Neuromuscular Blocking Drugs Flashcards
What is a neuromuscular blockade?
Reversible binding of nicotinic cholinergic receptors by drugs that prevent neuromuscular transmission by restricting ACh access to the receptors
T/F: Muscles relaxants = NMBD
False
Muscle relaxants include centrally acting drugs (benzodiazepines, guaifenesin, and A2 agonists)
NMBDs only act at the neuromuscular junction
T/F: the animal retains consciousness when given NMBD
True
Must ensure other analgesia/anesthesia is adequate
What are indications for NMBD ?
Microscopic ophthalmic surgery (intraocular or corneal)
Thoracic and diaphragmatic hernia repair —>complete paralysis improves IPPV
Orthopedic surgery —> eases stretching of muscles across fracture line
What are advantages to NMBD?
May be antagonized Produce predictable muscle relaxation Reduces required general anesthetic Less trauma Facilitate IPPV Facilitates endotracheal intubation
What are disadvantages to neuromuscular blockade?
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
How can you monitor anesthetic depth when using NMBD?
Somatic (cranial) reflexes are lots
Autonomic reflexes (tachycardia/hypertension) used as indicators of response to noxious stimulation
What is Recurarization ?
NMB-additive effect drugs (aminoglycosides and some antibiotics) administered post-op may cause full muscle paralysis again
How does muscle contraction occur?
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
T/F: NMBD reversibly occupy post synaptic nicotinic cholinoceptors and prevent neuromuscular transmission by restricting ACh access to these sites
True
What are the two classes of NMBDs?
Depolarizing (non-competitive)
-> structurally similar to ACh, depolarizes membrane until it is fatigued
Non-depolarizing (competive)
->antagonist blocking ACh interaction with the receptor
What is the order of muscle blockade ?
Face, muscles of expression Neck muscles Diaphragm Distal limbs Proximal limbs Abdominal muscles Intercostal muscles
Are NMBDs lipid or water soluble?
Water soluble —> do not cross lipid barriers/BBB
What drugs will potentiate the effects of NMBDs?
Inhalation anesthetic drugs
Injectable anesthetics
Aminoglycosides and some other antibiotics
Antiarrhythmic drugs
Diuretics
Mg
T/F: hyperthermia enhances and prolongs effect of NMBD
False
HYPOthermia potentiates effects
How does age effect NMBDs?
Younger more active animals require high doses
Delayed reversal in geriatrics
What is the only depolarizing NMBD in clinical use?
Succinylcholine
What are the advantages to Succinylcholine?
Rapid onset time (1min)
Very short duration (10mins)
—> ideal for intubation in humans
What adverse effects can succinylcholine have on the NMBD?
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
How are the effects of succinycholine terminated?
Diffusion out of the neuromuscular junction
Later metabolized by pseudo-cholinesterases
For the non-depolarizing NMBDs, what is their onset of action and duration of action?
3-5mins
All leasing 10-30mins except:
- pancuronium >30min
- rapacuronium <10min
T/F: non-depolarizing NMBD can be antagonized
True
What is the difference between atracurium and cis-atracurium?
Atracurium —> mixture of 10 isomers
Cis-atracurium —> single isomer
What are advantages to using atracurium ??
Rapid metabolism due to spontaneous degradation
Hydrolyzed by non specific tissue esterases
Hoffmann elimination - dependent on pH and temp
