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Critical Care > exam 1 > Flashcards

exam 1 Flashcards

1
Q

which necessary meds to hold prior to surgery for bleed risk?

A

ASA, NSAIDs 10-14 days before
Warfarin 4-5 days before
Dabigatran, rivaroxaban, apixaban 1-2 days before

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2
Q

when to stop taking alternative meds (valerian, st. john’s wort, garlic, gingko, ginseng, etc) prior to surgery

A

2 weeks before

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3
Q

components of virchow’s triad

A

hypercoagulable state
circulatory stasis
endothelial injury

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4
Q

venous stasis as defined in virchow’s triad

A

age >60, BMI>30, prolonged immobility, paralysis

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5
Q

injury as defined in virchow’s triad

A

surgery/trauma, ESPECIALLY involving spine, pelvis, knees

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6
Q

hypercoagulable state as defined in virchow’s triad

A

protein C or S deficiency, prior VTE, malignancy, antiphospholipid antibodies

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7
Q

3 risk factors for SMRD

A

respiratory failure requiring MV
coagulopathy (platelets <50,000, INR >1.5)
traumatic brain/spinal cord injury

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8
Q

when is prophylaxis for SMRD required?

A

ONLY if patient is mechanically ventilated, coagulopathic, or has TBI
not cost effective to prophylaxis for everyone

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9
Q

what are the consequences of unrelieved pain

A

inadequate sleep, agitation, stress response, chronic pain

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10
Q

what is the stress response to pain

A

increase catecholamines= vasoconstriction
hypercoagulopathy
immunosuppression
persistent catabolism

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11
Q

how do we assess pain in ICU?

A

patient reported is most reliable.
if patient cannot report: BPS, CPOT, or physiological indicators like HR, BP, RR

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12
Q

what is the gold standard for analgesia

A

multi modal
(opiates + non-opiates)

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13
Q

fentanyl use in therapy

A

preferred in acutely distressed & hemodynamically unstable patients. it has the most rapid onset, shortest duration.

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14
Q

morphine use in therapy

A

DO NOT give morphine if your patient has hypotension. associated with histamine release–> hypotension.

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15
Q

hydromorphone use in therapy

A

lacks histamine release; can be used in hemodynamically unstable patients

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16
Q

meperidine use in therapy

A

causes neuroexcitation: apprehension, tremors, delirium, seizures. interacts w/ MAOIs & SSRIs

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17
Q

codeine place in therapy

A

lacks analgesic potency

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18
Q

remifentanil place in therapy

A

very short duration so can be beneficial to do frequent neuro assessments for patients with neurological injuries

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19
Q

which opioids are preferred for renal insufficiency

A

fentanyl & hydromorphone

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20
Q

opioid ADEs

A

respiratory depression, hemodynamic instability (histamine release), sedation, hallucinations, GI

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21
Q

deleterious effects of agitation

A

dyssynchrony with the ventilator
increased oxygen consumption
inadvertent removal of devices, catheters, drains

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22
Q

what is the gold standard for assessment of sedation

A

Riker’s Sedation Assessment Scale (1-7)
1 is unresponsive and 7 is dangerously agitated
want them to be at 3-4

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23
Q

options for sedation

A

benzos (diazepam, lorazepam, midazolam)
propofol
dexmedetomidine
ketamine

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24
Q

MOA of benzos

A

bind to & enhance inhibitory effect of GABA
are sedative hypnotics & amnesiacs (NOT analgesics)

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25
Q

diazepam use for sedation

A

rapid onset & awakening
long acting metabolite can lead to prolonged sedation w/ repeat doses, acceptable for long term sedation & alcohol withdrawal

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26
Q

lorazepam use for sedation

A

slower onset, less useful with acute agitation

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27
Q

midazolam use for sedation

A

rapid onset, short duration, preferred for acute agitation

accumulation & prolonged sedation w/ obesity, low albumin (seniors), renal failure, CYP inhibitors

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28
Q

when can propofol be used for sedation?

