Vasopressors, Inotropes, and Drip Titration

Vasoactive drips are ICU bread-and-butter. You don’t have to be the one who decides to start them to be dangerous or safe with them — understanding what each drug does, why it was chosen, and how to titrate to a goal is what keeps the patient stable on your watch.

• •Vasopressors raise blood pressure mainly by increasing systemic vascular resistance (squeeze) — for vasodilatory/low-SVR shock.
• •Inotropes increase cardiac contractility and output (squeeze of the heart) — for low-output/cardiogenic shock.
• •Some agents do both; the “right” drug depends on whether the problem is tone, pump, or both.

• •α1 (alpha-1): on vascular smooth muscle → vasoconstriction → ↑ systemic vascular resistance (SVR) → ↑ blood pressure. This is the “squeeze.”
• •β1 (beta-1): on the heart → ↑ contractility (inotropy) and ↑ heart rate (chronotropy) → ↑ cardiac output. This is the “pump.”
• •β2 (beta-2): on vascular and bronchial smooth muscle → vasodilation (can LOWER diastolic BP) and bronchodilation.
• •Dopaminergic: dose-dependent (low = splanchnic/renal vasodilation; higher recruits β1 then α1).
• •V1 (vasopressin receptor): non-adrenergic vasoconstriction — works through a separate pathway, so it still squeezes when acidosis/catecholamine downregulation has blunted the adrenergic response.
• •PDE-3 inhibition (milrinone): raises intracellular cAMP → inotropy PLUS vasodilation (an “inodilator”) — independent of β-receptors, so it works even on β-blocked patients.

Doses below are typical adult starting points and ranges — your unit’s protocol, drug concentration, and weight-based vs fixed dosing govern. Always confirm against the order and the pump library.

• •Norepinephrine (α1 ≫ β1) — first-line vasopressor for most shock (septic, and many cardiogenic with adequate output): potent vasoconstriction with mild inotropy. Start ~0.05 mcg/kg/min (≈5 mcg/min); titrate to MAP, commonly up to ~0.5 mcg/kg/min (higher in refractory shock).
• •Epinephrine (β1/β2 at low dose, α1 added as dose rises) — vasopressor + inotrope; anaphylaxis, cardiac arrest, and refractory shock; more tachycardia/lactate. Infusion start ~0.01–0.05 mcg/kg/min (≈1–10 mcg/min); titrate.
• •Vasopressin (V1, non-adrenergic) — common FIXED-dose add-on in septic shock at 0.03 units/min (NOT titrated like a catecholamine; ~0.04 reserved for refractory shock). Added to norepinephrine rather than escalating it endlessly.
• •Phenylephrine (pure α1, no inotropy) — useful when tachycardia/arrhythmia limits other agents; can cause reflex bradycardia. Infusion start ~0.5 mcg/kg/min (≈40–100 mcg/min); push-dose boluses ~50–200 mcg.
• •Dobutamine (β1 ≫ β2) — inotrope that raises output but can LOWER blood pressure (β2 vasodilation); for low-output states with an adequate pressure. Start 2–5 mcg/kg/min, titrate to ~20.
• •Milrinone (PDE-3 inodilator) — inotropy plus systemic/pulmonary vasodilation; renally cleared and causes hypotension; used in advanced HF and RV failure / pulmonary hypertension. Infusion 0.125–0.75 mcg/kg/min (loading dose often omitted to avoid hypotension); reduce in renal dysfunction.
• •Dopamine (dose-dependent dopaminergic → β1 → α1) — more arrhythmia; generally less preferred than norepinephrine except select bradycardic/low-arrhythmia-risk patients. ~5–20 mcg/kg/min.

• •Septic/distributive (warm, vasodilated, low SVR): norepinephrine first, add vasopressin; treat the source.
• •Cardiogenic (cold, low output): often an inotrope (dobutamine/milrinone) ± a pressor (norepinephrine) to maintain perfusion — physician/ICU-directed, often with mechanical support considered.
• •A failing right ventricle (e.g., PE, PH): support perfusion pressure, consider an inodilator, and avoid worsening pulmonary pressures — specialist territory.

• •Titrate to an ordered hemodynamic goal — commonly a MAP ≥65 mmHg (individualized).
• •Central venous access is preferred for vasopressors; peripheral norepinephrine is acceptable short-term under protocol because extravasation can cause tissue necrosis — monitor the site.
• •Wean gradually as the patient improves — never stop a pressor abruptly (rebound hypotension).
• •Watch for tachy-/arrhythmias, digital/limb ischemia, and worsening lactate.

• •Using an inotrope (dobutamine/milrinone) as if it were a pressor and watching the BP fall further.
• •Pushing pressors hard in a hypovolemic patient instead of also addressing volume / the cause.
• •Forgetting milrinone is renally cleared and accumulates (prolonged hypotension) in renal dysfunction.
• •Abruptly stopping a drip, or missing peripheral extravasation.

• •Bedside ICU nurses run and titrate the drips to the ordered goals and watch the access site; you set/adjust the targets with the physician and act on trends and complications.