Exam 1 Flashcards
What is the ICU
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
types of intensive care units
MICU
SICU
CVICU
TICU
NSCU
PICU
NICU
Roles of clinical pharmacists role in the ICU
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
tpx considerations in critically ill patients
- 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
FAST HUGS BID meaning
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
FAST HUGS
F
why is it important?
considerations:
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
FAST HUGS
A
why is it important?
considerations:
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
FAST HUGS
S
why is it important?
considerations:
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
FAST HUGS
T
why is it important?
considerations:
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.
FAST HUGS
H
why is it important?
considerations:
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
FAST HUGS
U
why is it important?
considerations:
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
FAST HUGS
G
why is it important?
considerations:
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
FAST HUGS
S
why is it important?
considerations:
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
FAST HUGS
B
why is it important?
considerations:
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
FAST HUGS
I
why is it important?
considerations:
FAST HUGS
Indwelling catheters
why is it important?
monitor sites for signs of infection
assessing the lines or if they can be removed
considerations:
FAST HUGS
D
why is it important?
considerations:
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
Hypertensive crisis definition
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
hypertensive urgency
acute htn w. evidence of new or worsening target organ damage
hypertensive emrgency
pts w. acute condition of very high bp and evidence or new or worsening target organ dmaage
Examples of end organ dmaage
CV
Neurological
vascular
renal
liver
ocular
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
patho of hypertensive crisis
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
risk factors for hypertensive crisis
female sex
obesity
hypertensive/coronary heart disease
presence of somatoform disorder
higher number of antihipertensive agents at baseline
common causes
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
clinical presentation ofhtn crisis
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
mgt og htn urgency
timing:
lower bp slowly during first 24-48 hrs using oral meds
no need for icu admission
mgt of htn emergency
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
special considerations for htn emergencies
Aortic Disection
what is it
bp target:
iv a-htn selection:
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
special considerations for htn emergencies
Ischemic stroke
what is it
bp target:
iv a-htn selection:
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
special considerations for htn emergencies
Hemorrhagic stroke
what is it
bp target:
iv a-htn selection:
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
special considerations for htn emergencies
severe preeclampsia
what is it
bp target:
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
Vasodilators in HTN CRISIS
sodium nitroprusside
moa:
onset:
duration:
dosing:
AE:
clinical pearls
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
Vasodilators in HTN CRISIS
nitroglyceirin
moa:
onset:
duration:
dosing:
AE:
clinical pearls
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
Vasodilators in HTN CRISIS
hydralazine
moa:
onset:
duration:
dosing:
AE:
clinical pearls
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
Vasodilators in HTN CRISIS
BETA BLOCKERS
moa:
onset:
duration:
dosing:
AE:
clinical pearls
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
Vasodilators in HTN CRISIS
CCB
moa:
onset:
duration:
dosing:
AE:
clinical pearls
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
other agents for htn crisis
enaliprilat
fenoldopam: dopamine receptor agonst
DKA VS HHS
what is it?
most serious scute metabolic complications of diabetes
dka vs hhs
patho
dka: absolute insulin deficiency- has ketoacidosis
hhs: relative insulin deficiency-hyperosmolality
similar: hyperglycemia
causes of dka
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
clinical presentations
dka vs hhs
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
pillars of therapy for dka and hhs
IV FLUIDS
BICARB
INSULIN: REGULAR
POTASSIUM
pillas of theraoy
fluid managmt
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:
pillars of theraoy for dka and hhs
insulin theraoy
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
dka and hhs resolutions
dka:
bg<200
AND2 of following
serum bicarb>15
venous ph>7.3
aanion gap<12
hhs
normal osmolality AND
normal mental ststaus
tranition from iv sq insulin
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
pillars of therapy for dka and hhs
K mgt
mild-mod hyperkalemia is common
unsilin pushes k into cell, causing hypokalemia, also due to volume expansion and acidosis
- 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
pillars of theraoy for dka and hhs
bicarb
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
phosphate
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
complicaiton s of hyperglycemia crises treatment
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
approach to analgesia and sedation
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
analgesia
assess pain:
CPOT critical pain observation tool
CPOT significant pain>2
behavioral pain scale
agents for pain treatment
morphine
fentanyl
hydromorphone
pain treatment
morphine
onset
duration
dose
pearls
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
fentanyl
onset
duration
dose
pearls
onset: seconds
duration: 1-2 hrs
dose: 50-100 mcg
infusion: 25-300 mcg/hr
pearls
hepatic metabolism
cyp3a4 interaactions
tachyphylaxis
hydromorphone
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
Sedation
RASS score
richmond agitation sedation scale
goal is light sedation
sedation agents
propofol
moa:
pd
onset
duration
AE:
considerations
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
dexmedetomidine (presedex)
moa:
pd
onset
duration
AE:
considerations
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
sedation: benzos
midazolam
moa:
pd
onset:2-5 min
duration: 1-2 hrs
AE:
considerations:
lipophillic
acumulates in renal impairment
primary use for status epilepticus
sedation: lorazepam
moa:
pd
onset: 5-20 min
duration:2-6 hrs
AE:
considerations: propylene glycol acidosis
sedation: diazepam
moa:
pd
onset5-10 min
duration
AE: t1/2 44-100 hrs
considerations:
can taper quickly
sranding doses used in alcohol withdrawal
benzo drawbacks
increase delerium
increase time on ventilator
increase length of icu stay
when should benzos should reserved for in icu
status epilepticus
extreme alcohol withdrawl symptoms
serve ARDS requiring deep sedation
sedation: ketamine
indications:
moa: nmda antagonist
mu and kappa agonists
muscarining antagonist
inhibit reuptake of seretonin, NE and dopamine
ketamine dosing
respone is dose dependent for pain>anesthesia> and status epilepticus
ketamine
moa:
pd
onset
duration
AE:
considerations
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
Delerium
acute chages in mental sttaus w. inayttention, disorganized thinking
elerium risk factors modifiable and non modifiable
modifiable: benzo use
blood transfusions
non modifiable: increased age
dementia history
prior coma
pre icu emergency/ trauma
increase APACHE score
non pharm internventions for delerium
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
treatment of delerium
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
neuromuscular blockers indications
facitilate mechanical ventilation
minimize o2 consumption
acute respiratory distress sysndrome (ARDS)
increased muscle activity(tetany), meuroleptic malignant syndrome, antishivering
increased intracranial pressure
pros and cons of nmb
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
nmb monitoring for neuromuscular bockase
train of four using a peripheral nerve stimulatory
2 twitches=80-90% blockage->usual goal
non depolarization nmb agents
rocuronium, cistracurium
vercuronium
depolarizing nmb agent
succinylocholine
Plasma psuedo cholinesterase
