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PHRM 864 > Critical Care > Flashcards

Critical Care Flashcards

1
Q

absorption problems in ICU

A
  • gastric emptying / motility
  • enteral tube interactions (drugs)
  • GI injury / disease
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2
Q

criticially ill patients Vd of hydrophillic drugs

A

high because theyre pumped with fluids

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3
Q

hydrophillic drugs that are better absorbed with larger Vd

A

aminoglycosides

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4
Q

album and protein binding in critically ill patients is

A

decreased due to underlying stress

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5
Q

protein binding of what drugs is increased in critical illness

A

drugs binding alpha 1 acid glycoprotein

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6
Q

how is hepatic metabolism in critically ill pts

A

decreased

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7
Q

disease states associated with decreased renal elimination

A

shock
sepsis
organ failure
nephrotoxic drugs

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8
Q

disease states that may have increased renal elimination

A

burns
trauma

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9
Q

how do we detect changes in renal function

A

urine output

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10
Q

what is sepsis

A

life threatening organ dysfunction caused by response to infection

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11
Q

what can happen in sepsis

A

immune dysregulation
coagulation and thrombosis

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12
Q

what is most common pathogen that sepsis happens from

A

bacterial

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13
Q

most common sites of sepsis infection

A

blood, lungs, urinary tract

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14
Q

treatment of sepsis

A

supportive therapy
broad spectrum IV antibiotics

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15
Q

symptoms of septic shock

A

cardiovascular collpase
hypotension

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16
Q

drug classes given in septic shock

A

fluids
vasopressors
corticosteroids

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17
Q

fluids given in septic shock

A

crystalloids / colloids

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18
Q

vasopressors used in septic shock

A

norepinephrine preferred
can add vasopressin

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19
Q

goal mean arterial pressure in septic shock (MAP)

A

> 65 mm Hg

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20
Q

corticosteroid used in septic shock

A

IV hydrocortisone

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21
Q

what is acute respiratory distress syndrome (ARDS)

A

life threatening respiratory failure categorized by lung injury
25-40% mortality

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22
Q

risks for ARDS

A

sepsis, pnemonia, trauma, aspiration

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23
Q

treatment for ARDS

A

mechanical vent
corticosteroids dec mortality

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23
Q

FAST HUGS BID

A

F - feeding/fluids
A - analgesia
S - sedation
T - thrombophrophylaxis
H - HOB elevation
U - ulcer prophylaxis
G - glycemic control
S - spontaneous awakening trial
B - bowel regimen
I - indwelling catheters
D - de-escalation antiobiotics / delirium

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24
Q

risk factors for VTE

A

immobility
trauma, surgery, sepsis
cancer, obesity, VTE hx

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25
Q

who should receive VTE prophylaxis

A

everyone except:
- mobile
- very low risk
- contraindications

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26
Q

what do we use for thromboprophylaxis

A

UFH or LMWH
LMWH preferred

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27
Q

what if patient has contraindication to pharmacologic thromboprophylaxis

A

mechanical prophylaxis

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28
Q

UFH dose prophylaxis

A

5000 units SC q8h or q12h
no renal adjustments

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29
Q

enoxaparin dose prophylaxis

A

30 mg SC q12h
40 mg SC q24h
CrCl < 30: 30 mg SC q24h

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30
Q

monitoring for UFH and enoxaparin

A

bleeding
CBC (platelets for HIT)

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31
Q

stress ulcer happens how

A

lesions on mucosal layer of the GI caused by stress

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32
Q

are stress ulcers clinically importnat

A

not always, if bleeding important its deadly

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33
Q

risk factors for stress ulcers

A

shock
coagulopathy
liver disease
neurotrauma
burn
MECHANICAL VENTILATION
drugs

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34
Q

drugs with high risk for ulcer

A

NSAIDS, antiplatelets, anticoagulants

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35
Q

what do we use for stress ulcer prophylaxis (class)

A

PPI or H2RA
PPI may be better

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36
Q

H2RA drugs used for stress ulcer prophylaxis

A

famotidine
ranitidine

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37
Q

adverse reactions of H2RAs

A

potential thrombocytopenia

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38
Q

when do we d/c stress ulcer prophylaxis

A

once risk factor gone

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39
Q

side effect of PPI

A

increase risk c diff
nosocomial pnemonia

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40
Q

dosing consideration for H2RAs

A

renal adjustment

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41
Q

why do we keep glycemic control in ICU

A

hyperglycemia increased mortality
pts with stress / TPN can get even w/o diabetes

