Review on Neuromuscular Relaxants


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A small review on Non-Depolarizing NMBs.

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Review on Neuromuscular Relaxants

  1. 1. Neuromuscular Relaxants<br />
  2. 2. Endotracheal Intubation in E.R. and O.R.<br />Immobility at subconscious level.<br />Better surgical conditions of access.<br />0. Why do we need Relaxants?<br />
  3. 3. Motor Neurons’ Pathway.<br />The motor system consists of the pyramidal and extrapyramidal system. CorticoSpinal, CorticoNuclear and CorticoBulbar tracts all arise from the motor cortex and pass to muscle fibers in the extremities, face and eye. The corticospinal tract start in the motor center of the cerebral cortex. The motor impulses originates in the Giant pyramidal cells or Betz cells of the motor area, precentralgyrus, of cerebral cortex. These are the upper motor neurons (UMN) of the corticospinal tract. The axons of these cells pass in the depth of the cerebral cortex to the Corona radiata and then to the Internal Capsule passing through the posterior branch of internal capsule and continue to descend in the Midbrain and the Medulla Oblongata. In the lower part of Medulla oblongata 80 to 85% of these fibers decussate (pass to the opposite side) and descend in the White Matter of the Lateral funiculus of the spinal cord on the opposite side.<br />
  4. 4. Frontal lobe to Area 4 and 6.<br />Nerves pass through the Pyramidal and the extra- tracts.<br />Exit via the spinal nerves till reaching the MEP.<br />Action Potential triggers ACh. Release.<br />ACh. Binding & Ligand-Gated Na+ Channels open.<br />EPPs till full blown AP.<br />T-Tubule Propagation and contraction.<br />ACh. Hyhdrolysis by “true” AcetylCholineEstrase.<br />RAPID<br />I. Physiology<br />
  5. 5. Nerve synapses on muscle, SEM<br />Coloured scanning electron micrograph (SEM) of the junctions between a nerve cell (green) and a muscle fibre (red). The nerve cell (motor neuron) ends in a group of pads called end plates. The end plate holds neurotransmitter chemicals. When activated, the end plate releases a neurotransmitter, which is taken up by receptors on the muscle's side of the synapse. This makes the muscle contract. In neuromuscular synapses such as this, the neurotransmitter is the chemical acetylcholine.<br />
  6. 6. Either intervening at level of Motor Cortex and RAS.<br />Or at Local Nerve Block.<br />Or at Motor End Plate.<br />Physiologically similar to ACh; DepolarisingMRs.<br />Morphologically similar to ACh; Non-DepolarisingMRs.<br />II. Grand Scheme<br />
  7. 7. III. Depolarising M.R. – SuccinylCholine (sux)<br />
  8. 8. Given as an I.V., circulating in Blood.<br />SUX. Binding & Ligand-Gated Na+ Channels open.<br />EPPs till full blown AP.<br />T-Tubule Propagation and contraction = Fasiculations.<br />SUX. Hyhdrolysis by “Butyryl” Plasma AcetylCholineEstrase.<br />SLOW<br />IIIa. Mechanism of Action<br />
  9. 9. It remains attached to the receptors for MINUTES, during which the Ligand-Gated Na+ Channels remain opened. Na+ enters and K+ exits.<br />Since Ca+2 kinematics are independent of membrane polarity, It re-enters the Sarcoplasmic Reticulum, hence muscle flaccidity.<br />Thus muscle remains depolarized and flaccid. This is termed Phase I Block, and it’s entirely SUX-dependant. That is, reversible upon SUX removal.<br />
  10. 10. If Phase I block was maintained via continuous IV Infusion, Insensitivity of the Nicotinic receptors to normal A.Ch. develops and persists even after SUX. Washout. This is termed Phase II Block.<br />Thus Phase II block resembles the competitive inhibition of A.Ch. exerted by Non-Depolarising MR.<br />
  11. 11. IIIb. Indications<br />The Only MR having VERY rapid onset at 60 seconds, and VERY short duration of 5~10 minutes.<br />Thus indicated in situations needing rapid onset and/or short duration of Relaxation.<br />
  12. 12. Suxamethonium does not produce unconsciousness or anesthesia, and its effects may cause considerable psychological distress while simultaneously making it impossible for a patient to communicate. For these reasons, administration of the drug to a conscious patient is strongly contraindicated, except in necessary emergency situations, where awareness in diminished.<br />
