Vasopressors & Inotropes study guide previews.

Angiotensin II (Ang II) is an endogenous hormone in the renin-angiotensin-aldosterone system (RAAS) that plays a key role in vascular tone and blood pressure regulation. AT1 receptors (vascular smooth muscle) include Potent vasoconstriction leading to increased systemic vascular resistance (SVR) leading to increased MAP. Adrenal cortex include Stimulates aldosterone release leading to Na⁺ and water retention leading to increased intravascular volume. Sympathetic system & brain include Enhances norepinephrine release and central vasopressor tone and Acts downstream of ACE, so it’s effective even in patients with impaired RAAS or those taking ACE inhibitors.

Up to 80 ng/kg/min in first 3 hours, then max 40 ng/kg/min. High doses beyond 80 ng/kg/min are not recommended due to thrombotic risk.

Vasopressors are medications that induce vasoconstriction and elevate mean arterial pressure (MAP), primarily used in shock states to maintain organ perfusion. Inotropes increase myocardial contractility, helping in low-output states (e.g., cardiogenic shock, decompensated heart failure). In real-world critical care, the line between vasopressors and inotropes often blurs-many agents have both properties depending on the dose and patient physiology.

Vasopressors are medications that induce vasoconstriction and elevate mean arterial pressure (MAP), primarily used in shock states to maintain organ perfusion. Inotropes increase myocardial contractility, helping in low-output states (e.g., cardiogenic shock, decompensated heart failure). In real-world critical care, the line between vasopressors and inotropes often blurs-many agents have both properties depending on the dose and patient physiology.

Critical Care Vasopressors & Inotropes Comparison introduces the clinical pattern, physiology, and bedside decisions that matter for emergency and critical care practice.

Dobutamine is a synthetic catecholamine that acts primarily through β1-adrenergic receptor agonism leading to increased myocardial contractility (positive inotropy) and modest increased heart rate (chronotropy), β2-adrenergic receptor agonism leading to mild vasodilation (decreased SVR), and α1-agonism leading to dose-dependent; typically offset by β2 effects.

Receptor Selectivity (approximate relative potency) include β1:β2:α1 ≈ 5:1:0.5. Dobutamine is a racemic mixture include (−)-isomer = α1 agonist, weak β1 antagonist and (+)-isomer = β1 and β2 agonist, α1 antagonistThe combination results in net β1-dominant effect with mild vasodilation. The onset is usually -2 minutes. Monitoring includes cVP, MAP, ScvO₂/SvO₂, lactate, and mixed venous oxygen saturation. Advanced hemodynamics via thermodilution or non-invasive methods (e.g., NICOM, PiCCO, FloTrac) often used in titration.

Note includes the concept of "renal-dose dopamine" is no longer supported by evidence. Titrate dose based on hemodynamic goals, often guided by cardiac output, blood pressure, and perfusion indices.

Epinephrine (also known as adrenaline) is a potent endogenous catecholamine that acts on both alpha- and beta-adrenergic receptors. It is widely used in shock, cardiac arrest, and anaphylaxis, and plays a significant role in the management of refractory hypotension in the ICU.

Epinephrine is unique among vasopressors due to its mixed inotropic and vasopressor properties - making it both a pressor and an inotrope. Also used as an infusion in anaphylactic shock.

Levosimendan is a calcium sensitizer and inodilator that enhances myocardial contractility without increasing intracellular calcium or myocardial oxygen demand.

It acts via three key mechanisms include Calcium sensitization of troponin C leading to enhances myocardial contractility without increasing cytosolic calcium or oxygen consumption, Opening of ATP-sensitive potassium channels (K_ATP) in vascular smooth muscle leading to vasodilation (arterial and venous), Opening of mitochondrial K_ATP channels in cardiomyocytes leading to possible cardioprotective effects (anti-stunning, anti-apoptotic, anti-inflammatory), and "More squeeze, less cost": Increases inotropy with lower risk of ischemia compared to catecholamines.

Up to 7-10 days after a 24-hour infusion. Loading dose may cause hypotension-often omitted in hypotensive or unstable patients. Acute decompensated heart failure (Europe, South America, Asia). Weaning from inotropes or mechanical support (LVAD, ECMO, IABP). Not FDA-approved in the U.S., but available in >50 countries.

Midodrine is a prodrug that is metabolized in the liver to its active form, desglymidodrine, a selective α1-adrenergic receptor agonist. Desglymidodrine stimulates peripheral α1 receptors on arteriolar and venous smooth muscle leading to vasoconstriction. Increases systemic vascular resistance (SVR) and blood pressure. Does not cross the blood-brain barrier leading to no central adrenergic stimulation. No significant β-adrenergic, dopaminergic, or cardiac inotropic activity. Net effect include SVR leading to MAP (systolic and diastolic BP), without increasing HR or cardiac output.

