Neuromuscular blockade drug interactions

Factors Affecting Neuromuscular Blockade Drug Interactions... 

Propofol is primarily a hypnotic drug with substantial cardiorespiratory depressant actions and with no ability to produce neuromuscular blockade. While propofol lacks analgesic properties, its use permits lower doses of opioids. Likewise, less propofol is required for adequate hypnosis when it is administered with opioids. Thus, it is said that propofol and opioids interact synergistically. 

Drug interactions Co-administration of dinoprostone in patients receiving intravenous oxytocic agents such as oxytocin may result in uterine hyperstimulation and is therefore contraindicated. Severe hypertension has been reported when oxytocin was given 3 to 4 hours following prophylactic administration of a vasoconstrictor in conjunction with spinal anesthesia. Oxytocin may enhance the neuromuscular blockade of succinylcholine. 

Since mivacurium is metabolized by plasma cholinesterase, the interaction with the reversal drugs is unpredictable. On one hand, the neuromuscular blockade is antagonized because of increased acetylcholine concentrations in the synapse. On the other hand, mivacurium concentration may be higher because of decreased plasma cholinesterase breakdown of the muscle relaxant. The former effect usually dominates clinically, and mivacurium block is reversed by neostigmine. 

Interactions Inhaled anesthetics, especially isoflurane, strongly potentiate and prolong neuromuscular blockade. Aminoglycoside antibiotics and antiarrhythmic drugs potentiate and prolong the relaxant action of neuromuscular blockers to a lesser degree. 

In small doses, local anesthetics can depress posttetanic potentiation via a prejunctional neural effect. In large doses, local anesthetics can block neuromuscular transmission. With higher doses, local anesthetics block acetylcholine-induced muscle contractions as a result of blockade of the nicotinic receptor ion channels. Experimentally, similar effects can be demonstrated with sodium channel-blocking antiarrhythmic drugs such as quinidine. However, at the doses used for cardiac arrhythmias, this interaction is of little or no clinical significance. Higher concentrations of bupivacaine (0.75%) have been associated with cardiac arrhythmias independent of the muscle relaxant used. 

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