Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHRM 864 > Acute and Critical Care - Foster > Flashcards

Acute and Critical Care - Foster Flashcards

1
Q

why is oral absorption impaired/unpredictable in critically ill patients?

A

alterations of gastric emptying and motility due to opioids and c.diff (other infections)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how does fluid and hydration status affect distribution of medications?

A

hydrophilic drugs have a higher Vd in critically ill patients than in medical patients (surgery patients are receiving fluids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is metabolism altered in critically ill patients

A

usually some hepatic impairment; hepatic enzyme expression and activity may be decreased in some patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how is renal elimination altered in critically ill patients?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is sepsis?

A

organ dysfunction caused by dysregulated response to infection; immune dysregulations and coagulation and thrombosis leading to endothelial injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

general treatment strategy for sepsis

A

antibiotic therapy and source control; remove the cause of infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

treatment for septic shock (cardiovascular collapse/hypotension)

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the risks for ARDS (acute respiratory distress syndrome)

A
  • inflammatory lung injury –> eventually causing fibrosis of the lungs
  • pneumonia, sepsis, trauma, aspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how to treat ARDS?

A

mechanical ventilation with sedation, neuromuscular blockade, corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what ICU patients may not need thromboprophylaxis

A

very mobile and low risk OR contraindications to pharmacological prophhylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the prophylaxis dose for UFH

A

5000u SQ Q8H or Q12H
monitor for s/sx of bleeding and HIT
not adjusted renally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the prophylaxis dose for enoxaparin**

A

30mg SQ Q12H or 40mg SQ Q24H
monitor for s/sx of bleeding and HIT
renal dose <30 mL/min; 30mg SC Q24H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

prophylaxis for stress ulcers?

A

H2RAs
PPIs
Enteral feeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

famotidine prophylaxis dose

A

20 mg BID
crcl <30, 20mg P daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PPIs administration

A

enteral or parenteral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

omeprazole prophylactic dosing

A

20-40mg daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what patients may need SUP

A
  • mech vent
  • coagulopathy
  • chronic liver disease
  • shock
  • others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is BG target in ICU patients

A

144-180 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what can cause elevated BG in ICU patients?

A

underlying stress, steroids, TPN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

succinylcholine MOA

A

Depolarizing NMBA. binds and activates Ach receptor and causes sustained depolarization resulting paralysis. may cause initial muscle contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the indication for succinylcholine?

A

Rapid sequence intubation/ placement of a trach
NOT for sustained NMB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the adverse effects of succinylcholine?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MOA on nondepolarizing NMBAs

A

competitive inhibitor of Ach
- do not activate receptors/cause initial contractions

24
Q

What are the reversal agents for nondepolarizing NMBAs

A
  • acetylcholinesterase inhibitors (pyridostigmine, neostigmine)
  • sugammadex –reverses the curoniums
25
Q

what are the aminosteroidal NMBAs

A

pancuronium (slow onset and long duration)
vecuronium (intermediate onset and duration)
rocuronium (rapid onset and intermediate duration)

26
Q

What are the benzylisoquinolinium NMBAs

A

atracurium (intermediate onset and duration) (can cause histamine release and seizures)
cisatracurium (intermediate)

27
Q

Indications for NDNMBAs

A
  • 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
28
Q

ADRs for NDNMDA

A

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

29
Q

how to monitor sustained NMB

A
  • twitch monitoring (toxicity endpoint)
  • Should aim for ~80% suppression or 1-2 twitches
30
Q

adverse effects of over-sedation

A
  • increased time on mech vent
  • increased ICU and hospital LOS
  • obscure neurological function testing
31
Q

Treatment goals/ targets of sedation

A
  • light sedation
  • daily sedation interruption (sponto awakening trial)
32
Q

Scales to assess sedation?

A
  • RASS
    10 point scale
    -SAS
    1 (unarousable) to 7 (agitated)
  • Bispectral Index (uses an EEG in the operative setting)
33
Q

when is Bispectral index indicated?

A

IN patients with deep sedation and neuromuscular blockade
- for patients with known/suspected seizures

34
Q

Sedative drugs used in ICU

A
  • Benzos (lorazepam, midazolam, diazepam)
  • propofol
  • dexmedetomidine
35
Q

benzos MOA

A

bind to GABA
- hyperpolarize cells; make resistant to excitation

36
Q

benzos AE

A
  • respiratory depression
  • hypotension, tachycardia
  • withdrawal/ seizures – TAPER THE DOSE
  • delayed emergence from sedation
  • may require longer time on vent
  • may cause delirium
37
Q

lorazepam considerations

A
  • 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
38
Q

midazolam

A
  • 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
39
Q

propofol considerations

A

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)

40
Q

AE of propofol

A

apnea
hypotension/bradycardia
pain from infusion
increased triglycerides
infusion syndrome (rare)
- metabolic acidosis
- caution in doses >75-80mcg/kg/min
- withdrawal (taper dose)

41
Q

formulation of propofol

A

contains EDTA
take drug holiday after >7 days treatment to avoid electrolyte abnormalities

42
Q

When is propofol indicated?

A
  • when rapid wakening is important
  • neurotrauma (may help with ICP management)
  • recommended over benzos for critically ill patients on vent
  • used for procedural sedation
43
Q

dexmedetomidine MOA

A

alpha-2 agonist; inhibits noradrenalin release

44
Q

dexmedetomidine considerations

A
  • patients readily arousable
  • no respiratory depression
  • less delirium than benzos
  • should not be used when deep sedation is required
45
Q

dexmedetomidine pharmacokinetics

A
  • short half life
  • some elimination impairment in hepatic dysfunction
46
Q

dexmedetomidine use

A
  • no loading dose needed
  • only approved for short term
47
Q

dexmedetomidine AE

A
  • decreased BP with rapid administration
  • bradycardia and hypotension from loading dose
  • should not use in hemodynamic instability
48
Q

dexmedetomidine clinical use

A
  • recommended over benzos for critically ill mechanically ventilated adults
  • use limited by cardiovascular AE
  • lower incidence of delirium
49
Q

what are the two types of delirium?

A
  • hyperactive/agitated
  • hypoactive/lethargic
50
Q

what are the assessments for delirium?

A

ICDSC and CAM-ICU

51
Q

Prevention of delirium

A

early mobilization, optimization of sleep, hearing and vision, improving cognition and orientation

52
Q

what are the pharmacologic treatments for delirium

A

haloperidol
atypical antipsychotics: risperidone, olanzapine, quetiapine, aripiprazole
- may be used short-term only
dexmedetomidine- for delirium caused by agitation

53
Q

Haloperidol uses and AE

A
  • may provide mild sedation for acute agitation
  • no evidence for reduction of delirium duration
  • Prolongs QT interval
  • decreases seizure threshold
  • EPS
54
Q

Use/AE of atypical antipsychotics

A
  • may be safer than haloperidol
  • fewer EPS
  • should not use in patients at risk for torsades
  • olanzapine can cause NMS and hypotension
55
Q

treatment of delirium?

A
  • 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
56
Q

PAD Guidelines

A
  • sedation: less is more
  • light sedation preferred and only if required
  • daily interruptions of sedation
  • analgesia first!
57
Q

treatment algorithm

A
  • benzos last
  • dexmedetomidine: preferred in patients with delirium and agitation
    propofol: preferred in neurotrauma where rapid awakening is preferred and in cardiac surgery

PHRM 864 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions