.5 mg/kg
4mg/ kg (300 mg)
7mg/kg (500mg)

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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

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16
Q

Lidocaine onset

A

45-90 seconds

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17
Q

Lidocaine peak

A

1-2 minutes

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18
Q

Lidocaine duration of action

A

IV : 30-60 minutes

Infiltration : 60-240 minutes

Spinal : 30-60 minutes

Epidural : 60-120 minutes

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19
Q

Lidocaine metabolism

A

Hepatic

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20
Q

Lidocaine : special considerations

A

Infiltration : 0.5-1%

IVRA: 0.25-5%

Epidural : 1.5-2%

Spinal 1.5-5%

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21
Q

Propofol (diprovan) dosing

A

1.5-2.0 mg/kg

100-300mcg/kg/min

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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.

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23
Q

Propofol onset

A
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24
Q

Propofol peak

A

1 minute

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25
Q

Propofol duration of action

A

5-10 minutes

Vd: 3.5-4.5 L/kg

T1/2 : 0.5-1.5 hr

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26
Q

Propofol metabolism

A

Hepatic

Renal excretion

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27
Q

Propofol: special considerations

A

High lipid solubility

Discard 6 hours after injecting.

Pain with injection

Caution in the elderly and hypovolemic patients : hypotension.

Decreases ICP, CRMO2, and CBP.

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28
Q

Succinylcholine (ancentine) Dosing

A

1.0-1.5 mg/kg

Spasm: 0.25-1mg/kg

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29
Q

Succinylcholine mechanism of action

A

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.

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30
Q

Succinylcholine onset

A

30–60 seconds

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31
Q

Succinylcholine peak

A

60 seconds

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32
Q

Succinylcholine duration of action.

A

3-5 minutes

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33
Q

Succinylcholine metabolism

A

Plasma cholinesterases

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34
Q

Succinylcholine : special considerations

A

Dont give if trauma within last 24 hours

Caution in renal failure due to increased K+

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35
Q

Rocuronium (Zemuron) Dosing

A

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

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36
Q

Rocuronium MOA:

A

NMDR quaternary amniosteroid - competes for the cholinergic receptors at the motor endplate

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37
Q

Rocuronium onset :

A

45-60 seconds

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38
Q

Rocironium peak :

A

1-3 minutes

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39
Q

Rocuronium : DOA

A

15-150 minutes

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40
Q

Rocuronium metabolism

A

Hepatic

Renal

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41
Q

Rocuronium: special considerations

A

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)

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42
Q

Pancuronium (pavulon) dosing

A

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

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43
Q

Pancuromium MOA

A

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

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44
Q

Pancuromium onset

A

1-3 minutes

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45
Q

Pancuromium peak

A

3-5 minutes

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46
Q

Pan ironing DOA

A

40-65 minutes

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47
Q

Pancruonium metabolism

A

Hepatic

Renal - heavily dependent on kidneys for excretion

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48
Q

Pancuromium : special considerations

A

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.

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49
Q

Vecuronium dosing (norcuron)

A

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

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50
Q

Vecuronium MOA

A

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.

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51
Q

Vecuronium onset

A
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52
Q

Vecuronium peak

A

3-5 min

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53
Q

Vecuronium DOA

A

25-30 minutes.

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54
Q

Vecuronium metabolism

A

Hepatic. Small amount in kidneys.

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55
Q

Vecuronium : special considerations

A

Reconstitute with sterile water

Gtt 20 mg/ 100 ml for 0.2mg/ml

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56
Q

Atracurium dosing ( tracrium)

A

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

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57
Q

Atracurium MOA

A

NDMR that competes at cholinergic receptors at the motor end plate.

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58
Q

Atracurium onset

A
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59
Q

Atracurium peak

A

3-5 minutes

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60
Q

Atracurium DOA

A

20-35 minutes

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61
Q

Atracurium elimination

A

Hoffmann elimination - independent of renal elimination.

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62
Q

Atracurium : special considerations.

A

Laudenosine is a metabolite of Atracurium that can cause seizures.

Also causes histamine release and vasodilation/ tachycardia / bronchoscope, / laryngoscopes

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63
Q

Cisatracurium (nimbex) dosing

A

0.15-0.2 mg/kg

Bolus: 0.02-0.1 mg/kg

Gtt: 1-5 mcg/kg/min

Priming 1-2 mg

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64
Q

Cisatracurium MOA:

A

Isomer of Atracurium. Competes for cholinergic receptors at the motor end plate

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65
Q

Cisatracurium onset

A

90-120 seconds

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66
Q

Cisatracurium peak

A

3-7 minutes

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67
Q

Cisatracurium DOA:

A

20-35 minutes

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68
Q

Cisatracurium elimination

A

Hoffmann elimination

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69
Q

Cisatracurium : special considerations

A

Laudenosine is a metabolite of that can cause seizures

Histamine release can cause tachycardia hypotension broncho and laryngospasm.

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70
Q

Neostigmine dosing

A

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.

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71
Q

Neostigmine MOA

A

Reversal of NDMRs / treatment of MG, post op illeus, and urinary retention.

Inhibits hydrolysis of acetylcholine by inhibiting acetylcholinesterase at the esteric site

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72
Q

Neostigmine onset

A

3-5 minutes

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73
Q

Neostigmine peak

A

3-14 minutes

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74
Q

Neostigmine DOA

A

40-60 minutes.

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75
Q

Neostigmine metabolism

A

Hepatic / plasma esterases

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76
Q

Neostigmine : special considerations

A

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.

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77
Q

Pyridostigmine dosing

A

0.25 mg/kg

MAX DOSE 30 mg

Myasthenia Gravis tx : 60-1500 mg / day (avg 600 mg/day)

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78
Q

Pyridostigmine MOA

A

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.

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79
Q

Pyridostigmine Onset

A

3-8 minutes

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80
Q

Pyridostigmine Peak

A

5-10 minutes

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81
Q

Pyridostigmine DOA

A

30 min- 5hr.

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82
Q

Pyridostigmine metabolism

A

Plasma esterases

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83
Q

Pyridostigmine : special considerations

A

Give to reverse atropine toxicity

Crosses BBB (tertiary amine! )

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84
Q

Scopolamine dosing

A

IV: 0.3-0.6 mg

Patch delivers 1.5 mg (1mg over 72 hr)

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85
Q

Scopolamine MOA

A

Tertiary amine

Management of N/V associated with ovoid anesthesia /GA or motion sickness

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86
Q

Scopolamine onset

A

IV: immediate

TD:30 min.

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87
Q

Scopolamine peak

A

IV: 50-80 min
TD: 3 hr

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88
Q

Scopolamine DOA

A

IV:2 hr

TD : 3 days

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89
Q

Scopolamine metabolism

A

Hepatic/ renal

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90
Q

Scopolamine : special considerations

A

Lipid solubility allows for transdermal rout as well as greater CNS effects than atropine

Can cause sedation and amnesia

Crosses BBB.

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91
Q

Glycopyrrolate (robinul) dosing

A

0.2 mg for each 1 mg of Neo or 5 mg of Pyridostigmine

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92
Q

Glycopyrrolate MOA

A

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.

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93
Q

Glycopyrrolate Onset

A
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94
Q

Glycopyrrolate peak

A

5 minutes

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95
Q

Glycopyrrolate DOA

A

Vagal blockade : 2-3 hr.

Antisialogogue effect : 7 hr.

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96
Q

Glycopyrrolate metabolism

A

85% excreted unchanged in the urine within 48 hours.

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97
Q

Glycopyrrolate : special considerations

A

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.

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98
Q

Hydromorphone dosing

A

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

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99
Q

Hydromorphone MOA :

A

Opiate agonist that is a hydrogenated ketone Of morphine

7x more potent than morphine

Effects on CNS and organs containing smooth muscle.

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100
Q

Hydromorphone onset

A

IV:

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101
Q

Hydromorphone peak

A

IV: 5-20 minutes

Epidural : 30 minutes

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102
Q

Hydromorphone DOA

A

IV:2-4 hr

Epidural : 10-16 hr.

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103
Q

Hydromorphone metabolism

A

Hepatic

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104
Q

Hydromorphone : special considerations

A

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!

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105
Q

Remifentanyl (ultiva) Dosing

A

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.

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106
Q

Remifentanyl MOA

A

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.

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107
Q

Remifentanyl onset

A

30seconds.

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108
Q

Remifentanyl peak

A

3-5 min

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109
Q

Remifentanyl DOA

A

5-10 minutes

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110
Q

Remifentanyl metabolism

A

Plasma / tissue esterases

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111
Q

Remifentanyl : special considerations

A

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.

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112
Q

Morphine (duramorph) dosing

A

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.

