Critical Care: FASTHUGS BID and PADIS Flashcards
FASTHUGS BID
as a concept
aspects of critical care medicine that can be appplied bid to critically ill pts
what does FASTHUGS BID stand fore
- 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
Enteral vs parenteral feeding
- Enteral preferred to TPN
- Entereral: uses your gut, natural
- TPN: risk of infection and thromosis
Consequences of malnutrition in ICU
Malnutrition → impaired immune function →
- Increased susceptibility fo infetion
- Impaired wound healing
- Bacterial overgrowth in GI tract
- Increased risk for development of decubitus ulcers
Reasons a pt may be agitated in the ICU
- Anx, pain
- Lack of homeostsais
- Withdrawal
- BZD use
- Sleep-wake cycle disruption
Sedation assessment tools
- Richmond Agitation-Sedation Scale (RAS): light sedtion is supported in the guideliens for most situations
- Sedation Agittaion Scale (SAS)
ICU risk factors for VTE
- Central venous catheterization
- Immobility
- Trauma/burns
- Critical illness (sepsis)
who gets VTE ppx in ICU and what are the options
- 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)
Mechanical ventilation
endotracheal tube (ET) is placed into trachea through moouth and hooked up to a ventilator
VAP ppx
ventilator acquired PNA
- 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
Stress related mucosal damage (SRMD)
acute errosive, inflammatory upper GI insult associated with critical illness
- can lead to clincally significant bleedng
who qualfiies for SRMD ppx
stress related mucosal damage
- 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
SRMD ppx pharm
PPI, H2RA
hyperglycmia is common in ICU pts dt whaat risk factors
- Stress
- Meds (steroids, beta blockers, vasopressors)
- TPN or dextrose
glycemia control in ICU
- 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
spontaneous bbreathign trial
- 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
causes of constipation in critically iill pts
- immobility
- med ADR
- shock
constipation mangement in ICU
- monitor bowel movement QD
- if constipation occurs, add bowel regimen
- if pt on opioids, just have a standing order
causes of diarrhea in critically ill
- iinfectio (c. diff)
- feeds
- bowel regimen too good
Peripheral venous catheter
peripheral vein for venous access to admin IV therapy
CVC
terminate in superior vena cava
Arterial line
- in luen of artery to provide continuous display or accurate bp* and access frequent blood samples
- *important for pts on vasopressors
Foley
passes through urethra and into bladder to drain urine
Rectal tubes
fecal management; contain and divert fecal waste
benefits of precedex
- NO resp depreession
- effects similar to natural sleep
- anaglesic
- useful as adjunct therapy for EtOH withdrawal
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
benefits of ketamine
- favorable hemodynamics - no bradycardia and hypotension
- bronchodilator effects - NO resp depression
- opioid sparing
ketamine ADR
- emergence reaction (pretreat with benzo or propofol) - esp in dementia and schizo
- oral secretions (differentiate from infectious gunk)
- tachycardia
- HTN
delirium
acute changes in mental status with inattention, disorganized thinking, and altered level of consciousness not explained by pre-existing conditions
delirirum sequalae/consequences
- increased mortality
- cog impairment
- functional decline
- increase health system costs
- prolonged mechanical ventilation
- increased length of stay
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
fun fact: guidelines have NO recommendatios for pharm preventio - don’t do it
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
what drug class is used as paralytics
neuromusclar blockers
benefits of neuromuscular blockers
- inhibit diaphragmatic function and reduce chest wall rigidity
- reduce O2 consumptom
- eliminate work of breathing
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)
neuromuscular infusion monitoring
train of four using a peripheral nerve stimulator
- goal is 2 twitches
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
which do you treat first: pain or agitaiton?
pain
the agitation may be caused by pain
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
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
morphine onset and duration
- onset: 5-10 min
- duration: 3-6 hrs
fentanyl onset and duration
- onset: seconds
- duration: 1-2 hrs
hydromorphone onset and duration
- onset: 5 min
- duration: 2-4 hrs
ICU pain morphine dose
- bolus: 2-10 mcg
- infusion: 1-10 mcg/hr
ICU pain fentayl dose
- 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
ICU pain hydromorphone dose
- bolus: 0.5-2 mg
- infusion: 0.5-3 mg/hr
morphine considerations
- active metabolite
- accumulates in AKI -> do NOT use in AKI
morphine ADR
histamine release
- hypotension
- bradycardia
- urticaria - itching is a normal response, not an allergy
techincally possible for all opioids, seen often with morphine
fentanyl considerations
- hepatic metabolism
- CYP3A4 DDI
- pts can develop tolerance/tachyphylaxis
hydromorphone considerations
- good in renal impairment
- option if pt has fentyl tolerance
- minimal histamine relase
- available as PCA
Sedation assessment scale
RASS (richond agitation sedation scale)
- goal is generally -2 to 0 (light sedation)
sedative agents
- propofol
- precedex
- ketamine
- prn benzos (midazolam, lorazepa, diazepam) - boluses preferrred
propofol MOA
stimulate GABA and inhibit NMDA receptors
precedex MOA
alpha adrenergic agonst (like clonidine) -> decreased release of NE and DA in CNS
ketamine MOA
- NMDA antag
- mu and kappa agonsit
- muscarinic acetylcholine receptor antag
- inhibit reuptake of serotoin, NE, DA
propofol PD
effects
- hyponotic
- anxiolytic
- amnestic
- anticonvulsant - potentilaly first line in SE or severe EtOH withdrawal
NOT an analgesic
precedex PD
effects
analgesic and sedative
propofol onset and duraiotn
- onset < 1 min
- duration 10-15 min (extra rapid hepatic clearance)
quick on and off
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)
montior: BP, HR, TG, anion gap/lactate, CK
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
precedex ADR
- bradycardia
- hypotnsion
midazolam onset and duration
- onset 2-5 min
- duration 1-2 hrs
midazolam sedation dose
- bolus 2-4 mg
- infusion 1-4 mg/hr
midazolam consdierations
- lipophilic
- active metabolite
- accumulates in renal impairment
lorazepam onset and duration
- onset 5-20 min
- duration 2-6 hrs
lorazepam sedation dose
- bolus 1-2 mg
- infusion 0.5-4 mg/hr
lorazepam considerations
CAN use in hepatic/renal failure
lorazepam ADR
- propylene glycol acidosis (anion gap acidoss)
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
diazepam considerations
active metabolite
consequences of benzo sedatoin
- increased risk of delirium
- ncreased time on vent (dt resp depression adr)
- increase stay in ICU
when to use benzos for sedation
- SE
- extreme EtOH withdrwal
- severe ARDS requirng sedation
ARDS
a
acute respiratory distress syndrome
ketamine indications
- anesthesia
- pain
- rapid sequence intubation
- acute severe agitation
- SE
- treatment resitant depression
- PTSD
ketamine dosing for pain and associated onset and duration (formula specific)
0.15-0.5 mg/kg/hr
- IM onset: 10-15 min
- IM duration: 15-30 min
ketamine dosing for sedation and associated onset and duration (formula specific)
0.5-2 mg/kg/hr
(onset/duration)
- IV: within 30 seconds / 5-10 min
- IM: 3-4 min / 5-10 min
ketamine dosing for SE
> 2 mg/kg/hr
modifiable delirium risk factors
- benzo use
- blood transfusions
non-modifiable delirium risk factors
- old ae
- hx dementia
- prior coma
- pre-ICU emergeny surgery/trauma
- high APACHE score
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
