Exam 3 lecture 6 Flashcards
Monitoring sustained NMB (neuromuscular blockade)? How to avoid giving too much NMB?
it is challenging.
Toxicity endpoint- we want to avoid giving too much neuromuscular blocker. Side effect of giving too much neuromuscular blocker would be prolonged paralysis. Which means patient is on the ventilator longer, which means they cant get out of the ICU which means they are associated with ventilator associated pneumonia.
Peripheral nerve stimulation is how we avoid giving too much NMB (Otherwise known as train-of-four (TOF) assessment).
Define TOF assessment? What is the goal?
It is a series of electrical stimulations administered to patient (4 times) administered at 0.5 second intervals. It is administered on ulnar nerve. When there is no neuromuscular blockade, each time there is a stimulation, we see a twitch. As we increase neuromuscular blockade the number of twitches we see decrease.
3/4 twitches- 75% suppression, 2/4- 80% suppression, 1/4 -90%
Usually adjust dose to 1-2 twitches of train. This is a TOXICITY ENDPOINT
Define PADIS
Pain, agitation/sedation, delirium, immobility, sleep
Define pain and agitation
Pain- unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
Agitation- Condition characterized by apprehension, increased motor activity and autonomic arousal; may also be manifested by fearful withdrawal.
Agitation is a state of anxiety accompanied by motor restlessness
define delirium? What are the cardinal features?
Syndrome characterized by acute cerebral dysfunction with a change or fluctuation in baseline mental status, inattention and either disorganized thinking or altered level of consciousness.
Cardinal feature- disturbed level of consciousness and either a change of cognition or development of perceptual disturbance
What are the physiologic responses seen with pain?
-Increased sympathetic nervous system activation, raises catecholamine levels.
-Vasoconstriction, impaired tissue perfusion
- catabolism/hypermetabolism
-impaired wound healing
-immunosuppression
- can alter breathing patterns and mechanics
Biggest challenge of pain assessment? Gold standard for pain? What if patient is unable to self report?
Gold standard for pain management is whatever the patient says. Pain is usually treated poorly in hospitals.
If unable to self report- BPS (behavioral pain scale), CPOT (critical pain observation tool)
How should analgesia be used in ICU? What drugs to use in ICU for analgesia? What are the non opioid drugs we can use?
If we know a patient is going to undergo a painful procedure we do preemptive analgesia.
IV opioids preferred for non-neuropathic pain in critically ill patients
Non-opioid analgesics may ben used to decrease opioid requirements
-acetaminophen
- for neuropathic pain (Gabapentin, pregabalin)
potentially NSAIDs
Ketamine
What are the two most common analgesic drugs given in ICU? How are they given?
Morphine and fentanyl
Can be given as a bolus dose or a continuous infusion or combination
How frequent is agitation in critically ill patients? What are the adverse clinical outcomes?
Agitation- state of anxiety accompanied by motor restlessness. Frequent in critically ill pts.
Adverse clinical outcomes
- ventilator desynchrony
- inappropriate verbal behavior
- physical aggression
- Increased motor activity
- increases in O2 consumption
- inadvertent removal of devices
Underlying cause of agitation
Pain
mechanical ventilation
Delirium
hypoxia
Hypotension
Withdrawal
Treatment of agitation
non pcol- maintenance of patient comfort
Provide adequate analgesia
Frequent reorintation
Optimization of environment to maintain normal sleep pattern
Pcol- Sedatives may reduce stress of mechanical ventilation, relieve anxiety and prevent agitation related harm
- pcol sedation should be strated after providing adequate analgesia and treating reversible causes
Why is over sedation problematic
- increases time on mechanical ventilation
- increase ICU and hospital length stay
- obscure neurological function testing
What is the goal of treatement of agitation
Adequate sedation, but not oversedation
Less is best–> Light sedation
Daily sedation interruption (spontaneous awakening trial) used
Assessment if sedation>
Assessment is difficult in patients with altered level of mentation or inability to outwardly express anxiety
Most valid and reliable
- richmond-agitation sedation (RASS)
- Sedation- Agitation scale (SAS)
what do we use when we can not use a RASS or a SAS
BIS (Bispectral index)
What are sedative drugs used in the ICU
Benzodiazepines
- lorazepam, midazolam
propofol
Dexmedetomidine
What ideal properties do BZDs have to be ICU sedation agents? Who is more sensitive? What drusg commonly used?
Anxiolytic
Hypnotic/sedative effect
Amnestic effect
Anticonvulsant effect
Elderly are more sensitive.
Tolerance seen with chronic administration.
Drugs primarily used in ICU (lorazepam, midazolam)
adverse effects of BZDs
-Respiratory depression
-CVD effects (hypotension/tachycardia) but usually minimal especially compared to propofol
-Withdrawal possible
- Delayed emergence from sedation
a) occurs if patient is on benzo for a long time
b) Advanced age
C) Hepatic/renal insufficiency
compare BZDs to propofol and dexmedetomidine for duration of mechanical ventilation and association with delirium?
BZDs may be associated with longer duration of mechanical ventilation compared to propofol or dexmedetomidine.
Potential association with delirium!!
How can lorazepam be given? Compare lipid solubility with other BZDs. What effect does this half? Half life?
Lorazepam can be continuous or bolus.
It is the least lipid soluble BZD. So it takes a while to get through BBB. So it has a delayed onset and prolonged duration of effect.
Half life is longer than propofol and midazolam so it is less titratable.
how is lorazepam metabolized? How does this affect its action? How prone are they to drug i/a? How does the longer t 1/2 affect it?
Metabolized by glucuronidation–> not expected to accumulate in elderly
Because of glucuronidation, it tends to be prolonged in liver disease and ESRD
Least prone to drug i/a
long t 1/2 makes infusions less titrateable
potential association with delirium
What is a unique thing about lorazepam (EXAM)
IV formulation contains propylene glycol (PG) solvent
it is very toxic
We can look at osm gap to detect potential PG toxicity on patients with prolonged lorazepam exposure.
How is midazolam given? What is it metabolized by?
How long is t1/2?
When is this t1/2 altered?
continuous or IV
metabolized by CYP3A
T 1/2 is short, but is increased in elderly, hepatic disease, numerous drug interactions.
also prolonged in renal disease due to metabolite accumulation
Summarize midazolam (onset, when is it recomended, when is it not recommended, why does it have declining use in hospitals?
- fast onset
- recommended for short term use only, may be used for procedural sedation
not recommended for long term sedation due to unpredictable awakening time
declining use due to potential association with delirium
