Skeletal Muscle Relaxants

Skeletal Muscle Relaxants

1. Skeletal Muscle Relaxants Dr.M.Usman Khalid Dpt,ms-nmpt

2. Classification Neuromuscular Blockers Non Depolarizing: Long Acting e.g Tubocurarine Intermediate Acting e.g.Rocuronium Depolarizing ( Succinylcholine )

3. Spasmolytics Chronic Use: CNS Action e.g.Baclofen,Diazepam,Tizanidine Muscle Action: E.g.Dantrolene

4. Neuromuscular Blocking Drugs Pharmacokinetics: Given Parenterally,Highly Polar(Can’t cross BBB) High levels it may cause seizures

5. Mechanism of Action Prevents action of Ach at the skeletal muscle end plate They compete with Ach Some drugs may also directly plug the ion channel operated by Ach receptor Post tetanic potentiation is preserved,Tension during tetanus fades rapidly Larger muscles are more resistant to neuromuscular blockade

6. Depolarizing Neuromuscular Blocking Drugs Pharmacokinetics: Parenteral : short action inactivated by plasma esterases

7. Mechanism of action — Succinylcholine acts like a nicotinic agonist and depolarizes the neuromuscular end plate When given by continuous infusion, the effect of succinylcholine changes from continuous depolarization (phase I) to gradual repolarization with resistance to depolarization (phase II) ( ie , a curare-like block.

8. Reversal of Blockade Readily reversed by increasing the concentration of normal transmitter at the receptors. Neostigmine or pyridostigmine

9. Adverse effects Respiratory paralysis Autonomic ganglia stimulation Histamine release Muscle pain Hyperkalemia Increased intragastric and intraocular pressure

10. Non depolarizing drugs Mechanism of action: Competitive antagonists at skeletal muscle ACh -N receptor.

11. Pharmacokinetics: Parenteral use variable disposition Spontaneous inactivation ( atracurium , cisatracurium ) Plasma ChE ( mivacurium ) Hepatic metabolism ( rocuronium , vecuronium ) Renal elimination ( doxacurium , pancuronium , tubocurarine )

12. Adverse effects Histamine release ( mivacurium , tubocurarine ) Laudanosine formation ( atracurium ) Muscle relaxation is potentiated by inhaled anesthetics, aminoglycosides and possibly quinidine .

13. Spasmolytic drugs Mechanism of action: Three of the drugs ( baclofen , diazepam, and tizanidine ) act in the spinal cord. Baclofen acts as a GABA B agonist at both presynaptic and postsynaptic receptors, causing membrane hyperpolarization . Presynaptically , baclofen , by reducing calcium influx, decreases the release of the excitatory transmitter glutamic acid. At postsynaptic receptors, baclofen facilitates the inhibitory action of GABA.

14. Mechanism of action: Diazepam facilitates GABA-mediated inhibition via its interaction with GABA A receptors. Tizanidine , an imidazoline related to clonidine with significant α2 agonist activity, reinforces presynaptic inhibition in the spinal cord. Dantrolene : Weakens muscle contraction by reducing myosin- actin interaction.

15. Pharmacokinetics Oral Diazepam may also be given parenterally .

16. Adverse effects Sedation Muscle weakness CNS depression

17. JAZAK ALLAH!