neuromuscular blockers Flashcards
what types of cholinergic receptor antagonists are there?
-anti-muscarinic
-anti-nicotinic
>ganglion blockers (not clinically useful)
>neuromuscular blockers
properties of anti-muscarinics
Anti-Muscarinic
* Non-selective blockers of all M receptors (M1 – M5)
* Many clinically useful drug
properties of neuromuscular blockers. which are clinically useful?
- NM receptor blockade
- The only clinically useful nicotinic antagonists are those that block skeletal muscle type nAChRs (Nm)
on what part of the nervous system do neuromuscular blcokers act? what do they inhibit?
-work in the somatic nervous system
-inhibit skeletal muscle type nACHRs (Nm)
neuromuscular blocking drugs are structural analogues of what? How are they administered
Structural analogues of acetylcholine, given IV
what do Neuromuscular Blocking Drugs block, specifically?
- Block transmission between motor neurons & skeletal muscle by acting either as antagonists (“non-depolarizing block”) or agonists (“depolarizing block”) at the muscle-type nAChR
are animals conscious using Neuromuscular Blocking Drugs?
Animals are fully conscious unless an anesthetic is used concurrently
what type of Neuromuscular Blocking Drugs are used almost exclusively now
Non-depolarizing blockers
one of the most commonly used non-depolarizing neuromuscular blockers in veterinary medicine. What is its clinical use?
atracurium
To prevent eye movement during ocular surgery
-Can achieve complete muscle relaxation without the need for higher anesthetic doses
> Safer, with faster recovery than simply using higher anesthetic dose
what is the mechanism of action of atracurium?
Atracurium is chemically similar to ACh
-It competitively blocks AChRs at NMJ > causes intense relaxation/paralysis of voluntary muscle
-Intensity and duration depend on dosage
pharmacokinetics of atracurium? what does duration vary with?
- Must be injected IV because positively charged, highly polar > doesn’t cross membranes
- Maximum block occurs in ~3 min., duration varies with dosage (typically 20-30 min., ~1 h with higher dosages)
- Metabolized in blood by plasma esterases
- Can be injected periodically to maintain relaxation without extending recovery time (usual recovery time follows last dose)
main advantage of atracurium
Rapid reversal can be achieved with drugs that inhibit ACh esterase (e.g., neostigmine, edrophonium) > elevates ACh concentration
cautions of using atracurium or other NM blockers
N-M blockers do not produce sedative or analgesic effects, they just immobilize patients
Dose-dependent respiratory paralysis occurs
– use ventilator if necessary
order of paralysis of muscles from NM block
- Extraocular (main use)
- Neck, head, face, hands and feet
- Abdomen, arms and legs
- Eye blink
- Respiratory & diaphragm
Recovery occurs in reverse order
what is an important Depolarizing blocking agents (agonist)
Succinylcholine
what is Succinylcholine? what are its effects and uses? toxocity?
Depolarizing blocking agents (agonist)
* Similar but longer effects compared to ACh, but effect lasts only ~90 s
- Technically a nicotinic agonist (not antagonist) muscle tremors, then flaccid paralysis
Mechanism:
* Initial depolarization causes muscle contraction, but repolarization cannot occur so Na+ channels remain inactivated and no further impulse generation occurs > flaccid paralysis
Pharmacokinetics:
* Rapid onset, very short duration
* Metabolism by plasma pseudocholinesterase
Toxicity:
* Painful contractions may follow sole use; hypertension; tachycardia
* Malignant hyperthermia risk, as for volatile hydrocarbon inhalants
Avoid in recovery situations
**May be useful in getting horse to go down smoothly prior to euthanasia
atracurium potency, onset time, action time
potency: 2-3 (higher in horses)
onset: ~3 min
duration: long (~45 min, depends on dose)
general use of muscle relaxants. what forms are there?
- Decrease muscle tone & spasticity without completely inhibiting voluntary contractions
- **Used to alleviate painful muscle spasms associated with intervertebral disk disease, urethral obstructions, etc.
- *Centrally-acting & *peripherally-acting forms
important centrally acting muscle relaxants
Benzodiazepines
Methocarbamol
Guaifenesin
what are Benzodiazepines? what do they do and how?
centrally acting muscle relaxants
Benzodiazepines (e.g., Valium®)
Facilitates GABA activity in CNS (GABA is the major inhibitory NT in brain)
* Excellent muscle relaxation
* reduce spasms with disk disease, tetanus, urethral obstruction
* May cause CNS depression
* Other drugs may alter metabolism
what is Methocarbamol? what does it do and how?
centrally acting muscle relaxant
Methocarbamol (Robaxin®, Robaxacet®, etc.)
Mechanism unknown
* Efficacy uncertain
* May cause sedation, salivation, emesis, lethargy,
weakness, ataxia
* Contraindicated in various renal diseases
what is Guaifenesin? what is it used for?
centrally acting muscle relaxant
Inhibits interneurons in motor reflexes
* Used IV with injectable anesthetics for induction
what is Dantrolene? what is it used for?
peripherally-acting muscle relaxant
InhibitsCa2+ release from sarcoplasmic reticulum
* Used for urethral obstruction, equine rhabdomyolysis, *malignant hyperthermia
