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A18 Anesthesia
Induction Toronto Notes 2019
Plasma Cholinesterase
Plasma cholinesterase is produced by the liver and metabolizes SCh, ester local anesthetics, and mivacurium. A prolonged duration of blockade by SCh occurs with:
(a) decreased quantity of plasma cholinesterase, e.g. liver disease, pregnancy, malignancy, malnutrition, collagen vascular disease, hypothyroidism
(b) abnormal quality of plasma cholinesterase, e.g. normal levels but impaired activity of enzymes, genetically inherited
Muscle Relaxants
• twotypesofmusclerelaxants
1. depolarizing muscle relaxants: succinylcholine (SCh)
2. non-depolarizing muscle relaxants: rocuronium, mivacurium, vecuronium, cistracurium, pancuronium
• block nicotinic cholinergic receptors in NMJ
• provides skeletal muscle paralysis, including the diaphragm, but spares involuntary muscles such as the
heart and smooth muscle
• neverusemusclerelaxantswithoutadequatepreparationandequipmenttomaintainairwayand
ventilation
• muscle relaxation produces the following desired effects:
1. facilitates intubation
2. assists with mechanical ventilation
3. prevents muscle stretch reflex and decreases muscle tone 4. allows access to the surgical field (intracavitary surgery)
• nervestimulator(i.e.trainoffour)isusedintraoperativelytoassessthedegreeofnerveblock;notwitch response seen with complete neuromuscular blockade
Table 10. Depolarizing Muscle Relaxants (Non-Competitive): Succinylcholine (SCh)
Mechanism of Action
Intubating Dose (mg/kg)
Onset Duration Metabolism Indications
Side Effects
Mimics ACh and binds to ACh receptors causing prolonged depolarization; initial fasciculation may be seen, followed by temporary paralysis secondary to blocked ACh receptors by SCh
1-1.5
30-60 s – rapid (fastest of all muscle relaxants)
3-5 min – short (no reversing agent for SCh)
SCh is hydrolyzed by plasma cholinesterase (pseudocholinesterase), found only in plasma and not at the NMJ
Assist intubation
Increased risk of aspiration (need rapid paralysis and airway control (e.g. full stomach), hiatus hernia, obesity, pregnancy, trauma)
Short procedures
Electroconvulsive therapy (ECT)
Laryngospasm
1. SCh also stimulates muscarinic cholinergic autonomic receptors (in addition to nicotinic receptors; may cause bradycardia, dysrhythmias, sinus arrest, increased secretions of salivary glands (especially in children)
2. Hyperkalemia
Disruption of motor nerve activity causes proliferation of extrajunctional (outside NMJ) cholinergic receptors
Depolarization of an increased number of receptors by SCh may lead to massive release of potassium out of muscle cells
Patients at risk
3rd degree burns 24 h-6 mo after injury
Traumatic paralysis or neuromuscular diseases (e.g. muscular dystrophy) Severe intra-abdominal infections
Severe closed head injury
Upper motor neuron lesions
3. Can trigger MH (see Malignant Hyperthermia, A28)
4. Increased ICP/intraocular pressure/intragastric pressure (no increased risk of aspiration if competent
lower esophageal sphincter)
5. Fasciculations, post-operative myalgia – may be minimized if small dose of non-depolarizing agent
given before SCh administration
Known hypersensitivity or allergy, positive history of malignant hyperthermia, myotonia (m. congenita, m. dystrophica, paramyotonia congenital), high risk for hyperkalemic response
Known history of plasma cholinesterase deficiency, myasthenia gravis, myasthenic syndrome, familial periodic paralysis, open eye injury
Contraindications
Absolute Relative