Tuesday, March 15, 2016

Phenylephrine (pure alpha-1 agonist)

PulmCrit - March 14, 2016 - By Josh Farkas
This is the first of a series of four posts about vasopressors and hemodynamics. The first step is to explore the physiology of a pure alpha-1 agonist (phenylephrine).
Make no mistake, I’m not very fond of phenylephrine. I rarely use it (mostly for hypotensive atrial fibrillation). However, understanding phenylephrine is a prerequisite to understanding related vasopressors, particularly midodrine and norepinephrine.
Evidence regarding phenylephrine consists of a patchwork of often contradictory human and animal studies, based mostly on surrogate endpoints. Thus, this post is framed as an alternative viewpoint: a perspective which remains debatable.
  • Norepinephrine is similar to phenylephrine (norepinephrine is equivalent to phenylephrine plus some beta-1 stimulation). In some situations the two drugs may function in an identical fashion.
  • Like norephrine, phenylephrine can cause venoconstriction, thereby increasing venous return to the heart.
  • Phenylephrine can affect cardiac output in a variety of ways:
  • Increased preload may increase cardiac output
  • Increased afterload and reflex bradycardia may reduce cardiac output.
  • The effect of phenylephrine on cardiac output varies depending on the clinical context.
  • The most common mechanism whereby phenylephrine reduces cardiac output may be reflex bradycardia. Thus, an inappropriately low heart rate in a shocked patient on phenylephrine suggests that cardiac output is being suppressed.
  • Available evidence suggests that phenylephrine can improve renal function, particularly in hyperdynamic shock states (e.g. cirrhosis, sepsis)."