Other types of stimulation include tetanus and double burst. During tetanus the patient is stimulated for 5 s at 30–100 Hz. Fade will occur during tetanus during phase II of a depolarizing block and with the use of a non-depolarizer. Phase I will not demonstrate any fade. During double burst stimulation, the nerve is stimulated by two 50 Hz stimuli, separated by 750 msec. In a patient with partial paralysis, the second twitch will be weaker than the first.

Recovery is facilitated with the use of acetylcholinesterases. Acetylcholinesterases antagonize NMBs by increasing Ach. The three most commonly used acetylcholinesterases are neostigmine, pyridostigmine, and edrophonium. An antimuscarinic must be used along with one of the three aforementioned acetylcholinesterases to prevent undesirable cholinergic effects. Glycopyrrolate is administered with neostigmine and atropine is administered with edrophonium because of similarities in onset of activation [2].

Abductor pollicis is a better indicator of recovery of the muscles of the upper airway for reversal than orbicularis oculi or corrugator supercilii. Thus, train of four should be assessed at the abductor pollicis before reversal is administered [5]. Head lift for 5 s correlates with a train of four of 0.6 or less [10].

Neuromuscular blockers are agonized or antagonized by a variety of medications. Most antibiotics can cause blockade even without the use of a NMB. Magnesium enhances non-depolarizing NMBs but most likely antagonizes succinylcholine blockade. Calcium antagonizes muscle relaxation, whereas dantrolene enhances NMB by preventing release of calcium (recall that depolarization at the neuromuscular junction causes a surge of calcium release, leading to muscle contraction). Lithium can both enhance and antagonize NMBs secondary to its structural relationship to sodium and potassium. Local anesthetics enhance NMBs. Acute furosemide usage enhances dTC and succinylcholine. Acetazolamide antagonizes acetylcholinesterase. Steroids antagonize non-depolarizing NMBs. Antiestrogen medication potentiates non-depolarizing NMBs [3]. By decreasing the level of pseudocholinesterase, pregnancy, as well as hepatic and renal failure, prolongs the action of succinylcholine. This can lead to dangerous elevations of potassium levels secondary to the depolarization succinylcholine causes during phase I blockade. Acidosis, hypokalemia, and hypothermia prolong the effects of NMBs.