Neuromuscular Blockers Flashcards
MOA fo atracurium?
Isoquinoline. Non-depolarizing NMBA. Rapid initial distribution, slower elimination. Poor protein binding.
ADE of atracurium?
Strongly hepatically metabolized and can cause seizures.
MOA of pancuronium?
Steroidal Non-depolarizing NMBA.
ADE of pancuronium?
Pee out the panic (heart and piss). 80% renally eliminated. Has off target action on Cardiac M receptor.
MOA of vecuronium?
Steroidal non-depolarizing NMBA
ADE of vecuronium?
90% hepatically eliminated (also renal). No off target actions.
MOA of succinylcholine?
Depolarizing NMBA. Extremely short duration of action.
ADE of succinylcholine?
heart changes, hyperkalemia, intraocular pressure, myogloinuria and malignant hyeprthermia.
Increased risk for abnormally long duration with pseudocholinesterase defects.
Off target stimulation of ganglia, cardiac M receptors and Histamine release.
MOA of pyridostigmine?
parasympathomimetic and reversible AchE inhibitor.
ADE of pyridostigmine?
Can decrease heart rate, cause bronchospasms, increase GI peristalsis and bladder tone, pupillary constriction.
MOA of neostigmine?
AchE inhibitor prevents breakdown of Ach and counteracts all neuromuscular blocking agents except succinycholine. Parasympathomimetic
ADE of neostigmine?
headache, blurred vision, bradycardia. Usually given with atropine. GI symptoms
Contrast the mechanism and duration of action of depolarizing and non-depolarizing blockers in their interruption of skeletal muscle contraction.
Depolarizing blockers like succinylcholine, both occupy the Ach receptor and block the ion channel. Depolarizing may desensitize the end plate by occupying the receptor and cause persistent depolarization. They have a very rapid onset and short action of duration. Have more serious and life-threatening ADEs.
Non-depolarizing blockers like rocuronium bind competitively to the receptor at the motor end-plate to antagonize the action of Ach. Slower onset and longer duration than depolarizing agents.
What is TOF and how does it work?
TOF stands for train-of-four testing. It is commonly performed on ulnar nerve. Done by counting the number of twitches eliited thorugh electrodes along nerve paths. A stimulus is delivered as a group of 0.2 ms pulses spaced 500 ms apart. This pattern is repeated every 10 s. The number of contractions observed relfects the degree of blockade.
No NMBA -> 1 impulse = 1 contraction
Some NMBA –> 4th impulse begins to fade.
Why would you need muscarininc antagonists with AchE inhbitors?
TO reverse NMBA blockade, you only need the nicotinic cholinergic effects of the AchE drugs. Concurrent administration of the anticholinergic antimuscarinic agents prevents the muscarinic off target effects.
