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Critical Care/Hematology/Oncology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is the ICU

A

specialized section og a hospital that provides comprehensive care for persons who are critically ill
*achieve ATC monitoring and treatment
*staffed w. specially trained proffessionals
*contains sophisticated monitoring equiptment

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2
Q

types of intensive care units

A

MICU
SICU
CVICU
TICU
NSCU
PICU
NICU

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3
Q

Roles of clinical pharmacists role in the ICU

A

direct pt care:
interdisciplinary care rounds
code blue/ code stroke response
perform med hx
prevent and manage adverse drug events/ medication errors
PKPD monitoring
pt and caregiver education

indirect pt care:
policy and protocol development
formulary management
research
participation in committees

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4
Q

tpx considerations in critically ill patients

A
  1. pkpd changes
    *fluid shifts
    *renal and hepatic dysfunction

2.specific prophylaxis
*ventilator associated pna
stress ucer ppx
VTE ppx

3.nutrition considerations
*enteral vs parenteral

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5
Q

FAST HUGS BID meaning

A

pneumonic that emphasizes important aspects of critical care medicine that cna be applied twice daily to critically ill pts

“checklist”

Feeding
Aanalgesia
Sedation
Thromboembolism ppx

Head of Bed (VAP ppx)
Ulcer ppx
Glycemic control
Spontaneous breathing trial

Bowel regimen
Indwelling catheters
De-escalation of abx

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6
Q

FAST HUGS

F

why is it important?
considerations:

A

FAST HUGS

Feeding

why is it important?
*malnutrition can lead to impaired immune function-> leads to infections, delayed wound healing-> bacteria growth in gi tract

considerations:
emphasis on early enteral feedings: if the gut wks, use it
enteral preffered vs parenteral

parenteral may be necessary if gut is not working

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7
Q

FAST HUGS

A

why is it important?
considerations:

A

FAST HUGS

Analgensia

why is it important?
pain can be due to many underlying conditions :trauma, surgery, etc.
standard icu care: lines, turning/repositioning, physical therapy
*optimizes pt comfort and minimizes acute stress response, hypermetabolism, increased o2 consumption, hypercoagulability, and alterations in immune function

considerations:
assess pain w. icu validated pain scales such as…
Critical care pain observation tool (CPOT)
Behavioral Pain Scale
*types of pain (nciceptive pain vs neuropathic pain
*duration of pain: long term aents vs boluses
*home pain regimens

most common pain meds in icu
FENTANYL, hydrmorphone, morphine, oxycodone

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8
Q

FAST HUGS

S

why is it important?
considerations:

A

FAST HUGS

Sedation

why is it important?
icu pts can be sedated due to situations such as anxiety, pain, lack of homeostasis, withdrawal, benzo use, sleep wake cycle disruption

considerations:
sedatio should be assessed w. a validated tool
ex: Richmond Agitation Sedation Scale (RASS) or Sedation Agitation Scale(SAS)
*light sdation (RASS0-2) uppored in guidelines for most situations
propofol and dexmedetomidine are preffered sedative agents over ocntinuous benzos as benzo use associated w. more delerium and neurocognitive implications

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9
Q

FAST HUGS

T

why is it important?
considerations:

A

FAST HUGS

Thromboembolism PPX

why is it important?
*critically ill pts hve been shown to be at higher risk for vte than general med pts due to additional risk factors for vte in these pts such as
ex: central venous catherization, immobility, trauma/burns, sepsis

considerations:
vte ppx should be given to all pts in icu
initiation of dependent on risk vs benefits
options: LWMH (enoxaparin 40mg SQ daily or 30 mg SQ BID or unfractioned heparin in pts w. renal dysfunction (5000 units SQ q8h)
*high bleed risk pts, nonharm vte ppx such as compresion socks, pneumatic compression device. or combo of nonpharm and pharm can be initiated.

