Lecture on Vasopressors and Inotropes

Presenter

• Andrew Straznitskas, PharmD, BCCCP
• Clinical Pharmacist, Medical ICU, NYC H+H/Bellevue

Adrenergic Receptors

• Vasopressors: Act on systemic vasculature causing vasoconstriction, increasing systemic vascular resistance (SVR)
• Inotropes: Act on myocardium, increasing heart rate (HR) and contractility, thus increasing cardiac output (CO)
• Vasodilators: Act on systemic vasculature causing vasodilation, reducing SVR

Key Vasopressors and Inotropes

Norepinephrine (Levophed)

• Effects: Potent vasoconstriction (primary), enhances cardiac contractility and HR (secondary)
• Dose: 2-30 mcg/min or 0.05-0.5 mcg/kg/min
• Clinical Use: Septic shock, cardiogenic shock, undifferentiated shock
• Notes: Preferred over dopamine, can cause tachycardia/tachyarrhythmias

Phenylephrine (Neosynephrine)

• Effects: Pure alpha agonist causing vasoconstriction
• Dose: 20-200 mcg/min, bolus dose 100-200 mcg Q3-5min
• Clinical Use: Septic shock (intolerant to norepinephrine), anesthetic-induced hypotension, aortic/mitral stenosis
• Notes: Least arrhythmogenic, potential for reflex bradycardia

Vasopressin (Vasostrict)

• Effects: V1 receptor causes vasoconstriction, V2 receptor reabsorbs water from renal ducts
• Dose: 0.03 units/min
• Clinical Use: Adjunct in refractory shock, reduces norepinephrine requirement
• Notes: Effective in severe acidosis, not arrhythmogenic

Epinephrine (Adrenalin)

• Effects: Potent vasoconstriction and increased contractility/HR
• Dose: 1-20 mcg/min or 0.01-0.5 mcg/kg/min
• Clinical Use: Refractory shock, adjunct agent, cardiogenic shock, anaphylaxis, cardiac arrest
• Notes: Arrhythmogenic, causes hyperglycemia, inhibits insulin secretion

Dopamine (Inotropin)

• Effects: Dose-dependent (renal blood flow, cardiac contractility, vasoconstriction)
• Dose: 2.5-20 mcg/kg/min
• Clinical Use: Mostly obsolete, ACLS for symptomatic bradycardia
• Notes: High arrhythmogenicity, increased myocardial oxygen demand

Dobutamine (Dobutrex)

• Effects: Increases contractility/HR, causes systemic vasodilation
• Dose: 2.5-20 mcg/kg/min
• Clinical Use: Shock with low CO, decompensated heart failure
• Notes: May cause hypotension and arrhythmias

Milrinone (Primcor)

• Mechanism: Phosphodiesterase-3 inhibitor
• Effects: Increases intracellular cAMP, enhances contractility/HR, causes vasodilation
• Dose: 0.125-0.75 mcg/kg/min
• Clinical Use: Low CO shock, decompensated heart failure
• Notes: Hard to titrate in unstable patients, arrhythmogenic

Isoproterenol (Isuprel)

• Effects: Pure beta agonist, increases contractility/HR
• Dose: 1-10 mcg/min
• Clinical Use: Bradyarrhythmias, heart block, Torsade de Pointes
• Notes: Restricted to cardiology

Administration

• Peripheral administration may risk infiltration and extravasation injury
• Start centrally when possible; peripheral use should be short-term
• Use largest available IV site and least concentrated formulation

Management of Extravasation

• Phentolamine: Alpha-blocker, preferred antidote
• Terbutaline: Beta-agonist, secondary option
• Nitroglycerin Ointment: For mild injuries

Key Points

• Maintain euvolemia, assess fluid status regularly
• Hypoxia and acidemia can reduce catecholamine effects
• Vasopressins are effective in acidosis
• Correct hypocalcemia to improve responsiveness

Questions

• Address any clarifying questions and concerns related to the use and management of vasopressors and inotropes.