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Therapeutics 3 > Critical Care > Flashcards

Critical Care Flashcards

1
Q

common causes of pain for ICU patients

A 
surgery
trauma
burns
cancer
procedural
etc.
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2
Q

Consequences of untreated pain

A 
insufficient sleep
psychiatric problems
PTSD
higher risk of chronic pain
lower QOL possible
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3
Q

IV fentanyl onset

A

1-2 minutes

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4
Q

IV Fentanyl metabolite

A

no metabolite

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5
Q

IV fentanyl accumulation

A

accumulates with hepatic impairment

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6
Q

IV Fentanyl other information

A

less hypotension than morphine

-infuse at 0.7-10 ug/kg/hr

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7
Q

IV Hydromorphone onset

A

5-15 minutes

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8
Q

IV hydromorphone metabolite

A

no active metabolite

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9
Q

IV hydromorphone accumulation

A

accumulates with hepatic and renal failure

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10
Q

IV hydromorphone other information

A

therapeutic option in patients tolerant to morphine and fentanyl

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11
Q

IV morphine onset

A

5-10 minutes

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12
Q

IV morphine metabolite

A

6- and 3- glucuronide

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13
Q

IV morphine accumulation

A

accumulates with hepatic and renal failure

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14
Q

IV morphine other information

A

causes histamine release!! pts will experience itching

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15
Q

role of APAP and NSAIDS in ICU

A

adjunctive pain therapy to reduce opioid need

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16
Q

how is neuropathic pain treated?

A

enterally administered gabapenten and carbamazepine in patients with sufficient GI absorption and motility

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17
Q

Underlying causes of agitation

A 
pain
delirium
hypoxemia
hypoglycemia
hypotension
withdrawal
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18
Q

what should be done to minimize agitation prior to administering sedatives

A

maintenance of patient comfort
provision of adequate analgesia
frequent reorientation
optimization of environment to maintain normal sleep patterns

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19
Q

Midazolam onset
metabolite accumulation
duration

A

O: 2-5 minutes
M: yes, in renal failure
D: 2h

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20
Q

Midazolam ADRs and monitoring

A

Respiratory depression

Hypotension

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21
Q

Midazolam DOC situation

A

when rapid onset is needed

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22
Q

Lorazepam Onset
Metabolite accumulation
duration

A

O: 15-20 minutes
M: none
D: 6-8 hours

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23
Q

Lorazepam ADRs and monitoring

A

respiratory depression
hypotension
propylene-glycol-related acidosis
nephrotoxicity

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24
Q

Lorazepam DOC situation

A

patients with hepatic impairment

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25
Q

Propofol onset
metabolite accumulation
duration

A

O: 1-2 minutes
M: none
D: 3-10 minutes

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26
Q

Propofol ADRs and monitoring

A 
pain on injection
hypotension
respiratory depression
hypertriglyceridemia
pancreatitis
allergic reaction
propofol-related infusion syndrome (deep sedation with propofol associated with significantly longer emergence times than with light sedation)
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27
Q

Propofol DOC situation

A

when rapid awakening is needed

to lower intracranial pressure

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28
Q

Dexmedetomidine onset
metabolite accumulation
duration

A

O: 5-10 minutes
M: none
D: 1-2 hours

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29
Q

Dexmedetomidine ADRs and monitoring

A

bradycardia
hypotension
hypertension with loading dose
loss of airway reflexes

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30
Q

Dexmedetomidine DOC situation

A

when minimal respiratory depression is desired

or pt needs to be easily arousable

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31
Q

all anti-agitation medication ADRs

A

respiratory depression

may build up in hepatic insufficiency

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32
Q

all opioid analgesic ADRs

A

respiratory depression
GI
CNS
hemodynamic effects

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33
Q

cardinal features of delirium

A

disturbed level of consciousness with reduced ability to focus, sustain, or shift attention
either a change in cognition or the development of a perceptual disturbance
other symptoms such as sleep disturbances, abnormal psychomotor activity, or emotional disturbances

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34
Q

risk factors of delirium

A

age
genetics
exposure to opioids or sedatives (iatrogenic factors)
prolonged physical restraint or immobilization (environmental factors)
Base line risk factors (pre-existing dementia, history of hypertension, history of alcoholism, or high severity of illness at administration)

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35
Q

outcomes associated with delirium

A

increased mortality
increased hospital LOS
increased cost of care
increased long-term cognitive impairment consistent with dementia-like state

