exam 1 Flashcards
(146 cards)
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
2
Q
when to stop taking alternative meds (valerian, st. john’s wort, garlic, gingko, ginseng, etc) prior to surgery
A
2 weeks before
3
Q
components of virchow’s triad
A
hypercoagulable state
circulatory stasis
endothelial injury
4
Q
venous stasis as defined in virchow’s triad
A
age >60, BMI>30, prolonged immobility, paralysis
5
Q
injury as defined in virchow’s triad
A
surgery/trauma, ESPECIALLY involving spine, pelvis, knees
6
Q
hypercoagulable state as defined in virchow’s triad
A
protein C or S deficiency, prior VTE, malignancy, antiphospholipid antibodies
7
Q
3 risk factors for SMRD
A
respiratory failure requiring MV
coagulopathy (platelets <50,000, INR >1.5)
traumatic brain/spinal cord injury
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
9
Q
what are the consequences of unrelieved pain
A
inadequate sleep, agitation, stress response, chronic pain
10
Q
what is the stress response to pain
A
increase catecholamines= vasoconstriction
hypercoagulopathy
immunosuppression
persistent catabolism
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
12
Q
what is the gold standard for analgesia
A
multi modal
(opiates + non-opiates)
13
Q
fentanyl use in therapy
A
preferred in acutely distressed & hemodynamically unstable patients. it has the most rapid onset, shortest duration.
14
Q
morphine use in therapy
A
DO NOT give morphine if your patient has hypotension. associated with histamine release–> hypotension.
15
Q
hydromorphone use in therapy
A
lacks histamine release; can be used in hemodynamically unstable patients
16
Q
meperidine use in therapy
A
causes neuroexcitation: apprehension, tremors, delirium, seizures. interacts w/ MAOIs & SSRIs
17
Q
codeine place in therapy
A
lacks analgesic potency
18
Q
remifentanil place in therapy
A
very short duration so can be beneficial to do frequent neuro assessments for patients with neurological injuries
19
Q
which opioids are preferred for renal insufficiency
A
fentanyl & hydromorphone
20
Q
opioid ADEs
A
respiratory depression, hemodynamic instability (histamine release), sedation, hallucinations, GI
21
Q
deleterious effects of agitation
A
dyssynchrony with the ventilator
increased oxygen consumption
inadvertent removal of devices, catheters, drains
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
23
Q
options for sedation
A
benzos (diazepam, lorazepam, midazolam)
propofol
dexmedetomidine
ketamine
24
Q
MOA of benzos
A
bind to & enhance inhibitory effect of GABA
are sedative hypnotics & amnesiacs (NOT analgesics)
25
diazepam use for sedation
rapid onset & awakening
long acting metabolite can lead to prolonged sedation w/ repeat doses, acceptable for long term sedation & alcohol withdrawal
26
lorazepam use for sedation
slower onset, less useful with acute agitation
27
midazolam use for sedation
rapid onset, short duration, preferred for acute agitation
accumulation & prolonged sedation w/ obesity, low albumin (seniors), renal failure, CYP inhibitors
28
when can propofol be used for sedation?
ONLY in intubated patients.
IF THE PATIENT IS BREATHING ROOM AIR, NO PROPOFOL.
29
properties of propofol
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
30
what are the complications with propofol
hypertriglyceridemia, increased pancreatic enzymes (bad bad pancreatitis)
respiratory depression
hypotension, bradycardia, propofol infusion syndrome (think about michael jackson)
31
dexmedetomidine place in therapy for sedation
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
32
dexmedetomidine MOA
selective alpha 2 agonist with sedative and opioid sparing effects with a rapid onset and short duration
33
dexmedetomidine ADE
transient hypertension w/ rapid admin, bradycardia, hypotension w/ maintenance infusion
34
ketamine MOA
noncompetitive NMDA receptor antagonist w/ sedative & opioid sparing effects
35
ketamine onset/duration
rapid onset & short duration
36
ketamine ADEs
dose dependent emergence reactions, respiratory depression w/ rapid IV, airway complications, increased ICP, dependence
37
how to choose a sedative?