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10
Q

FAST HUGS

H

why is it important?
considerations:

A

FAST HUGS

Head of Bed

what is mechanical ventilation?
helps pt to breath when they cant on their own
ET tube placed into trachea through the mouth. this tube then hooked up to ventilatorwhich blows o2 rich air into lungs and removing co2 from lungs

why is it important?
ventilator associated pneumonia ppx
specific to pts recieveing mechanical ventilation.

considerations:
elevating head of bed to 30-45 degree angle reduces risk of gi reflux and nosocomial pneumonia
apply antiseptic mouthwash (chlorhexidine 0.12%) topiccaly oral cavity 3x daily to maintain oral hygeine to prevent bacterial growth w. trach tube

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11
Q

FAST HUGS

U

why is it important?
considerations:

A

FAST HUGS

Ulcer ppx

why is it important?
criticaly ill pts deelop stress related mucosal damage (SMRD), potentially leading to clinically significant bleeding

SMRD: acute erosive inflammatory upper gi insult to the upper gi tract associated w. critical illness
*mortality 50-70%, incidence as decreased due ot stress ulcer ppx

considerations:
Risk factors for GI bleeding
*majr: 1 requires ppx
mechanical ventilation >48hrs OR
coagulopathy INR>1.5 PTT>2X ULN, or platelets <50,000/mm^3

minor: 2 or more requires ppx
*drugs tht increase risk of bleeding (steroids, warfarin, heparin
*shock, sepsis, hypotension, vasopressors
*hepatic/renal failure
multiple trauma
burns>35% of BSA
organ tansplant
head or spinal trauma

Stress ulcer ppx
*PPIs( protonix 40 mg daily), h2ra (famotidine)
continue until rik factors have resolved

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12
Q

FAST HUGS

G

why is it important?
considerations:

A

FAST HUGS

Glycemic control

why is it important?
hyperglycemia common in critically ill ( even w.o hx of DM) due to multiple facors such as stress and meds (steroids, BB, vasopressors) exogenous glucose tpn

GLYCEMIC CONTROL decreases the incidence of complications such as decrease wound healing and increased inection risk

considerations:
GLUCOSE GOAL in ICU: 140-180 mg/dL i n the acutely ill .
trial showed worsed outcomes w. conventional glycemic control of 80-110 mg/dL

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13
Q

FAST HUGS

S

why is it important?
considerations:

A

FAST HUGS

Spontaneous Breathing Trial

why is it important?
mechanical ventialtion associated w. many complications, so d/c of MV at earliest opportunity is an important goal

considerations:
performed on pts on mechanical ventilation and assesses the pts ability to breah on minimal or no ventilatory support

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14
Q

FAST HUGS

B

why is it important?
considerations:

A

FAST HUGS

Bowel regimen

why is it important?
constipation can occur for a # of reasons in critically ill ( immobility, effects of meds, shock)

considerations:
monitor bowel movements
opioid pt can be put on bowel regimen preemptively
OPTIONS: DOCUSATE, SENNOSIDES, peg: BISACODYL SUPPOSITORIES, ENEMAS, MAGNESIUM CTRATE FOR RESCUE OPTIONS
reasons for diarrhea in icu: INfection, feeds, aggressive bowel regimens

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15
Q

FAST HUGS

I

why is it important?
considerations:

A

FAST HUGS

Indwelling catheters

why is it important?
monitor sites for signs of infection
assessing the lines or if they can be removed

considerations:

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16
Q

FAST HUGS

D

why is it important?
considerations:

A

FAST HUGS

De-escalaion of abx

why is it important?
broad spectrum abx are common in critical care units

considerations:
applying abx stewardship .
de-escalating abx as appropriate based on culture or results
*setting appropriate abx duration to ovoid under or overuse of abx

