Intubation/Anesthesia/Analgesia

Question 1

RSI

Answer 1

• Rapid Sequence Intubation
• For patients at risk for aspiration or impending loss of airway to maintain/protect airway
• Induction => Paralytics

Question 2

Induction Medication Options

Answer 2

• Etomidate
• Ketamine
• Midazolam
• Propofol

Question 3

Etomotide

Answer 3

• Onset 10-30 sec
• 4-10 min duration
• AE: hemodynamically neutral, adrenal insufficiency, myoclonic activity

Question 4

Ketamine

Answer 4

• Onset: 45-60 sec
• Duration: 10-20 min
• AE: Increased HR/BP (Caution with heart disease, hypertensive), Increased intraocular pressure and ICP, bronchodilator

Question 5

Midazolam

Answer 5

• 60-90 sec onset
• Duration: 30-80 min
• AE: Hypotension, respiratory depression, paradoxical agitation, doses and patient response can very

Question 6

Propofol

Answer 6

• 15-45 sec onset
• Duration: 5-10 min
• AE: Hypotension, myocardial depressant/decreased SVR, caution with egg allergy, reduces ICP

Question 7

Paralytic Medications and Options

Answer 7

• Used to relax oropharyngeal airway and diphragmatic muscles in order to facilitate passage of an endotracheal tube
• May not be indicated if there is an absence of a gag reflex
• Options: Succinylcholine, rocuronium, vecuronium

Question 8

Succinylcholine

Answer 8

• Depolarizing
• 30-60 sec onset
• Duration: 6-10 min
• AE: rhabdomyolysis, hyperkalemia, fasciculation, elevated IOP, malignant hyperthermia (rare), caution in NM disease

Question 9

Rocuronium

Answer 9

• Nondepolarizing
• 45-60 sec onset
• Duration: 45-70 min
• Longer onset compared to succinylcholine and few adverse effects

Question 10

Vecuronium

Answer 10

• Nondepolarizing
• 120-180 sec onset
• Duration: 40-60 min
• Longer onset compared to succinylcholine and few adverse effects

Question 11

Post Intubation Sedation and Analgesia

Answer 11

• Initiated immediately upon securing the airway
• Durations of most sedatives are shorter than some paralytics, used to avert a patient being intubated or paralyzed/intubated without sedation
• Adequate analgesia should be provided prior to initiation of sedation

Question 12

Pain Assessment in ICU

Answer 12

• More likely to have patients experiencing pain and unable to vocalize it
• Monitor routinely in these patients
• Communicating patient: NRS scale
• Non-communicative: BPS or CPOT
• Patient self-assessment is gold standard, vital signs can be used to cue for further pain assessment but can’t be only method to assess pain

Question 13

Pain Treatment

Answer 13

• Individualized therapy, use minimum effective doses, and AE such as constipation or N/V require adjunctive treatment
• Administer preemptive analgesia and/or non-pharm interventions to alleviate pain prior to painful procedures
• IV opioids are first line for non-neuropathic pain: when properly titrated all IV opioids are equally effective

Question 14

Meperidine

Answer 14

• Generally avoided, potential for neurotoxicity
• Use limited to control shivering
• Naloxone should be made available for emergent reversal

Question 15

Neuropathic Pain

Answer 15

• Enterally administrated gabapentin or carbamazepine in addition to IV opioids
• Consider complementary, non-pharm interventions like music therapy or relaxation

Question 16

Fentanyl

Answer 16

• Fastest onset/duration
• Accumulates in hepatic impairment
• May accumulate in more obese patients, no MAOIs within 14 days, and watch out for CYP3A4 interactions
• AE: respiratory depression, tachyphylaxis, constipation, chest wall rigidity/laryngospasm

Question 17

Morphine

Answer 17

• Longer onset/duration to fentanyl, similar to hydromorphone
• Accumulates in renal and hepatic impairment
• Avoid in hemodynamic instable patients due to histamine release
• AE: respiratory depression, constipation

Question 18

Hydromorphone

Answer 18

• Longer onset/duration to fentanyl, similar to morphine
• Accumulates in hepatic impairment
• Generally used as PCA at UNMH
• AE: Respiratory depression, constipation

Question 19

Agitation/Sedation

Answer 19

• Occurs frequently with adverse outcomes
• Generally approach prior to sedatives: identify/treat underlying cause of agitation and treat pain first!!!
• Analgesia first sedation should be used for mechanically ventilated adult ICU patients
• Provide non-pharm: environment optimization for comfort and to maintain normal sleep patterns and frequent reorientation (control light/noise, cluster patient care activities, decrease stimuli at night)

Question 20

Measuring Sedation Depth

Answer 20

• Most validated/reliable scales are SAS and RASS
• Depth of sedation: light = arousable and can follow commands, deep = unresponsive to painful stimuli
• Light sedations are preferred unless CI for better clinical outcomes and physiological stress response

Question 21

Managing Sedation

Answer 21

• Either daily interruption of light target level sedation in mechanically ventilated patients
• Daily sedation interruption: allow for neurological function assessment and can help with drug accumulation/overdose (not for all patients)
• D/C all sedative and analgesics, monitor patient’s responsiveness/awareness for opening eyes/maintaining eye contact/squeezing hand or sticking out tongue/ wiggling toes
• Restart medications at half dose
• Both reduce ventilation time; daily interruption has shown to decrease LOS

Question 22

Choice of Sedative

Answer 22

• Non-benzo sedatives are preferred over benzos in mechanically ventilated patients
• One of the “modifiable” risk factors for delirium
• BZD have adverse outcomes (increased ventilation, LOS, and delirium development)
• Additional considerations: patient specific factors, pharmacology, and cost

Question 23

Times to Use Benzo

Answer 23

• Seizures

- Alcohol or benzo withdrawal

Question 24

PRIS

Answer 24

• Propofol Infusion Syndrome
• Rare but high mortality and can continue after infusion is D/C
• Associated with prolonged, high dose administration by mitochondrial dysfxn, impaired fatty acid oxidation, diversion of carb metabolism, and propofol metabolite accumulation

Question 25

PRIS Presentation

Answer 25

• Metabolic acidosis: ABG
• Hypertriglyceridemia: TGA
• Hypotension: BP, increase vasopressors
• Arrhythmias: EKG
• Rhabdomyolysis: Troponin/CK
• Acute renal injury: SCr, urine output
• Hyperkalemia: Chem7

Question 26

PRIS Treatment

Answer 26

• D/C propofol

- Supportive treatment

Question 27

Propylene Glycol Toxicity

Answer 27

• Diluent in parenteral lorazepam formulations, accumulation more likely with high lorazepam infusions
• Lower doses can cause toxicity as well like propofol
• Presentation: metabolic acidosis, AKI, or seizures
• Serum osmol gap > 10-12 may help identify accumulation