A

ONLY in intubated patients.
IF THE PATIENT IS BREATHING ROOM AIR, NO PROPOFOL.

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29
Q

properties of propofol

A

IV general anesthetic with sedative hypnotic & amnesiac properties (NO analgesic properties)
rapid onset, short duration
predictable awakening times & no PK changes in renal/hepatic insufficiency

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30
Q

what are the complications with propofol

A

hypertriglyceridemia, increased pancreatic enzymes (bad bad pancreatitis)
respiratory depression
hypotension, bradycardia, propofol infusion syndrome (think about michael jackson)

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31
Q

dexmedetomidine place in therapy for sedation

A

for short term use (<24 hours) in patients initially receiving MV
often used in peri-extubation period (getting the tube out)
there is no respiratory depression so can give to someone who is not intubated

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32
Q

dexmedetomidine MOA

A

selective alpha 2 agonist with sedative and opioid sparing effects with a rapid onset and short duration

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33
Q

dexmedetomidine ADE

A

transient hypertension w/ rapid admin, bradycardia, hypotension w/ maintenance infusion

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34
Q

ketamine MOA

A

noncompetitive NMDA receptor antagonist w/ sedative & opioid sparing effects

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35
Q

ketamine onset/duration

A

rapid onset & short duration

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36
Q

ketamine ADEs

A

dose dependent emergence reactions, respiratory depression w/ rapid IV, airway complications, increased ICP, dependence

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37
Q

how to choose a sedative?

A

nonbenzos may be preferred in MV adult ICU pt

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38
Q

gold standard for assessment of delirium in ICU

A

ICDSC
intensive care delirium screening checklist

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39
Q

options for non-alcohol withdrawal delirium

A

quetiapine, olanzapine, haloperidol

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40
Q

options for alcohol withdrawal delirium

A

benzodiazepines, phenobarbital, propofol, ketamine, dexmedetomidine

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41
Q

allergy considerations with propofol

A

egg, soy, soybean

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42
Q

how do neuroleptics work for delirium

A

stabilizing effect on cerebral function via antagonizing dopamine mediated transmission at the cerebral synapses, basal ganglia
inhibits hallucinations/delusions, diminishes interest int eh environment

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43
Q

indication for neuroleptics

A

ICU-related delirium if patient exhibits harmful behavior to themselves or healthcare professionals

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44
Q

which antipsychotics reduce duration of delirium in adult ICU patients

A

atypicals: quetiapine, olanzapine
older (haloperidol) does not

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45
Q

antipsychotic ADEs

A

QT prolongation, EPS, sedation

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46
Q

VTE prophylaxis

A

use LMWH for very high risk, otherwise heparin

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47
Q

SRMD prophylaxis

A

options are antacids, sucralfate, H2RAs, PPIs

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48
Q

SSI prophylaxis

A

typically IV cefazolin or vancomycin 30-60 minutes before & for a duration of 24 hours post operation

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49
Q

perioperative cardiac complication prophylaxis

A

beta blockers should be continued in patients undergoing surgery who are receiving beta blockers for treatment of conditions (goal HR 65)

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50
Q

opioid- induced constipation

A

usually start with senna, miralax after trial of fiber, fluids, mobility, d/c constipating meds

save opioid antagonists as a last line.

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51
Q

systole

A

contraction

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52
Q

diastole

A

relaxation

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53
Q

preload

A

pressure/volume of ventricle before contraction

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54
Q

afterload

A

resistance to preload

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55
Q

goal MAP in ICU

A

> 65

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56
Q

MAP= __ x __

A

CO x TPR

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57
Q

indicators of right ventricular function

A

CVP, RVEDP

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58
Q

indicators of left ventricular function

A

PCWP, LVEDP

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59
Q

indicators of afterload

A

SVRI, PVRI

60
Q

SvO2

A

goal >70%
evaluates tissue oxygenation

61
Q

complications with pulmonary artery catheter

A

infection, arrhythmia, thrombosis, bleeding

62
Q

complications with central venous catheter

A

infection, thrombosis, bleeding

63
Q

hypovolemic shock

A

SVR ↑
CI, PCWP↓

64
Q

cardiogenic shock

A

CI ↓
SVR, PCWP↑

65
Q

septic shock

A

CI, SVR, and PCWP↓

66
Q

how much of total body water is extracellular

A

1/3

67
Q

how much of extracellular water is interstitial fluid

A

75%

68
Q

how much of extracellular water is intravascular fluid (blood)

