PRESSORS

In this episode of AudioBoards, we break down the practical use of vasopressors in the ICU through a physiology-first approach. We walk through the four major shock types—hypovolemic, distributive, cardiogenic, and obstructive—and connect each to appropriate hemodynamic targets and management strategies. The discussion covers when to start vasopressors, how to choose first-line agents like norepinephrine, and when to add adjuncts such as vasopressin, epinephrine, dobutamine, or milrinone.

Transcript

Welcome back to AudioBoards. Today we’re covering one of the most important topics in critical care: vasopressors in the ICU. This is a subject that can feel overwhelming at first because there are multiple medications with different effects, but the goal today is to turn it into a structured way of thinking rather than memorization.

I’ll be honest, vasopressors always feel like a long list of drugs I’m supposed to memorize. Norepinephrine, epinephrine, dopamine… it just blends together.

That’s exactly why people struggle with it. If you start with the drugs, it feels random. But if you start with physiology, it all becomes organized.

Let’s start simple:

Mean arterial pressure, or MAP, equals cardiac output multiplied by systemic vascular resistance.

So when blood pressure drops, one of two things is happening—the pump is failing, the pipes are dilated, or both.

So it’s really just cardiac output or SVR?

Exactly. And cardiac output itself is heart rate times stroke volume. Stroke volume depends on preload, contractility, and afterload.

Every vasopressor or inotrope is just targeting one of those variables. Once you see that, the entire ICU pressor board makes sense.

But before we even talk drugs, we have to ask: why is the patient hypotensive?

Right, because shock isn’t just low blood pressure.

Exactly. Shock is inadequate tissue perfusion leading to organ dysfunction.

And we classify it into four types: hypovolemic, distributive, cardiogenic, and obstructive.

Each one behaves differently, so pressors are not a universal fix.

So in some cases, pressors might not even be the right answer?

Exactly. For example, in hemorrhagic shock, giving norepinephrine doesn’t solve the problem—you need blood and hemorrhage control.

Or in tension pneumothorax, no amount of vasoconstriction fixes the mechanical obstruction.

Pressors are supportive. They buy time, not cure disease.

That makes sense. So they improve blood pressure, but not necessarily perfusion?

Right. They improve perfusion pressure, not always actual tissue perfusion.

Think of MAP like pressure in a hose. If there’s no volume in the system—like severe hypovolemia—tightening the hose doesn’t create flow.

That’s why fluids usually come first when volume loss is suspected.

But in septic shock, we don’t always wait too long for fluids, right?

Exactly. In septic shock, we give crystalloid first when appropriate. But if MAP stays below about 65 mmHg despite fluids, we don’t delay vasopressors.

The key is balance—don’t delay pressors in profound shock, but don’t skip resuscitation either.

And the goal isn’t just hitting 65?

No, and this is critical.

The goal is restoring oxygen delivery to tissues.

A “normal” MAP means nothing if lactate is rising, urine output is dropping, mental status is worsening, or the skin is poorly perfused.

You treat the patient, not the number.

 Before we go into the drugs, can we go over receptors quickly? That part always helps.

Absolutely—this is the foundation.

Alpha-1 receptors cause vasoconstriction—arterial and venous. That increases SVR, increases MAP, improves venous return, and increases afterload. Think: squeezing the pipes.

Beta-1 receptors act on the heart—they increase heart rate and contractility, which increases cardiac output. Think: stronger and faster pump.

Beta-2 receptors cause vasodilation and bronchodilation.

Dopamine receptors have been overemphasized historically—“renal-dose dopamine” does not protect kidneys and is no longer recommended.

Vasopressin is different. It works on V1 receptors and causes vasoconstriction independent of catecholamines. That’s especially useful in septic shock when patients become catecholamine-resistant.

So if I had to remember just one vasopressor, what should it be?

Norepinephrine. No question. It’s first-line for almost all shock states, especially septic shock.

And Why is it so preferred?

Because it’s balanced. Strong alpha-1 effects increase SVR and MAP, and moderate beta-1 activity supports cardiac output. Minimal beta-2 means less unwanted vasodilation.