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113
Q

Morphine MOA:

A

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

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114
Q

Morphine onset

A

IV:

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115
Q

Morphine peak

A

IV: 5-20 min

Epidural / spinal : 90 min.

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116
Q

Morphine DOA

A

IV:2-7 hr.

Epidural / spinal 6-24 hr.

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117
Q

Morphine ,metabolism

A

Hepatic / renal

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118
Q

Morphine : special considerations.

A

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.

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119
Q

Sufentanyl citrate: (sufenta) dosing

A

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

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120
Q

Sufentanil citrate : MOA

A

Thienyl analogue of fentanyl with 5-7 x the analgesia potency.

Attenuates the hemodynamics response to DVL and surgical manipulation

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121
Q

Sufentanil citrate : onset

A

IV :1-3 min

Epidural / spinal :4-10 min

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122
Q

Sufentanil citrate : peak

A

IV :3-5 min

Epidural / spinal :

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123
Q

Sufentanil citrate : DOA

A

IV: 20-45 minutes

Epidural / spinal : 2-4 hr.

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124
Q

Sufentanil citrate : metabolism

A

Hepatic

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125
Q

Sufentanil citrate : special considerations

A

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.

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126
Q

Meperidine (Demerol) : dosing

A

Analgesic : 25-100 mg

Post op shivering : 12.5-25 mg

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127
Q

Meperidine : MOA

A

Premedication , analgesia , and tx of post op shivering.

Synthetic opioid agonist 1/10th as potent as morphine.

Direct myocardial depressant at high doses.

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128
Q

Meperidine : onset

A
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129
Q

Meperidine : peak

A

5-20 minutes

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130
Q

Meperidine : DOA

A

2-4 hr

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131
Q

Meperidine : metabolism

A

Hepatic

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132
Q

Meperidine : special considerations.

A

Active metabolite - NORMEPERIDINE - can Cause seizures!!!

DO NOT GIVE TO A PATIENT TAKING AN MAOI.

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133
Q

Ketorlac (toradol) : dosing

A

15-30 mg QID

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134
Q

Ketorlac: MOA

A

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.

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135
Q

Ketorlac: onset

A
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136
Q

Ketorlac : peak

A

1-3 hours.

137
Q

Ketorlac : DOA

A

3-7 hours.

138
Q

Ketorlac : metabolism

A

Hepatic / renal

91% renal dependent.

139
Q

Ketorlac: special considerations.

A

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
Q

Narcan (naloxone) : dosing

A
  1. 5-1mcg/kg/ min Q3-5 min.
  2. 04-0.4 mg

Gtt : 4-5 mcg/kg/hr

141
Q

Narcan : MOA

A

Pure opioid antagonist - competes and displaces narcotics at receptor sites

Reverses all narcotic properties including analgesia

Can cause tachycardia , HTN, plum edema.

142
Q

Narcan: onset

A

1-2 minutes

143
Q

Narcan: peak

A

5-15 minutes.

144
Q

Narcan : DOA

A

1-4 hours.

145
Q

Narcan : metabolism

A

Hepatic

Conjugation with glucuronic acid to form naloxone 3 glucuronide

146
Q

Narcan: special considerations.

A

May antagonize the anti hypertensive effects of clonidine

147
Q

Flumazinil (romazicon) : dosing

A

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
Q

Flumazinil : MOA

A

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
Q

Flumazinil : onset

A

1-2 minutes

150
Q

Flumazinil : peak

A

2-10 minutes.

151
Q

Flumazinil : DOA

A

45-90 minutes.

152
Q

Flumazinil : metabolism

A

Hepatic

153
Q

Flumazinil : special considerations

A

Precipitates Benzo withdrawal

Increased risk of seizures in those with concurrent tricyclics OD. May provoke panic attack

154
Q

Etomidate: dosing

A

0.1- 0.4mg/ kg

Gtt : 0.25-1.0 mg/min

155
Q

Etomidate: MOA

A

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
Q

Etomodate : onset

A

30-60 seconds.

157
Q

Etomidate : peak

A

1 minute

158
Q

Etomidate : DOA

A

3-10 minutes.

159
Q

Etomidate : metabolism

A

Hepatic

160
Q

Etomidate: special considerations.

A

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
Q

Ketamine : dosing

A

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
Q

Ketamine : MOA

A

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
Q

Ketamine : onset

A
164
Q

Ketamine : peak

A

1 minute

165
Q

Ketamine : DOA

A

5-15 minutes.

