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A meta-analysis reported that the incidence of residual neuromuscular paralysis was 41% in patients receiving intermediate neuromuscular blocking agents during anaesthesia. [1] It is possible that > 100,000 patients annually in the USA alone, are at risk of adverse events associated with undetected residual neuromuscular blockade. [5]
A depolarizing neuromuscular blocking agent is a form of neuromuscular blocker that depolarizes the motor end plate. [15] An example is succinylcholine. Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine.
The British Journal of Anaesthesia published an article in 2015 in which the incidence of residual neuromuscular blockade could be reduced to zero if sugammadex is used as the reversal agent and the correct dosage is selected with the use of neuromuscular monitoring. [17]
Neuromuscular monitoring is recommended when neuromuscular-blocking drugs have been part of the general anesthesia and the doctor wishes to avoid postoperative residual curarization (PORC) in the patient, that is, the residual paralysis of muscles stemming from these drugs. [citation needed]
Postanesthetic shivering is one of the leading causes of discomfort in patients recovering from general anesthesia. It usually results due to the anesthetic inhibiting the body's thermoregulatory capability, although cutaneous vasodilation (triggered by post-operative pain) may also be a causative factor.
Vecuronium is in the aminosteroid neuromuscular-blocker family of medications and is of the non-depolarizing type. [2] It works by competitively blocking the action of acetylcholine on skeletal muscles. [2] The effects may be reversed with sugammadex or a combination of neostigmine and glycopyrrolate. To minimize residual blockade, reversal ...
The main complication resulting from pseudocholinesterase deficiency is the possibility of respiratory failure secondary to succinylcholine or mivacurium-induced neuromuscular paralysis. Individuals with pseudocholinesterase deficiency also may be at increased risk of toxic reactions, including sudden cardiac death, associated with recreational ...
Effective neuromuscular block by non-depolarizing neuromuscular drugs occurs only when 70-80% of acetylcholine receptors are occupied by the drug. [11] This is because at this occupancy rate, junctional potential cannot reach the threshold value required for muscle contraction. Diagram of nicotinic receptor (Acetylcholine receptor)