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17
Q

Hypertensive crisis definition

A

umbrella term wihch encompasses htn emergency or emergency

acute ocndition of very high bp w. eithwe a SBP>180 MMHG, DBP>120 mm hg
or both

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18
Q

hypertensive urgency

A

acute htn w. evidence of new or worsening target organ damage

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19
Q

hypertensive emrgency

A

pts w. acute condition of very high bp and evidence or new or worsening target organ dmaage

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20
Q

Examples of end organ dmaage

CV
Neurological
vascular
renal
liver
ocular

A

CV
*acute pulmonary edema
*acute lv dysfunction
*acute MI

Neurological
*htn encephalopathy
*intracranial bleeding
cerebral infarction

vascular
*acute aortic disectin
*eclampsia/preeclampsia

renal
*AKI

liver
*elevated LFTs
*acute liver failure

ocular
*retinopathy
*retinal hemmorhage

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21
Q

patho of hypertensive crisis

A

acute elevation of bp-> overwhelms andcauses failure of autoregulation system->abrupt increase in bp/vasoconstriction-> mechanical stress and endothelial injury, further contributing to ischemia and target organ damage

RAAS activation leads to further vasoconstriction and thus generting a vicious cycle of continuous injury and subsequent ischemia-> also leads to vascular permeability->leakage of plasma into the vascular wall->activates platelets and coagulation cascade->creating prothrombotic state->leads to further ischemia and organ damage

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22
Q

risk factors for hypertensive crisis

A

female sex

obesity

hypertensive/coronary heart disease

presence of somatoform disorder

higher number of antihipertensive agents at baseline

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23
Q

common causes

A

non adherance w. prescribed therpay

abrupt withdrawal of certain a-htn-> rebound htn (clonidine, bb)

subatnce abuse (cocaine, amphetamines, ecstasy

drug induced interactions (seretonin syndrome

drug-food: tyramine containing foods w. MAOIs

drug disease state interactions: nsaids, sympathomimetics in pts. w. htn

withdrwal(alcohol, opioids, benzos

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24
Q

clinical presentation ofhtn crisis

A

pts may appear asymptomatic (htn urgency) or asymptomatic (emergency)

symptoms
*headahce
N&V
epistaxis
sob
chest pain
dizziness
paresthesia
vision changes

Signs:
focal neurological defecrs
crackles on lung auscultation
increased Scr, bun,lfts
new/worseninf hematuria, proteinuria
ekg changes
changes on fundoscopic examination of the eye
changes on ct of the head (bleed)
mri evidence of cva

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25
Q

mgt og htn urgency

A

timing:
lower bp slowly during first 24-48 hrs using oral meds
no need for icu admission

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26
Q

mgt of htn emergency

A

timing:
1st hour
*decreas DBP by 10-15% or map by 25% w. goal of DBP?100 mmhg

2-6 hr
*SBP 160 mmhg and/or dbp 100-110

6-24 hrs
*maintain baove goals

24-48 hrs
*gradually decrease bp to normal (outpt goal)

requires IV a-htn and icu admission

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27
Q

special considerations for htn emergencies

Aortic Disection

what is it
bp target:
iv a-htn selection:

A

special considerations for htn emergencies

Aortic dissection

what is it: tear that ocurs in inner layer of weakened area of aorta. disrupts normal blood flow to the body

bp target: SBP<120 mmhg w.in first hour,ideally within first 20 min (and hr <60 bpm)

iv a-htn selection: BB (esmolol)then vasodilator (nicardipine, clevidipine, nitroprusside

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28
Q

special considerations for htn emergencies

Ischemic stroke

what is it
bp target:
iv a-htn selection:

A

special considerations for htn emergencies

what is it: blood clot blocks or narrows an artery of the brain, reducing or impeding bloodflow

bp target:BP<185/110 before tpa and <180/05 during tpa infusion.
if no tpa-SBP <220 mmhg

iv a-htn selection:nicardipine, clevidipine, labetalol
AVOID SODIUM NITROPRUSSIDE

