PADIS Flashcards

1
Q

How does the peripheral pathophys of pain work? What are the 2 peipheral fibres?

A
  • Painful stimulus causes cell damage
  • Damage received by nociceptors, turning noxious stimuli into impulses and transmit along peripheral nerve fibres (A delta fibers or C fibres)
  • A DELTA –> Thermal or mechanical cellular changes transmit pain quickly through densely myelinated fibres. Result in “prickling” or “sharp” pain
  • C FIBRES –> Less myelinated, transmit chemical changes in cellular environment. Associated with “dull”, “aching”, or “diffuse” pain
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2
Q

How does central pathophys of pain work?

A

Neurotransmitters (Substance P) carry impulses across synapse from PNS to the central nervous system.

  • Impulse enters dorsal horn of spinal cord and travels along spinothalamic tract
  • Pain interpreted at the CEREBRAL CORTEX
  • Body produces endorphins to reduce the pain, produced in the brainstem and travel down the spinal cord and block the transmission of pain
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3
Q

What do synthetic opioid analgesics mimic?

A

Mimic action of natural endorphins produced at the brainstem and travel down the spinal cord binding to nerve receptor sits to block pain transmission

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4
Q

What is the pain assessment hierarchy?

A

1) Self report (NRS, non-verbal communications)
2) Behavioural pain assessment tool
3) Minimize emphasis of physiological indicators of pain

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5
Q

What are valid physiological indicators of pain?

A

NO VALID PHYSIOLOGIC INDICATORS.

Changes may arise from multiple causes associated with catecholamine release, difficult to isolate to pain. They can be used as a CUE to begin pain assessment

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6
Q

How is morphine used for pain management?

A

For acute pain, mod-severe

Dose: 2-4mg IVP
Onset: 5 min
Duration: 4-5 hrs

For hemodynamically stable pts, causes histamine release that can cause hypotension (especially with hypovolemia). Can cause resp. depression

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7
Q

How is hydromorphone used for pain management?

A

For acute pain, mod-severe

Dose: 0.2-1mg IVP
Onset: 5 mins
Duration: 3-4 hrs

Less side effects than morphine (pruritus, sedation, N/V), approx 10 times stronger than morphine

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8
Q

How is fentanyl used for pain management?

A

For acute pain, mod-severe

Dose: 25-100mcg IVP (MCG)
Onset: 1-2min
Duration: 30-60 min

For hemodynamically unstable pts, procedural analgesic, renal impairment, no histamine release, more rapid onset than morphine but drug accumulation in liver.

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9
Q

What are 2 routes opiates can be administered in ICU?

A

1) Intravenous
2) Epidural

-Push, continuous infusion, patient controlled analgesic

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10
Q

When is epidural opiate route recommended?

A

For pts with abdominal aortic surgery and traumatic rib fractures

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11
Q

What is sedation?

A

State where pt is calm, relaxed, and relatively pain free. Used in management of anxiety, agitation, and short turn procedural intervention

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12
Q

What is agitation?

A

Excessive, usually non purposeful motor activity associated with muscle tone and catecholamine release

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13
Q

What is anxiety?

A

Prolonged state of apprehension in response to real or perceived fear

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14
Q

How can sedation be assessed?

A

Riker Sedation Agitation Scale (SAS)

EEG or Bispectral Index (BIS) record brain wave activity illustrating sedation

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15
Q

How is midazolam / versed used for sedation?

A

Acute rapid sedation, short term / immediate use

Onset: Short half life, shortest acting benzo
Metabolism: Liver, metabolite causes hypotension

-If used as continuous infusion, short acting benefits are lost and drug accumulates in fatty tissue. Tolerance can develop and risk of delirium

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16
Q

How is propofol used for sedation?

A

Useful for neuro pts requiring waking for assessment, post op, short term, or long term use, management of increased ICP

Onset: Short acting, rapid onset
Metabolism: Liver (rapidly metabolized)

-Does not have analgesic properties, monitor triglyceride levels after 2 days of use, associated with hypotension

17
Q

Why must we balance sedation?

A

Prolonged sedation = delayed weaning

Inadequate sedation = anxiety, agitation

18
Q

How do we avoid over-sedation?

A

1) Daily sedation interruption

2) Light sedation

19
Q

What are symptoms of sedation withdrawal?

A
  • Increased HR, BP, RR
  • Irritability, anxiety, delirium
  • Confusion, short term memory issues
20
Q

How are Alpha 2 agonists used?

A

Can be used as a sedative as they inhibit effects of norepinephrine. Traditionally used as anti-hypertensive but also has sedative and anxiolytic properties.

  • Used to wean off sedatives and opioids, or in withdrawal syndrome
  • Clonidine, dexmedetomidine are examples
21
Q

Why is it important to manage delirium?

A
  • Increased length of ICU stay, hospital stay
  • Increased mortality
  • Long term cognitive impairment
22
Q

What is delirium?

A

Syndrome characterized by acute onset of cerebral dysfunction associated with:

1) Disturbed LOC
2) Change in cognition

23
Q

What are the 3 subtypes of delirium?

A

1) Hypoactive (Lethargy, decreased LOC)
2) Hyperactive (Agitation, restlessness)
3) Mixed (fluctuation)

24
Q

What is the pathophys of delirium?

A

Unknown, but possibly imbalance of neurotransmitters such as serotonin, acetylcholine, or dopamine

25
What are risk factors for delirium?
- Pre-existing dementia - Hypertension - Alcoholism - High severity of illness - Coma - Benzo use - Sleep deprivation
26
What are the most valid pain scales in ICU?
- BPS | - CSPOT
27
What is the recommendation for first line analgesic therapy?
IV opioids. Use non-opioid analgesics to reduce opioid side effects. Use gabapentin or carbamazepine in conjunction to IV opioids for neuropathic pain.
28
Should procedural pain be pre-treated?
Yes, pre-treat procedural pain
29
What are the most valid scales for assessing sedation?
RASS and SAS, suggest using brain function monitors for pts on NMBA
30
What are the most valid delirium scales?
CAM-ICU and ICDSC
31
What is the most important intervention to reduce the incidence and duration of delirium?
Early mobilization
32
Should prophylactic meds be given to prevent delirium?
No. Most important to mobilize early and protect pt sleep cycles
33
What should be held in pts with baseline QT prolongation?
Anti-psychotics like haloperidol
34
What is the risk of ICU acquired weakness? What is the primary recommendation as intervention to reduce?
Occurs in 25-50% of pts, associated with impairments to long term survival, functioning and quality of life. Mobilization is primary intervention.
35
What is the effect of sleep disruption?
Associated with distress, delirium, increased length of mechanical ventilation, immune dysfunction, cognitive decline