A

25%

69
Q

what is hydrostatic pressure

A

outward driving force of fluid created by SV

70
Q

what is protein oncotic (osmotic) pressure

A

inward pulling force of fluid exerted across capillary membrane

71
Q

what is capillary permeability

A

prevents plasma proteins and other molecules from crossing into interstitial fluid

72
Q

what is the goal CI

A

> 2.2

73
Q

what are the crystalloids

A

D5W, sodium chloride, lactated ringers, plasma lyte

74
Q

sodium chloride components

A

154 mEq/L of Na & Cl
intravascular to interstitial fluid distribution 1:3
redistributes in minutes

75
Q

use of sodium chloride

A

fluid resuscitation in hypovolemic or septic shock

76
Q

ADEs of sodium chloride

A

hypernatremia, fluid overload, hyperchloremic metabolic acidosis

77
Q

generally, components of lactated ringers

A

sodium, potassium, chloride, calcium, lactate in different equivalents
intravascular to interstitial fluid distribution ratio 1:3, redistributes in minutes

78
Q

uses of lactated ringers/potential advantages over NS?

A

used for fluid resuscitation in hypovolemic or septic shock; no clinical advantages over NS except in preventing hyperchloremic acidosis

79
Q

adverse effects of lactated ringers

A

fluid overload, hyponatremia, aggravation of preexisting hyperkalemia or lactic acidosis

80
Q

general composition of albumin

A

protein colloid, at least 96% albumin

comes in 5% or 25% products, but expensive

intravascular to interstitial fluid distribution ratio 1:1, redistributes in 5-6 hours

81
Q

uses for albumin

A

hypovolemic or septic shock

82
Q

albumin side effects

A

fluid overload, potential protein overload, anaphylaxis, infectious complications

83
Q

when are packed red blood cells used

A

only when Hgb <7 gm/dL

84
Q

when are platelets used

A

only when platelet count <10,000

85
Q

when is fresh frozen plasma used

A

only for coagulopathy: reversal of warfarin

86
Q

what are some general complications/adverse effects of blood products such as PRBC, platelets, FFP

A

viral transmission (CMV, hepatitis, HIV)
transfusion reactions aka anaphylaxis
hyperkalemia, hyperphosphatemia
dilutional coagulopathy
immunosuppressive
metabolic alkalosis, hypocalcemia, decrease Hgb affinity for oxygen

87
Q

sympathetic adrenergic receptor in the HEART

A

B1 receptor (+ chronotropic and ionotropic activity)

88
Q

sympathetic adrenergic receptors in the VASCULATURE

A

a1/a2: vasoconstriction
b2: vasodilation

89
Q

general points to know for epinephrine

A

think lots of B1 (increased heart rate and force)
and lots of a1 (vasoconstrict/SQUEEZE)
leads to severe hypoperfusion & tissue ischemia, severe tachycardia, severe arrhythmias
save for SECOND line septic shock/cardiogenic shock
FIRST line for anaphylaxis

90
Q

general points to know for norepinephrine

A

1st line septic shock, 2nd line cardiogenic shock.
ADEs: severe hypoperfusion & tissue ischemia, tachycardia, tachyarrhythmias. to a less potent extent than epi

91
Q

general points to know for phenylephrine

A

it is all about the SQUEEZE (a1)– doesn’t have those B1 effects so we can use it when patients have a high HR.

FIRST line in tachycardia with septic shock. Second line in tachycardia with cardiogenic shock.

ADEs are hypoperfusion and tissue ischemia (less than NE)

92
Q

general points to know for dopamine

A

has a little more “kick” than norepi, biggest takeaway is higher incidence of arrhythmia.

