Critical Care: FASTHUGS BID and PADIS Flashcards

1
Q

FASTHUGS BID

as a concept

A

aspects of critical care medicine that can be appplied bid to critically ill pts

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2
Q

what does FASTHUGS BID stand fore

A
  • Feeding
  • Analgesia
  • Sedation
  • Thrombo 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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3
Q

Enteral vs parenteral feeding

A
  • Enteral preferred to TPN
    • Entereral: uses your gut, natural
    • TPN: risk of infection and thromosis
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4
Q

Consequences of malnutrition in ICU

A

Malnutrition → impaired immune function →
- Increased susceptibility fo infetion
- Impaired wound healing
- Bacterial overgrowth in GI tract
- Increased risk for development of decubitus ulcers

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5
Q

Reasons a pt may be agitated in the ICU

A
  • Anx, pain
  • Lack of homeostsais
  • Withdrawal
  • BZD use
  • Sleep-wake cycle disruption
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6
Q

Sedation assessment tools

A
  • Richmond Agitation-Sedation Scale (RAS): light sedtion is supported in the guideliens for most situations
  • Sedation Agittaion Scale (SAS)
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7
Q

ICU risk factors for VTE

A
  • Central venous catheterization
  • Immobility
  • Trauma/burns
  • Critical illness (sepsis)
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8
Q

who gets VTE ppx in ICU and what are the options

A
  • VTE ppx to all ICU pts (unless high bleed risk duh)
  • Pharm options
    • lovenox 40mg QD or 30mg BID
    • heparin 5000U Q8H - esp in renally impaired pts
    • pts with high bleed risk, can do mechanical ppx (stockings)
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9
Q

Mechanical ventilation

A

endotracheal tube (ET) is placed into trachea through moouth and hooked up to a ventilator

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10
Q

VAP ppx

ventilator acquired PNA

A
  • Elevate head and thorax above the bed at 30-45 degree angle → reduced GI reflux and nosocomial PNA
  • Apply anti-septic mouthwash (chlorhexidine) topically to oral caity TID → prevent bacterial growth in ET
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11
Q

Stress related mucosal damage (SRMD)

A

acute errosive, inflammatory upper GI insult associated with critical illness
- can lead to clincally significant bleedng

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12
Q

who qualfiies for SRMD ppx

stress related mucosal damage

A
  • 1 of the following
    • Mechanical ventialtion > 48 hrs
    • INR > 1.5
    • PTT >2x ULN
    • Plts < 50
  • 2 of the following
    • Drugs with increased bleed risk: steroids, warfarin, treatment heparin
    • Shock, sepsis, hypotension, vasopressors
    • Hepatic or renal failure
    • Multiple traumas or head or spinal
    • Burns >35% BSA
    • Organ transplant
    • Hx of upper GI bleed or PUD

situations that would make you do a double take if pt on anticoag

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13
Q

SRMD ppx pharm

A

PPI, H2RA

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14
Q

hyperglycmia is common in ICU pts dt whaat risk factors

A
  • Stress
  • Meds (steroids, beta blockers, vasopressors)
  • TPN or dextrose
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15
Q

glycemia control in ICU

A
  • Maintain BG of 140-180 (ICU pts may not tolerate hypoglycemia well dt delayed detection → do NOT impleemnt strict controls)
  • non diabetics: insulin SS - if pt needs a lot each day, can consider long acting insulin
  • diabetcs: cotinue home long acting if pt is eating, but at a reduced dose because they likely are eating less (and less sugary foods) in hospital
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16
Q

spontaneous bbreathign trial

A
  • performed on pts on mechanical ventilation to assess their ability to breathe with little to no ventaltion support
  • Mechanical ventilatoin has many complications and it is important to get pts off it ASAP
  • Perform QD
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17
Q

causes of constipation in critically iill pts

A
  • immobility
  • med ADR
  • shock
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18
Q

constipation mangement in ICU

A
  • monitor bowel movement QD
  • if constipation occurs, add bowel regimen
  • if pt on opioids, just have a standing order
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19
Q

causes of diarrhea in critically ill

A
  • iinfectio (c. diff)
  • feeds
  • bowel regimen too good
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20
Q

Peripheral venous catheter

A

peripheral vein for venous access to admin IV therapy

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21
Q

CVC

A

terminate in superior vena cava

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22
Q

Arterial line

A
  • in luen of artery to provide continuous display or accurate bp* and access frequent blood samples
    • *important for pts on vasopressors
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23
Q