Compared to dopamine, it’s more predictable and causes fewer arrhythmias.

Okay, so norepinephrine first. When do we add vasopressin?

Usually as a second-line agent in septic shock.

In prolonged shock, endogenous vasopressin gets depleted. So adding it helps restore vascular tone without increasing catecholamine dose.

It works via V1 receptors, has no beta activity, and doesn’t really affect heart rate.

A common dose is 0.03 units per minute.

And epinephrine?

Epinephrine is more aggressive. It hits alpha, beta-1, and beta-2 receptors.

So it increases SVR, heart rate, contractility, and cardiac output.

It’s useful in refractory septic shock, cardiac arrest, and anaphylaxis.

But it comes with tradeoffs—tachycardia, arrhythmias, increased myocardial oxygen demand, and lactate elevation from beta-2 stimulation.

Phenylephrine seems simpler—just squeeze vessels?

Exactly. Pure alpha-1 agonist.

It raises blood pressure but can reduce cardiac output because afterload increases. It can also cause reflex bradycardia.

So it’s not first-line in septic shock.

It’s more useful in specific cases like tachyarrhythmias or anesthesia-related hypotension with good cardiac function.

Dopamine used to be everywhere.

It did, but not anymore.

Dose-dependent effects sound nice in theory, but in practice it’s unpredictable and increases arrhythmia risk.

Now it’s rarely used, except in select cases like symptomatic bradycardia with hypotension when other options aren’t available.

What about dobutamine?

Dobutamine is an inotrope, not a vasopressor.

It mainly stimulates beta-1 receptors, increasing cardiac output.

So it’s useful in cardiogenic shock—low ejection fraction, low cardiac index, poor perfusion.

But it can drop blood pressure?

Because of beta-2 effects, it can reduce SVR, so hypotension can worsen. That’s why we often pair it with norepinephrine.

And milrinone?

Milrinone is different—it’s a phosphodiesterase-3 inhibitor.

It increases contractility, causes vasodilation, and reduces pulmonary vascular resistance.

It’s especially helpful in right ventricular failure, pulmonary hypertension, and patients on chronic beta-blockers.

But it can cause hypotension and has a long half-life, especially in renal dysfunction.

Can we put this all together by shock type?

Yes—that’s where it finally clicks.

In septic shock: fluids first, then norepinephrine. Add vasopressin if escalating, epinephrine if refractory, and dobutamine if cardiac output is still low.

In cardiogenic shock: norepinephrine for perfusion pressure, plus dobutamine or milrinone for contractility. Consider mechanical support if needed.

In hypovolemic shock: replace volume first—blood, fluids, hemorrhage control. Pressors only if still hypotensive afterward.

In obstructive shock: fix the obstruction—PE, tamponade, or tension pneumothorax. Pressors are only a bridge.

In neurogenic shock: loss of sympathetic tone causes vasodilation and bradycardia. Norepinephrine is usually best.

So what do we actually do at the bedside?

Step one: recognize shock early.

Step two: give fluids if appropriate.

Step three: if MAP stays below about 65 mmHg, start norepinephrine—don’t keep giving repeated fluid boluses that don’t work.

And we titrate to numbers or the patient?

The patient. Always.

We look at lactate, urine output, mental status, capillary refill, and skin perfusion—not just MAP.

And we don’t need to wait for a central line anymore?

Correct. Peripheral norepinephrine is safe when given through a good large-bore IV in a proximal vein with close monitoring.

Don’t delay treatment in shock waiting for central access.

Once pressors are running, you reassess constantly—blood pressure trends, urine output, lactate, rhythm, and signs of ischemia.

Rising pressor requirements usually mean worsening shock, not undertreatment.

And every vasopressor carries risks—arrhythmias, ischemia, and tissue injury. The goal is always the lowest effective dose for the shortest time.

Thanks for listening to AudioBoards. Stay tuned for more educational content in our next episode! The views and opinions expressed on the AudioBoards Podcast do not necessarily reflect those of our employers. This podcast is for educational purposes only and should not be used to diagnose or treat any medical conditions. It is not a substitute for professional medical advice. Always consult a qualified, board-certified healthcare provider for any medical concern.