3rd line in septic shock due to arrythmia potential.

ADEs: tachyarrhythmia, ischemic limb necrosis

93
Q

general points to know for vasopressin

A

ADH analog with peripheral vasoconstriction effects, used in septic shock to reduce vasopressor doses as an ADJUNCT role– NEVER MONOTHERAPY

ADEs: cardiac, digital, and splachnic hypoperfusion

94
Q

things that increase preload

A

fluids, pressors

95
Q

thinks that decrease preload

A

diuretics, venous vasodilators (nitroglycerin, ACEi)

96
Q

things that increase afterload

A

pressors

97
Q

things that decrease afterload

A

arterial vasodilators (nitroprusside, ACEi, BB, CCBs, alpha blockers, phosphodiesterase inhibitors)

98
Q

things that increase contractility

A

positive inotropes (dobutamine, dopamine, digoxin, PDE inhibitors)

99
Q

things that decrease contractility

A

negative inotropes: beta blockers, CCBs

100
Q

definition of sepsis

A

life threatening organ dysfunction caused by dysregulated host response to infection

101
Q

definition of septic shock

A

sepsis + vasopressors to maintain MAP>65 and serum lactate <2 despite adequate volume resuscitation

102
Q

most common cause of sepsis

A

bacterial, gram positive>negative

103
Q

sepsis risk factors

A

immunocompromised, hospital patients, preexisting infection, trauma, very young, very old

104
Q

general pathophysiology of sepsis

A

bug in blood–> cytokines go crazy–> fluid leaks & the heart becomes stunned

105
Q

overview of treatment strategies for sepsis

A

initial resuscitation (fluids, pressors)
antimicrobial agents within 1 hour
CIRCI
glycemic control (<180)

106
Q

key points for antimicrobial coverage in sepsis

A

draw cultures before giving abx
give abx <1 hr from diagnosis
empiric 1 or more agents, generally try to cover pseudomonas, MRSA
reassess regimen in 48-72 hours to narrow coverage. when pathogen identified, d/c double coverage. duration 7-10 days

107
Q

key points for critical illness related corticosteroid insufficiency (CIRCI)

A

don’t need cosyntropin stimulation test
hydrocortisone 50 mg IV q6h only for septic shock patients that are not responding to fluid resuscitation & vasopressors, continue until d/c pressors & taper by 1/2 dose every 2 days if duration >7 days

108
Q

indication of hospital-related hyperglycemia (BG)

A

random BG>180

109
Q

key points for regular insulin sliding scale (RISS)

A

treats hyperglycemia AFTER it has occurred
causes rapid changes in BG (hyper & hypo)
reserve for: supplement to usual diabetes meds, 24h in patients with unknown insulin requirements

110
Q

key points for long acting insulin NPH, lantus

A

really just don’t use for acutely ill ICU patients.

111
Q

key points for regular insulin continuous infusion

A

favorable PK, takes current BG into consideration, has safety measures, effective & user friendly. consider for patients expected to be on infusion >3 days (mechanical ventilation as indicator), 2 consecutive BG>180 in 24h, moderate insulin sliding scale failed to control

112
Q

goal BG

A

<180

113
Q

3 things that DKA must have

A

D: hyperglycemia
K: ketosis
A: acidosis

114
Q

general pathogenesis of DKA

A

insulin deficiency/reduced glucose uptake (stems from noncompliance of insulin, or infection)
free fatty acid formation & ketone production
hyperglycemia acidosis & neurological injury

115
Q

signs and symptoms of DKA

A

MENTAL STATUS CHANGES
n/v, polyuria, polydipsia

116
Q

lab findings in DKA

A

BG>200
arterial pH<7.35
urine/serum ketone positive

117
Q

DKA treatment: IV fluids

A

normal saline first hour
0.45% normal saline (unless Na<135)

D5W added to replacement fluids when BG<200: hyperglycemia corrects faster than ketoacidosis. know this.

