NMBD Reversal Agents (Exam IV) Flashcards
- What type of NMBD reversal is Edrophonium?
- What is its trade name?
- What anticholinergic agent is given with it?
- What receptor does it work on?
- What is the MOA?
- Acetylcholinesterase inhibitor
- Enlon
- Atropine
- nACHr
- Competitive antagonist. Inhibits the destruction of acetylcholinesterase at the NMJ.
- What type of NMBD reversal is Neostigmine?
- What is its trade name?
- What anticholinergic agent is given with it?
- What receptor does it work on?
- What is the MOA?
- Acetylcholinesterase inhibitor
- Bioxiverz
- Glycoprrolate
- nAChr
- Competitive antagonist. Inhibits the destruction of acetylcholinesterase at the NMJ.
- What type of NMBD reversal is atropine?
- What other reversal agent is it given with?
- What receptor does it work on?
- What is the MOA?
- Anticholinergic
- Edrophonium
- mAChr
- Competitive inhibitor of ACh at post ganglionic sites.
- What type of NMBD reversal is glycoprrolate?
- What is the trade name?
- What other reversal agent is it given with?
- What receptor does it work on?
- What is the MOA?
- Anticholinergic
- Robinol
- Neostigmine, pyridostigmine
- mAChr
- Competitive inhibitor of ACh at post ganglionic sites.
- What type of NMBD reversal is sugammadex?
- What is the trade name?
- What type of chemical forces or bonds does it use?
- What is the MOA?
- Aminosteroid curare reversal
- Bridion
- Van der walls, hydrophobic, and hydrogen bonding
- Forms a complex with aminosteroid NMBDs (Roc > Vec > panc) reducing the amount of available nAChr at the NMJ. It encapsulates the aministeroid using intermolecular forces.
Which NMBD reversal agents are lipid soluble?
- Edrophonium
- Neostigmine
- Atropine
- Glycopyrrolate
Which NMBD reversal agents are highly water soluble?
- Sugammadex
- What is the normal dose of edrophonium?
- Max dose?
- Onset?
- Duration?
- 0.5 - 1mg/kg
- MAX = 1 - 1.5mg/kg
- Onset = 1-2 minutes
- Duration = 5-15 minutes
- What is the normal dose of Neostigmine?
- Max dose?
- Onset?
- Duration?
- 40 - 70mcg/kg (Use total body weight to calculate) Or 0.04mg - 0.07mg/kg
- MAX = 5mg
- Onset = 5-10 minutes
- Duration = 60 minutes
- What is the normal dose of Atropine?
- Onset?
- Duration?
- 7-10mcg/kg
- Onset = 1-2 minutes
- Duration = 5 minutes
- What is the normal dose of Glycopyrrolate?
- Max dose?
- Onset?
- Duration?
- 7-15mcg/kg given over 2 minutes
- MAX = 1mg
- Onset = 1 minute
- Duration = 60 minutes
- What is the normal dose of Sugammadex for a moderate block?
- Deep block?
- Extreme block?
- Onset?
- Duration?
- Moderate block (TOF 2/4) = 2mg/kg (use total body weight).
- Deep block (TOF 0/4, or 1-2 posttetanic count) = 4mg/kg (use total body weight)
- Extreme block (TOF 0/4) = 8-16mg/kg (Use total body weight)
- Onset = 1-4 minutes
- Duration = 1.5-3 hours
What 2 NMBD reversals use total body weight for dosage calculations?
- Neostigmine
- Sugammadex
How is Edrophonium metabolized?
- Hepatic 30-50%
- Renal 75%
How is Neostigmine metabolized?
- Hepatic 30-50%
- Renal 50%
How is Atropine metabolized?
Hepatic 50-87%
Renal 13-50%
How is Glycopyrrolate metabolized?
hepatic through hydrolysis
How is Sugammadex metabolized?
Renal 70% in 6 hours and 90% in 24 hours
When giving Edrophonium and atropine, which one do you give first?
- Give the atropine first, wait for the heart rate to start climbing to an increase of 20%, then give the edrophonium and the heart rate will go back down to normal.
- Edrophonium can drop heart rate very first because it is so fast acting.
What are the side effects of acetylcholinesterase inhibiting NMBD reverasals (Edrophnium and neostigmine)?
