Critical Care: FASTHUGS BID and PADIS Flashcards

(80 cards)

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
benefits of precedex
- **NO resp depreession** - effects similar to natural sleep - anaglesic - useful as adjunct therapy for EtOH withdrawal
26
disadvantages of precedex
- 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
27
benefits of ketamine
- favorable hemodynamics - no bradycardia and hypotension - bronchodilator effects - NO resp depression - opioid sparing
28
ketamine ADR
- emergence reaction (pretreat with benzo or propofol) - esp in dementia and schizo - oral secretions (differentiate from infectious gunk) - tachycardia - HTN
29
delirium
acute changes in mental status with inattention, disorganized thinking, and altered level of consciousness not explained by pre-existing conditions
30
delirirum sequalae/consequences
- increased mortality - cog impairment - functional decline - increase health system costs - prolonged mechanical ventilation - increased length of stay
31
non-pharm delirim prevention
- 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 ## Footnote fun fact: guidelines have NO recommendatios for pharm preventio - don't do it
32
indications for paralytic admin
- 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
33
what drug class is used as paralytics
neuromusclar blockers
34
benefits of neuromuscular blockers
- inhibit diaphragmatic function and reduce chest wall rigidity - reduce O2 consumptom - eliminate work of breathing
35
disadvantages of neuromuscular blockde
- 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
neuromuscular infusion monitoring
train of four using a peripheral nerve stimulator - goal is 2 twitches
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neuromuscular blocker agents
- 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
which do you treat first: pain or agitaiton?
pain | the agitation may be caused by pain
39
what is the pain assessment tool and what is the associated treatment goal
CPOT (critical care pain observatio tool) - score > 2 indicates significant pain - goal is < 2
40
what are our pain meds in ICU
- 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
morphine onset and duration
- onset: 5-10 min - duration: 3-6 hrs
42
fentanyl onset and duration
- onset: seconds - duration: 1-2 hrs
43
hydromorphone onset and duration
- onset: 5 min - duration: 2-4 hrs
44
ICU pain morphine dose
- bolus: 2-10 mcg - infusion: 1-10 mcg/hr
45
ICU pain fentayl dose
- bolus: 50-100 mcg - infusion: 25-300 mcg/hr ## Footnote if doing an opioid infusion (which isn't preferred over bolus), fentayl is drug of choice
46
ICU pain hydromorphone dose
- bolus: 0.5-2 mg - infusion: 0.5-3 mg/hr
47
morphine considerations
- active metabolite - accumulates in AKI -> do NOT use in AKI
48
morphine ADR
histamine release - hypotension - bradycardia - urticaria - itching is a normal response, not an allergy ## Footnote techincally possible for all opioids, seen often with morphine
49
fentanyl considerations
- hepatic metabolism - CYP3A4 DDI - pts can develop tolerance/tachyphylaxis
50
hydromorphone considerations
- good in renal impairment - option if pt has fentyl tolerance - minimal histamine relase - available as PCA
51
Sedation assessment scale
RASS (richond agitation sedation scale) - goal is generally -2 to 0 (light sedation)
52
sedative agents
- propofol - precedex - ketamine - prn benzos (midazolam, lorazepa, diazepam) - boluses preferrred
53
propofol MOA
stimulate GABA and inhibit NMDA receptors
54
precedex MOA
alpha adrenergic agonst (like clonidine) -> decreased release of NE and DA in CNS
55
ketamine MOA
- NMDA antag - mu and kappa agonsit - muscarinic acetylcholine receptor antag - inhibit reuptake of serotoin, NE, DA
56
propofol PD | effects
- hyponotic - anxiolytic - amnestic - anticonvulsant - potentilaly first line in SE or severe EtOH withdrawal | NOT an analgesic
57
precedex PD | effects
*analgesic* and sedative
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propofol onset and duraiotn
- onset < 1 min - duration 10-15 min (extra rapid hepatic clearance) | quick on and off
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propofol ADR
- 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) ## Footnote montior: BP, HR, TG, anion gap/lactate, CK
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propofol considerations
- 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
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precedex ADR
- bradycardia - hypotnsion
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midazolam onset and duration
- onset 2-5 min - duration 1-2 hrs
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midazolam sedation dose
- bolus 2-4 mg - infusion 1-4 mg/hr
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midazolam consdierations
- lipophilic - active metabolite - accumulates in renal impairment
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lorazepam onset and duration
- onset 5-20 min - duration 2-6 hrs
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lorazepam sedation dose
- bolus 1-2 mg - infusion 0.5-4 mg/hr
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lorazepam considerations
CAN use in hepatic/renal failure
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lorazepam ADR
- propylene glycol acidosis (anion gap acidoss)
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diazepam onset and duration
- onset 5-10 min - duration: long, its half life is 44-100 hrs | basiclaly tapers itself off with such a long half life
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diazepam considerations
active metabolite
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consequences of benzo sedatoin
- increased risk of delirium - ncreased time on vent (dt resp depression adr) - increase stay in ICU
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when to use benzos for sedation
- SE - extreme EtOH withdrwal - severe ARDS requirng sedation
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ARDS ## Footnote a
acute respiratory distress syndrome
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ketamine indications
- anesthesia - pain - rapid sequence intubation - acute severe agitation - SE - treatment resitant depression - PTSD
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ketamine dosing for **pain** and associated onset and duration (formula specific)
0.15-0.5 mg/kg/hr ## Footnote - IM onset: 10-15 min - IM duration: 15-30 min
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ketamine dosing for **sedation** and associated onset and duration (formula specific)
0.5-2 mg/kg/hr ## Footnote (onset/duration) - IV: within 30 seconds / 5-10 min - IM: 3-4 min / 5-10 min
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ketamine dosing for **SE**
> 2 mg/kg/hr
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modifiable delirium risk factors
- benzo use - blood transfusions
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non-modifiable delirium risk factors
- old ae - hx dementia - prior coma - pre-ICU emergeny surgery/trauma - high APACHE score
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pharm options for delirium
- 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