Foley

A

passes through urethra and into bladder to drain urine

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24
Q

Rectal tubes

A

fecal management; contain and divert fecal waste

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25
Q

benefits of precedex

A
  • NO resp depreession
  • effects similar to natural sleep
  • anaglesic
  • useful as adjunct therapy for EtOH withdrawal
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26
Q

disadvantages of precedex

A
  • risk of hypotension
  • light sedatve (RASS score -3 or lower unlikely)
  • risk of wthdrwa lwith pronlonged use (HTN, tachycardia)
  • case reports of drug inducd fever
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27
Q

benefits of ketamine

A
  • favorable hemodynamics - no bradycardia and hypotension
  • bronchodilator effects - NO resp depression
  • opioid sparing
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28
Q

ketamine ADR

A
  • emergence reaction (pretreat with benzo or propofol) - esp in dementia and schizo
  • oral secretions (differentiate from infectious gunk)
  • tachycardia
  • HTN
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29
Q

delirium

A

acute changes in mental status with inattention, disorganized thinking, and altered level of consciousness not explained by pre-existing conditions

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30
Q

delirirum sequalae/consequences

A
  • increased mortality
  • cog impairment
  • functional decline
  • increase health system costs
  • prolonged mechanical ventilation
  • increased length of stay
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31
Q

non-pharm delirim prevention

A
  • re-orient patiet
  • use of hearing aids or galsses
  • limit noise and light at night
  • encoruage natural sleep-wake sycle
  • early mobilization
  • family presence
  • music therapy
  • limit use of benzos and anticholinergics

fun fact: guidelines have NO recommendatios for pharm preventio - don’t do it

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32
Q

indications for paralytic admin

A
  • facilitate mechanical ventilation (intubation)
  • minimize O2 consumption in pts with ARDS
  • increased muscle activity (tetany, NMS)
  • increased intracranial pressure or intra-abdominal preassures
  • surgical procedures
  • rapid sequece intubation
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33
Q

what drug class is used as paralytics

A

neuromusclar blockers

34
Q

benefits of neuromuscular blockers

A
  • inhibit diaphragmatic function and reduce chest wall rigidity
  • reduce O2 consumptom
  • eliminate work of breathing
35
Q

disadvantages of neuromuscular blockde

A
  • pt canNOT communicate
  • no analgesic or sedative properties
  • increased risk of DVT and skin breakdown
  • corneal abrasion risk -> give artificial tears Q2H
  • critical illness polyneuropathy

GIVE HEAVY HEAVY SEDATION (precedex doesn’t cut it)

36
Q

neuromuscular infusion monitoring

A

train of four using a peripheral nerve stimulator
- goal is 2 twitches

37
Q

neuromuscular blocker agents

A
  • non-depolarizing agents (can be used IV drip): cistaracurium, rocuronium, vecuronium
  • depolarizing agent: succinylcholine (usually used for sedation, it doesn’t come in a drip)

avoid succinylcholin in pts with malignant hyperthermia or hyper K

38
Q

which do you treat first: pain or agitaiton?

A

pain

the agitation may be caused by pain

39
Q

what is the pain assessment tool and what is the associated treatment goal

A

CPOT (critical care pain observatio tool)
- score > 2 indicates significant pain
- goal is < 2

40
Q

what are our pain meds in ICU

A
  • opioids: morphine, fentanyl, hydromorphone
  • APAP - liver caution
  • NSAID - increased risk of GI bleed and caution in AKI
  • methadone - slow titration to avoid QTc prolongation
  • gabapentin - onset can be days
  • ketamine
41
Q

morphine onset and duration

A
  • onset: 5-10 min
  • duration: 3-6 hrs
42
Q

fentanyl onset and duration

A
  • onset: seconds
  • duration: 1-2 hrs
43
Q

hydromorphone onset and duration

A
  • onset: 5 min
  • duration: 2-4 hrs
44
Q

ICU pain morphine dose

A
  • bolus: 2-10 mcg
  • infusion: 1-10 mcg/hr
45
Q

ICU pain fentayl dose

A
  • bolus: 50-100 mcg
  • infusion: 25-300 mcg/hr

if doing an opioid infusion (which isn’t preferred over bolus), fentayl is drug of choice

46
Q

ICU pain hydromorphone dose

A
  • bolus: 0.5-2 mg
  • infusion: 0.5-3 mg/hr
47
Q

morphine considerations

A
  • active metabolite
  • accumulates in AKI -> do NOT use in AKI
48
Q

morphine ADR

A

histamine release
- hypotension
- bradycardia
- urticaria - itching is a normal response, not an allergy

techincally possible for all opioids, seen often with morphine

49
Q

fentanyl considerations

A
  • hepatic metabolism
  • CYP3A4 DDI
  • pts can develop tolerance/tachyphylaxis
50
Q

hydromorphone considerations

A
  • good in renal impairment
  • option if pt has fentyl tolerance
  • minimal histamine relase
  • available as PCA
51
Q