Adjust dose in renal impairment; risk of accumulation and hypertension. FDA-Approved include Symptomatic orthostatic hypotension in patients with autonomic failure (e.g., multiple system atrophy, pure autonomic failure, diabetic neuropathy). Off-Label / Critical Care Uses include Adjunct to wean from IV vasopressors in ICU patients (e.g., norepinephrine), Hepatorenal syndrome (as part of vasoconstrictor + albumin protocol), and Neurogenic shock or spinal cord injury-induced hypotension. Severe organic heart disease, acute renal failure, urinary retention, pheochromocytoma, thyrotoxicosis.

Supine hypertension (very common), CAD, arrhythmias, renal impairment. Supine hypertension is a major risk - patients should remain upright after dosing.

Milrinone is a phosphodiesterase-3 (PDE3) inhibitor, which leads to increased intracellular cyclic adenosine monophosphate (cAMP) in both cardiac myocytes and vascular smooth muscle. In vascular smooth muscle leading to increased cAMP leading to vasodilation of arterial and venous beds. 5 - 4 hours (longer in renal impairment). Primarily renal (unchanged drug - dose accumulation in renal dysfunction). Dose reduction required in renal dysfunction (e.g., start at 0.125-0.25 mcg/kg/min and titrate carefully).

Acute decompensated heart failure (ADHF), especially in patients on chronic β-blockers. Low-output cardiac states post-cardiac surgery or in cardiogenic shock. Bridge to transplant, VAD, or decision in advanced heart failure. Severe hypotension, volume depletion, or arrhythmias; renal failure. Avoid or use lower doses in hypotensive or vasoplegic states unless a vasopressor is added.

Norepinephrine (NE), also known as noradrenaline, is a first-line vasopressor used in the management of shock, particularly septic shock. It is a catecholamine that acts primarily on α-adrenergic receptors, causing vasoconstriction, and to a lesser extent on β1-receptors, which support cardiac output.

Norepinephrine is recommended by major critical care guidelines (e.g., Surviving Sepsis Campaign) as the vasopressor of choice in most cases of distributive shock. α1-adrenergic agonist (strong) include Causes peripheral vasoconstriction, increasing systemic vascular resistance (SVR) and thus raising blood pressure. β1-adrenergic agonist (moderate) include Increases myocardial contractility and heart rate, though less than epinephrine or dopamine and Norepinephrine increases MAP by raising SVR more than it increases cardiac output. Initial Dose (Continuous Infusion) include 01-0.05 mcg/kg/min, 05-1 mcg/kg/min, and Maximum doses vary by institution, but can go up to 3 mcg/kg/min in extreme cases.

Titration include Adjust every 2-5 minutes based on MAP goal (usually ≥ 65 mmHg) and Titrate slowly to effect, watching for signs of ischemia or excessive vasoconstriction. Preparation include Comes in premixed bags (e.g., 4 mg in 250 mL D5W or NS) and Administer via central line to avoid extravasation, especially at higher doses.

Phenylephrine is a pure α1-adrenergic agonist used as a vasopressor to increase blood pressure by inducing peripheral vasoconstriction. Unlike catecholamines such as norepinephrine or epinephrine, phenylephrine has no β-adrenergic activity - meaning it does not directly affect heart rate or contractility.

It is generally considered a second- or third-line agent, and is particularly useful when tachycardia or arrhythmia makes β-stimulation undesirable. α1-receptor agonist leading to systemic arterial and venous vasoconstriction leading to increased systemic vascular resistance (SVR) leading to increased mean arterial pressure (MAP). No β1 or β2 activity leading to no direct effect on heart rate or contractility. Phenylephrine increases afterload without affecting cardiac output, which can be problematic in patients with poor left ventricular function.

Often used temporarily in anesthesia or procedural sedation. Use if tachycardia or arrhythmias limit other pressors.

Vasopressin And RV Dysfunction introduces the clinical pattern, physiology, and bedside decisions that matter for emergency and critical care practice.

Vasopressin, also known as arginine vasopressin (AVP) or antidiuretic hormone (ADH), is an endogenous hormone that plays a major role in fluid balance and vascular tone. In critical care, vasopressin is used as a second-line vasopressor, often added to norepinephrine in the treatment of vasodilatory shock, especially septic shock.

Unlike catecholamines, vasopressin acts via non-adrenergic receptors, which is helpful in catecholamine-refractory hypotension. In shock states, vasopressin helps raise mean arterial pressure (MAP) by constricting peripheral vessels and augmenting intravascular volume via water retention. No titration - vasopressin is usually added as an adjunct to norepinephrine. Some centers may use up to 0.04 units/min, but higher doses increase risk of ischemia. Administration includes continuous IV infusion via central line (preferred).