166
Q

Ketamine metabolism

A

Hepatic

167
Q

Ketamine : special considerations.

A

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
Q

Esmolol : dosing (BREVIBLOC)

A

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
Q

Esmolol : MOA

A

Treatment of SVT and HTN.

Cardio selective beta blocker with rapid onset and short DOA.

At high doses can affect beta 2 rcp.

170
Q

Esmolol : onset

A

1-2 min

171
Q

Esmolol : peak

A

5 min

172
Q

Esmolol : DOA

A

10-20 minutes.

173
Q

Esmolol : metabolism

A

Hydrolized BY RBC esterases

174
Q

Esmolol Special considerations

A

None

175
Q

Hydralazine : dosing (APRESOLINE)

A
  1. 1-2 mg/kg

2. 5-40 mg.

176
Q

Hydralazine MOA

A

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
Q

Hydralazine onset

A

5-20 min

178
Q

Hydralazine peak

A

10-80 min

179
Q

Hydralazine DOA

A

2-4 hours.

180
Q

Hydralazine metabolisim

A

Hepatic acetylation

Higher doses requires in rapid acetylators.

181
Q

Hydralazine special considerations

A

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
Q

Labatelol (NORMODYNE TRANDATE) : dosing

A

2.5-20 mg over 2 min.

Gtt : 0.5-2 mg/min

Max cumulative dose 1-4 mg/kg.

183
Q

Labatelol MOA

A

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
Q

Labatelol : onset

A

2-5 minutes

185
Q

Labatelol peak action

A

5-15 min

186
Q

Labatelol DOA

A

2-4 hours

187
Q

Labatelol metabolism

A

Hepatic

188
Q

Labatelol : special considerations

A

Crosses placenta

189
Q

Metoprolol : dosing (LOPRESSOR)

A

2.5-5 mg

MAX DOSE :15 mg

190
Q

Metoprolol : MOA

A

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
Q

Metoprolol : onset

A

Immediate

192
Q

Metoprolol : peak

A

20 min

193
Q

Metoprolol DOA

A

5-8 hours

194
Q

Metoprolol metabolism

A

Hepatic

195
Q

Metoprolol special considerations

A

Broncho spasm at high doses. Abrupt withdrawal can lead to rebound HTN and tachycardia dt up regulation of rcp.

196
Q

Methyl dopa (ALDOMET) : dosing

A

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
Q

Methyl dopa : MOA

A

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
Q

Methyl dopa : onset

A

1-2 hr.

199
Q

Methyl dopa : peak

A

4-6 hours

200
Q

Methyl dopa : DOA

A

10-16 hours

201
Q

Methyl dopa metabolism:

A

Hepatic

202
Q

Methyl dopa : special considerations

A

Crosses BBB. Contraindicated in hepatic dz. first line therapy for PIH.

Reduces the MAC of VAs.

203
Q

Phenylepherine : dosing

A

0.5-1 mcg/kg

50-100 mcg bolus

204
Q

Phenylephrine MOA

A

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
Q

Phenylephrine onset

A
206
Q

Phenylephrine peak

A
207
Q

Phenylephrine DOA

A

15-20 min

208
Q

Phenylephrine metabolism

A

Hepatic

209
Q

Phenylephrine special considerations

A

Tachyphylaxis may occur

210
Q

Ephedrine : dosing

A

2.5- 10 mg

MAX : 150 mg / 24 hr.

211
Q

Ephedrine MOA

A

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
Q

Ephedrine onset

A

Immediate

213
Q

Ephedrine peak

A

2-5 minutes

214
Q

Ephedrine DOA

A

10-60 min.

215
Q

Ephedrine metabolism

A

Hepatic / renal

216
Q

Ephedrine special considerations

A

Tachyphylaxis may occur once catcholemine stores are depleted.

217
Q

Ondansetron dosing (ZOFRAN)

A

4 mg IV/ PO Q4-8h.

218
Q

ZOFRAN MOA

A

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
Q

ZOFRAN onset

A
220
Q

ZOFRAN peak

A

Variable

221
Q

ZOFRAN DOA

A

12-24 hours

222
Q

ZOFRAN metabolism

A

Hepatic

223
Q

ZOFRAN special considerations

A

Expensive.

224
Q

Metroclopramide dosing (REGLAN)

A

10 mg IV

Peds; 0.1 mg/kg.

