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28 Cards in this Set

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  • Back

depolarization of muscle fibers occurs when...

ACH combines w/Nm receptors

Muscle relaxation occurs when...

ACH hydrolyzed by acetylcholinesterase. This terminates ACH action.

centrally acting skeletal muscle relaxant

inhibits skeletal muscle contraction by blocking conduction within spinal cord

Peripheral skeletal muscle relaxant

inhibit at NMJ or within contractile process

when skeletal muscle relaxation desired

spastic diseases (MS, CP)


spinal cord damage (trauma, paraplegia)


injuries when pain accompanies muscle overexertion


surgical, orthopedic procedures, intubation (bronchoscopy)


2 types neuromuscular blockers

nondepolarizing (curare, pancuronium)


depolarizing (succinylcholine)

Non depolarizing blockers mechanism of action

occupy Nm sites, ACH cant combine w/receptors, depolarization cant occur

prototype non-depolarizing drug

Curare

Modern non-depolarizing drugs end in

-curium


-curomium

non depolarizing drug examples

Mivacurium (duration 10-20 mins)


Pancuronium bromide (duration 30+ mins)


Rocuronium bromide (Zemuron) (up to 30 mins)


Atracurium besylate (30 mins)


Cisatracurium besylate (NImbex) (30 mins)


Curare (duration up to 60 mins)

Depolarizing blockers

produces paralysis by 1st causing nerve transmission (observed as fasciculations), then inhibiting it (no response to ACH)

Succinylcholine

only available depolarizing neuromuscular blocking drug

ACH

neurotransmitter in NMJ

nondepolarizing blockers administration

IV

Recovery of muscle function from nondepolarizing blocker

as drug is metabolized, excreted

Vagolytic action

inhibition of Vagus nerve to heart, causing tachycardia (counteraction to vagal tone that causes bradycardia)

Succinylcholine

can produce ventricular arrhythmias, changes in BP


Can cause muscle breakdown and life threatening arrhythmias and cardiac arrest in children


potentiated by digitalis, diuretics

atracurium


mivacurium


succinylcholine

cause release of histamine from mast cells, can lead to bronchospasms, increased secretions in sensitive patients (asthma)

Major toxicity associated with neuromuscular blockers

paralysis of respiratory muscles, life threatening

skeletal muscle paralysis caused by non depolarizing blockers reversed with?

neostigmine


edrophonium


Sugammadex

1st in new class


selective relaxant binding agent (SRBA)


reverses neuromuscular blockade of nondepolarizing blockers by encapsulating, chelating the blocker.


special affinity for rocuronium

Succinylcholine OD

No Known antidote


drug must be metabolized

Malignant hyperthermia

drastic increase in body temp


can be caused by normal dose succinylcholine in combination w/inhalation anesthetic

Dantrolene

direct acting peripheral skeletal muscle relaxant


perevents actin, myosin from interacting, preventing muscle contraction. Blocks release of calcium ions


Acts within muscle cell at calcium storage centers

Sarcoplasmic reticulum

organelle in muscle cell releases calcium ions during contraction, absorbs calcium ions during relaxation

Dantrolene clinical indications

malignant hyperthermia, spastic conditions (MS, CP, spinal cord injuries)


relaxes spastic skeletal muscle


interferes w/calcium release

Dantrolene adverse effects

dizziness, vomiting, fatigue, weakness


potential for hepatoxicity


Contraindications- hepatitis, cirrhosis, other hepatic diseases


Can be potentiated by alcohol, antiarrhythmics (lidocaine, procainamide, quinidine) antibiotics, general anesthetics, narcotic analgesics, tranquilizers, sedatives

Spasmolytics

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