Acute and Critical Care - Foster Flashcards
why is oral absorption impaired/unpredictable in critically ill patients?
alterations of gastric emptying and motility due to opioids and c.diff (other infections)
how does fluid and hydration status affect distribution of medications?
hydrophilic drugs have a higher Vd in critically ill patients than in medical patients (surgery patients are receiving fluids)
how is metabolism altered in critically ill patients
usually some hepatic impairment; hepatic enzyme expression and activity may be decreased in some patients
how is renal elimination altered in critically ill patients?
renal dysfunction due to shock, or sepsis related organ failure and/or nephrotoxic drugs.
HD is common in ICU
trauma and burns may be associated with increased renal elimination
what is sepsis?
organ dysfunction caused by dysregulated response to infection; immune dysregulations and coagulation and thrombosis leading to endothelial injury
general treatment strategy for sepsis
antibiotic therapy and source control; remove the cause of infection.
treatment for septic shock (cardiovascular collapse/hypotension)
fluids (lactated ringers) (crystalloids, colloids)
- vasopressors: norepi, phenylephrine, epi, dopamine (can add-on vasopressin)
- may use dobutamine (inotrope)
- use corticosteroids
- target MAP >65 mmHg (use BP to determine MAP)
What are the risks for ARDS (acute respiratory distress syndrome)
- inflammatory lung injury –> eventually causing fibrosis of the lungs
- pneumonia, sepsis, trauma, aspiration
how to treat ARDS?
mechanical ventilation with sedation, neuromuscular blockade, corticosteroids
what ICU patients may not need thromboprophylaxis
very mobile and low risk OR contraindications to pharmacological prophhylaxis
what is the prophylaxis dose for UFH
5000u SQ Q8H or Q12H
monitor for s/sx of bleeding and HIT
not adjusted renally
what is the prophylaxis dose for enoxaparin**
30mg SQ Q12H or 40mg SQ Q24H
monitor for s/sx of bleeding and HIT
renal dose <30 mL/min; 30mg SC Q24H
prophylaxis for stress ulcers?
H2RAs
PPIs
Enteral feeding
famotidine prophylaxis dose
20 mg BID
crcl <30, 20mg P daily
PPIs administration
enteral or parenteral
omeprazole prophylactic dosing
20-40mg daily
what patients may need SUP
- mech vent
- coagulopathy
- chronic liver disease
- shock
- others
what is BG target in ICU patients
144-180 mg/dL
what can cause elevated BG in ICU patients?
underlying stress, steroids, TPN
succinylcholine MOA
Depolarizing NMBA. binds and activates Ach receptor and causes sustained depolarization resulting paralysis. may cause initial muscle contractions
what is the indication for succinylcholine?
Rapid sequence intubation/ placement of a trach
NOT for sustained NMB
what are the adverse effects of succinylcholine?
Apnea– need to be ready to intubate
- deep aching muscle pain
- hyperkalemia
- contraindicated in major burns, crush injury, and upper motor neuron disease due to hyperkalemia risk
- increased intracranial and intraocular pressure
MOA on nondepolarizing NMBAs
competitive inhibitor of Ach
- do not activate receptors/cause initial contractions
What are the reversal agents for nondepolarizing NMBAs
- acetylcholinesterase inhibitors (pyridostigmine, neostigmine)
- sugammadex –reverses the curoniums
what are the aminosteroidal NMBAs
pancuronium (slow onset and long duration)
vecuronium (intermediate onset and duration)
rocuronium (rapid onset and intermediate duration)
What are the benzylisoquinolinium NMBAs
atracurium (intermediate onset and duration) (can cause histamine release and seizures)
cisatracurium (intermediate)
Indications for NDNMBAs
- mech vent patients with acute lung injury or ARDS
- not required in all mech vent patients
- in the OR (promote muscle relaxation)
- rapid sequence intubation when succinylcholine is contraindicated
- manage increased ICP
- prevent/treat shivering in hypothermia
- sepsis; decrease oxygen consumption
ADRs for NDNMDA
paralysis of respiratory muscles/apnea
(need to prevent extubation)
inadequate pain and sedation
- patients must be optimized on sedative and analgesic drugs
- muscle weakness
- may interact with steroids
- need DVT prophylaxis and ocular lubricants
how to monitor sustained NMB
- twitch monitoring (toxicity endpoint)
- Should aim for ~80% suppression or 1-2 twitches
adverse effects of over-sedation
- increased time on mech vent
- increased ICU and hospital LOS
- obscure neurological function testing
Treatment goals/ targets of sedation
- light sedation
- daily sedation interruption (sponto awakening trial)
Scales to assess sedation?
