Vasopressors for Nurses

Reading Time: 5 minutes
Picture of Tyler Jones
Tyler Jones
Critical Care Nurse Practitioner in Cleveland, Ohio. With a passion for teaching, POCUS and shock. I am a Husband to an amazing Wife/Nurse, dog father, world traveler and volunteer high school baseball coach.

The Pre-brief

Vasopressors are one of the most prominent therapies in the intensive care unit. These medications are designed to enhance CO or vascular tone (SVR). Broadly speaking, they can be grouped as either  inotropes or vasoconstrictors.


The adrenal glands and neurons release catecholamines in response to emotional or physical stress. These “fight or flight” hormones elicit sympathetic responses such as: increase the force of contraction on muscles, increase the contraction of arterioles, and stimulate gluconeogenesis and catabolism of fats. 

The stimulation of muscle contractility is known as an inotropic effect. Inotropes aid in the contractility of the heart and can increase CO by raising stroke volume, heart rate, or both (remember, CO = SV x HR). 

Vasoconstriction increases SVR. These combined or individually increase the MAP, allowing for better end-organ targets’ perfusion.

The Receptors that Dominate 

Alpha-adrenergic receptors cause vasoconstriction, intestinal relaxation, and pupil dilation.

Alpha 1 receptors: stimulate vascular smooth muscle contraction (Increasing SVR).

Alpha 2 receptors are a feedback loop that causes the contraction of smooth muscle (Increasing SVR) when antagonized.

Beta-adrenergic receptors are responsible for the increase in the force of contraction of the heart and the relaxation of bronchial smooth muscle.

Beta 1 receptors: specific to heart muscle contraction and increased inotropy (Increases CO)

Beta 2 receptors: specific to smooth muscle relaxation such as the bronchioles in airways, increasing calcium uptake.

Vasopressin targets: V1 and V2. (Note: non-catecholamine receptors)

V1: Act on the splanchnic, renal, and coronary circulation as a potent vasoconstrictor (increase SVR).

V2: Present in the renal collecting duct prevents diuresis and promotes retention of Na+ and water (Increases vascular volume in order to increase CO).


Most frequently used Vasopressors and their Mechanisms


Solely an alpha agonist and strictly causes systemic arterial constriction with little to no beta-adrenergic stimulation. It can cause reflex bradycardia and potentially a decrease in CO. Be leary in those patients you know have a reduced ejection fraction

It can be used as a pre-made, push-dose pressor due to its stability compared to other pressors. Push dosing is typically 50 to 100 mcg per dose and can repeat every 1-2 minutes. Non-weight based infusion starts at 10-35 mcg/minute. Weight-based dosing is 0.5 mcg/kg/min with titration up to 6 mcg/min, though in theory there is no “ceiling” dose of vasopressors. The onset of action is immediate with a half-life around 5 minutes.

Norepinephrine (Levophed) 

Norepinephrine stimulates alpha 1, alpha 2, and Beta 1 receptors. This stimulation will increase contractility and vasoconstriction (↑ CO & SVR). Alpha effects are stronger than beta in norepinephrine. Bedside warriors should watch for tachyarrhythmias, tissue necrosis, and ischemia. (These last two items should be monitored for the use of any vasoconstrictors). 

Norepinephrine can be titrated based on weight base or non-weight base. Weight base titrations are initiated at 0.05 mcg/kg/min and titrated 0.01-0.05 mcg/kg/min every 1-15 minutes for effect. Non-weight-base is initiated at 5 mcg/minute, titrated typically 1-5 mcg every 1-15 minutes. The onset of action is very rapid and the half-life of norepinephrine is around 2.5 minutes.


Stimulates Alpha 1, alpha 2, Beta 1, and beta 2 adrenergic receptors. More Beta 1 action than the previous norepinephrine where cardiac stimulation is enhanced. However, you need to remember that it increases myocardial oxygen demand. As nurses, we need to be aware that epinephrine can cause an increase in lactic acidosis, dysrhythmias, tachycardia, necrosis, and ischemia. However, the lactate production with epinephrine is not necessarily pathological.