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36
Q

appropriate treatment for delirium

A

atypical antipsychotics may reduce duration

no proof that haloperidol will do the same

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37
Q

neuromuscular blocker MOA

A

block ACh from bonding to receptors, blocking motor function

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38
Q

indications for NMB therapy

A

adult ICU patients to manage ventilation
treat muscle spasms
manage increased ICP
decrease O2 consumption
ONLY use when all other means have been tried with no success. for LIFE SAVING MEASURES or to PREVENT NEGATIVE PERMANENT CONSEQUENCES
**optimize sedatives and analgesics before therapy initiation

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39
Q

Pancuronium duration

A

long - 90 minutes

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40
Q

pancuronium elimination

A

mainly Renal

some hepatic

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41
Q

Pancuronium ADRs and monitoring

A

Vagolytic (increases HR)

caution in renal failure and cirrhosis, can decrease clearance and increase half life

42
Q

vecuronium duration

A

intermediate - 25-30 minutes

43
Q

vecuronium elimination

A

mainly hepatic

some renal

44
Q

vecuronium ADRs and monitoring

A

more commonly produces prolonged blockade upon discontinuation
may be more likely if given with corticosteroids

45
Q

Cisatracurium duration

A

intermediate

46
Q

Cisatracurium elimination

A

hoffman and hydrolysis (not renal/hepatic)

47
Q

Cisatracurium ADRs and monitoring

A

lower risk of cardio effects
lower risk of mast cell degranulation
duration should not be effected by renal/hepatic dysfunction

48
Q

Preload

A

what is coming into the heart

measured by PAOP or PCWP. Also SV

49
Q

Contractility

A

How effectively the heart pumps

Measured by CI or CO

50
Q

Afterload

A

what pressure the heart pumps blood out against

Measured by SVR

51
Q

example causes of Hypovolemic shock

A 
severe external or internal bleeding
profound fluid loses from GI sources
urinary losses
burns
capillary leak
trauma
AAA
vomiting
diarrhea
third-spacing
52
Q

changes that happen in Hypovolemic shock

A

low volume in body, decreased SV

body compensates by tachycardia and reflex increases in SVR and CO

53
Q

example causes of cardiogenic shock

A

Massive MI

Severe CHF

54
Q

changes that happen in cardiogenic shock

A

low contractility, CO, the heart has trouble pumping

get overload of blood in heart and cardio system backs up

55
Q

example causes of distributive shock

A

sepsis
anaphylactic shock
spinal cord injury

56
Q

changes that happen in distributive shock

A

every vessel is dilated, blood doesn’t get through well, it pools up instead of being pushed through. SVR is low

57
Q

goals of treating hypovolemic shock

A

restore effective circulating blood volume

manage underlying cause

58
Q

Examples of crystalloids

A

lactated ringer’s

NS

59
Q

advantages of crystalloids

A

relatively low volume expansion
widely available
low cost
rapid delivery

60
Q

disadvantages of crystalloids

A

possible fluid overload, more fluid required than colloids

may lead to leakage, edema, electrolyte disturbances, and dilution of anticoagulation factors

61
Q

amount of crystalloid to be given

A

1-2 L in the first hour

2-4 L or more total

62
Q

examples of colloids

A

albumin
dextran
netastarch

63
Q

advantages of colloids

A

recommended when patients require substantial amounts of crystalloids because not as much volume is needed with colloids
better at keeping volume in veins, less third-spacing

64
Q

disadvantages of colloids

A

expensive
takes longer to administer
hetastarch and dextran are not recommended for sepsis

65
Q

hetastarch and dextran ADRs

A

increased risk of bleeding and anaphylactoid reactions

66
Q

amount of colloids to be given

A

500-1000 ml

67
Q

norepinephrine

A

first line therapy

primary effect through vasoconstriction

68
Q

norepinephrine ADRs

A

tissue necrosis
arrhythmias
potentially lower mortality

69
Q

Dopamine

A

only consider for use if pt has low risk of tachyarrhythmias or bradycardia
effect is dose dependent, mostly increases SV and HR

70
Q

Dopamine and Renal Protection

A

low-dose dopamine (<3 mcg/kg/min) can improve renal function in patients with inadequate urine output despite high filling pressures and volume overload
controversial

71
Q

Dopamine ADRs

A

tissue necrosis with extravasation
arrhythmias
tachycardia

72
Q

vasopressin

A

direct vasoconstrictor without inotropic or chronotropic effects
acts at alpha-receptors
may add to NE therapy to maintain BP or decrease NE dose