- **CNS **= miosis
- CV = bradycardia, dysrhythmias, asystole, decreased SVR
- Pulm = Bronchoconstriction, increased airway resistance, increased salivation
- **GI = hyperperistalsis, PONV, increased gastric fluid secretion
*** Overall, increased parasympathetic nervous system activity
What are the side effects of anticholinergic NMBD reverasals (Atropine and glycopyrrolate)?
- **CNS **= mydriasis
- CV = tachycardia, dysrhythmias, asystole, increased SVR
- Pulm = Bronchodilation, decreased airway resistance, decreased salivation
- **GI **= dry mouth, decreased proximal gastric emptying, decresed antral contractility, slower gastric emptying, constipation
- GU = urinary retention
What are the side effects of Sugammadex?
- Nausa/vomitting
- Dry mouth
- Bradycardia
- Dizziness
- Pruritis
- uticaria
- anaphylaxis
- Decreased renal excretion with ESRD and HD patients
- Potential for no therapeutic effect
What is a nickname for edrophonium?
Fast eddie
True/False
Glycopyrrolate crosses the blood brain barrier?
False, it does not cross the blood brain barrier
What happens with NMBD reversal agents when a patient has decreased kidney function, ESRD, or renal failiure?
Their plasma clearance of the drug is decreased which will prolong duration of action of the reversal.
- When should you administer neostigmine during emergence?
- How long, generally, until NMJ blockade is fully reversed with neostigmine?
- 5-10 minutes before the case is over, when they are suturing the faschia.
- 20-30 min
Do AChE inhibitors work with deep neuromuscular blockade?
No, due to the ceiling effect.
Reversal of NMJ blockade is dependent on these 6 factors:
- Depth of block
- Drug choice (neo vs edro)
- Dose
- Rate of plasma clearance
- Anesthetic agent and depth (remember some of our volitiles also provide NMB)
- Patient conditions: metabolic acidosis, respiratory acidosis, hypothermia.
What drugs would be coupled with NMBD reversal agents to prevent adverse side effects from these drugs?
Anti-cholinergic / Anti-muscarinics
- Atropine
- Glycopyrrolate
Differentiate between no block, moderate block, and deep block.
- No block: 4/4 twitches on TOF (no NMBD reversal needed, or give 20% neostigmine and glycopyrrolate)
- Moderate: 2/4 twitches on TOF. (give 50% neostigmine and glycopyrrolate)
- Deep: No twitches to TOF (AChE wont work due to ceiling effect)
If you’re concerned about someone’s cardiac status due to existing disease, which Anticholinergic drug would you use?
Glycopyrrolate
What common side effects are seen right after atropine administration?
- Mydriasis
- Tachycardia
How long does glycopyrrolate need to be administered over?
2 - 5 min
What reversal drug is very specific to rocuronium?
Sugammadex
What should be known about sugammadex’s organic structure and physical properties?
- γ-cyclodextrin
- Dextrose units from starch (Can still be given to diabetic patients without throwing them into DKA)
- Very H₂O-soluble
- Binds to the free drug (NMDB) in the plasma. Does not bind to a receptor.
What drugs does sugammadex work with?
Roc > Vec > Pancuronium
* Aminosteroid NMBDs
What is the E ½ time of sugammadex?
2 hours
What drugs/conditions are relative contraindications to sugammadex?
- Contraceptives (innactivates birth control for 7 days)
- Toremifene (displaces roc from sugammadex)
- Coagulopathy - will cause elevated PTT, PT, and INR
- ESRD (excreted renally)
- What is the mechanism of persistant NM blockade?
- What is the intervention?
- Happens when acetylcholinesterase is maximally inhibited and no further acetylcholinesterase is effective. Typically caused by the ceiling effect.
- Intervention = sedation and post op ventilation (could be either bipap or re-intubation).
When should tetany be used?
When you aren’t getting any train of 4 response for NMBD reversal
What is recurarization?
Resumption of NMJ blockade after period of reversal
What s/s would indicate recurarization?
Say you just brought the patient to PACU.
- ↓ SpO₂
- ↓ respiratory effort
- Floppy/uncoordinated
- Unresponsive
- unable to lift head/neck
- Pharyngeal collapse and respiratory obstruction (worst case scenario.
What drug and dose would be a good choice for a recurarizing patient in the PACU?
Why might this be a good choice?
- Neostigmine 0.05 mg/kg IV
- Longer duration of action
What reversal drug is specific to mivacurium?
Purified human plasma cholinesterase
What reversal drug is specific to gantacurium?
Cystiene
