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Appendix > ICU drugs > Flashcards

ICU drugs Flashcards

1
Q

This is the time dependency of a drug; relationship between the dose of a drug and its plasma/tissue concentration;

A

pharmacokinectics

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2
Q

What is pharmacokinectics?

A

relationship between dose of a drug and tissue concentration

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3
Q

This is what the body does to the drug; absorption, distribution, metabolism, and elimination;

A

pharmacokinectics

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4
Q

What is pharmacodynamics?

A

how plasma concentration of a drug exerts its effect on the body

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5
Q

This is what the drug does to the body;

A

pharmacodynamics

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6
Q

General anesthesia encompasses three parts:

A

unconsciousness (and amnesia)
analgesia
muscle relaxation

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7
Q

These drugs commonly used for unconsciousness and amnesia:

A

propofol
ketamine
etomidate

benzos/barbs

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8
Q

How does propofol work?

A

inhibits synaptic transmission thru its effects on GABA receptor

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9
Q

This drug is used for unconsciousness and is an alkylated phenol that inhibits synaptic transmission thru its effects on GABA receptor:

A

propofol

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10
Q

Why is propofol use attractive in smokers and asthmatics?

A

has bronchodilator properties

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11
Q

Why do we use propofol cautiously in pts with hypovolemia and CAD?

A

causes hypovolemia

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12
Q

Onset of action of propofol?

A

less than a minute

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13
Q

Propofol is metabolized by?

A

liver

cleared 60% by liver, 40% by kidneys

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14
Q

Half life of propofol?

A

biphasic

initially 40 minutes
terminal half life 4-7 hrs

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15
Q

Adverse reactions of propofol?

A 
local pain at injection site
hypotension
myoclonus
QT prolongation (rare)
green urine (rare)
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16
Q

Propofol safe in pregnancy?

A

yes

crosses the placenta

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17
Q

Propofol effects on the brain?

A

decrease in cerebral blood flow
decrease in intracranial pressure
decrease in cerebral oxygen consumption

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18
Q

Propofol use for status epilepticus?

A

used off label for status epilepticus

suppresses seizure activity

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19
Q

Propofol also exerts anti-emetic effects post-op, how?

A

depresses chemoreceptor trigger zone and vagal nuclei

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20
Q

Cardiovascular effects of propofol?

A

causes vasodilation by inhibitis SNS vasoconstriction

can cause hypotension when given as a bolus

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21
Q

What is PRIS?

A

propofol infusion syndrome

rare side effect of prolonged prop infusion (>4 mg/kg/hr >24 hrs)

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22
Q

Clinical side effects of PRIS?

A

metabolic acidosis
hyperkalemia
hyperlipidemia
rhabdomyolysis

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23
Q

Onset of PRIS?

A

usually within 4 days of initial treatment

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24
Q

How do we manage PRIS?

A

discontinue prop

supportive care

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25
Q

Mortality of PRIS?

A

33%

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26
Q

Most commonly used IV benzos?

A

diazepam
lorazepam
midazolam

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27
Q

What do we use benzos for?

A

anxiety and amnesia

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28
Q

MOA of benzos?

A

inhibit synaptic transmission at GABA receptor

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29
Q

Can cause hyperlipidemia, pancreatitis, and local injection site pain;

A

prop

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30
Q

Does propofol have analgesic effects?

A

NO

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31
Q

Main disadvantages of prolonged propofol use?

A

high cost

dose-related hypotension

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32
Q

Mechanism of this syndrome thought to be decreased fatty acid metabolism coupled with damage to mitochondria resulting in cardiac and peripheral myocyte dysfunction:

A

PRIS

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33
Q

Do benzos have analgesic effects?

A

NO

they are sedative anxiolytic

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34
Q

3 main benzos?

A

diazepam
lorazepam
midazolam

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35
Q

Diazepam AKA?

A

valium

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36
Q

How do benzos work?

A

increase frequency of Cl channel opening at GABA-A receptors

neuron becomes hyper-polarized, reduced neuron excitability

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37
Q

This benzo has short onset of action and short half-life,;

A

diazepam (valium)

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38
Q

Dose of diazepam (valium) for anxiety?

A

PO: 2-10 mg 2-4x/day
IV: 2-10 mg Q 3-4 hrs

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39
Q

Lorazepam AKA?

A

ativan

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40
Q

ATIVAN AKA?

