Exam 1

Question 1

What is the ICU

Answer 1

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

Question 2

types of intensive care units

Answer 2

MICU
SICU
CVICU
TICU
NSCU
PICU
NICU

Question 3

Roles of clinical pharmacists role in the ICU

Answer 3

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

Question 4

tpx considerations in critically ill patients

Answer 4

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

Question 5

FAST HUGS BID meaning

Answer 5

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

Question 6

FAST HUGS

F

why is it important?
considerations:

Answer 6

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

Question 7

FAST HUGS

A

why is it important?
considerations:

Answer 7

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

Question 8

FAST HUGS

S

why is it important?
considerations:

Answer 8

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

Question 9

FAST HUGS

T

why is it important?
considerations:

Answer 9

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.

Question 10

FAST HUGS

H

why is it important?
considerations:

Answer 10

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

Question 11

FAST HUGS

U

why is it important?
considerations:

Answer 11

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

Question 12

FAST HUGS

G

why is it important?
considerations:

Answer 12

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

Question 13

FAST HUGS

S

why is it important?
considerations:

Answer 13

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

Question 14

FAST HUGS

B

why is it important?
considerations:

Answer 14

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

Question 15

FAST HUGS

I

why is it important?
considerations:

Answer 15

FAST HUGS

Indwelling catheters

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

considerations:

Question 16

FAST HUGS

D

why is it important?
considerations:

Answer 16

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

Question 17

Hypertensive crisis definition

Answer 17

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

Question 18

hypertensive urgency

Answer 18

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

Question 19

hypertensive emrgency

Answer 19

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

Question 20

Examples of end organ dmaage

CV
Neurological
vascular
renal
liver
ocular

Answer 20

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

Question 21

patho of hypertensive crisis

Answer 21

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

Question 22

risk factors for hypertensive crisis

Answer 22

female sex

obesity

hypertensive/coronary heart disease

presence of somatoform disorder

higher number of antihipertensive agents at baseline

Question 23

common causes

Answer 23

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

Question 24

clinical presentation ofhtn crisis

Answer 24

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

Question 25

mgt og htn urgency

Answer 25

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

Question 26

mgt of htn emergency

Answer 26

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

Question 27

special considerations for htn emergencies Aortic Disection what is it bp target: iv a-htn selection:

Answer 27

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

Question 28

special considerations for htn emergencies Ischemic stroke what is it bp target: iv a-htn selection:

Answer 28

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

Question 29

special considerations for htn emergencies Hemorrhagic stroke what is it bp target: iv a-htn selection:

Answer 29

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

Question 30

special considerations for htn emergencies severe preeclampsia what is it bp target:

Answer 30

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

Question 31

Vasodilators in HTN CRISIS sodium nitroprusside moa: onset: duration: dosing: AE: clinical pearls

Answer 31

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

Question 32

Vasodilators in HTN CRISIS nitroglyceirin moa: onset: duration: dosing: AE: clinical pearls

Answer 32

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

Question 33

Vasodilators in HTN CRISIS hydralazine moa: onset: duration: dosing: AE: clinical pearls

Answer 33

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

Question 34

Vasodilators in HTN CRISIS BETA BLOCKERS moa: onset: duration: dosing: AE: clinical pearls

Answer 34

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

Question 35

Vasodilators in HTN CRISIS CCB moa: onset: duration: dosing: AE: clinical pearls

Answer 35

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

Question 36

other agents for htn crisis

Answer 36

enaliprilat fenoldopam: dopamine receptor agonst

Question 37

DKA VS HHS what is it?

Answer 37

most serious scute metabolic complications of diabetes

Question 38

dka vs hhs patho

Answer 38

dka: absolute insulin deficiency- has ketoacidosis hhs: relative insulin deficiency-hyperosmolality similar: hyperglycemia

Question 39

causes of dka

Answer 39

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

Question 40

clinical presentations dka vs hhs

Answer 40

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

Question 41

pillars of therapy for dka and hhs

Answer 41

IV FLUIDS BICARB INSULIN: REGULAR POTASSIUM

Question 42

pillas of theraoy fluid managmt

Answer 42

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:

Question 43

pillars of theraoy for dka and hhs insulin theraoy

Answer 43

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

Question 44

dka and hhs resolutions

Answer 44

dka: bg<200 AND2 of following serum bicarb>15 venous ph>7.3 aanion gap<12 hhs normal osmolality AND normal mental ststaus

Question 45

tranition from iv sq insulin

Answer 45

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

Question 46

pillars of therapy for dka and hhs K mgt

Answer 46

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

Question 47

pillars of theraoy for dka and hhs bicarb

Answer 47

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

Question 48

phosphate

Answer 48

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

Question 49

complicaiton s of hyperglycemia crises treatment

Answer 49

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

Question 50

approach to analgesia and sedation

Answer 50

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

Question 51

analgesia

Answer 51

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

Question 52

agents for pain treatment

Answer 52

morphine fentanyl hydromorphone

Question 53

pain treatment morphine onset duration dose pearls

Answer 53

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

Question 54

fentanyl onset duration dose pearls

Answer 54

onset: seconds duration: 1-2 hrs dose: 50-100 mcg infusion: 25-300 mcg/hr pearls hepatic metabolism cyp3a4 interaactions tachyphylaxis

Question 55

hydromorphone

Answer 55

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

Question 56

Sedation

Answer 56

RASS score richmond agitation sedation scale goal is light sedation

Question 57

sedation agents propofol moa: pd onset duration AE: considerations

Answer 57

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

Question 58

dexmedetomidine (presedex) moa: pd onset duration AE: considerations

Answer 58

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

Question 59

sedation: benzos midazolam

Answer 59

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

Question 60

sedation: lorazepam

Answer 60

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

Question 61

sedation: diazepam

Answer 61

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

Question 62

benzo drawbacks

Answer 62

increase delerium increase time on ventilator increase length of icu stay

Question 63

when should benzos should reserved for in icu

Answer 63

status epilepticus extreme alcohol withdrawl symptoms serve ARDS requiring deep sedation

Question 64

sedation: ketamine

Answer 64

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

Question 65

ketamine dosing

Answer 65

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

Question 66

ketamine moa: pd onset duration AE: considerations

Answer 66

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

Question 67

Delerium

Answer 67

acute chages in mental sttaus w. inayttention, disorganized thinking

Question 68

elerium risk factors modifiable and non modifiable

Answer 68

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

Question 69

non pharm internventions for delerium

Answer 69

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

Question 70

treatment of delerium

Answer 70

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

Question 71

neuromuscular blockers indications

Answer 71

facitilate mechanical ventilation minimize o2 consumption acute respiratory distress sysndrome (ARDS) increased muscle activity(tetany), meuroleptic malignant syndrome, antishivering increased intracranial pressure

Question 72

pros and cons of nmb

Answer 72

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

Question 73

nmb monitoring for neuromuscular bockase

Answer 73

train of four using a peripheral nerve stimulatory 2 twitches=80-90% blockage->usual goal

Question 74

non depolarization nmb agents

Answer 74

rocuronium, cistracurium vercuronium

Question 75

depolarizing nmb agent

Answer 75

succinylocholine Plasma psuedo cholinesterase