225
Q

REGLAN MOA

A

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
Q

REGLAN onset

A

1-3 min

227
Q

REGLAN peak

A
228
Q

REGLAN DOA

A

1-2 hours

229
Q

REGLAN metabolism

A

Renal

230
Q

REGLAN special considerations.

A

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
Q

Diphenhydramine dosing (Benadryl)

A

10-50 mg IV
25-50 PO
Max dose is 400 mg.

232
Q

Benadryl MOA

A

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
Q

Benadryl onset

A
234
Q

Benadryl peak

A

1-3 hr

235
Q

Benadryl DOA

A

4-6 hr

236
Q

Benadryl metabolism

A

Hepatic

237
Q

Benadryl special considerations

A

Sry mouth, pvc,photophobia, mydriasis, sedation.

Give slowly IV as you can see exhibitory CNS effects.

238
Q

Famotadine dosing (PEPCID)

A

20mg IV q12 hr.

239
Q

Pepcid MOA

A

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
Q

Pepcid onset

A
241
Q

Pepcid peak

A

30min - 3 hr.

242
Q

Pepcid DOA

A

10-12 hr

243
Q

Pepcid metabolism

A

Renal

244
Q

Pepcid special considerations.

A

DOES NOT CHANGE THE PH OD GASTRIC CONTENTS PRESENT UPON TIME OF ADMINISTRATION.

very effective when used with an h1 antagonists

245
Q

Promethazine hydrochloride dosing (PHENERGAN)

A

12.5-50 mg q4-6h

246
Q

PHENERGAN MOA

A

Phenothiazine derivative does not possess neuroleptic or antipsychotic activity.

H1 rcp antagonist with sedative , antiemetic, anticholinergic,and anti motion sickness effects.

247
Q

PHENERGAN onset.

A

2-5 minutes

248
Q

PHENERGAN peak

A
249
Q

PHENERGAN DOA

A

2-8 hr

250
Q

PHENERGAN metabolism

A

Hepatic

251
Q

PHENERGAN special considerations

A

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
Q

Ranitidine dosing (ZANTAC)

A

50 mg q1-2hr. Give at HS and 2 hr prior to surgery.

150-300 mg PO.

253
Q

Zantac MOA

A

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
Q

Zantac onset

A
255
Q

Zantac peak

A

1-2 hr

256
Q

Zantac DOA

A

6-8 hr

257
Q

Zantac metabolism

A

Hepatic

258
Q

Zantac special considerations

A

None

259
Q

Dexamethasone dosing (DECADRON)

A

0.2 mg/kg

max 12 mg.

260
Q

DECADRON MOA

A

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
Q

DECADRON onset

A

1-2 minutes

262
Q

DECADRON peak

A

12-24 hr

263
Q

DECADRON DOA

A

36-54 hr

264
Q

DECADRON metabolism

A

Hepatic

265
Q

DECADRON special considerations

A

Does. It cause sodium or water rentention.

Caution in DM

HPA Axis suppression

266
Q

Furosemide dosing (LASIX)

A

0.1-1 mg/kg

10-40 mg IV bolus

267
Q

LASIX MOA

A

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
Q

LASIX onset

A

5-15 minutes

269
Q

LASIX peak

A

20-60 minutes

270
Q

LASIX DOA

A

2 hr

271
Q

LASIX metabolism

A

Renal

272
Q

LASIX special considerations

A

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
Q

Doxapram dosing (DOXPRAM)

A

0.5-1.5mg/kg may repeat Q5 min

Max dose 2mg/kg

274
Q

Doxapram MOA

A

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
Q

Doxapram onset

A

20-40’seconds

276
Q

Doxapram peak

A

1-2 min

277
Q

Doxapram DOA

A

5-12 minutes

278
Q

Doxapram metabolism

A

Hepatic

279
Q

Doxapram special considerations

A

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
Q

Mannitol dosing (OSMITROL)

A

0.25-1 g/kg

281
Q

Mannitol MOA

A

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
Q

Mannitol onset

A

Dieresis :15-60 min

Decrease ICP :

283
Q

Mannitol peak

A

Diuretic :1 hr

Decrease ICP –

Decrease IOP 1-2 hr.

284
Q

Mannitol DOA

A

Diuretic 3-8 hr.

Decrease ICP :3-8 hr

Decrease IOP : 4-6 hr.

285
Q

Mannitol metabolism

A

Renal

286
Q

Mannitol special considerations

A

Can worse. Or Induce pulmonary edema, intracranial hemorrhage, hypertension or rebound increase in ICP.

