Today we’re going to talk about vasopressin.
Those of you who have been nursing a bit will remember when vasopressin, 40 units, IV as a bolus dose was the ACLS recommendation for the second medication to give during a cardiac arrest. The first? Epinephrine, as always. “All dead people get epi,” at least if we’re following the recommendation of the AHA. As I said before, there’s some controversy.
But we aren’t here to talk about epinephrine. Let’s look at vasopressin. The chart I posted over catecholamines is useful, but vasopressin wasn’t on it. That’s because vasopressin isn’t an alpha-1/beta-1/beta-2 drug. Nor does it metabolize into a drug that accesses those receptor sites.
Vasopressin is anti-diuretic hormone. It is necessary for life in humans and animals, and it works on the V1 and V2 receptor sites. The first is located on the membrane of a vascular smooth muscle cell and mediates vasoconstriction in much the same way as angiotensin II. The second receptor regulates water excretion by increasing water reabsorption.
Vasopressin is used to restore vascular tone in vasodilatory shock. We usually use it in sepsis, but also in vasoplegic syndromes and advanced heart failure. It’s the drug we reach for when shock is resistant to catecholamines.
There are several ways vasopressin performs its magic. We mentioned vasoconstriction and increasing water reabsorption. Other effects include modulating endrogenous nitric oxide and potentiating adrenergic agents to promote vasoconstriction.
Platelets are affected by stimulation of the V1 receptor site to provoke an increase in intracellular calcium levels. This facilitates thrombosis, but the amount of variability in aggregation response is so large it’s not possible to point to vasopressin as a cause of coagulopathy.
V1 receptor agonism doesn’t affect every part of the kidney in the same way, but selectively affects the inner (but not the outer) medulla blood flow rate, and contracts the efferent arterioles but not the afferent arterioles.
DDAVP is a selective form of vasopressin which affects only the V2 receptors, causing a release of von Willebrand factor and vasodilation in the kidney alone. Although V2 receptors are found elsewhere, for reasons most mysterious it doesn’t seems to have effects outside the renal circulation.
The vasopressin receptors are relatively resistant to downregulation. The interaction of vasopressin with arrestins, when combined with this resistance, allows vasopressin to (purportedly) bypass the downregulated myocardial adrenergic receptors.
Vasopressin is dosed in 0.01-0.04 units per minute or 0.1-0.4 units per hour. Either way, it’s particularly helpful in hypoxic/acidotic states, as well as those resistant to sympathomimetics. It’s not generally titrated–for sepsis or vasoplegic syndromes, we generally place it at 0.03 units/min and leave it. It increases MAP without affecting inotropy, as a general rule.
Although the cardiac effects of vasopressin are complex and conflicting, a few common uses have emerged over the last ten years. One is the pairing of milrinone and vasopressin. In cases of severe advanced heart failure requiring the use of inotropic agents, plus the necessity to bypass downregulated receptor sites, added to the need for diuresis in the presence of relative hypotension, vasopressin has emerged as a superior agent for maintaining vascular tone and perfusion.
It’s also an excellent choice for blood pressure support in PAH, as it avoids vasoconstriction in pulmonary circulation.
Consider adding vasopressin to levophed in refractory hypotension, particularly in septic shock. In those patients the levophed dose can get so high it blocks perfusion of the capillary beds. Starting vasopressin in these patients can allow you to reduce the rate of levophed infusions to much more reasonable levels.
Another use is in post-operative cardiac surgery patients. Maintenance on bypass circuitry for surgery has multiple effects on a patient’s physiology, which can evidence themselves in a vasoplegic scenario post-operatively. Vasopressin can prevent cardiovascular collapse in this patient population without adversely affecting inotropy.