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42
Q

BG target in ICU

A

144-180

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43
Q

what kind of insulin should we not use in ICU

A

long acting

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44
Q

what does spontaneous awakening trial help prevent

A

oversedation
promotes weaning from mechanical vent

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45
Q

what is succinylcholine and how does it work

A

depolarizing NMBA
binds ACh receptor and prevents ACh from binding so muscle contraction can’t occur
- may cause initial muscle contraction

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46
Q

dose onset and duration of succinylcholine

A

1.5 mg/kg
onset: 1 min
duration: 3-5 min

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47
Q

how is succinylcholine eliminated

A

neither renal or hepatic

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48
Q

what is succinylcholine used for

A

rapid intubation
NOT sustained neuromuscular blockade

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49
Q

what can we preadminister before succinylcholine so we don’t have initial contractions

A

non-depolarizing NMBA imediatley prior

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50
Q

succinylcholine ADRs

A

apnea
hyperkalemia
muscle contractions
incr intracranial pressure
incr intraocular pressure

51
Q

succinylcholine contraindications

A

burn
crush victim
upper neuron disease (ALS)

52
Q

what are non-depolarizing NMBAs

A

competitively block ACh receptors
do not cause muscle contractions

53
Q

classes of non-depolarizing agents

A

aminosteroidal
benzylisoquinolinium

54
Q

reversal agents for non-depolarizing NMBAs

A

ACh esterase inhibs (stigmines)
suggamedex

55
Q

non-depolarizing NMBA ending

A

-oniums

56
Q

who gets non-depolarizing NMBAs in mechanical vent

A

not everyone
often in ARDS - continuous administration

57
Q

indications for NDNMBAs

A

mechanical vent ARDS common
contraindication to succ: burn, crunch, neuron dx
operative
increased intracranial pressure
hypothermia

58
Q

adverse effects of NDNMBAs

A

apnea
inadequate pain and sedation
prolonged paralysis
DVT
ocular dryness

59
Q

what must patients be on before sedative given

A

optimized on analgesia and sedative

60
Q

drug interaction with NMBAs

A

corticosteroids

61
Q

whats the efficacy endpoint in NMB

A

are we seeing improvement

62
Q

how do we monitor the toxicity endpoint in NMBAs

A

peripheral nerve stimulation, twitch monitor
more twiches = less suppression
4/4 < 75%
3/4 75%
2/4 80%
1/4 90%
0/4 100%

63
Q

how many twitches do we want to dose adjust to

A

1-2 twitches

64
Q

what is delirium

A

acute onset of cerebral dysfunction with
change in baseline mental status
inattention
disorganized thinking
altered level of consciousness

65
Q

cardinal feautre of delirium

A

disturbed level of consciousness/attention
and
change in cognition or development hallucinations /delusions

66
Q

gold standard for pain if pt can communicate

A

what the pt says

67
Q

pain scale if pt cant commuicate

A

behavioral pain scale (BPS)
critical care pain oversavation tool (CPOT)
proxy - caretaker suggestion

68
Q

what pain meds preferred for non-neuropathic pain

A

IV opioids, can cause sedation

69
Q

non-opioids used to decrease opioid requirement

A

tylenol
ketamine (post surgery)
gapapentin/pregabalin
NSAID - bleed risk tho

70
Q

how do we give opioids IV

A

bolus or continuous

71
Q

causes of agitation in ICU

A

pain
mechanical vent
hypoxia
hypotension
withdrawal EtOH, drugs
delirium

72
Q

nonpharm treatment of agitation

A

patient comfort
analgesia
reorientation
optimization of sleep environment

73
Q

who gets sedatives in agitation

A

adjunct for anxiety/agitation
non-pharm supplement
many on mechanical vent, not all

74
Q

what should we not use sedative for

A

restraint
coercion
discipline
convenience
retaliation
“you dont like them”

75
Q

pharm treatment of agitation can be given after what

A

analgesia and reversible physiollogic causes treated

76
Q

why is over sedation dangerous

A

longer time on vent
longer time in ICU
no neruological testing

77
Q

sedation goal

A

calm but arousable so can follow simple commands

78
Q

how do we assess sedation and titrate subjectively

A

richmond agitation sedation scale (RASS)
sedation agitation scale (SAS)

