review on neuromuscular relaxants
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Neuromuscular Relaxants
Endotracheal Intubation in E.R. and O.R.Immobility at subconscious level.Better surgical conditions of access.
0. Why do we need Relaxants?
Motor Neurons’ Pathway.
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, precentral
gyrus, 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.
Frontal lobe to Area 4 and 6.Nerves pass through the Pyramidal and the extra- tracts.Exit via the spinal nerves till reaching the MEP.Action Potential triggers ACh. Release.ACh. Binding & Ligand-Gated Na+ Channels
open.EPPs till full blown AP.T-Tubule Propagation and contraction.ACh. Hyhdrolysis by “true” AcetylCholine Estrase.
RAPID
I. Physiology
Nerve synapses on muscle, SEM
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.
Either intervening at level of Motor Cortex and RAS.
Or at Local Nerve Block.Or at Motor End Plate.
Physiologically similar to ACh; Depolarising MRs.
Morphologically similar to ACh; Non-Depolarising MRs.
II. Grand Scheme
III. Depolarising M.R. – Succinyl Choline (sux)
Given as an I.V., circulating in Blood.SUX. Binding & Ligand-Gated Na+
Channels open.EPPs till full blown AP.T-Tubule Propagation and contraction
= Fasiculations.SUX. Hyhdrolysis by “Butyryl” Plasma
AcetylCholine Estrase.
SLOW
IIIa. Mechanism of Action
It remains attached to the receptors for MINUTES, during which the Ligand-Gated Na+ Channels remain opened. Na+ enters and K+ exits.
Since Ca+2 kinematics are independent of membrane polarity, It re-enters the Sarcoplasmic Reticulum, hence muscle flaccidity.
Thus muscle remains depolarized and flaccid. This is termed Phase I Block, and it’s entirely SUX-dependant. That is, reversible upon SUX removal.
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.
Thus Phase II block resembles the competitive inhibition of A.Ch. exerted by Non-Depolarising MR.
IIIb. Indications
The Only MR having VERY rapid onset at 60 seconds, and VERY short
duration of 5~10 minutes.
Thus indicated in situations needing rapid onset and/or short duration of
Relaxation.
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.
Tracheal Intubation, especially in E.R. and if expected difficult intubation.
Short procedures necessiating relaxation; as Oesopho-, Gastro- and Bronchoscopes.
A premedication in ECT. (Short duration)
Can be used in Second Stage of delivery.
To alleviate severe laryngospasm.
Myotonia Congenita, 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.
Myotonica Dystrophia. (Myotonia associated with severe wasting of the muscles)
IIIc. Contraindications
Patients with Congenital or Idiosyncratic properties;
Patients with burns or neuromuscular disorders, as this predisposes to severe Hyperkalimia, up to cardaic arrest.
Patients having previous history of Anaphylaxis following SUX administration.
Patients having previous history of Malignant Hyperthermia following SUX administration.
Patients having previous history of Prolonged apnea following SUX administration. This indicates weak or absent activity of ButyrylCholineEstrase.
MUSCLE FASICULATIONS, that can surmount in acute Rhabdomyolysis.
Post-operative muscle pains.CARDIOVASCULAR; +ABP, -HR, and even
asystole. Latter can also be caused by Hyperkalimia.
OCCULAR; +IOP, practically dangerous if asscociated with ocular traumas. (which is a probability considering its use in E.R. for ETT)
ABDOMINAL; +Intragastric pressure due to Fasiculation of Abdominal muscles.
IIId. Complications
CRANIAL; Hyper-metabolism due to fasciculations produces +PaCO2 , thus increased Blood flow and +ICP.
HYPERKALIMIA. Mainly due to continuous opening of Na+ channels, thus Its massive Influx is electrically equated with a massive K+ efflux.Exaggerated in Burns and Neuromuscular disorders.
MALIGNANT HYPERTHERMIA. Has an AD susceptibility determination. Can occur with other gas anesthetics too.
PROLONGED APNEA following SUX administration. Usually means weak or absent activity of ButyrylCholineEstrase.Since this enzyme is produced by the liver,
Hepatic disorders (cirrhosis), and malnutrition can lead to a decrease in its activity.
Can also occur with Phase II Block.ANAPHYLAXIS; with massive Histamine
release.
Pretreatment of the patient with a small dose Non-Depolarising MR can attenuate many of the side
effects mentioned above.
The recent arrival of the cyclodextrin SUGAMMADEX 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.
Thank You
Clinical Uses of MRs
Following Induction of Anaesthesia and administrating the MR, Ventilation continues via face mask, and Intubation can be done upon relaxation of the muscles.
Cough. Hiccough and abdominal wall tightening are all signs of inadequate dose of the relaxant.
They should be differentiated from signs of inadequate dose of the anaesthetic, such as limb movement in response to surgical stimulation.
Rapid Tracheal Intubation; Suxamethonium or Rocuronium.
Haemodynamic Instability; Vecuronium.Renal and Hepatic Dysfunction; Atracurium.In Myasthenia Gravis; AVOID MR; but if
essential, use 1/10 the dose of Atracurium, and titrate.
In Asthmatics; AVOID Histamine releasing drugs.
Choice of the MR.
Normal Tidal volume.Maintain open eyes.Sustain tongue protrusion.Maintain head lift for 5 seconds.Maintain firm hand grip.Effective Coughing.Return of full muscle activity by nerve
stimulators.
Clinical Criteria of Adequate MR Recovery
Shallow respiration and Cyanosis.Jerky movement of extremities.Restless patient.Diplopia.Inability to raise head or extrude tongue.By nerve stimulators.
Clinical Signs of Incomplete MR Recovery
Depolarizing vs. Non- Depolarizing MR
Depolarising Non - Depolarising
Onset Rapid Slow
Duration Short Long
Fasiculations Yes No
Use of AntiCholineEstrase
Increase Block Reverse Block
Antidote No Yes
Effect of repeated use
Phase II Block No
Nerve Stimulators
Special features Different features
Thank You
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