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RUSVM Anesthesiology > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

What is a neuromuscular blockade?

A

Reversible binding of nicotinic cholinergic receptors by drugs that prevent neuromuscular transmission by restricting ACh access to the receptors

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2
Q

T/F: Muscles relaxants = NMBD

A

False

Muscle relaxants include centrally acting drugs (benzodiazepines, guaifenesin, and A2 agonists)

NMBDs only act at the neuromuscular junction

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3
Q

T/F: the animal retains consciousness when given NMBD

A

True

Must ensure other analgesia/anesthesia is adequate

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4
Q

What are indications for NMBD ?

A

Microscopic ophthalmic surgery (intraocular or corneal)

Thoracic and diaphragmatic hernia repair —>complete paralysis improves IPPV

Orthopedic surgery —> eases stretching of muscles across fracture line

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5
Q

What are advantages to NMBD?

A 
May be antagonized 
Produce predictable muscle relaxation 
Reduces required general anesthetic 
Less trauma
Facilitate IPPV 
Facilitates endotracheal intubation
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6
Q

What are disadvantages to neuromuscular blockade?

A

Requires mechanical ventilation

Difficulty monitoring anesthetic depth

Risk of transecting nerves because you lose twitch response with nerve is touched

Complexity of monitoring blockade
Unpredictable responses

Recuarization
Histamine release

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7
Q

How can you monitor anesthetic depth when using NMBD?

A

Somatic (cranial) reflexes are lots

Autonomic reflexes (tachycardia/hypertension) used as indicators of response to noxious stimulation

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8
Q

What is Recurarization ?

A

NMB-additive effect drugs (aminoglycosides and some antibiotics) administered post-op may cause full muscle paralysis again

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9
Q

How does muscle contraction occur?

A

Action potential arrives at pre-junctional A-alpha motor neurons

Nerve terminal depolarizer

ATP converted to cAMP —> Ca2+ influx to nerve terminal causing ACh release into synaptic cleft

ACh binds receptors on muscle resulting in muscle cell AP and contraction

Acetylcholinesterase metabolizes ACh

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10
Q

T/F: NMBD reversibly occupy post synaptic nicotinic cholinoceptors and prevent neuromuscular transmission by restricting ACh access to these sites

A

True

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11
Q

What are the two classes of NMBDs?

A

Depolarizing (non-competitive)
-> structurally similar to ACh, depolarizes membrane until it is fatigued

Non-depolarizing (competive)
->antagonist blocking ACh interaction with the receptor

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12
Q

What is the order of muscle blockade ?

A 
Face, muscles of expression 
Neck muscles 
Diaphragm 
Distal limbs 
Proximal limbs 
Abdominal muscles 
Intercostal muscles
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13
Q

Are NMBDs lipid or water soluble?

A

Water soluble —> do not cross lipid barriers/BBB

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14
Q

What drugs will potentiate the effects of NMBDs?

A

Inhalation anesthetic drugs

Injectable anesthetics

Aminoglycosides and some other antibiotics

Antiarrhythmic drugs

Diuretics

Mg

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15
Q

T/F: hyperthermia enhances and prolongs effect of NMBD

A

False

HYPOthermia potentiates effects

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16
Q

How does age effect NMBDs?

A

Younger more active animals require high doses

Delayed reversal in geriatrics

17
Q

What is the only depolarizing NMBD in clinical use?

A

Succinylcholine

18
Q

What are the advantages to Succinylcholine?

A

Rapid onset time (1min)
Very short duration (10mins)
—> ideal for intubation in humans

19
Q

What adverse effects can succinylcholine have on the NMBD?

A

Muscle fasciculation, muscle contraction —> post op pain/ malignant hyperthermia /myopathy

Cardiac arrhythmia: bradycardia or sinus arrest

Elevated IOP/ICP/ intra-abdominal pressures

May cause histamine release

20
Q

How are the effects of succinycholine terminated?

A

Diffusion out of the neuromuscular junction

Later metabolized by pseudo-cholinesterases

21
Q

For the non-depolarizing NMBDs, what is their onset of action and duration of action?

A

3-5mins

All leasing 10-30mins except:

  • pancuronium >30min
  • rapacuronium <10min
22
Q

T/F: non-depolarizing NMBD can be antagonized

A

True

23
Q

What is the difference between atracurium and cis-atracurium?

A

Atracurium —> mixture of 10 isomers

Cis-atracurium —> single isomer

24
Q

What are advantages to using atracurium ??

A

Rapid metabolism due to spontaneous degradation
Hydrolyzed by non specific tissue esterases

Hoffmann elimination - dependent on pH and temp

25
Q

What are disadvantages of atracurium?

A

May cause histamine release at high doses —> inject diluted and slowly

Laudanosine —> metabolite is a CNS stimulant

26
Q

What advantages does Cis-atracurium have over atracurium?

A

More potent: smaller dose will have same effect

Reduced adverse effects like histamine release and seizures

27
Q

What is the first NMBD that is free of adverse cardiovascular effects?

A

Vecuronium

28
Q

Where are vecuronium and rocuronium eliminated?

A

Liver

Partly by kidney

29
Q

Rocuroniums effects can be terminated by what??

A

Cyclo-dextrin based, Sugammadex

30
Q

How can you monitor the neuromuscular blockade??

A

Extent of muscle relaxation recorded by peripheral nerve stimulator —> record and number of twitches in the innervated muscle group

31
Q

Why is neuromuscular blockade monitoring recommended?

A

Allows for tighter titration of NMBD

Residual blockage may lead to post-op muscle weakness and fatal hypoventilation

(Cannot determine residual blockage on clinical signs alone)

32
Q

What nerves do you stimulate in a dog/cat to monitor neuromuscular blockade??

A

Peroneal nerve

Ulnar nerve

33
Q

What nerves do you stimulate when monitoring neuromuscular blockade in horse?

A

Facial nerve

Superficial peroneal nerve

34
Q

What is the single twitch stimulation pattern?

A

Single stimuli applied at 0.1-1Hz

1Hz used before NMBD to determine pre-relaxant response (control)

Degree of relaxation = post-NMBD response / pre-relaxant response

35
Q

What is the train of four stimulation pattern ?

A

Delivery of 4 supramaximal stimulus (2Hz over 2seconds)

Degree of relaxation= ratio of intensity of twitch 4 / twitch 1

—> serves as own control
—> no blockade: t1/T4= 1

Ratio below 0.7 implies blockade

36
Q

How can NMBD be antagonized??

A

Anti-cholinesterases
—> edrophonium
—> neostigmine

37
Q

When antagonizing NMBDs, what must you concurently administer with the anti-cholinesterase

A

Anticholinergic drugs (atropine/glycopyrolate)

ACh levels will rise when choliesterase are inhibited

—> bradycardia, bronchoconstriction, GI hypermotility

38
Q

What NMBD antagonist is a selective muscle relaxant binding agent and does not inhibit cholinesterase

A

Sugammadex (cyclodextrin)

—> doesnt inhibit choliesterase—> no buildup of ACh—> less PSNS effects—> no bradycardia

RUSVM Anesthesiology (32 decks)

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