73
Q

vasopressin ADRs

A 
arrhythmias
tachycardia
increased CO
chest pain
MI
vasoconstriction
venous thrombosis
74
Q

epinephrine

A

alpha and beta agonist
increases cardiac index and peripheral vasoconstriction (increased SVR)
may be added to NE if needed to maintain BP

75
Q

epinephrine ADRs

A 
angina
arrhythmia
chest pain
flushing
HTN
palpitation
tachycardia
vasoconstriction
ventricular ectopy
v-fib
76
Q

dobutamine

A 
inotrope
increases CO (HR and contractility)
vasodilation
B1 and B2 agonists
minimally works at a1
reserved for pts with systolic BP >90, severe HF, MI, or cardio shock
decreased preload
77
Q

dobutamine ADRs

A

tachycardia

arrhythmia

78
Q

dobutamine use with milrinone

A

may be used, but as last line!!

milrinone causes severe hypotension, arrhythmias, and thrombocytopenia

79
Q

define SIRS

A 
patient has two of the following
temp 38*C
HR > 90
Resp > 20
WBC > 12,000 or < 4,000 or > 10% bands
80
Q

define sepsis

A

SIRS + infection

81
Q

define severe sepsis

A

sepsis + organ dysfunction in 1 or more organs

82
Q

septic shock

A

sepsis + hypotension unresponsive to fluids

83
Q

what causes sepsis

A 
pulmonary causes
GI causes
GU causes
blood stream infections
all count for majority of sepsis cases
84
Q

risk factors for sepsis

A 
age
cancer
immunodeficiency
chronic organ failure
genetic factors
bacteremic patients
polymorphisms in genes that regulate immunity
85
Q

general approach to treatment of sepsis

A

early goal-directed resuscitation of septic patients during the first 6 hours after recognition
early administration of broad-spec anti-infective therapy
hydrocortisone for septic shock patients refractory to resuscitation and vasopressors
glycemic control via insulin infusion ith BG goal of 140-180
adjunctive therapies (nutrition, DVT ppx, stress ulcer ppx, sedation for mechanically ventilated patients

86
Q

monitoring parameters and goals for initial resuscitation monitoring

A

central venous pressure: 8-12 mmHg, 12-15 for intubated patients
Mean arterial pressure 65 or greater
urine output 0.5 ml/kg/h or more
central venous 70% or mixed venous oxygen saturation 65% or greater

87
Q

risk factos for VTE

A 
age > 50
prior history of VTE
venous stasis
vascular injury
hypercoagulable states
drug therapy (estrogen, chemo, etc)
88
Q

unfractionated heparin dose, frequency, and route (for ppx)

A

5000 units 2-3 times daily subQ

89
Q

does unfractionated heparin require renal adjustment?

A

no

90
Q

Enoxaparin dose, frequency, and route (for ppx)

A

40mg daily subQ

91
Q

does enoxaparin require renal adjustment?

A

yes - 30mg daily subQ

92
Q

Fragmin (dalteparin) dose, frequency, and route

A

5000 units daily subQ

93
Q

does Fragmin require renal adjustment?

A

yes - monitor anti-Xa levels at CrCl <30 ml/min

94
Q

Arixtra (fondaparinux) dose, frequency, and route

A

2.5mg daily subQ

95
Q

does Arixtra require renal adjustment?

A

yes - use caution in patients with CrCl 30-50, do not use in pts with CrCl <30

96
Q

Monitoring parameters for all VTE ppx agents

A

PT, aPTT, thrombocytopenia, excessive bleeding, CBC, SCr
Heparin - monitor hemoglobin and hematocrig
Enoxaparin - monitor anti-Xa levels (PT and aPTT not necessary)

97
Q

Stress-related mucosal disease (SRMD) risk factors

A

Coagulopathy
mechanical ventilation for > 48 hours
Hypotension

98
Q

Agents used for SRMD ppx

A

PPI - hard to give to NG tube patients. Risk of C. diff infection may be enhanced
H2RA - limited with low CrCl, confusion, or thrombocytopenia

99
Q

how to measure Mean Arterial Pressure (MAP)

A

((2*diastolic) + systolic)/3

100
Q

Can epidurals be used in anticoag patients?

A

NO!!! can cause paralysis if the patient bleeds into spinal space

Therapeutics 3 (8 decks)

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