Lecture 8 Intro to Analgesia Techniques Part 1 Flashcards
1
Q
What are the 6 nsaids given in class
A
- Carprofen
- Deramaxx
- Meloxicam
- Robenacoxib
- Phenylbutazone
- Flunixin Meglumine
2
Q
- What species do we use fentanyl intra-op
- Is it dose dependent MAC sparing?
- Cause bradycardia or tachycardia?
- How do we treat this?
A
- Dogs & cats
- Dose dependent MAC sparing (up to ~65%)
- Bradycardia
- Glycopyrrolate, Atropine if also hypotensive
3
Q
What must you monitor with fentanyl
A
•Monitor EtCO2, IPPV
4
Q
What is MLK?
A
- Morphine, lidocaine, ketamine
- A Multimodal Analgesia
5
Q
- What part of pain pathway does morphine work on?
- Is it better for somatic or visceral pain?
A
- transduction, modulation, perception
- Visceral pain, ‘backbone’ of most/all analgesic protocols
6
Q
- What part of pain pathway does lidocaine work on?
- What properties does it have for the MLK combination (its job)
A
- transduction*, transmission, modulation
- Properties:
- Anti-inflammatory, central analgesic properties with CRI
- ‘Prokinetic’ agent in horses due to anti-inflammatory properties (↓ TNF)
- Neuroprotection (?)
7
Q
how does lidocaine ↓ cardiac/cerebral ischemia-reperfusion injury ?
A
↓ cardiac/cerebral ischemia-reperfusion injury by preventing intracellular Na+ overload & through its anti-inflammatory properties
8
Q
- What type of drug is ketamine
- How does it block pain?
- What does it to do MAC of ISO?
A
- NMDA receptor antagonist
- Somatic Pain => bones, joints, ligaments, skin
- ↓ Central sensitization & ‘wind-up’
- ↓ MAC ISO ~ 10%
9
Q
Explain how central sensitization happens
A
- Frequent/severe activation of Aδ & C nociceptors =>
- ↑ excitatory neurotransmittors (glutamate, Substance P) =>
- Activates NMDA, NK, AMPA receptors =>
- ↑ signal molecules, gene expression, neuroplasticity
- Aβ mechanoreceptors activated => nonpainful stimuli contribute to pain response => 2⁰ hyperalgesia
10
Q
How does Ketamine stop Central Sensitization
A
Blocks NMDA receptors ↓ central sensitization, wind-up, 2⁰ hyperalgesia, chronic pain
11
Q
How does ketamine cause neuroprotection
A
- via NMDA blockade
- ↓Ca influx =>
- ↑Cell integrity
- ↑Cell survival
- ↑Regeneration
12
Q
Can MLK be bolused?
A
DO NOT BOLUS!
13
Q
How much does MLK decrease MAC of ISO?
A
- many patients ~1% ISO
- ↓ MAC of ISO by 45%
14
Q
How do you recover patients on MLK
A
- Wean from IPPV, continue to monitor EtCO2
- 10 minutes O2 support after vaporizer off
- Monitor SpO2, keep >93-95% with O2 supplementation
- +/- Partial reversal if prolonged O2 dependence
- 0.1ml (1mg) Butorphanol + .9ml NaCl
- Give in .2ml (.2mg) increments
- 0.1ml (1mg) Butorphanol + .9ml NaCl
15
Q
- What is HLK?
- What is the difference clinically to MLK?
A
- Hydromorphone, lidocaine, ketamine
- Clinical impression:
- less sedation
- more vocalization/dysphoria at recovery