118
Q

DKA treatment insulin

A

regular insulin 0.1 u/kg bolus, then 0.1 u/kg/hr CI

goal: reduce BG 50-75 mg/dL/hr

reduce infusion to 0.05 u/kg/hr when BG 200

119
Q

when to hold insulin

A

if K<3.3

120
Q

when to supplement potassium

A

10 mEq if 3.0-4.9
20 mEq if <3.0

121
Q

when to supplement bicarbonate

A

if pH<6.9

122
Q

when to supplement phosphate

A

if PO4<1

123
Q

when is neuromuscular blockade indicated in ICU

A

intubation
ventilator dysynchrony
ICP/tetanus

*despite maximal sedation/etc

124
Q

depolarizing NMBA

A

succinylcholine

125
Q

nondepolarizing NMBA

A

pancuronium, vecuronium, rocuronium, cisatracurium, atracurium

126
Q

key points succinylcholine

A

rapid onset, short duration
caution in renal patients (HYPERKALEMIA), hepatic patients
really caution for hyperkalemia, muscle pain, rhabdo, hyperthermia

127
Q

key points pancuronium

A

long acting
disadvantage is hepatic metabolism, renal excretion, cardiovascular side effects (increases HR & BP)

128
Q

key points vecuronium

A

intermediate acting
no vagolytic activity (doesn’t increase HR), advantage
but hepatic metabolism, renal excretion, associated with prolonged blockade

128
Q

key points rocuronium

A

short acting, faster onset than vec, longer duration than sux, minimal side effects: rare arrhythmias, respiratory. disadvantage is cost & biliary excretion

129
Q

key points atracurium

A

intermediate acting
no dose adjustments for renal/hepatic & minimal CV effects
disadvantage is higher dose= histamine release (hypotension) & neuroexcitation (seizures)

130
Q

key points cisatracurium

A

intermediate acting
no CV effects
less histamine release & neuroexcitation
no renal/hepatic dosage adjustments
recovery times similar to atra, better than vec

use in ICU limited due to slow onset 3-6 minutes

131
Q

how to choose NMBA in ICU?

A

length of paralysis
renal/hepatic function, BP, HR of patient

132
Q

ideal NMBA?

A

rapid onset & offset, complete recovery
minimal ADEs, drug interactions
low cost
doesn’t exist

133
Q

monitoring NMBA

A

measure degree of NM blockade via Train of Four, movement, cough, respiratory efforts
daily measure of neuro function

134
Q

complications of NMBA

A

skeletal muscle weakness
HR, BP
ketatitis & corneal abrasion
DVT/PE
tachyphylaxis

135
Q

NMBA reversal agents

A

neostigmine, glycopyrollate, sugammadex

136
Q

PONV definition

A

n/v within 24 hr of surgery

if its more than 24 hr think of other causes

137
Q

consequences of PONV

A

discomfort, electrolytes, dehydration, suture dehiscence

138
Q

3 broad mechanisms of nausea/vomiting

A

CTZ
vestibular
GI path

139
Q

receptors involved in nausea/vomiting

A

serotonin, dopamine, acetylcholine, histamine, neurokinin

140
Q

PONV risk factors

A

non smoking females with history of motion sickness or PONV
general anesthesia, nitrous, opioids, neostigmine
surgery duration >60 mins
Gi, OB/GYN, ENT, neuro surgeries

141
Q

what if 2 risk factors for PONV

A

monotherapy

142
Q

what if 3+ risk factors for PONV

A

combo therapy

143
Q

nonpharm for PONV

A

reduce baseline risks: local, no nitrous or neostigmine, NSAIDs instead of opioids

144
Q

which agents may be used for PONV and which ones are first line

A

anticholinergics (scopolamine)
phenothiazines (prochlorperazine)
antihistamines (diphenhydramine)
butyrophenones (droperidol)
benzamides (metoclopramide)

first lines:
serotonin antagonist (ondansetron)
corticosteroids (dexamethasone)
neurokinin antagonists (aprepitant)

145
Q

what if failed prophylaxis for PONV

A

treatment with an agent not used in prophylaxis

Critical Care (1 decks)

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