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29
Q

special considerations for htn emergencies

Hemorrhagic stroke

what is it
bp target:
iv a-htn selection:

A

special considerations for htn emergencies

what is it: rupture of weakened blood vessel causing bleeding into the surrounding brain

bp target: if SBP 150-220 mmhg: lowrring to <140 mmhg in 60 min is generally safe
if SBP >220 mmhg: lower w. infusion and monitor

iv a-htn selection:
clevidipine, labetalol, nicardipine
AVOID SODIUM NITROPRUSSIDE (due to increased intracranial pressure

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30
Q

special considerations for htn emergencies

severe preeclampsia

what is it
bp target:

A

special considerations for htn emergencies

severe pre-eclampsia or eclampsia

what is it: severe new onset-htn after 20 week sgestation (SBP>160MMHG) or DBP>100+ proteinuris

eclampsia: a convulsive condition progressed by pre-eclampsia

bp target:SBP<140MMHG in 60 min

IV a-htn: hydralazine, labetalol, nicardipine

avoid RASS inhibitors or sodium nitroprusside . not safe for fetus

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31
Q

Vasodilators in HTN CRISIS

sodium nitroprusside

moa:
onset:
duration:
dosing:
AE:
clinical pearls

A

Vasodilators in HTN CRISIS

moa: breaks own nitric oxide->relaxation/dilation of vascular smooth muscle
direct venous an darterial vasodilator

onset:<2 min

duration:1-10min

dosing: IV infusion 0.25-10mcg/kg/min

AE:hypotension(potent), n/v, muscle twitching, cyanide toxicity (accumulation occurs at higher does >2mcg/kg/min) an dlonger trt duration

clinical pearls: caution in pt . high intracranial pressure, ckd

32
Q

Vasodilators in HTN CRISIS

nitroglyceirin
moa:
onset:
duration:
dosing:
AE:
clinical pearls

A

Vasodilators in HTN CRISIS

moa: converted to nitric oxide, acitvates guanylate cyclase, increase cGMP in smooht muscle->dephosphorylation of myosin light chains->vasodilation

onset: immediate

duration: 3-5 min

dosing: 5-200 mcg iv infusion

AE:hypotension, headache, methemblobulinemia, tolerance w. prolonged use

clinical pearls: most often utilized in situations w. coronary ischemia

33
Q

Vasodilators in HTN CRISIS

hydralazine

moa:
onset:
duration:
dosing:
AE:
clinical pearls

A

Vasodilators in HTN CRISIS

hydralazine

moa: direct acting smooth muscle relaxant

onset: 10-80 min

duration: up to 12 hours
dosing: 10-20 mg iv infusion q4-6 hrs

AE: hypotension, tachycardia, flushing, headache

clinical pearls: unpredictable pk profile
safe for use in pregnancy

34
Q

Vasodilators in HTN CRISIS

BETA BLOCKERS
moa:
onset:
duration:
dosing:
AE:
clinical pearls

A

Vasodilators in HTN CRISIS

moa:bblock binding of neurotransmitters norepinephrine and epinephrine to beta adrenergic receptors

most commonly used:

Labetalol
onset: 5-10 min
duration: 180-360 min
dosing: bolus: 10-20 mg IV q10 min
infusion: initiate at 0.5-2 mg/min

AE: hypotension, bradycardia/heartblock, orthostatic hypotension

clinical pearls: most htn emergencies, safe in pregnancy, caution in acute HF

metoprolol
onset: 5-15 min
duration: 120-360 min
dosing: bolus: 5-15 mg iv q5-15 min
infusion: initiate at 0.5-2 mg/min

AE: hypotension, bradycardia/heartblock,

clinical pearls: caution in acute HF

Esmolol
onset: 1-2 min
duration: 10-20 min
dosing: bolus: 250-500 mcg/kg/min
infusion: 50-100 mcg/kg/min

