Lecture 4 Flashcards
Anticholinergics may also be called: (4)
Cholinergic antagonists
Cholinergic-blocking agents
Parasympatholytics
Vagolytics
3 categories of Anticholinergics
Antimuscarinics
Ganglionic Blockers
Neuromuscular Blockers
5 Antimuscarinics
Atropine Glycopyrrolate (Robinul) Benzotropine (Cogentin) Propantheline Scopolamine
Example of Ganglionic Blocker
Trimethophan (Arfonad)
2 Types of Neuromuscular Blockers
Non-depolarizing
Depolarizing
4 Non-depolarizing neuromuscular blockers
Vecuronium
Cisatracurium (Nimbex)
Pancuronium (Pavulon)
Rocuronium (Zemuron)
Example of Depolarizing Neuromuscular Blocker
Succinylcholine (Anectine)
2 functions of antimuscarinics
Block muscarinic function
Block sympathetic cholinergic receptors
Atropine is a _____
Antimuscarinic
Atropine adult dose
0.4 to 1.0 mg
May repeat every 3-5 minutes up to 3x for bradycardia
Robinul adult dose
0.2 to 0.6 mg
Patients with advanced heart disease often have _____.
increased parasympathetic tone
lower heart rate, lower contractility
What are 3 disease processes antimuscarincs are most commonly used?
Symptomatic bradycardia
PEA/electromechanical dissociation
AV block
What else might antimuscarins be used for?
Adjunct Parkinson's Disease therapy Motion sickness (dramamine) Opthalmic examinations (dilate eyes) Excessive GI hypermotility (lomotil) Urinary urge incontinence
Robinul is a _____.
antimuscarinic
Common side effects of antimuscarinics:
Blind as a bat (dilated pupils)
Red as a beet (vasodilation)
Hot as a hare (hyperthermia)
Dry as a bone (dry skin)
Mad as a hatter (hallucinations/agitation)
Bloated as a Toad (ileus, urinary retention)
And the heart runs alone (tachycardia)
Why do antimuscarinics cause tachycardia?
They knock out vagus nerve parasympathetic tone to the heart.
Ganglionic blockers are rarely used for: (3)
HTN Crises
Dissecting aortic aneurysms
Reduce bleeding during neurosurgery
Dramine is a _____.
antimuscarinic
What are the effects of ganglionic blockers?
Profound hypotension
Profound constipation
Negative chronotrope and inotrope (no reflex tachycardia)
How do ganglionic blockers cause profound hypotension?
Due to loss of sympathetic tone on vessels and histamine release
Lomotil is an _____.
Antimuscarinic
Trimethophan (Arfonad)
- Route
- Duration
- Adult Dose
IV
5-15 minutes
Bolus = 1 to 3 mg
Infusion = 0.5 to 6.0 mg/min
When are neuromuscular blocking agents mostly used?
During surgery to prevent patient movement.
What is the most important thing to remember when administering a neuromuscular blocker?
They do not sedate, tranquilize, or anesthetize the patient
All neuromuscular blockers have some structural resemblance to _____.
ACh
What started the development of neuromuscular blockers?
Curare then tubocurare was developed clinically
The nondepolarizing neuromuscular blockers acts as ____ to ACh.
Antagonists
All nondepolarizing neuromuscular blocking agents are given ___.
IV
What factors cause variation in non-depolarizing neuromuscular blockers?
Half-life length
Metabolism
Propensity to cause histamine release
Non-depolarizing neuromuscular blockers are antagonized by _____.
Acetylcholinesterase inhibitors
What types of drugs are synergistic with non-depolarizing neuromuscular blockers?
Calcium-channel blockers Halogenated hydrocarbon gas anesthetics Aminoglycoside antibiotics (b/c they inhibit ACh release)
The depolarizing neuromuscular blockers acts as ____ to ACh.
Agonists
Depolarizing neuromuscular blockers act as a _______.
Non-competitive antagonist
Explain the 2 phases of depolarizing neuromuscular blockers.
Phase 1 = membrane depolarizes, causing an initial discharge that produces transient small twitches (fasciculations) followed by flaccid paralysis
Phase 2 = membrane repolarizes, but receptor is desensitized to the effect of ACh.
Duration of SUX?
Less than 8 minutes
Shorter than any of the non-depolarizing blockers
SUX is broken down by _____ when circulating in the plasma.
Pseudocholinesterase
The _____ neuromuscular blockers acts as antagonists to ACh.
Nondepolarizing
SUX is terminated by when it diffuses away from the neuromuscular junction to be metabolized and allow ___ back to its receptors.
ACh
There is little pseudocholinesterase at the _____.
Neuromuscular junction
SUX is historically linked to _____ when used with gas anesthetic Halothane (Fluothane).
malignant hyperthermia
Prolonged apnea is seen when SUX is given to patients with ______.
Genetic pseudocholinesterase deficiency
Genetic pseudocholinesterase deficiency is most commonly found in:
Persian Jewish
Indian Hindu
The _____ neuromuscular blockers acts as agonists to ACh.
Depolarizing
SUX is historically linked to malignant hyperthermia when used with ______.
Gas anesthetic Halothane (Fluothane)
1 side effect of SUX
Hyperkalemia
Why may SUX cause hyperkalemia?
Potassium cellular pumps are locked “open”
What patients would you be especially considerate of giving them SUX?
Patients with electrolyte problems
Burn patients
_____ neuromuscular blockers reach the neuromuscular junction, block receptors and cause persistent depolarization.
Depolarizing
_____ neuromuscular blockers = AKA stabilizers
Non-depolarizing
_____ neuromuscular blockers effect can be antagonized by reversible inhibitors
Non-depolarizing
_____ neuromuscular blockers stimulat action potential initially for a short while then flaccid paralysis is followed.
Non-depolarizing
_____ neuromuscular blockers effect cannot be antagonized.
Depolarizing
_____ neuromuscular blockers compete with receptors to cause them not to depolarize and the action potential is stopped.
Non-depolarizing
What is the paralyzation process with Depolarizing Neuromuscular Blockers?
First large muscles (abdominal and limb)
Next short muscles (face, ear, nose)
Last respiratory muscles
_____ neuromuscular blockers directly lead to flaccid paralysis.
Non-depolarizing
What is the paralyzation process with Non-Depolarizing Neuromuscular Blockers?
First short muscles
Next large muscles
Last respiratory muscles