Epinephrine, based on weight, starts at 0.01 mcg/kg/min and can be titrated by 0.01-0.05 mcg/kg/min every 1-15 minutes for effect. Non-weight-based titrations start at 6-8 mcg/min and Epinephrine onset is 1-2 minutes with a half-life of 2 minutes. As the dose of epinephrine is increased, the vasoconstrictor effects predominate over the inotropic effects. Generally speaking, above a dose of 0.1 mcg/kg/min, the beta effects have been “maxed out”, and you are just adding SVR to the system.

Epinephrine can also be used for bradycardia and anaphylaxis.


Vasopressin is helpful in vasodilatory shock states, typically used in conjunction with norepinephrine. Systemic blood pressure is augmented through the retention of sodium, prevention of diuresis, decrease UOP, and an increase in SVR. The predominant effect on BP is through vasoconstriction. Another appealing use of vasopressin is in patients with right heart failure or pulmonary vasodilation, as vasopressin is generally considered to have little or no effect on pulmonary vascular resistance.

At the bedside, we need to be aware that vasopressin increases the afterload to the heart (as does any pure vasoconstrictor), potentially reducing cardiac output and a decrease in UOP due to the retention of sodium. Vasopressin dosing typically starts at 0.03 units/minute, if targeted perfusion is not met it can be titrated up to 0.05 units/minute.

What is this Midodrine?

If you are ever in the ICU, working with dialysis patients, or on the regular nursing floor, you potentially could have seen midodrine used. But what is it exactly? 

Midodrine is a vasoconstrictor that can be given orally. It has an active metabolite that is an alpha 1 agonist that vasoconstrictors (it behaves like a weaker version of phenylephrine). This metabolite creates arteriole and venous tone and increases SVR. Midodrine was initially designed for syncope and orthostatic hypotension but often is used as a supplement to intravenous vasopressors. Santer et al, recently studied the effect of Midodrine in this setting. It was shown that there is no significant decrease in time to vasopressor weaning. If you want to know if the Juice Worth the Squeeze visit this article.

As bedside nurses, we need to be aware that Midodrine can cause significant reflex bradycardia and a decrease in CO. Be careful with patients with heart failure with reduced ejection fraction.

The Debrief:

  • It is essential to know the reason why we use vasopressors in each situation.
  • Alpha-adrenergic agonists are mainly vasoconstrictors and increase SVR.
  • Beta-adrenergic agonists increase inotropy and bronchodilation.
  • Vasopressin for distributive shock exerts effects on the kidney and vascular smooth muscle.
  • Watch for potential arrhythmias and adverse events that can come from vasopressors.
  • Part of that elevated lactate could be coming from your vasopressors, particularly epinephrine, though this is not necessarily pathological.
  • When patients do not respond to initiate therapy, it is important to investigate why this may be: is our diagnosis wrong, is there cardiac dysfunction, etc. This will require collaboration with your APPs, pharmacists, and physicians at the bedside.


  1. Anstey MH, Wibrow B, Thevathasan T, et al. Midodrine as adjunctive support for treatment of refractory hypotension in the intensive care unit: a multicenter, randomized, placebo-controlled trial (the MIDAS trial). BMC Anesthesiol. 2017;17(1):47. Published 2017 Mar 21. doi:10.1186/s12871-017-0339-x
  2. Beta-Adrenoceptor Agonists (β-agonists). Image for Cardiovascular Pharmacology Concepts, Richard E Klabunde Ph.D. (2012, October 26).
  3. Holmes, C.L., Landry, D.W. & Granton, J.T. Science Review: Vasopressin and the cardiovascular system part 1 – receptor physiology. Crit Care 7, 427 (2003).
  4. Holmes, C.L., Landry, D.W. & Granton, J.T. Science Review: Vasopressin and the cardiovascular system part 2 – clinical physiology. Crit Care 8, 15 (2003).
  5. Overgaard CB, Dzavík V. Inotropes and vasopressors: a review of physiology and clinical use in cardiovascular disease. Circulation. 2008;118(10):1047-1056. doi:10.1161/CIRCULATIONAHA.107.728840
  6. Santer P, Anstey MH, Patrocínio MD, et al. effect of midodrine versus placebo on time to vasopressor discontinuation in patients with persistent hypotension in the intensive care unit (MIDAS): an international randomized clinical trial. Intensive Care Med. 2020;46(10):1884-1893. doi:10.1007/s00134-020-06216-x


More Posts

Related Posts

Would love your thoughts, please comment.x