AE: hypotension, bradycardia/heartblock,

clinical pearls: drug of choice in aortic dissection. caution in acute hf

35
Q

Vasodilators in HTN CRISIS

CCB
moa:
onset:
duration:
dosing:
AE:
clinical pearls

A

Vasodilators in HTN CRISIS

CCB

moa: bind to and block voltage gated L type caclium channels found on smooth muscles of arterial vessels-> vasodilation

2 most common: clevedipine, nicardipine

clevedipine
onset:2-4 min
duration:5-15 min
dosing:
AE:hypotension, headache, tachycardia, hypertriglyceridemia

clinical pearls: most htn emergensies, caution w. coronary ischemia. CI w. soybean/eggs

nicardipine:
onset: 5-10 min
duration:15-30 min
dosing:
AE: hypotension, tachyardia, headache, flushing, local phlebitis

clinical pearls: most hypertensive emergencies, not generally utilized in acute hf . caution w. coronary ischemia

36
Q

other agents for htn crisis

A

enaliprilat

fenoldopam: dopamine receptor agonst

37
Q

DKA VS HHS

what is it?

A

most serious scute metabolic complications of diabetes

38
Q

dka vs hhs

patho

A

dka: absolute insulin deficiency- has ketoacidosis

hhs: relative insulin deficiency-hyperosmolality

similar: hyperglycemia

39
Q

causes of dka

A

infection (common uti and pna)

MI

medications (ggc)
noncompliance w. therapy

poor “sick day” mgt

pancreatitis

drug/alcohol abuse

new onset T1DM

inadequatedose of insulin

40
Q

clinical presentations
dka vs hhs

A

onset:
dka: hours to days
hhs:several days to weeks

clinical picture:
dka: polydypsia, polyuria, polupjagia, weightloss, weakness, kussmal respirations, n/v abdominal pain
hhs: vomiting, dehydration , seizures, hemiparesis

glucose:
dka:>250
hhs:>600

acidosis:
dka: acidosis
hhs: normal

anion gap
dka: >12
hhs:variable

ketones
dka:positive
hhs: negative

serum osmolality
dka:<320
hhs:>320

41
Q

pillars of therapy for dka and hhs

A

IV FLUIDS

BICARB

INSULIN: REGULAR

POTASSIUM

42
Q

pillas of theraoy

fluid managmt

A

initial: 15-20 ml/kg for first hour

subsequent….

severe hypovolemia:
admin ns @1L/hr

mild dehydratrion:
serumna normal or high->1/2 ns (250-500ml/hr) depending on hydraiton status

low serum na-> ns 250-500 ml/hr depending on hydration status

cartiogenic shock: utilize vasopressors and monitor hemodynamics closely

once bg gets to…
dka: 200
hhs300

change to 1/2 ns/d5w at 150-250 ml/hr:

43
Q

pillars of theraoy for dka and hhs

insulin theraoy

A

regular insulin drip: short t1/2, easy titration

dosing: 0.1 U/kg iv bolus->0.1 u/kg/hr continuous infusion

or
0.12u/kg/hr continuous infusion (IV BOLUS

low dose insulin infusions should drop insulin 50-75 mg/dl

when pt reaches dka<200
hhs<300, infusion rate hsould be dropped to 0.02-0.05

GOAL: DKA: 150-200 until resolition of dka
HHS: 200-300 until pt is mentally alert

q1hr glucose checks

44
Q

dka and hhs resolutions

A

dka:
bg<200
AND2 of following
serum bicarb>15
venous ph>7.3
aanion gap<12

hhs
normal osmolality AND
normal mental ststaus

45
Q

tranition from iv sq insulin

A

start sq insulin and overlap w. iv fo r1-2 hrs

if hx of dm: can go back to prior insulin dose (maybe reduced dose)

unsulin naive: multidose regimen w. basal (glargine+detemir)+ bolus (lispro, aspart, glisine) started at 0.5-0.8 u /kg/day

