Vasopressors for Nurses

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

Phenylephrine

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.

Epinephrine

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

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.