As NICU nurses, it’s essential that we are knowledgeable about caring for both the most stableandthe most unstable infants. When I think about some of the sickest babies I’ve taken care of, many of them required inotropes and vasoconstrictors. These medications can feel intimidating and often take time to truly understand.

Let’s review them together. Whether you're encountering these medications for the first time or have years of experience managing them, understanding the nuanced differences in how these drugs work (especially in our vulnerable NICU population) directly impacts patient outcomes.

Before the Drips: Understanding Receptors

Before we dive into the drugs themselves, it’s important to review and understand thereceptorsthese medications act on.

Adrenergic receptorsare located throughout the body: in the heart, lungs, blood vessels, kidneys, nerves and more. When activated, they produce different physiologic responses. For example,dopaminergic receptors respond to dopamine, and their effects vary based ondoseandpatient population(preterm infants respond differently than term infants).

Dopaminergic Receptors

• Increase renal and mesenteric blood flow

Alpha Receptors

• α₁:Vasoconstriction and increased systemic vascular resistance (SVR)

• α₂:Inhibits norepinephrine, acetylcholine, and insulin release

Beta Receptors

• β₁:Increases heart rate (HR), contractility, and renin release

• β₂:Vasodilation, relaxation of smooth muscle, bronchodilation, increased glucagon release, and glycogenolysis

Vasopressin (V) Receptors

• V₁:Vasoconstriction and increased SVR

• V₂:Water reabsorption (antidiuretic effect)
  

A helpful memory aid I’ve learned is:

• “1” affects the heart(we have one heart)

  • think chronotropy, inotropy

• “2” affects the lungs(we have two lungs)

  • think bronchodilation, smooth muscle relaxation
    
    

Of course, this doesn’t cover everything—but itisa useful starting framework.

Inotropes vs. Vasopressors: What’s the Difference?

• Inotropesincrease cardiac contractility
  

• Vasopressorsincrease peripheral vasoconstriction, which raises SVR

Many medications haveboth inotropic and vasoactive effects, which is why understanding physiology (not just blood pressure) is so important.

Let’s review the most commonly used agents.

Dopamine

Dopamine is one of the most commonly used and studied inotropes/vasopressors in the NICU. Its effects aredose-dependent.

Low Dose – Dopaminergic Receptors

• Term infants:2–4 mcg/kg/min

• Preterm infants:0.5–2 mcg/kg/min

• Increases renal and mesenteric perfusion

Moderate Dose – β₁ Receptors

• Term infants:5–10 mcg/kg/min

• Preterm infants:2–6 mcg/kg/min

• Increases inotropy (contractility) and chronotropy (HR)

• May lose inotropic effect after ~8–12 hours due to depleted norepinephrine stores

High Dose – α₁ Receptors

• Term infants:>10 mcg/kg/min

• Preterm infants:5–15 mcg/kg/min

• Peripheral vasoconstriction, increased SVR, glycogenolysis

Important consideration:
Premature infants haveimmature adrenergic receptor regulation, which means they may demonstrateincreased alpha activity at lower dosescompared to term infants.

Clinical Pearl:In very sick or premature infants, the norepinephrine stores can be depleted in as little as8–12 hours. If you find yourself constantly needing to increase the dose to maintain the same BP. The baby may have hit a ceiling, and it might be time to suggest a direct-acting agent like Epinephrine.

Adverse Effects of Dopamine

• Tachycardia

• Hyperglycemia

• Tissue ischemia

• Decreased endocrine function

  • Hypothyroxinemia of prematurity

• Increased pulmonary vascular resistance (PVR)

⚠️Avoid dopamine in infants with PPHN, as it may worsen pulmonary hypertension.
Interestingly, this same effect can make dopamine helpful in cases of ahemodynamically significant PDA.

Dobutamine

Dobutamine is a commonly used inotrope for treatinghypoperfusion due to myocardial insufficiency or elevated PVR. It is often preferred in patients withpoor myocardial contractility and normal SVR. One important consideration is that dobutamineincreases myocardial oxygen demand.