287
Q

Methylene blue dosing

A

1-2 mg/kg

288
Q

Methylene blue MOA

A

Treatment of drug induced methomoglobinemia,dye effect to delineate body structure and fistula and confirm rupture of amniotic membranes. Urinary antiseptic.

289
Q

Methylene blue onset

A

Immediate

290
Q

Methylene blue peak

A
291
Q

Methylene blue DOA

A

Varies

292
Q

Methylene blue metabolism

A

Renal

293
Q

Methylene blue special considerations

A

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
Q

Indigo carmine dosing

A

40 mg

295
Q

Indigo carmine MOA

A

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
Q

Fentanyl dosing

A 
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
Q

Indigo carmine metabolism

A

Appears in the urine within 10 minutes of injection

Biological t1/2 4-5 min.

298
Q

Indigo carmine special considerations

A

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
Q

Oxytocin dosing

A

0.5- 10 u/ min
10-40 u/1000 l
10 u/250 cc NS.

300
Q

Oxytocin MOA

A

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
Q

Oxytocin onset

A

IV immediate

IM: 3-5 min.

302
Q

Oxytocin DOA

A

IV : 1 hr

IM : 2-3 hr.

303
Q

Oxytocin metabolism

A

Hepatic / renal

304
Q

Oxytocin. Special considerations

A

May cause HTN. Arrhythmia and transient hypotension and reflex tachycardia fetal distress and water retention.

305
Q

Protamine sulfate dosing

A

1mg/ 100 units of heparin

306
Q

Protamine MOA

A

Reversal of heparin/ anti coagulation OD. The positive charged alkaline protamine binds to the negative charge of heparin rendering it Inactive.

307
Q

Nitrous Oxide : Dosing

A

MAC 10% (104)

BG : 0.46

308
Q

Nitrous Oxide MOA

A

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
Q

Nitrous oxide metabolism

A

Exhalation

310
Q

Nitrous Oxide Special considerations:

A

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
Q

Desfulrane Dosing :

A

MAC : 6.6
BG: 0.42
VP 669

312
Q

Desfulrane MOA :

A

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
Q

Desflurane Metabolism

A

exhalation

15-20% hepatic

314
Q

Desflurane Special considerations:

A

may cause coughing, breath holding, salivation, and layrngospasm.

Avoid as an induction agent.

315
Q

Sevoflurane Dosing:

A

MAC 2.0
BG 0.65
VP 170

316
Q

Sevoflurane MOA

A

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
Q

Sevoflurane Metabolism:

A

Exhalation

3 % hepatic

318
Q

Sevoflurane Special considerations:

A

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
Q

Isoflurane Dosing:

A

MAC : 1.17
BG 1.4
VP 240

320
Q

Isoflurane MOA

A

Produces general anesthesia through interactions with the CNS cellular membranes.

volatile agent, nonflammable halogenated methyl ethyl ether.

321
Q

Isoflurane metabolism

A

Exhalation

0.2% hepatic

322
Q

Isoflurane Special considerations

A

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
Q

Nitrous Oxide : Dosing

A

MAC 10% (104)

BG : 0.46

324
Q

Nitrous Oxide MOA

A

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
Q

Nitrous oxide metabolism

A

Exhalation

326
Q

Nitrous Oxide Special considerations:

A

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
Q

Desfulrane Dosing :

A

MAC : 6.6
BG: 0.42
VP 669

328
Q

Desfulrane MOA :

A

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
Q

Desflurane Metabolism

A

exhalation

15-20% hepatic

330
Q

Desflurane Special considerations:

A

may cause coughing, breath holding, salivation, and layrngospasm.

Avoid as an induction agent.

331
Q

Sevoflurane Dosing:

A

MAC 2.0
BG 0.65
VP 170

332
Q

Sevoflurane MOA

A

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
Q

Sevoflurane Metabolism:

A

Exhalation

3 % hepatic

334
Q

Sevoflurane Special considerations:

A

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
Q

Isoflurane Dosing:

A

MAC : 1.17
BG 1.4
VP 240

336
Q

Isoflurane MOA

A

Produces general anesthesia through interactions with the CNS cellular membranes.

volatile agent, nonflammable halogenated methyl ethyl ether.

337
Q

Isoflurane metabolism

A

Exhalation

0.2% hepatic

338
Q

Isoflurane Special considerations

A

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.

Anesthesia (1 decks)

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