Neo-Synephrine is the trade name for phenylephrine. It is a pure alpha receptor agonist and has both venous and arterial constrictive effects. Because Alpha1 receptors have been discovered in the myocardium, it is also possible that it has positive inotropic effects.

In our current culture of patient safety, it is important to avoid commonly used medical abbreviations so that medical errors can be prevented.

For example, the term neo is often used in the operating room and intensive care unit (ICU) to refer to the drug Neo-Synephrine; however, it could also reasonably be interpreted as neostigmine, another commonly used drug in the operating room and ICU. To avoid this confusion and to decrease the risk of a medication error, the use of the brand name Neo-Synephrine should be abandoned.


Acutely, phenylephrine causes an increase in venous return (preload) due to its venous constrictive effects; it increases after load as well. In normal individuals, it does not affect cardiac output. However, in patients with ischemic heart disease, it can decrease cardiac output.

Other uses for phenylephrine or Neo-Synephrine include reversing right-to-left shunt flow in patients with tetralogy of Fallot and terminating supraventricular tachycardias (SVTs) as it can cause reflex vagal stimulation in response to elevated blood pressure. In this last circumstance, Neo-Synephrine is particularly useful as it treats both the arrhythmia and the hypotension.

Phenylephrine or Neo-Synephrine is given as either an intravenous (IV) bolus or infusion; bolus doses are 1 to 10 mcg/kg, or in 50- to 100-mcg boluses in adults. As an Neo-Synephrine IV infusion, it is usually mixed as 10 to 15 mg in 250 mL and dosed as 0.15 to 0.75 mcg/kg/min. For use in pediatric patients with tetralogy of Fallot, IV bolus doses are 5 to 50 mcg/kg.


Neostigmine (marketed under the trade name Prostigmin) is a reversible acetylcholinesterase inhibitor. It is used clinically in the treatment of myasthenia gravis, glaucoma, and atony of the gastrointestinal and urinary tracts. In the operating room and ICU settings, it is commonly used to reverse nondepolarizing neuromuscular blockade.

Although it antagonizes neuromuscular blocking agents at nicotinic receptors, it has muscarinic effects as well. Its adverse effects result from its action at these receptors: bradycardia and bradyarrhythmias; increased salivation; increased bowel motility; and possibly bronchospasm.

To counteract these adverse effects, neostigmine is typically given in conjunction with an anticholinergic agent–either atropine or glycopyrrolate.

The dose of intravenous neostigmine required to reverse neuromuscular blockade is greater in long-acting neuromuscular blockers than short-acting blockers.

For example, 40 to 50 mcg/kg of neostigmine is required to reverse a 90% block produced by pancuronium or d-tubocurarine, whereas 20 to 30 mcg/kg is needed for atracurium, vecuronium, and rocuronium, and 5 mcg/kg is needed for mivacurium. Because neostigmine dosage has a ceiling effect, administering greater than 0.07 mg/kg has little benefit.

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