Emergency Medicine Hub / Resuscitation & Critical Care • 3 min read • 3 sections

Vasopressors, Inotropes & Hemodynamic Monitoring in Shock

Comprehensive emergency management of undifferentiated and refractory shock syndromes: receptor pharmacodynamics of vasopressors and inotropes, titration strategies, peripheral line safety, extravasation antidote administration, and dynamic assessment of fluid responsiveness (Passive Leg Raise, VTI, IVC collapsibility).

Resuscitation Quick Actions • First 2 Minutes

High-Acuity

First-Line Pressor (Septic/Distributive Shock)

Norepinephrine infusion starting at 2-5 mcg/min, titrate rapidly q2-3min to MAP >= 65 mmHg (typical range 5-30 mcg/min).

Second-Line Pressor

Vasopressin fixed dose at 0.03 units/min (do NOT titrate; spares adrenergic toxicity and restores V1 vascular tone in acidic states).

Third-Line/Inodilator Addition

Epinephrine 2-10 mcg/min for ongoing hypoperfusion, or Dobutamine 2.5-20 mcg/kg/min if myocardial dysfunction persists despite adequate MAP.

Pure Alpha-1 Vasoconstrictor

Phenylephrine 50-300 mcg/min; indicated in hyperdynamic sepsis with tachyarrhythmias preventing norepinephrine use, or severe aortic stenosis.

Peripheral Pressor Safety

Norepinephrine and phenylephrine are safe through a dedicated, ultrasound-confirmed 18G/20G peripheral IV in the forearm/antecubital fossa for up to 24-48 hours. Monitor site every 1-2 hours.

Extravasation Emergency

Stop infusion immediately. DO NOT remove catheter. Aspirate remaining drug. Infiltrate Phentolamine 5-10 mg diluted in 10 mL NS through catheter and subcutaneously around blanching area within 12 hours. Apply topical 2% nitroglycerin paste as adjunct.

Vasopressors & Inotropes

Norepinephrine (first-line in septic/cardiogenic shock), Epinephrine, Vasopressin (fixed 0.03 U/min), Phenylephrine, Dobutamine, Milrinone, Angiotensin II.

Fluid Responsiveness Assessment

Dynamic measures like Passive Leg Raise test (PLR with cardiac output rise >=10-15%) and stroke volume variation.

Bottom-Line Clinical Pearl

Norepinephrine is the first-line vasopressor for septic, cardiogenic, and undifferentiated distributive shock. In refractory vasodilatory shock, add Vasopressin (fixed 0.03 units/min, no titration) followed by Epinephrine. Assess fluid responsiveness with dynamic measures (Passive Leg Raise test), not static CVP or flat-leg ultrasound.

CRITICAL PROTOCOL: Peripheral Vasopressor Extravasation Management

Vasopressor extravasation causes intense alpha-1-mediated vasoconstriction, ischemic necrosis, and limb gangrene. If extravasation occurs:

1. Do not remove the IV cannula immediately. Aspirate as much extravasated drug as possible.

2. Administer Phentolamine (alpha-1 blocker): 5 to 10 mg diluted in 10 mL normal saline injected through the catheter, and multiple subcutaneous wheel injections surrounding the area of pallor/ischemia.

3. If phentolamine is unavailable, apply 1-2 inches of 2% topical nitroglycerin paste to the ischemic area or infiltrate subcutaneous Terbutaline (1 mg in 10 mL NS).

Vasopressor & Inotrope Receptor Profiles & Dosing

Agent	Receptor Activity	Hemodynamic Effect	Standard Dosing & Titration	Primary Clinical Indications
Norepinephrine (Levophed)	Alpha-1 (++++), Beta-1 (++)	Marked vasoconstriction + modest inotropy; minimal tachycardia	2 to 40 mcg/min (titrate q2-3 min to MAP >= 65)	First-line for septic, cardiogenic, and undifferentiated distributive shock
Epinephrine (Adrenaline)	Beta-1 (++++), Beta-2 (++), Alpha-1 (++++ at higher dose)	Potent inotropy + chronotropy + peripheral vasoconstriction	1 to 20 mcg/min (0.01-0.5 mcg/kg/min)	Anaphylactic shock, cardiogenic shock with bradycardia, refractory septic shock
Vasopressin	V1 vascular smooth muscle (++++), V2 renal	Pure vasoconstriction; preserves SVR during profound acidosis	Fixed 0.03 units/min (NO titration)	Second-line adjuvant in vasodilatory septic shock to reduce norepinephrine requirements
Phenylephrine	Alpha-1 (pure)	Pure vasoconstriction; induces reflex bradycardia	40 to 300 mcg/min (0.5-5 mcg/kg/min)	Tachyarrhythmias limiting norepinephrine, neurogenic shock, procedural hypotension
Dobutamine	Beta-1 (++++), Beta-2 (++), Alpha-1 (+/-)	Potent inotropy + mild chronotropy; peripheral vasodilation (inodilator)	2.5 to 20 mcg/kg/min (titrate q10-15 min)	Cardiogenic shock with adequate MAP, low cardiac output state, severe RV failure
Milrinone	Phosphodiesterase-3 (PDE3) inhibitor	Inotropy + pulmonary/systemic vasodilation; non-adrenergic	0.25 to 0.75 mcg/kg/min (renally cleared; reduce in AKI)	Cardiogenic shock with pulmonary hypertension; beta-blocker overdose
Angiotensin II (Giapreza)	AT1 receptor agonist	Potent vasoconstriction and aldosterone release	20 ng/kg/min, titrate up to 80 ng/kg/min	Refractory high-output distributive shock; vasoplegia after cardiopulmonary bypass

Dynamic Assessment of Fluid Responsiveness

Static parameters such as Central Venous Pressure (CVP) and baseline IVC diameter do not reliably predict fluid responsiveness. Only 50% of critically ill patients respond to volume expansion with an increase in stroke volume (>10-15%). Dynamic tests evaluate cardiopulmonary interactions:

* Passive Leg Raise (PLR) Test: The gold-standard bedside challenge. Place patient in semi-recumbent 45° position, then tilt bed flat while elevating legs 45°. This acts as an endogenous auto-transfusion of ~300-500 mL of blood from the lower extremities. Measure continuous cardiac output (via arterial line waveform, Doppler velocity time integral [VTI] across aortic valve on echocardiogram, or bioreactance). An increase in cardiac output or stroke volume >= 10-15% within 60-90 seconds proves fluid responsiveness. Reversible immediately upon returning to semi-recumbent posture. * Inferior Vena Cava (IVC) Collapsibility/Distensibility Index: - Spontaneously breathing patient (Collapsibility): $(IVC_{max} - IVC_{min})/IVC_{max} > 50\%$ suggests volume responsiveness (sniff test). - Mechanically ventilated patient (Distensibility): Fully passive, no spontaneous efforts, Vt >= 8 mL/kg: $(IVC_{max} - IVC_{min})/IVC_{min} > 15-18\%$ indicates volume responsiveness.

Hemodynamic Monitoring Pitfalls

Pouring fluids into non-responsive cardiogenic/septic patients: Fluid overload worsens ARDS, increases mortality, and precipitates right ventricular distension and failure.
Titrating vasopressin: Vasopressin must be maintained at a fixed dose of 0.03 U/min; titrating it up causes severe splanchnic, mesenteric, and digital ischemia.
Using Dopamine as first-line: Dopamine is associated with significantly increased tachyarrhythmias and excess mortality in cardiogenic and septic shock compared to norepinephrine.

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