  13. 13. Tracheal Intubation, especially in E.R. and if expected difficult intubation.<br />Short procedures necessiating relaxation; as Oesopho-, Gastro- and Bronchoscopes.<br />A premedication in ECT. (Short duration)<br />Can be used in Second Stage of delivery.<br />To alleviate severe laryngospasm.<br />
  14. 14. MyotoniaCongenita, a Channelopathy; hereditary disease that is caused by mutations in the chloride, sodium or potassium ion transport channels in the muscle membrane, leading to difficulty in relaxing the muscle, or Myotonia.<br />MyotonicaDystrophia. (Myotonia associated with severe wasting of the muscles)<br />IIIc. Contraindications<br />
  15. 15. Patients with Congenital or Idiosyncratic properties;<br />Patients with burns or neuromuscular disorders, as this predisposes to severe Hyperkalimia, up to cardaic arrest.<br />Patients having previous history of Anaphylaxis following SUX administration.<br />Patients having previous history of Malignant Hyperthermia following SUX administration.<br />Patients having previous history of Prolonged apnea following SUX administration. This indicates weak or absent activity of ButyrylCholineEstrase.<br />
  16. 16. MUSCLE FASICULATIONS, that can surmount in acute Rhabdomyolysis.<br />Post-operative muscle pains.<br />CARDIOVASCULAR; +ABP, -HR, and even asystole. Latter can also be caused by Hyperkalimia.<br />OCCULAR; +IOP, practically dangerous if asscociated with ocular traumas. (which is a probability considering its use in E.R. for ETT)<br />ABDOMINAL; +Intragastric pressure due to Fasiculation of Abdominal muscles.<br />IIId. Complications<br />
  17. 17. CRANIAL; Hyper-metabolism due to fasciculations produces +PaCO2 , thus increased Blood flow and +ICP.<br />HYPERKALIMIA. Mainly due to continuous opening of Na+ channels, thus Its massive Influx is electrically equated with a massive K+ efflux.<br />Exaggerated in Burns and Neuromuscular disorders.<br />MALIGNANT HYPERTHERMIA. Has an AD susceptibility determination. Can occur with other gas anesthetics too.<br />
  18. 18. PROLONGED APNEA following SUX administration. Usually means weak or absent activity of ButyrylCholineEstrase.<br />Since this enzyme is produced by the liver, Hepatic disorders (cirrhosis), and malnutrition can lead to a decrease in its activity.<br />Can also occur with Phase II Block.<br />ANAPHYLAXIS; with massive Histamine release.<br />
  19. 19. Pretreatment of the patient with a small dose Non-Depolarising MR can attenuate many of the side effects mentioned above.<br />
  20. 20. The recent arrival of the cyclodextrinSUGAMMADEX may well render suxamethonium obsolete. Sugammadex can be used to 'instantly' reverse the effects of longer-acting muscle relaxants, particularly rocuronium. This means that rocuronium can be given in sufficiently high dose to work quickly, and then reliably reversed when necessary, all without the unwelcome side effects of suxamethonium.<br />
  21. 21. Thank You<br />
  22. 22.
  23. 23. Clinical Uses of MRs<br />
  24. 24. Following Induction of Anaesthesia and administrating the MR, Ventilation continues via face mask, and Intubation can be done upon relaxation of the muscles.<br />Cough. Hiccough and abdominal wall tightening are all signs of inadequate dose of the relaxant.<br />They should be differentiated from signs of inadequate dose of the anaesthetic, such as limb movement in response to surgical stimulation.<br />
  25. 25. Rapid Tracheal Intubation; Suxamethonium or Rocuronium.<br />Haemodynamic Instability; Vecuronium.<br />Renal and Hepatic Dysfunction; Atracurium.<br />In Myasthenia Gravis; AVOID MR; but if essential, use 1/10 the dose of Atracurium, and titrate.<br />In Asthmatics; AVOID Histamine releasing drugs.<br />Choice of the MR.<br />
  26. 26. Normal Tidal volume.<br />Maintain open eyes.<br />Sustain tongue protrusion.<br />Maintain head lift for 5 seconds.<br />Maintain firm hand grip.<br />Effective Coughing.<br />Return of full muscle activity by nerve stimulators.<br />Clinical Criteria of Adequate MR Recovery<br />
  27. 27. Shallow respiration and Cyanosis.<br />Jerky movement of extremities.<br />Restless patient.<br />Diplopia.<br />Inability to raise head or extrude tongue.<br />By nerve stimulators.<br />Clinical Signs of Incomplete MR Recovery<br />
  28. 28. Depolarizing vs. Non- Depolarizing MR<br />
  29. 29. Thank You<br />