46
Q

pillars of therapy for dka and hhs

K mgt

A

mild-mod hyperkalemia is common

unsilin pushes k into cell, causing hypokalemia, also due to volume expansion and acidosis

  1. check K before intiaiting insulin

a: if k <3.3: hold insulin and replerw @20-30 meq until k>3.3

if k3.3-5.3: 20-30 meq given w. every l of fluid

if k>5.2: do not give k until it falls below ULN

check k q4-6 hrs

47
Q

pillars of theraoy for dka and hhs

bicarb

A

use ocntrversial

risks: kypokalemia
decrease in tissue o2 take
cerebral edema
paradoxal cns acidemia

only indicated in pts w. ph <6.9:
100 mmol (2 ampules) in 400mL of h20 +20 meq of kcl

48
Q

phosphate

A

hyperglycemic crises cause elevated serum phosphate

insulin therpay decreases phosphate

rcts fail to show beneficial effect

indicated only in (cardiac dysfunction, anemia, respiratory depression, serum phos ocncentration <1:

cREFUL repletion 20-30 meq /L of fluids

49
Q

complicaiton s of hyperglycemia crises treatment

A

a)hypoglycemia: check q 1-2 hrs whil eon IV insulin infusion

hypokalemia: bmps sheck q4-6 hrs while insulin infusion is running

hyperchloremic non anion gap secondary to infusion og Cl containing fluids during treatment

cerbral edema: occurs 1-3% of dka episodes in children

rare in adults

prevention: avoid excessive hgydration
treatment: mannitol

50
Q

approach to analgesia and sedation

A

Analgesia: treat an dprevent pain first. give boluses or infusion of opioids, have breakthorugh prn opioids

ll
i
v
deation: ig agitiation ot controlled by opioids, then can use propofol, dexmedetomidine or ketamine.
or prn boluses of benzos

delerium:
screan and identify early
mompharm interventions
consider pharm options

51
Q

analgesia

A

assess pain:
CPOT critical pain observation tool
CPOT significant pain>2

behavioral pain scale

52
Q

agents for pain treatment

A

morphine
fentanyl
hydromorphone

53
Q

pain treatment

morphine

onset
duration
dose
pearls

A

onset :5-10 min

duration: 3-6 hrs

dose: bolus: 2-10 mg
infusion: 1-10mg/hr

pearls:
active metabolite 6-
accumulates in renal impairment

histmaine release (hypotension, bronchospasm, urticaria

54
Q

fentanyl

onset
duration
dose
pearls

A

onset: seconds

duration: 1-2 hrs

dose: 50-100 mcg
infusion: 25-300 mcg/hr

pearls
hepatic metabolism
cyp3a4 interaactions
tachyphylaxis

55
Q

hydromorphone

A

onset: 5 min

duration: 2-4 hrs
dose: 0.-2 mg
0.5-3 mg

pearls:
good in renal impairment
optional fo rfentanyl tolerance
minimal histamine release
available as PCA

56
Q

Sedation

A

RASS score

richmond agitation sedation scale

goal is light sedation

57
Q

sedation agents

propofol

moa:
pd
onset
duration
AE:
considerations

A

moa: stimulates gaba and inhibits nmda receptors

pd: hypnotic, anti anxiety, amnestic, anticonvulsant

onset:<1 min

duration: 10-15 min

AE: resp. depression, hypotension, bradycardia, decrease CO, hypertriglyceridemia, propofol related infusion syndrome (PRIS)

considerations
NO analgesic properties
highly lipid soluble
LIPID EMUlsions
avoid in pts w. egg allergy,s ulfites or soybean allergies
monitor bp, hr, trg

