EP 90: Managing Vasopressors

In today’s episode, we are going to talk about the most common vasopressors we use in the ICU. Those being norepinephrine, epinephrine, phenylephrine, vasopressin, and dopamine.


Vasopressors are a powerful class of drugs that induce vasoconstriction, they elevate mean arterial pressure (MAP). Vasopressors differ from inotropes, inotropes increase cardiac contractility. Keep in mind that many drugs have both vasopressor and inotropic effects. 

  • Vasopressors are a group of medicines that contract (tighten) blood vessels and raise blood pressure.
  • They’re used to treat severe low blood pressure, especially in a critical care setting.
  • When blood pressure is continuously low it can lead to organ damage and even death.
  • Most commonly used on patients who are in shock, undergoing surgery, or during an emergency.

Vasopressor Considerations

  • Alpha 1 adrenergic receptors
    • Located primarily in the skin and GU tract and ultimately decrease blood flow to these organs when activated.
    • Activation of these receptors will result in vasoconstriction and an increase in peripheral vascular resistance and systemic arterial blood pressure.
  • Alpha 2 adrenergic receptors
    • Contribute both to control of sympathetic tone and to local and regional blood flow in the peripheral vasculature. 
    • Sits alongside the more plentiful α1-adrenergic receptor.
  • Beta 1 adrenergic receptors
    • Located near the SA node, AV node, and cardiac myocytes (make up the heart muscle).
    • Activation causes an increased heart rate (chronotropic effect), automaticity, and contractility (inotropic effect). 
  • Beta 2 adrenergic receptors
    • Located in the tissues of the GI tract, bronchi, uterus, pancreas, striated muscle (cardiac), blood vessels, coronary arteries, and hepatic artery.
    • Activation causes smooth muscle relaxation, vasodilation and increases perfusion, and increased cardiac contractility. 
  • Dopamine receptors
    • Present throughout the body, dopamine is a precursor to epinephrine and norepinephrine
    • Activation causes vasodilation, increased myocardial contraction, and increases cardiac output without changing heart rate

Depending on the size of the extravasation, bring 5 to 10 mg of phentolamine to the bedside. This will need to be reconstituted and further diluted to 0.5 mg/mL in normal saline. Treatment of the extravasation will involve the nurse administering the phentolamine intradermally around the site of the extravasation.


NEO-SYNEPHRINE hydrochloride produces vasoconstriction that lasts longer than that of epinephrine. Its action on the heart contrasts sharply with that of epinephrine and ephedrine, in that it slows the heart rate and increases the stroke output, producing no disturbance in the rhythm of the pulse. Phenylephrine is a powerful postsynaptic alpha-receptor stimulant with little effect on the beta receptors of the heart.


  • Neo causes a rise in systolic and diastolic pressures.
  • Reflex bradycardia that can be blocked by atropine.
  • Cardiac output is slightly decreased and peripheral resistance is considerably increased. Circulation time is slightly prolonged, and venous pressure is slightly increased. 
  • Most vascular beds are constricted leading to renal splanchnic, cutaneous, and limb blood flow reduction but coronary blood flow is increased. 
  • Pulmonary vessels are constricted, and pulmonary arterial pressure is raised.


  • Severe hypotension
  • Septic shock
  • Cardiogenic shock
  • Situations where levo causes tachyarrhythmias

The drug is a powerful vasoconstrictor with properties very similar to norepinephrine but almost completely lacking the chronotropic and inotropic actions on the heart that norepinephrine provides.,Indications%20and%20Usage,drug%20induced%20hypotension%20or%20hypersensitivity.


The majority of norepinephrine effects are going to lead to an activation of the alpha 1, alpha 2, and beta 1 receptors. Levophed functions as a peripheral vasoconstrictor (alpha-adrenergic action) and as an inotropic stimulator of the heart and dilator of coronary arteries (beta-adrenergic action)


  • Increases heart rate
  • Increase BP through an increase in cardiac output and systemic vascular resistance. 
  • Vasoconstriction of arteries and veins (alpha 1 and alpha 2)
  • Increase in heart contractility (beta 1 mediated).
  • Increases blood flow to skeletal muscle.
  • Reduces blood flow to the gastrointestinal system.
  • Inhibits voiding of the bladder and gastrointestinal motility.


  • Severe hypotension
  • Septic shock
  • Cardiogenic shock


Stimulates alpha 1 and 2, and beta 1, and 2 adrenergic receptors. Epinephrine is usually given as a last resort drip or pushed during a code. It has the shortest half-life of all the vasopressors. 


  • Relaxation of the smooth muscle of the bronchial tree
  • (increasing myocardial oxygen consumption)
  • Increased heart rate and contractility (beta 1)
  • Vasoconstriction in most arteries and veins (alpha 1 and 2)
  • Low concentrations cause vasodilation of muscle and liver vasculature (Beta 2)
  • High concentrations cause vasoconstriction (alpha mediated)
  • Cardiac output is increased but with a small change in MAP due to a decrease in systemic vascular resistance (Beta 2 mediated)
  • Increase in myocardial oxygen consumption


  • Anaphylactic shock
  • Cardiogenic shock
  • Cardiac arrest
  • Inotropic support


Vasopressin doesn’t act on the same receptors as the prior pressors. Vasopressin is a peptide hormone that acts on 2 major sites, V1 which is the blood vessels and V2 are the kidneys. 


  • V1 is responsible for the constriction of blood vessels through an increase in systemic vascular resistance leading to an increase in MAP
  • V2 is responsible for regulating extracellular fluid volume. Activation causes fluid reabsorption leading to an increase in blood volume causing an increase in MAP. 


Dopamine is a precursor of norepinephrine and stimulates norepinephrine release. At low doses, dopamine stimulates the heart and decreases systemic vascular resistance. At high doses, dopamine’s vasodilation effect becomes vasoconstriction as lower affinity α-receptors bind to the dopamine. Dopamine also binds to D1 receptors in the kidney, producing vasodilation.


  • Stimulates both adrenergic and dopaminergic receptors.
  • Lower doses
    • Mainly dopaminergic stimulating producing renal and mesenteric vasodilation.
  • Higher doses
    • Both dopaminergic and beta1-adrenergic stimulating and produce cardiac stimulation and renal vasodilation.
  • Larger doses
    • Stimulate alpha-adrenergic receptors causing vasoconstriction


  • Hemodynamic support
    • Acute heart failure and cardiogenic shock
  • Acute renal failure

Know what vasopressors are by watching this full episode 👇👇👇


00:00 – Intro
00:55 – Topic Intro
02:29 – Vasopressor’s main job
05:48 – Alpha 1 adrenergic receptors
06:14 – Alpha 2 adrenergic receptors
06:42 – Beta 1 adrenergic receptors
07:08 – Beta 2 adrenergic receptors
07:40 – Dopamine receptors
10:47 – Phenylephrine
13:00 – Norepinephrine
17:45 – Vasopressin
22:15 – Epinephrine
24:30 – Dopamine
30:25 – Checking the maps
35:07 – Matt’s First ICU patient on vasopressors – Don’t let your drips run dry!
37:15 – Wrapping up the show
38:40 – Announcements
40:08 – End of show

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