Sedation assessment scale

A

RASS (richond agitation sedation scale)
- goal is generally -2 to 0 (light sedation)

52
Q

sedative agents

A
  • propofol
  • precedex
  • ketamine
  • prn benzos (midazolam, lorazepa, diazepam) - boluses preferrred
53
Q

propofol MOA

A

stimulate GABA and inhibit NMDA receptors

54
Q

precedex MOA

A

alpha adrenergic agonst (like clonidine) -> decreased release of NE and DA in CNS

55
Q

ketamine MOA

A
  • NMDA antag
  • mu and kappa agonsit
  • muscarinic acetylcholine receptor antag
  • inhibit reuptake of serotoin, NE, DA
56
Q

propofol PD

effects

A
  • hyponotic
  • anxiolytic
  • amnestic
  • anticonvulsant - potentilaly first line in SE or severe EtOH withdrawal

NOT an analgesic

57
Q

precedex PD

effects

A

analgesic and sedative

58
Q

propofol onset and duraiotn

A
  • onset < 1 min
  • duration 10-15 min (extra rapid hepatic clearance)

quick on and off

59
Q

propofol ADR

A
  • resp depression - MUST be intubated
  • hypotension - can give to pts in shock, if pt hypotensive dt sedation and NOT shock, switch off propofol
  • bradycardia
  • dereased cardiac output
  • hyper TG
  • propofol related infusion sundrome (extreme acidossi)

montior: BP, HR, TG, anion gap/lactate, CK

60
Q

propofol considerations

A
  • highly lipid soluble -> long term admin can lead to sautration of peripheral tissues -> takes longer to clear
  • lipid emultoin -> provides 1.1 kcal/mL
  • avoid in pts with egg, sulfites, soy bean allergies
61
Q

precedex ADR

A
  • bradycardia
  • hypotnsion
62
Q

midazolam onset and duration

A
  • onset 2-5 min
  • duration 1-2 hrs
63
Q

midazolam sedation dose

A
  • bolus 2-4 mg
  • infusion 1-4 mg/hr
64
Q

midazolam consdierations

A
  • lipophilic
  • active metabolite
  • accumulates in renal impairment
65
Q

lorazepam onset and duration

A
  • onset 5-20 min
  • duration 2-6 hrs
66
Q

lorazepam sedation dose

A
  • bolus 1-2 mg
  • infusion 0.5-4 mg/hr
67
Q

lorazepam considerations

A

CAN use in hepatic/renal failure

68
Q

lorazepam ADR

A
  • propylene glycol acidosis (anion gap acidoss)
69
Q

diazepam onset and duration

A
  • onset 5-10 min
  • duration: long, its half life is 44-100 hrs

basiclaly tapers itself off with such a long half life

70
Q

diazepam considerations

A

active metabolite

71
Q

consequences of benzo sedatoin

A
  • increased risk of delirium
  • ncreased time on vent (dt resp depression adr)
  • increase stay in ICU
72
Q

when to use benzos for sedation

A
  • SE
  • extreme EtOH withdrwal
  • severe ARDS requirng sedation
73
Q

ARDS

a

A

acute respiratory distress syndrome

74
Q

ketamine indications

A
  • anesthesia
  • pain
  • rapid sequence intubation
  • acute severe agitation
  • SE
  • treatment resitant depression
  • PTSD
75
Q

ketamine dosing for pain and associated onset and duration (formula specific)

A

0.15-0.5 mg/kg/hr

  • IM onset: 10-15 min
  • IM duration: 15-30 min
76
Q

ketamine dosing for sedation and associated onset and duration (formula specific)

A

0.5-2 mg/kg/hr

(onset/duration)
- IV: within 30 seconds / 5-10 min
- IM: 3-4 min / 5-10 min

77
Q

ketamine dosing for SE

A

> 2 mg/kg/hr

78
Q

modifiable delirium risk factors

A
  • benzo use
  • blood transfusions
79
Q

non-modifiable delirium risk factors

A
  • old ae
  • hx dementia
  • prior coma
  • pre-ICU emergeny surgery/trauma
  • high APACHE score
80
Q

pharm options for delirium

A
  • start with opioids - maybe it was pain induced
  • precedex
  • melatonin - maybe they can’t sleep
  • APS (quetiapine, haldol, olanzapine)

keep in mind that all these kinda suck and prevention is where it’s at