Lecture 15 (Exam 4) - NMBD Reversal Agents Flashcards
Castillo talked about this case study where everything went wrong and the patient died.
Flip card to learn how to NOT fuck around find out. 😮💨
These are the factors that were identified that led to the patient’s death.
*They pulled out the ETT without fully reversing the patient.
* Intubation skills were not on fleek.
* The team did not communicate with one another.
What are sugammadex’s side-effects?
Dose related: nausea/vomitting, pruritis, urticaria
Anaphylaxis
Marked bradycardia
Doesn’t work ??
(same type of reaction with protamine. Give full dose of suggamadex but slowly.)
Slide 32
Why do we use monitoring with reversal agents?
Our assessment alone (quantitative) does not suffice as you can see by the 44% of residual block therefore we will use monitoring to assess any residual block to ⬆ safety :)
Slide 4
When is the best time to get a baseline TOF?
Immediately before giving your intubating dose of NMBA. (post lido, opioids and propofol –> like we do in SIM 😁)
Slide 7
List the 5 NMBA reversal drugs.
List the 2 Anti-Cholinergic Agents we use.
Why do we give these in conjunction?
What is the one NMBA Reversal that does not require a conjunction med?
Edrophonium, Neostigmine, Physostigmine, Pyridostigmine, Sugammadex
Atropine and glycopyrrolate
We give an anti-cholinergic to blunt the S/E of the reversal agent. (bradycardia, n/v, pruritic, urticaria, etc.)
NMBA are AChe, so there will be in an increase in ACh. The ACh is what causes the SE
Sugammadex
Slide 8
List some cautions for sugammadex.
- Oral contraceptives (Binds w/ progesterone for 7 days. Make sure you tell your patients to use other forms of birth control!)
- Toremifene (non-steroidal anti-estrogen) –> displaced by suggamadex (for pt’s with hx of breast cancer)
- Coagulopathy/Bleeding –> Heparin/LMWH, elevated PTT, PT, INR
-
Recurarizaiton –> does not happen w/ appropriate dosage unless lower than recommended dosage given.
(Less than recommended dosage of suggamadex is not enough to reverse the paralytic agent, hence pt will continue to have NMB)
Slide 34
What is NMB reversal agents MOA?
They are Acetylcholinesterase (AChE) inhibitors that allow ACh to remain longer at the NMJ thus allowing it to compete with our previously given NMB on the nACh-r.
Also called Cholinergic Agents or Competitive Antagonists (technically this should be Indirect Competitive Antagonists…but w/e)
Slide 9
You have already given sugammadex (Bridion) as your NMB reversal to your patient after the surgeon has already closed up the belly. While the surgery tech is counting the sponge, he finds out that one sponge is missing. He looks for it everywhere, even in the trash can. He did not find it. Now, the surgeon thinks that the sponge might have been left in the abdomen and need to open up the belly again.
How long do you have to wait before you give another dose of rocuronium and how much dosage do you need to give?
5 minutes and administer a dose of 1.2 mg/Kg rocuronium
Slide 33
In previous patient, assume you gave neostigmine instead of sugammadex in the same situation.
Now how long do you need to wait before you give another dose of roc and vec?
What are the dosages of rocuronium and vecuronium would you give?
4 hours wait time after reversal with neostigmine for another dose of NMB
Give 0.6mg/kg rocuronium or 0.1 mg/kg vecuronium
Slide 33
Where is our desired site of action for NMB reversal agents?
What is the reason we may see side effects?
The NMJ.
We may see side effects because we give these meds IV –> systemic distribution inhibiting AChE causing an increase in ACh
AChE is available: preganglionic (SNS & PNS and NMJ
Slide 10
What does AChE do again? & how does it do it? (enzyme reaction)
What subunit(s) on the nACh-r does ACh bind to?
Catalyzes rapid hydrolysis of ACh
ACh binds to the alpha subunits (2)
Slide 10
Your patient has 0/4 twitches. What will you do?
A. Give MAX doses of all the reversals
B. Give 50 mcg/kg Neostigmine
C. Give 1 mg/kg Edrophonium
D. Go to lunch since they aren’t gonna move
E. Just wait…
E. Just wait you impatient swine.
- if you give a reversal this can prolong the blockade bc of the CEILING EFFECT
DO NOT give reversals when your patient is in a DEEP block!