Dosing and Effects

Low Dose – β₁ and β₂ Receptors

• <5 mcg/kg/min

• Increases HR, contractility, and stroke volume

Higher Dose – α₁ Effects

• 5–15 mcg/kg/min

• Increased peripheral vasoconstriction and SVR
  

Dobutamine increases intracellular calcium, which drives increased contractility, HR, and stroke volume.

Adverse Effects to Monitor

• Tachycardia

• Increased urine output

• Electrolyte imbalances

• Increased myocardial oxygen demand
  
  

Learn more in my Shock & Vasoactive Drugs Mini Course

Epinephrine

Epinephrine (adrenaline) is anendogenous catecholamineproduced by the adrenal glands and is a powerful inotropeandvasopressor.

Atlow doses, epinephrine can act similarly to dobutamine by augmenting myocardial function.

Low Dose – β₁ and β₂ Receptors

• 0.01–0.1 mcg/kg/min

• Increased HR, contractility, lusitropy, and coronary artery dilation

• Decreased SVR

High Dose – α₁ and α₂ Receptors

• 0.1 mcg/kg/min

• Increased peripheral vasoconstriction and SVR

• Coronary vasoconstriction

Adverse Effects

• Tachycardia

• Hyperglycemia

• Lactic acidosis

• Hypokalemia

• Myocardial ischemia

• Peripheral ischemia and limb necrosis
  

Norepinephrine

Norepinephrine is another endogenous catecholamine that primarily affectsvascular tone and blood pressure. It preferentially causessystemic vasoconstriction over pulmonary vasoconstriction, making it useful in distributive shock (like septic shock) states.

Dosing

• Initiation: 0.05–0.1 mcg/kg/min

• Maximum: 2 mcg/kg/min

Receptor Activity

• α₁ and α₂ stimulation

• Minimal β₂ activity

Because of this profile, norepinephrine tends to causefewer metabolic side effects(like hyperglycemia and lactic acidosis) compared to epinephrine.

Adverse Effects to Monitor

• Tachycardia

• Peripheral ischemia

• Acidosis (especially at higher doses)
  

Vasopressin

Vasopressin is anendogenous neuropeptide, also known asantidiuretic hormone (ADH). It plays a key role in osmolarity and fluid homeostasis and is often used when hypotension persists despite inotropes, vasopressors, or steroids.

Dosing

• 0.01–0.12 units/kg/hr

Receptor Activity

• V₁a:Vasoconstriction and increased SVR

• V₂:Water reabsorption and increased plasma volume

Because vasopressin has antidiuretic effects,decreased urine outputis expected.

Adverse Effects

• Thrombocytopenia

• Elevated liver enzymes

• Hyponatremia

• Cutaneous ischemia and necrosis
  

Milrinone

Lastly, let’s talk aboutmilrinone(even though it’s not technically an inotrope or a vasopressor… and neither was vasopressin 😉).

Milrinone is aphosphodiesterase-3 inhibitorthat prevents the breakdown of cAMP and cGMP, leading tovasodilation and improved myocardial relaxation and contractility. It also provides lusitropy (diastolic relaxation), enhancing LV filling.

One major advantage of milrinone is that itdoes not increase myocardial oxygen demand, making it ideal for infants with congenital heart disease, especially post-operatively.

Loading doses may be used but should be administeredslowly (over 1–3 hours)to prevent hypotension.