79
Q

how do we assess sedation for patients on a NMBA or if we cant use typical scales

A

bispectral index (BIS): EEG

80
Q

benzos used in ICU

A

lorazepam
midazolam

81
Q

benzos adverse effects

A

respiratory depression
withdrawal
prolonged sedation/duration
delirium association

82
Q

onset and duration of lorazepam

A

long duration
delayed onset
less titratable

83
Q

lorazepam elimination

A

not renally or hepatially eliminated
no dose accumulation

84
Q

IV formulation of lorazepam has what solvent

A

propylene glycol

85
Q

how can we detect prpylene glycol toxicity

A

calculate osm gap
high dose lorazepam

86
Q

lorazepam not a good choice if what

A

want to wake quickly

87
Q

midazolam metabolized how

A

CYP3A

88
Q

midazolam halflife and duration

A

short halflife
unpredicitible duration

89
Q

midazolam reccommended over loraZepam for what

A

quick sedation
short term use

90
Q

propofol onset and offset

A

quick onset
quick offset

91
Q

propofol given as what

A

infusion

92
Q

propofol popular in wht

A

surgery
general anesthesia
neurosurgery dec ICP

93
Q

propofol dosage form

A

emulsion
lipid vehicle
watch for hypertriglyceridemia
safe in egg/soy allergy

94
Q

adverse effects of propofol

A

apnea
hypotension
bradycardia
pain upon infusion
hypertriglyceridemia
propofol infusion syndrome
allergic reactions

95
Q

what is propoofol infusion syndrome

A

acidosis
bradycardia
lipidemia
- associated with high mortality

96
Q

propofol not reccoemmended for who

A

high doses in peds

97
Q

what should we monitor in propofol

A

triglyerides after 48 hours
caloric intake - 1.1 kcal/mL
propofol infusion syndrome

98
Q

propofol affect on body

A

CNS depression

99
Q

dexmedetomidine class

A

alpha 2 agonist
decrease NE release in CNS

100
Q

dexmed level of sedation

A

light sedation, can wake pts up

101
Q

dexmed differences

A

some analgesia and dec opioid requirement
light sedation
anxiolysis like Benzos
no respiratory depression

102
Q

dexmed halflife

A

short, titratable

103
Q

dexmed elimination

A

hepatic, might have to dose reduce

104
Q

how do we administer dexmed

A

NO loading dose
just do infusion

105
Q

adverse effects with dexmed

A

bradycardia
hypotension
increase BP with rapid admin

106
Q

who should we not use dexmed in

A

hypovolemic
shock
hemodynamically unstable

107
Q

which sedative has least delirium

A

dexmed

108
Q

types of delirium

A

hyperactive - agitated
hypoactive - calm, sedated

109
Q

who gets delirium

A

80% of mechanical vent patients

110
Q

delirium can cause what after ICU

A

cognitive impairment
mortality maybe

111
Q

delirium risk factors

A

benzos use
blood transfusions
older age
dementia
severity of illness

112
Q

assessmnet scales used for delirium

A

ICDSC
CAM-ICU

113
Q

nonpharm way to decrease delirium

A

early mobilization
optimization of sleep
optimization of hearing/vision

114
Q

when do we use drugs in delirium

A

no prophylaxis
no routine treatment
short term with significant stress

115
Q

what drugs used in delirium

A

dexmed
haloperidol
atypical antipsychotics

116
Q

what drug can we used in delirium if we cant get them off the vent

A

dexmed

117
Q

haloperidol usea

A

mild sedation for agitation/delirium

118
Q

haloperidol dosing

A

NO continuous infusion
every 1 hour boluses

119
Q

haloperidol risk

A

QT prolongation - torsades
high dose IV
seizure
EPS
NMS

120
Q

atypical antipsychotics benefit in delirium

A

safety benefit
decreased risk of torsades but still could cause torasad and QT

121
Q

atypical antipsychotics used

A

risperidone
olanzapine
quetiapine

122
Q

adverse effects antipsychotics

A

Qt prolong
torasad

123
Q

which med used for stress with delirium

A

antipsychotics

124
Q

which med for acute agitaiton with delirium

A

haloperidol

PHRM 864 (23 decks)

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