Slide 11
Persistent NM blockade occurs when what two things occur?
Acetylcholinesterase is maximally inhibited and no further anti cholinesterase is effective
Slide 21
What can you do as an anesthesia provider if your patient experiences persistent NM blockade/recurarization?
Sedation and post-op ventilation
Slide 21
What are three metabolic patient conditions that influence NMBD reversal?
Metabolic Acidosis
Respiratory Acidosis
Hypothermia
Slide 22
What are the five factors influencing NMBD reversal?
- Intensity of block
- The NMBD used
- Continued volatile anesthetics
- The reversal agent used
- Patient conditions (Hypothermia, acidosis)
Slide 22
Purified human plasma cholinesterase has worked with reversing which NMB drug previously?
Mivacurium
Slide 23
In the past, Cysteine has worked well with what drug for NMBD reversal?
Gantacurium
Slide 23
Sugammadex selectively binds with drugs that have which chemical compound?
Aminosteroid = sugammadex
Slide 23
Sugammadex is renally excreted due to its high _________ solubility.
Water
Slide 25
What is the chemical make-up of Sugammadex?
γ-cyclodextrin
Slide 25
True or False: The main mechanism of action of Sugammadex is in the NMJ.
False.
The main MOA is throughout encapsulating “free drug” in the PLASMA.
Slide 26
Sugammadex can be used to reverse which drugs?
Rocuronium > Vecuronium > > Pancuronium
Slide 26
The reversal that accompanies Sugammadex administration is caused by…
Encapsulation of the free drug in circulation
Slide 26
What are some unintended s/e of our NMBD reversal agents?
1. CV
2. Pulmonary
3. GI
4. Eyes
- CV: Bradycardia, dysrhythmias, asystole, ↓SVR (M2 receptor - inhibitory)
- Pulmonary: Bronchoconstriction, increased airway resistance, increased salivation (M3 receptors; Beta2 dilates)
- GI: Hyperperistalsis, enhanced gastric fluid secretion, PONV (M2 receptor [inhibits the down-regulation provided by M2])
- Eyes: Miosis (M3 receptor is stimulated causing constriction)
“SLUDGE-M”
(slide 18)
Using 10mcg/kg:
Answer:
- 100kg x 10mcg = 1000mcg
- 1mg = 1000mcg
- 1000mcg = 1mg
= 5ml
100 kg x 10 mcg/kg=1000 mcg
1000 mcg x 1 mg/1000mcg= 1mg
1 mg x 1 ml/0.2mg = 5 mL
(slide 20)
How much Suggamadex do we give a patient presenting with 2 out of 4 twitches with T04 stimulation?
2mg/kg for a moderate block
(Slide 28)
How much Suggamadex do we give a patient presenting with 1-2 post-tetanic counts but has no twitch responses to T04 stimulation?
4mg/kg for a deep block
(Slide 28)
ChatGPT explanation: When a deep neuromuscular block is present, and no twitches are elicited on TOF stimulation, post-tetanic stimulation can be applied. This involves giving a burst of high-frequency stimulation (tetanus), followed by single twitches at a slower frequency. The number of twitches observed after this tetanic stimulation is the PTC.
Having 1-2 post-tetanic counts while observing no twitches on TOF indicates profound neuromuscular blockade but not a complete block. Some recovery has occurred since tetanic stimulation can temporarily increase the availability of calcium ions in the muscle cells, making it possible to elicit a few twitches. However, the absence of twitches on TOF stimulation suggests that the block is still too deep for the muscle to respond to the less intense TOF stimuli.
Check out this cool chart comparing recovery times with use of Suggamadex vs. Neostigmine with reversal of Rocuronium.
Slide 30
Check out another cool chart comparing recovery times with use of Suggamadex vs. Neostigmine with reversal of Vecuronium.
Slide 31
What are the clinical duration of response times (in mins) of the following that were given in slide 39, Table 12-2?
Intermediate-acting:
- Rocuronium
- Vecuronium
- Cisatracurium
- Atracurium
Intermediate-acting:
- Rocuronium = 36
- Vecuronium = 44
- Cisatracurium = 45
- Atracurium = 46
(slide 39, Table 12-2)