- RASS
10 point scale
-SAS
1 (unarousable) to 7 (agitated) - Bispectral Index (uses an EEG in the operative setting)
when is Bispectral index indicated?
IN patients with deep sedation and neuromuscular blockade
- for patients with known/suspected seizures
Sedative drugs used in ICU
- Benzos (lorazepam, midazolam, diazepam)
- propofol
- dexmedetomidine
benzos MOA
bind to GABA
- hyperpolarize cells; make resistant to excitation
benzos AE
- respiratory depression
- hypotension, tachycardia
- withdrawal/ seizures – TAPER THE DOSE
- delayed emergence from sedation
- may require longer time on vent
- may cause delirium
lorazepam considerations
- IV preferred for severe/acute agitation
- delayed onset and longer duration
- not expected to accumulate in elderly, but may accumulate in liver and renal failure
- may cause acidosis/nephrotoxicity due to propylene glycol in injection
- monitor osmol gap. gap >10 may mean toxicity
midazolam
- rapid onset and shorter t1/2 than lorazepam.
- metabolized by CYP 3A
- drug interactions, increase t1/2 in the elderly and hepatic disease
- metabolites may accumulate
- not recommended for long-term sedation
- may be used for procedures and rapid sedation
propofol considerations
binds to GABA, facilitates global CNS depression
- rapid onset and offset
- can be used for general anesthesia
- procedural sedation
- may saturate tissues but no active metabolites
- metabolized through the liver, highly protein bound
- no dose adjustment for renal or hepatic dysfunction
- may cause increased triglycerides; check these
- incompatible with other fluids; requires dedicated IV catheter
- phospholipid emulsion (1.1 kcal/mL) (risk of infection)
AE of propofol
apnea
hypotension/bradycardia
pain from infusion
increased triglycerides
infusion syndrome (rare)
- metabolic acidosis
- caution in doses >75-80mcg/kg/min
- withdrawal (taper dose)
formulation of propofol
contains EDTA
take drug holiday after >7 days treatment to avoid electrolyte abnormalities
When is propofol indicated?
- when rapid wakening is important
- neurotrauma (may help with ICP management)
- recommended over benzos for critically ill patients on vent
- used for procedural sedation
dexmedetomidine MOA
alpha-2 agonist; inhibits noradrenalin release
dexmedetomidine considerations
- patients readily arousable
- no respiratory depression
- less delirium than benzos
- should not be used when deep sedation is required
dexmedetomidine pharmacokinetics
- short half life
- some elimination impairment in hepatic dysfunction
dexmedetomidine use
- no loading dose needed
- only approved for short term
dexmedetomidine AE
- decreased BP with rapid administration
- bradycardia and hypotension from loading dose
- should not use in hemodynamic instability
dexmedetomidine clinical use
- recommended over benzos for critically ill mechanically ventilated adults
- use limited by cardiovascular AE
- lower incidence of delirium
what are the two types of delirium?
- hyperactive/agitated
- hypoactive/lethargic
what are the assessments for delirium?
ICDSC and CAM-ICU
Prevention of delirium
early mobilization, optimization of sleep, hearing and vision, improving cognition and orientation
what are the pharmacologic treatments for delirium
haloperidol
atypical antipsychotics: risperidone, olanzapine, quetiapine, aripiprazole
- may be used short-term only
dexmedetomidine- for delirium caused by agitation
Haloperidol uses and AE
- may provide mild sedation for acute agitation
- no evidence for reduction of delirium duration
- Prolongs QT interval
- decreases seizure threshold
- EPS
Use/AE of atypical antipsychotics
- may be safer than haloperidol
- fewer EPS
- should not use in patients at risk for torsades
- olanzapine can cause NMS and hypotension
treatment of delirium?
- only use antipsychotics for short term treatment where delirium is associated with significant stress and anxiety
- use dexmedetomidine for delirium/agitation precluding weaning of vent/extubation
PAD Guidelines
- sedation: less is more
- light sedation preferred and only if required
- daily interruptions of sedation
- analgesia first!
treatment algorithm
- benzos last
- dexmedetomidine: preferred in patients with delirium and agitation
propofol: preferred in neurotrauma where rapid awakening is preferred and in cardiac surgery