nonbenzos may be preferred in MV adult ICU pt
38
gold standard for assessment of delirium in ICU
ICDSC
intensive care delirium screening checklist
39
options for non-alcohol withdrawal delirium
quetiapine, olanzapine, haloperidol
40
options for alcohol withdrawal delirium
benzodiazepines, phenobarbital, propofol, ketamine, dexmedetomidine
41
allergy considerations with propofol
egg, soy, soybean
42
how do neuroleptics work for delirium
stabilizing effect on cerebral function via antagonizing dopamine mediated transmission at the cerebral synapses, basal ganglia
inhibits hallucinations/delusions, diminishes interest int eh environment
43
indication for neuroleptics
ICU-related delirium if patient exhibits harmful behavior to themselves or healthcare professionals
44
which antipsychotics reduce duration of delirium in adult ICU patients
atypicals: quetiapine, olanzapine
older (haloperidol) does not
45
antipsychotic ADEs
QT prolongation, EPS, sedation
46
VTE prophylaxis
use LMWH for very high risk, otherwise heparin
47
SRMD prophylaxis
options are antacids, sucralfate, H2RAs, PPIs
48
SSI prophylaxis
typically IV cefazolin or vancomycin 30-60 minutes before & for a duration of 24 hours post operation
49
perioperative cardiac complication prophylaxis
beta blockers should be continued in patients undergoing surgery who are receiving beta blockers for treatment of conditions (goal HR 65)
50
opioid- induced constipation
usually start with senna, miralax after trial of fiber, fluids, mobility, d/c constipating meds
save opioid antagonists as a last line.
51
systole
contraction
52
diastole
relaxation
53
preload
pressure/volume of ventricle before contraction
54
afterload
resistance to preload
55
goal MAP in ICU
>65
56
MAP= __ x __
CO x TPR
57
indicators of right ventricular function
CVP, RVEDP
58
indicators of left ventricular function
PCWP, LVEDP
59
indicators of afterload
SVRI, PVRI
60
SvO2
goal >70%
evaluates tissue oxygenation
61
complications with pulmonary artery catheter
infection, arrhythmia, thrombosis, bleeding
62
complications with central venous catheter
infection, thrombosis, bleeding
63
hypovolemic shock
SVR ↑
CI, PCWP↓
64
cardiogenic shock
CI ↓
SVR, PCWP↑
65
septic shock
CI, SVR, and PCWP↓
66
how much of total body water is extracellular
1/3
67
how much of extracellular water is interstitial fluid
75%
68
how much of extracellular water is intravascular fluid (blood)
25%
69
what is hydrostatic pressure
outward driving force of fluid created by SV
70
what is protein oncotic (osmotic) pressure
inward pulling force of fluid exerted across capillary membrane
71
what is capillary permeability
prevents plasma proteins and other molecules from crossing into interstitial fluid
72
what is the goal CI
>2.2
73
what are the crystalloids
D5W, sodium chloride, lactated ringers, plasma lyte
74
sodium chloride components
154 mEq/L of Na & Cl
intravascular to interstitial fluid distribution 1:3
redistributes in minutes
75
use of sodium chloride
fluid resuscitation in hypovolemic or septic shock
76
ADEs of sodium chloride
hypernatremia, fluid overload, hyperchloremic metabolic acidosis
77
generally, components of lactated ringers
sodium, potassium, chloride, calcium, lactate in different equivalents
intravascular to interstitial fluid distribution ratio 1:3, redistributes in minutes
78
uses of lactated ringers/potential advantages over NS?
used for fluid resuscitation in hypovolemic or septic shock; no clinical advantages over NS except in preventing hyperchloremic acidosis
79
adverse effects of lactated ringers
fluid overload, hyponatremia, aggravation of preexisting hyperkalemia or lactic acidosis
80
general composition of albumin
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
uses for albumin
hypovolemic or septic shock
82
albumin side effects
fluid overload, potential protein overload, anaphylaxis, infectious complications
83
when are packed red blood cells used
only when Hgb <7 gm/dL
84
when are platelets used
only when platelet count <10,000
85
when is fresh frozen plasma used
only for coagulopathy: reversal of warfarin
86
what are some general complications/adverse effects of blood products such as PRBC, platelets, FFP
viral transmission (CMV, hepatitis, HIV)
transfusion reactions aka anaphylaxis
hyperkalemia, hyperphosphatemia
dilutional coagulopathy
immunosuppressive
metabolic alkalosis, hypocalcemia, decrease Hgb affinity for oxygen
87
sympathetic adrenergic receptor in the HEART
B1 receptor (+ chronotropic and ionotropic activity)
88
sympathetic adrenergic receptors in the VASCULATURE
a1/a2: vasoconstriction
b2: vasodilation
89
general points to know for epinephrine
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
general points to know for norepinephrine
1st line septic shock, 2nd line cardiogenic shock.
