Vasopressin, otherwise known as antidiuretic hormone (ADH), is a peptide hormone synthesized in the hypothalamus and released by the posterior pituitary gland. Its physiologic effects include vascular smooth muscle constriction (via V1 receptors, PLC-IP3 and calcium pathway) and free water retention (via V2 receptors, cAMP/PKA pathway).
Peruse the literature, and you’ll find many trials comparing vasopressin to other pressors (norepinephrine, epinephrine) and other adjuncts like hydrocortisone in pathologies like septic shock. In general, vasopressin might be a better alternative for patients who have hyperdynamic features, tachycardia, impending renal failure, and pulmonary hypertension (vaso tends to spare pulmonary vascular beds). However, most of these studies show no morbidity/mortality benefits favoring the use of vasopressin.
One of the best things about vasopressin is that it tends to work in acidotic environments and potentiates other vasoactive agents. If a penetrating trauma rolls into the stat operating room, I don’t need a blood gas to tell me that the patient is usually anemic and acidotic. As part of my resuscitative efforts, I’ll work in a few units of vasopressin with fluids to help maintain perfusion pressure while correcting the acidosis.
I can think of multiple instances in my residency where I knew vasoplegia was the problem and conventional pressors like norepinephrine simply weren’t getting the job done. Bolusing a few units of vaso seemed to do the trick. 🙂 Keep this important medication in mind during vasoplegia and shock!