19. Classification Of Skeletal Muscle Relaxants A- Neuromuscular blocking agents: 1. According to their mechanism of action into: a) Competitive or b) depolarizing neuromuscular blockers. 2. According to their duration of action : into: a) Long-acting agents (more than 35 minutes) e.g. d-tubocurarine b) Intermediate-acting agents (20-35 minutes) e.g. gallamine, atracurium c) Short-acting agents (less than 20 minutes) e.g. succinyl choline, mivacurium 3. According to their route of elimination from the body into: a) Agents eliminated via kidney e.g. gallamine (95%), pancuronium (80%) b) Agents eliminated via liver e.g. d-tubocuranine (60- 70%) c) Agents eliminated via plasma cholinesterase enzyme, e.g. succinylcholine. d) Agents spontaneously broken down (Hofmann elimination) e.g. atracurium.
20. B- Antispasticity agents Which are used to decrease painful muscle spasms. According to their site of action, they are divided into : 1- Central muscle relaxants: Their site of action is the spinal cord and subcortical areas of the brain. They do not directly relax spastic muscles. They include benzodiazepine 2- Direct muscle relaxants: They do not act on central synapses or neuromuscular junction. They act directly on skeletal muscles e.g. dantrolene
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22. ATRACURIUM (TRACIUM): 1- potent as tubocurarine 2- It has a shorter duration of action (~30 min). 3- It is spontaneously broken down in the plasma by a non-enzymatic chemical process “Hofmann’s degradation”. Thus it is non-cumulative. It could be used in patients with either liver and/or kidney disease. 4- It is the relaxant of choice in fragile patients and in renal failure. 5- It is a weak histamine releaser , but has no effect on autonomic ganglia or on cardiac muscarinic receptor 6- Dose: 0.5 mg/kg
23. Drug Interactions A- Synergists: a) inhalational anaesthetics e.g. ether, halothane, isoflurane, act synergistically with competitive blockers. Consequently their doses should be reduced.. b) Some antibiotics, e.g. aminoglycosides as streptomycin, neomycin inhibit acetylcholine release from cholinergic nerves by competing with calcium ions. The paralysis could be reversed by administration of calcium ions. . c) Local anaesthetics e.g . procaine may block neuromuscular transmission through a stabilizing effect on the nicotinic receptor ion channels.
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36. Mechanism Of Action Depolarization block ■ Succinylcholine has a similar effect to acetylcholine on the motor end plate receptors (open the sodium channel and cause depolarization of the motor end plate) but instead of producing transient depolarization, it produces prolonged depolarization which is associated with transmission failure. Thus it produces initial stimulation of the muscle which is manifested as fasciculation of the muscle followed by muscle paralysis ■ Succinylcholine stimulates the nicotinic receptors in sympathetic and parasympathetic ganglia (NN) and the muscarinic receptors (M2) in the SAnode of the heart. ■ Histamine release , particularly in larger doses.
37. Side Effects: 1- Succinylcholine apnoea: Occasionally succinylcholine produces prolonged apnoea due to lack of normal plasma (pseudo) cholinesterase levels. This may be the result of: a) Genetic abnormality in the enzyme: i- Its activity may be lower than normal or ii- Abnormal variant of pseudocholinesterase (atypical form of the enzyme) that may be totally unable to split succinylcholine. b) Acquired low level of pseudocholinesterase activity occurs in: i- Severe liver disease. ii- Malnutrition. iii- Exposure to insectisides. iv- Cancer patients. Treatment: a) Artificial respiration until the muscle power returns. b) Fresh blood or plasma transfusion to restore cholinesterase enzyme level. c) No specific antidote is available.
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49. Peripheral nerve stimulator electrodes were positioned over the ulnar nerve on the volar side of the wrist, so that the distal electrode was positioned where the proximal skin crease crossed the radial side of the flexor carpi ulnaris muscle. The proximal electrode was placed 2-3 cm proximal to the distal electrode. Viby Mogensen first reported that the use of neuromuscular blocking agents was followed by residual paralysis in 42% patients even after administration of reversal. Study conducted by Ali showed that TOF ratio of 75% correlated well with adequate clinical recover including sustained head lift for 5 seconds or more.
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