ADEs: severe hypoperfusion & tissue ischemia, tachycardia, tachyarrhythmias. to a less potent extent than epi
91
general points to know for phenylephrine
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
general points to know for dopamine
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
general points to know for vasopressin
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
things that increase preload
fluids, pressors
95
thinks that decrease preload
diuretics, venous vasodilators (nitroglycerin, ACEi)
96
things that increase afterload
pressors
97
things that decrease afterload
arterial vasodilators (nitroprusside, ACEi, BB, CCBs, alpha blockers, phosphodiesterase inhibitors)
98
things that increase contractility
positive inotropes (dobutamine, dopamine, digoxin, PDE inhibitors)
99
things that decrease contractility
negative inotropes: beta blockers, CCBs
100
definition of sepsis
life threatening organ dysfunction caused by dysregulated host response to infection
101
definition of septic shock
sepsis + vasopressors to maintain MAP>65 and serum lactate <2 despite adequate volume resuscitation
102
most common cause of sepsis
bacterial, gram positive>negative
103
sepsis risk factors
immunocompromised, hospital patients, preexisting infection, trauma, very young, very old
104
general pathophysiology of sepsis
bug in blood--> cytokines go crazy--> fluid leaks & the heart becomes stunned
105
overview of treatment strategies for sepsis
initial resuscitation (fluids, pressors)
antimicrobial agents within 1 hour
CIRCI
glycemic control (<180)
106
key points for antimicrobial coverage in sepsis
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
key points for critical illness related corticosteroid insufficiency (CIRCI)
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
indication of hospital-related hyperglycemia (BG)
random BG>180
109
key points for regular insulin sliding scale (RISS)
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
key points for long acting insulin NPH, lantus
really just don't use for acutely ill ICU patients.
111
key points for regular insulin continuous infusion
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
goal BG
<180
113
3 things that DKA must have
D: hyperglycemia
K: ketosis
A: acidosis
114
general pathogenesis of DKA
insulin deficiency/reduced glucose uptake (stems from noncompliance of insulin, or infection)
free fatty acid formation & ketone production
hyperglycemia acidosis & neurological injury
115
signs and symptoms of DKA
MENTAL STATUS CHANGES
n/v, polyuria, polydipsia
116
lab findings in DKA
BG>200
arterial pH<7.35
urine/serum ketone positive
117
DKA treatment: IV fluids
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
DKA treatment insulin
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
when to hold insulin
if K<3.3
120
when to supplement potassium
10 mEq if 3.0-4.9
20 mEq if <3.0
121
when to supplement bicarbonate
if pH<6.9
122
when to supplement phosphate
if PO4<1
123
when is neuromuscular blockade indicated in ICU
intubation
ventilator dysynchrony
ICP/tetanus
*despite maximal sedation/etc
124
depolarizing NMBA
succinylcholine
125
nondepolarizing NMBA
pancuronium, vecuronium, rocuronium, cisatracurium, atracurium
126
key points succinylcholine
rapid onset, short duration
caution in renal patients (HYPERKALEMIA), hepatic patients
really caution for hyperkalemia, muscle pain, rhabdo, hyperthermia
127
key points pancuronium
long acting
disadvantage is hepatic metabolism, renal excretion, cardiovascular side effects (increases HR & BP)
128
key points vecuronium
intermediate acting
no vagolytic activity (doesn't increase HR), advantage
but hepatic metabolism, renal excretion, associated with prolonged blockade
128
key points rocuronium
short acting, faster onset than vec, longer duration than sux, minimal side effects: rare arrhythmias, respiratory. disadvantage is cost & biliary excretion
129
key points atracurium
intermediate acting
no dose adjustments for renal/hepatic & minimal CV effects
disadvantage is higher dose= histamine release (hypotension) & neuroexcitation (seizures)
130
key points cisatracurium
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
how to choose NMBA in ICU?
length of paralysis
renal/hepatic function, BP, HR of patient
132
ideal NMBA?
rapid onset & offset, complete recovery
minimal ADEs, drug interactions
low cost
doesn't exist
133
monitoring NMBA
measure degree of NM blockade via Train of Four, movement, cough, respiratory efforts
daily measure of neuro function
134
complications of NMBA
skeletal muscle weakness
HR, BP
ketatitis & corneal abrasion
DVT/PE
tachyphylaxis
135
NMBA reversal agents
neostigmine, glycopyrollate, sugammadex
136
PONV definition
n/v within 24 hr of surgery
if its more than 24 hr think of other causes
137
consequences of PONV
discomfort, electrolytes, dehydration, suture dehiscence
138
3 broad mechanisms of nausea/vomiting
CTZ
vestibular
GI path
139
receptors involved in nausea/vomiting
serotonin, dopamine, acetylcholine, histamine, neurokinin
140
PONV risk factors
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
what if 2 risk factors for PONV
monotherapy
142
what if 3+ risk factors for PONV
combo therapy
143
nonpharm for PONV
reduce baseline risks: local, no nitrous or neostigmine, NSAIDs instead of opioids
144
which agents may be used for PONV and which ones are first line
anticholinergics (scopolamine)
phenothiazines (prochlorperazine)
antihistamines (diphenhydramine)
butyrophenones (droperidol)
benzamides (metoclopramide)
first lines:
serotonin antagonist (ondansetron)
corticosteroids (dexamethasone)
neurokinin antagonists (aprepitant)
145
what if failed prophylaxis for PONV
treatment with an agent not used in prophylaxis
