Neuromuscular Blockers Flashcards
What is the action of NMBs?
Prevents muscle contraction by interfering with the transmission of an action potential from the nerve ending to the muscle
What are NMBs used for?
Facilitates endotracheal intubation, decreases muscle tone for optimal operating conditions, alleviates muscle activity with ECT, allow balanced anesthesia without patient movement, assist in controlled ventilation in ICU patients.
Where do NMBs work?
The neuromuscular junction between the nerve and muscle
_______ influx causes vesicles to adhere to the ________ ________ and rupture to release ________ into the cleft
Calcium influx causes vesicles to adhere to the presynaptic membrane and rupture to release acetylcholine into the cleft
ACh diffuses across _____ _____ to the _______ receptor located on the motor end plate.
ACh diffuses across the synaptic cleft to the nicotinic (cholinergic) receptor located on the motor end plate.
ACh binds with the ______ sites on the postsynaptic receptor, causing the opening of the _____ ______. Then what happens to Na and K ions?
ACh binds with the alpha sites on the postsynaptic receptor, causing the opening of the ion channel.
The sodium and potassium ions move through the channel causing depolarization of the motor end plate membrane (change in transmembrane potential from -90mV to -45 mV- the threshold potential.
-Sodium comes in, potassium goes out.
What causes a muscle contraction?
The action potential spreading over the surfaces of the muscle fibers.
Muscle contraction is initiated by _______-_______ _______
muscle contraction is initiated by excitation-contraction coupling.
What happens with ACh after muscle contraction?
ACh quickly diffuses away from the end plate region or is metabolized (hydrolyzed) by acetylcholinesterase (AChE), a local acetylcholine enzyme
Where is AChE contained?
In the postsynaptic membrane
What does it mean when a muscle repolarizes?
It relaxes
What happens if there is too much or too little of Ca when releasing acetylcholine?
ACh release is calcium-dependent and triggered by increases in the concentrations of free Ca ions in the nerve terminals.
-Too much Ca, too much contraction.
-Too little Ca, not enough contraction.
What is the process of Ca triggering ACh release?
A nerve action potential activates adenylate cyclase in membranes of nerve terminals leading to the formation of cyclic adenosine monophosphate (cAMP), which subsequently opens Ca ion channels, causing synaptic vesicles to fuse with the nerve membrane and release ACh.
What is the primary transmitter for neuromuscular junctions?
Acetylcholine
What is the principle site of neuromuscular blocking agents?
Neuromuscular junctions
What inhibits release of ACh?
Magnesium. This is why we treat high Ca with magnesium sulfate.
Acetylcholine is rapidly _______ by _________ to ______ _____ and _______
Acetylcholine is rapidly hydrolyzed by acetylcholinesterase to acetic acid and choline.
-Happens in less than <15 ms
What happens after choline is formed from the breakdown of ACh?
It returns to nerve ending to be used to synthesize more ACh.
What are the ACh receptors?
Presynaptic (prejunctional), extrajunctional, and postsynaptic
What are presynaptic receptors?
These are on the nerve ending and they affect neurotransmitter release. Ion channel opening allows the flow of sodium only.
-activation of these mobilizes additional ACh for subsequent release (so blocking these receptors causes a decrease in ACh release)
-This is the receptor where you see a fade on the TOF