0 Neuromuscular transmission can be blocked by inhibiting the production and release of acetylcholine or its interaction with receptors.
0 These drugs only block nicotinic receptors at neuromuscular junctions.
0 Sensitivity to these drugs increases in conditions such as myasthenia gravis, hypokalemia, hyponatremia, hypocalcemia, hypermagnesemia, antibiotics (aminoglycosides, polymyxin B, lincosamides, tetracyclines), inhalation anesthetics / local anesthetics and class I antiarrhythmics, lithium, hypothermia, acidosis.
Depolarizing Block
Before this type of block, fasciculations due to depolarization occur.
Not antagonized by anticholinesterases.
While its effects are potentiated by acetylcholine, isoflurane, enflurane, alkalosis, hypothermia and Mg+2; It becomes antagonized in the presence of ether, halothane, acidosis.
Depolarizing blocking agents are decametonium and suxamethonium.
Hyperkalemia and bradycardia are the most important disadvantages.
Succinyl choline
It gives symptoms of non-depolarizing block at high doses.
It causes vagal stimulation and bradycardia.
Increases serum potassium.
Increases intraocular pressure.
It causes muscle pain in the postoperative period.
It increases saliva and gastric secretion.
It is broken down by pseudocholinesterase synthesized in the liver and found in plasma.
Genetic defect of pseudocholinesterase
Prolonged apnea
Malignant hyperthermia may occur.
The duration of action is prolonged in liver failure.
Non-depolarizing Block
• It prevents acetylcholine from reaching the receptor and depolarization.
• No fasciculation is seen before the block.
• They become antagonized by anticholinesterases. (Neostigmine, edrophonium, physostigmine, pyridostigmine).
• Long-acting: Pancuronium, pipecuronium, doxacurium, gallamine, methocurine
• Medium-acting: Atracurium, cisatracurium, vecuronium, rocuronium
• Short-acting: Mivacurium, gantacurium
• Histamine Release: tubocurarine > methocurine > atracurium > mivacurium
Pancuronium Bromide
It releases minimal histamine or not.
A very small amount crosses the placenta.
It makes vagal block.
Does not cross the blood-brain barrier.
It should not be used in renal failure.
Stimulates the myocardium, raises blood pressure and heart rate.
It does not accumulate in the body.
Atracurium Desylate
It is excreted from the body by Hofman elimination (it is spontaneously broken down in the body under physiological conditions).
It does not change the CVS.
Does not affect intracranial pressure and intraocular pressure.
It is the muscle relaxant to be chosen in anephric patients.
cisatracurium
It is the stereoisomer of atracurium.
Causes histamine release, does not cause hemodynamic changes, 3-4 times stronger than atracurium.
It is decomposed by Hofmann degradation.
It is not affected by end-organ disease or old age.
Vecuronium Bromide
It has no effect on the cardiovascular system. It is the only nondepolarizing muscle relaxant that does not have a cardiovascular effect.
It can be used in kidney failure.
Its effect increases most with enflurane.
rocuronium
The intubation dose is 0.6 mg/kg in 60-90 seconds, good or excellent intubation condition.
Its effect is about 25-30 minutes.
Sugamadex is used to reverse its effect.
Properties of the depolarizing block
• It develops with the effect of depolarizing relaxants, agonist and mimicking acetylcholine. During the block, sodium channels remain open and the muscle fiber does not respond to other stimuli.
• Fasciculations due to depolarization are seen before the block.
• It cannot be antagonized by anticholinesterases, on the contrary, it deepens.
• Tachyphylaxis develops due to its effect.
• It is potentiated by the effects of acetylcholine, isoflurane, enflurane, respiratory alkalosis, hypothermia and magnesium.
• Antagonized by ether, halothane, acidosis and nondepolarizing relaxants.
Characteristics of the nondepolarizing block
• It develops when nondepolarizing muscle relaxants prevent the depolarization of the motor endplate by preventing acetylcholine from reaching the receptor.
• No faciculation is seen before the block.
• Antagonized by anticholinesterases.
• It is potentiated by the effect of inhalation anesthetics, magnesium and hypothermia (below 33 °C) and antagonized by mild hypothermia.
• Acidosis increases the depth and duration of the block.
• Adrenaline, succinylcholine and acetylcholine block decreases.
• Paralytic muscle fiber responds directly to electrical and mechanical stimuli.
Factors that increase neuromuscular blockade
Medicines
• Volatile anesthetics
• Antibiotics: Aminoglycosides, polymyxin B
• Neomycin, tetracycline, clindamycin
• Dantrolene
• Verapamil
• Furosemide
• Lidocaine
Electrolytes and acid-base disturbance
• Hypermagnesemia
• Hypocalcemia
• Hypokalemia
• Respiratory acidosis
heat
• Hypothermia