A

lorazepam

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41
Q

This benzo has slow onset, intermediate half life and most useful for medium to long-term sedation:

A

lorazepam (ativan)

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42
Q

Lorazepam and the elderly?

A

can accumulate in older pts with renal and hepatic dysfunction causing prolonged sedation

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43
Q

Midazolam AKA?

A

versed

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44
Q

Benzo of choice for acutely agitated pts?

A

midazolam (versed)

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45
Q

Rapid onset, short acting benzo?

A

midazolam (versed)

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46
Q

Benzos when used with opioids tend to cause what?

A

respiratory depression

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47
Q

This is an imidazole derivative used to IV induction?

A

etomidate

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48
Q

Etomidate is rapidly and completely hydrolized to inactive metabolites, thus;

A

results in rapid awakening

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49
Q

Where does etomidate work?

A

GABA receptor

50
Q

Effect of etomidate on BP and HR?

A

very iittle compared to propofol

51
Q

What does ketamine do?

A

produces amnesia + analgesia

52
Q

MOA of ketamine?

A

blocks NMDA receptors

53
Q

What can ketamine cause in pts with CAD?

A

can increase HR and BP and cause ischemia in pts with CAD

54
Q

Why is ketamine useful in asthmatic pts?

A

direct bronchodilator effect

55
Q

Half life of ketamine?

A

10-15 mins

56
Q

Ketamine elimination depends on?

A

liver CYP450 metabolism

57
Q

Most common side effects of ketamine?

A

nausea/vomiting

58
Q

Do we use ketamine in head trauma?

A

NO

causes increased intracranial pressure

59
Q

IV NSAID that produces analgesia by blocking COX:

A

ketorloac

60
Q

Ketorolac blocks what?

A

COX-1 & COX-2

61
Q

Side effects of ketorolac?

A

gastric bleeding
platelet dysfunction
liver/kidney damage

62
Q

Analgesic and anti-pyretic that acts on CNS:

A

IV acetaminophen

63
Q

Site of action of IV acetaminophen?

A

CNS

not peripherally

64
Q

Addition of benzos to ketamine infusion has been shown to decrease what side effects?

A

delirium and hallucinations assc w/ketamine

65
Q

What is dexmedetomidine?

A

sedative with analgesic properties

66
Q

MOA of dexmedetomidine?

A

a2-adrenergic agonist

67
Q

Side effects of dexmedetomidine?

A

hypotension

bradycardia

68
Q

What are the 3 opioids used in ICU setting?

A

fentanyl
morphine
hydromorphone

69
Q

Advantages of fentanyl over morphine?

A

more rapid onset of action (600x more lipid soluble)

less risk of hypotension (fentanyl does not cause histamine release)

fent does not have active metabolites

70
Q

Opioids are primarily metabolized in the ?

A

liver

and metabolites excreted in urine

71
Q

Maintenance dose of morphine should be adjusted to 50% in pts with renal failure, why?

A

MS has several active metabolites that accumulate in the kidney

72
Q

Does fentanyl need to be adjusted for pts with renal failure?

A

no, it does not have metabolites

73
Q

How does MS cause hypotension?

A

promotes release of histamine

causes systemic vasodilation

74
Q

Onset of morphine?

A

5-10 minutes

75
Q

Onset of fentanyl?

A

1-2 minutes

76
Q

Why is fentanyl better than morphine?

A

more lipid soluble

more rapid onset of action

no active metabolites

no need for renal adjustment

no histamine release–> no hypotension

77
Q

Advantages of hydromorphone over morphine?

A

hydromorphone does not cause histamine release

does not need to be adjusted in renal failure

78
Q

Meperidine (demerol) is an opioid analgesic no longer used in ICU, why?

A

potential for neurotoxicity

normeperidine is a metabolite that causes CNS excitation, myoclonus, delirium

79
Q

Cardiovascular effects of opioids?

A

decrease HR and BP due to decrease in SNS activity

BP responds to fluid boluses or pressor boluses

80
Q

Opioid effects in GI motility?

A

depressed GI motility via opioid receptors in GI tract

81
Q

How do opioids cause vomiting?

A

stimulate chemoreceptor trigger zone

82
Q

Why are IV doses of ketorlac preferred over IM?

A

IM doses can cause hematomas

83
Q

Recommended dosage of ketorolac?

A

30 mg IV Q 6 hrs

reduce it to 15 mg IV Q 6 hrs for elderly or pts with body weight <50kg

84
Q

Adverse rxns with ketorolac?

