Vasopressin is the exogenous, parenteral form of antidiuretic hormone (ADH) that may be used for several conditions in the intensive care unit (ICU), including the treatment of central diabetes insipidus and as a vasopressor agent in shock.
Endogenous vasopressin dose is an important stress hormone and plays a critical role in maintaining volume hemostasis. However, its beneficial physiological effects may be offset when there is excess hormone in the circulation.
It is important to understand vasopressin’s mechanism of action and to be able to recognize which ICU patients may suffer adverse effects from the use of this drug.
Endogenous vasopressin dose is synthesized in neurosecretory cells of the hypothalamus and excreted by the posterior pituitary gland in response to decreases in blood volume and increases in serum osmolality.
Vasopressin Receptors are primarily located in vascular smooth muscle (V1) and the renal collecting duct (V2) and the Vasopressin Receptors act to stimulate vasoconstriction and increase free water reabsorption, respectively.
These are normal compensatory mechanisms designed to maintain vascular tone and circulatory homeostasis during periods of low cardiac output.
In patients with congestive heart failure, however, chronic activation of this neurohormonal axis contributes to the progression of disease through an increase in afterload and water retention with vasopressin dose .
Moreover, giving vasopressin infusions to patients with existing heart failure will cause an acute increase in systemic vascular resistance and pulmonary capillary wedge pressure, possibly resulting in a further decrease in cardiac output.
Therefore, caution should be used when administering exogenous vasopressin in patients with known heart failure in the ICU.
Another adverse effect of excessive vasopressin dose in the circulation is the potential for mesenteric hypoperfusion.
When vasopressin dose stimulates the contraction of vascular smooth muscle, this effect is often most prominent in the capillaries and small arterioles or venules of the splanchnic circulation.
This vasoconstriction can cause a major redistribution of blood flow away from the bowel mucosa that can result in ischemia and produce its associated signs, including hyperlactatemia.
Along with the concurrent decrease in cardiac output and global oxygen delivery, high doses of exogenous vasopressin may produce or exacerbate mesenteric ischemia and has been shown to increase gut pCO2 in tonometry studies.
In order to avoid detrimental reductions in mesenteric blood flow associated with extra vasopressin dose, other vasopressors should be considered first-line agents in shock.
This includes norepinephrine, epinephrine, and dopamine, which do not compromise regional blood flow or tissue oxygenation at normal levels.
Vasopressin dose should be used only as a supplementary vasopressor to these agents at a continuous low-dose infusion (0.04 U/min) and should not be titrated as a single agent.
One final note is that vasopressin analogue desmopressin (DDAVP) is the treatment of choice for central diabetes insipidus, given that it has a longer duration of action and causes less stimulation of smooth muscle than vasopressin dose.