58
Q

dexmedetomidine (presedex)

moa:
pd
onset
duration
AE:
considerations

A

moa: a2 agonist, depresses release of NE and dopamine in cns

indications: procedural sedation and for sedarion for mechanical ventilarion NOT>24 hrs

pd: sedative and analgesic properties

onset
duration
AE: bradycardia, hypotension

considerations:
no resp depression.effects are similar to naturallly occuring sleep
opioid sparing effexts
useful as adjunct therapy for alcohol withdrawal

. risk of hypotension
RAAS score of -3 unoikeyl, risk of withdrawal w. prolonged use
drug induced fever

59
Q

sedation: benzos

midazolam

A

moa:
pd
onset:2-5 min
duration: 1-2 hrs
AE:
considerations:
lipophillic
acumulates in renal impairment
primary use for status epilepticus

60
Q

sedation: lorazepam

A

moa:
pd
onset: 5-20 min
duration:2-6 hrs
AE:
considerations: propylene glycol acidosis

61
Q

sedation: diazepam

A

moa:
pd
onset5-10 min
duration
AE: t1/2 44-100 hrs
considerations:
can taper quickly
sranding doses used in alcohol withdrawal

62
Q

benzo drawbacks

A

increase delerium
increase time on ventilator
increase length of icu stay

63
Q

when should benzos should reserved for in icu

A

status epilepticus

extreme alcohol withdrawl symptoms
serve ARDS requiring deep sedation

64
Q

sedation: ketamine

A

indications:

moa: nmda antagonist
mu and kappa agonists
muscarining antagonist
inhibit reuptake of seretonin, NE and dopamine

65
Q

ketamine dosing

A

respone is dose dependent for pain>anesthesia> and status epilepticus

66
Q

ketamine
moa:
pd
onset
duration
AE:
considerations

A

moa:
pd
onset: iv anesthesia = withiin 30 seconds
im: anesthetic effect. 3-4 min, analgesia 15 min

durationiv anesthetic: 5-10 min. recovery 1-2 hours
im anethetic: 12-25 min
analgesia 15-20 min, recovery 1-2 hours

AE:emergence reaction(hallucinations and agitation), oral secretions, tachycardia, HTN

considerations
favorable hemodynamic,
bronchodilator effects
opioid sparing effects

67
Q

Delerium

A

acute chages in mental sttaus w. inayttention, disorganized thinking

68
Q

elerium risk factors modifiable and non modifiable

A

modifiable: benzo use
blood transfusions

non modifiable: increased age
dementia history
prior coma
pre icu emergency/ trauma
increase APACHE score

69
Q

non pharm internventions for delerium

A

reorient patient
us eof hearing aids or glasses
lmimit nois eand light
encourage sleep wake cycle
early mobilization
family presence
music therapy
limit use of benxos and anti-ach

70
Q

treatment of delerium

A

guidelines do not suggest ANY PHARM agent in PREVENTION OF delerium

suggest dexedemotidine for delerium in mechannically ventalated pts where agitation is precluding weaning/exubation (lo recommendation)
suggets not routinely using haloperido, or hmg-coA reductase inhibitor to treat delerium

71
Q

neuromuscular blockers indications

A

facitilate mechanical ventilation

minimize o2 consumption

acute respiratory distress sysndrome (ARDS)

increased muscle activity(tetany), meuroleptic malignant syndrome, antishivering
increased intracranial pressure

72
Q

pros and cons of nmb

A

pros: inhibit diaphragmatic function and reduce chest wall rigidity

reduces oxygen consumption

elimnates work of breathing

cons:
pt cannot communicate
no analgesic or sedative properties
increase risk of dvt and skin breakdown
corneal abrasian risk
critical illness polyneuropathy

73
Q

nmb monitoring for neuromuscular bockase

A

train of four using a peripheral nerve stimulatory

2 twitches=80-90% blockage->usual goal

74
Q

non depolarization nmb agents

A

rocuronium, cistracurium
vercuronium

75
Q

depolarizing nmb agent

A

succinylocholine
Plasma psuedo cholinesterase

Critical Care/Hematology/Oncology (4 decks)

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