A

gastric mucosal injury

upper GI bleed

renal function impairment

85
Q

Maximum daily dose of ibuprofen?

A

3.2 grams

86
Q

Maximum allowed dose of IV acetaminophen?

A

4 grams daily

***to prevent acetaminophen hepatoxicity

87
Q

How do we measure agitation in the ICU?

A

sedation agitation scale SAS

richmond agitation severity score RASS

88
Q

Preferred benzo for rapid sedation?

A

midazolem (versed)

89
Q

Onset of action of midazolem (versed)?

A

1-2 minutes due to its high lipid solubility

90
Q

Effects of midazolam (versed) last how long?

A

1-2 hrs (cleared rapidly from blood stream and taken avidly into tissue)

91
Q

Why do we limit midazolam (versed) infusion to less than 48 hrs?

A

prevents excessive sedation from drug accumulation in tissues

92
Q

Lorazepam (ativan) is a longer acting drug that midazolam, with effects up to?

A

6 hrs after a single dose

93
Q

The IV preparation of lorazepam contains what?

A

propylene glycol (a solvent which increased drug solubility)

its toxic when it accumulates

94
Q

Midazolam vs loparezepam, which has a metabolite?

A

midazolam has a metabolite –> cleared by the kidneys

95
Q

Why can changes in renal function affect midazolam?

A

has a metabolite that’s cleared by the kidneys

96
Q

Benzos are metabolized where?

A

liver

97
Q

Onset of action of midazolam vs lorazepam:

A

midazolam; 2-5 mins

lorazepam; 15-20 mins

98
Q

Toxicity assc with midazolam vs lorazepam:

A

midazolam; metabolite toxicity in renal impaired pts

lorazepam; propylene glycol toxicity

99
Q

What is propylene glycol toxicity seen with lorazepam?

A

IV preparations of lorazepam contain propylene glycol to enhance solubility

converted to lactic acid in the liver

causes; lactic acidosis, delirium, hypotension, multi-organ failure

100
Q

AN unexplained metabolic acidosis after > 24 hrs of lorazepam should prompt evaluation for?

A

serum lactate levels

raise suspicion for propylene glycol toxicity

101
Q

Onset of action of prop?

A

1-2 minutes

102
Q

Arousal after prop wears off?

A

10-15 mins

103
Q

Adverse effects of prop?

A

Hypotension
Hyperlipidemia
PRIS
respiratory depression

104
Q

Why can we use propofol in pts with intracranial injuries?

A

reduces intracranial pressures

allows for frequent arousal to check mental status

105
Q

How is propofol dose?

A

dose for IBW

not adjusted for renal failure or moderate liver failure

106
Q

Prop is suspended in what?

A

10% lipid emulsion to enhance plasma solubility

107
Q

Green urine with prop?

A

rare

due to phenolic metabolites

108
Q

Prop well known for producing what?

A

resp depression
hypotension

(should be ideally started in pt’s that are vented)

109
Q

How to avoid risk of PRIS?

A

avoid prop infusion rates > 5mg/kg/hr for more than 48 hrs

110
Q

This is an a2-receptor agonist that produces sedative, amnestic and mild analgesic effect;

A

dexmedtomidine

111
Q

Onset of action of dex?

A

5-10 mins

time to arousal; 6-10 mins

112
Q

Does dex cause respiratory depression like prop?

A

NO

113
Q

What’s so nice about dex?

A

patients can be aroused even though they’re sedated., don’t need to stop the infusion

when awake pt’s can communicate and follow commands

114
Q

Why is dex good for vented pts?

A

sedation can be continued from transition period from mechanical ventilation to spontaneous breathing

115
Q

Adverse effects of dex?

A

dose dependent decrease in HR, BP

116
Q

How does haldol work?

A

produces its sedative and antipsychotic effects by blocking dopamine receptors in brain

117
Q

Onset of haldol?

A

10-20 mins

lasts 3-4 hrs

118
Q

Does haldol cause respiratory depression?

A

NO

hypotension rare

119
Q

Extrapyramidal effects of haldol?

A

rare with IV administration (seen with PO)

rigidity, spasmodic rxns

120
Q

Neuroleptic malignant syndrome seen with what drug?

A

IV haldol

rare

(fever, muscle rigidity, rhabdo)

121
Q

Why do we avoid haldol in pts with prolonged qtC?

A

haldol prolongs Qtc

causes polymorphic vtach like torsades

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