Adverse Effects

• Hypotension (highest risk during initiation or with low intravascular volume)

• Tachycardia

• Arrhythmias

• Thrombocytopenia

Back to Basics: Nursing Considerations for Managing Drips

When caring for infants receiving inotropes and vasoactive medications, some “basic” nursing considerations are critical:

• Alwaysdouble-check the dose and rate with another RN

• These medications are given ascontinuous infusions

• If a drug is discontinued,do not rapidly flush the lumenit was infusing through (this can cause an unintended bolus)

• Monitor the infusion site closely—many of these drugs can causeischemia or necrosiswith extravasation

• Ideally, administer via acentral line; if not available, monitor peripheral sites extremely closely

• Useinline filterswhen indicated to prevent air embolism, precipitates, or bacterial contamination

• If unsure whether a medication requires a filter,check the package insert or contact pharmacy

• Always follow yourinstitutional policies

Remember: These medications require both knowledge and experience. New nurses - don't hesitate to ask questions. Experienced nurses - your insights during bedside teaching moments are invaluable for growing our next generation of NICU nurses.

Let’s do a case study:

The Scenario:

You are caring for Baby Sofia, a 24-weeker on Day of Life 3. She has a confirmed E. coli positive blood culture. She is intubated and requires increasing support. Despite a normal saline bolus, her MAPs are 22 mmHg (her gestational age is 24).

Current Status:

• Medication:Dopamine is infusing at 10 mcg/kg/min.

• Assessment:She is tachycardic (HR 185), her pulses are weak, and her lactic acid is climbing (4.2 mmol/L).

• The team wants to increase the Dopamine to 15 or 20 mcg/kg/min to get her pressures up.

Based on the physiology of a 24-weeker, why might the nurse suggest stopping the Dopamine titration and switching to Epinephrine instead?

A) Dopamine causes significant sedation in micro-preemies, making it hard to assess their neuro status.

B) Preterm infants have immature receptors and may have depleted their norepinephrine stores, making "direct-acting" Epinephrine more effective.

C) Epinephrine is the only medication that can be safely given through a peripheral IV in an emergency.

The Answer: B

As we discussed in the "Dopamine" section, Dopamine is an indirect-acting catecholamine. It works by telling the baby's brain/adrenals to release their own stored norepinephrine.

A 24-weeker on Day 3 is physiologically fragile. She likely doesn't have much norepinephrine stored up. If you keep cranking the Dopamine up, you're eventually going to deplete the stores of norepinephrine.

Epinephrine is direct-acting. It doesn't make the adrenals release catecholamines; it hits the alpha and beta receptors directly.

Nursing Pearl:When you make this switch, watch the Blood Glucose. Epinephrine can cause hyperglycemia because it tells the liver to dump glucose for energy. Don't be surprised if you need to adjust your dextrose infusion or start frequent glucose checks.

Shock & Vasoactive Drugs Minicourse

If you found this interesting and want to go deeper intoinotropes, vasopressors, and shock physiology, check out myShock & Vasoactive Drugs online minicourse.

What questions do you have about these drugs? Ask away! I love hearing from you.

Stay curious,

Amanda

© 2025 This content is for educational purposes and should complement, not replace, your unit's policies and procedures.

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Reference:

Beaulieu, M. J. (2013). Vasopressin for the treatment of neonatal hypotension.Neonatal Network,32(3), 209–212.https://doi.org/10.1891/0730-0832.32.3.209

Hébert, A., Ford, S., Lakshminrusimha, S., Rios, D. R., Bhombal, S., Moore, S. S., & Altit, G. (2025). Physiology-guided vasoactive therapy in neonates: Rethinking dopamine as first-line.Journal of Perinatology. Advance online publication.https://doi.org/10.1038/s41372-025-02407-w

Jnah, A. J., Barnes, J., & Dias, P. L. (2026). Hypotension and shock. In A. J. Jnah (Ed.),Neonatal pharmacology: A case-based approach(pp. 401–448). [Publisher Name—Note: Usually National Association of Neonatal Nurses or similar].

Odackal, N. J., Crume, M., Naik, T., & Stiver, C. (2024). Cardiac development and related clinical considerations.NeoReviews,25(7), e401–e414.https://doi.org/10.1542/neo.25-7-e401

Schmaltz, C. (2009). Hypotension and shock in the preterm neonate.Advances in Neonatal Care,9(4), 156–163.https://doi.org/10.1097/ANC.0b013e3181af5388