PODCAST: Vasopressors

פוסט זה זמין גם ב: עברית

We go over the essential and complex topic of vasopressors in the ED.

Hosts:
Brian Gilberti, MD
Catherine Jamin, MD

Show Notes

Introduction

  • Host: Brian Gilberti, MD
  • Guest: Catherine Jamin, MD
    • Associate professor of Emergency Medicine at NYU Langone Health
    • Vice Chair of Operations
    • Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine
  • Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED

What Are Vasopressors and When to Use Them

  • Two primary mechanisms to increase blood pressure:
    1. Increasing systemic vascular resistance via vasoconstriction
    2. Increasing cardiac output via augmenting inotropy and chronotropy
  • Indicators for vasopressor use:
    • MAP <65, systolic BP <90, or significant drop from baseline BP
    • Signs of organ dysfunction like altered mental status, decreased urine output, elevated lactate
    • Fluid resuscitation either ineffective or contraindicated (e.g., in CHF patients)

Commonly Used Vasopressors in the ED

  • Norepinephrine
  • Epinephrine
  • Vasopressin
  • Phenylephrine

Norepinephrine

  • Mechanism: Stimulates alpha-1 (vasoconstriction) and beta-1 receptors (increases inotropy & chronotropy)
  • Starting Dose: 10 mcg/min, titrate to MAP >65
  • Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min
  • Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic)
  • Pros: Can be infused peripherally via large bore IV

Vasopressin

  • Mechanism: Activates V1a receptors causing vasoconstriction
  • Dose: Fixed, non-titratable dose of 0.04 units/min
  • Situational Preference: Second-line in septic shock
  • Concerns: Potential for peripheral ischemia

Phenylephrine

  • Mechanism: Stimulates alpha-1 receptors causing vasoconstriction
  • Starting Dose: 100 mcg/min, titrate to MAP >65
  • Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation
  • Concerns: Increases afterload, can worsen low cardiac output states

Epinephrine

  • Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors
  • Starting Dose: 5-10 mcg/min, titrate to MAP >65
  • Situational Preference: Anaphylactic shock, septic cardiomyopathy
  • Limitations: Can induce tachycardia, may elevate lactate levels

Escalation Strategy in Refractory Shock

  • Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine
  • Consider POCUS, lactate, central venous saturation, and acid-base status

Peripheral Pressors

  • Can safely be administered peripherally via large bore IVs in proximal upper extremity
  • Sites: Cephalic or basilic veins
  • Adverse Events: Low at 1.8% based on meta-analysis
  • Actions in case of extravasation: Phentolamine injection, nitroglycerin paste

Push-Dose Pressors

  • Primarily Phenylephrine (peri-intubation, during procedures)
  • Also Epinephrine for peri-code situations
  • Doses: Epi – 5-20 mcg every 2-5 min

Take-Home Points

  • Most used medications are going to be norepinephrine, vasopressin, phenylephrine, and epinephrine.
  • Consider these medications if there are signs of end-organ dysfunction, there is a considerable delta in baseline BP, systolic is less than 90 and/or MAP is less than 65
  • Norepinephrine is a good pressor for a lot of the situations that we encounter in the emergency department, such as septic shock, undifferentiated shock and hypovolemic shock.
  • Vasopressin is commonly the second we reach for in most of these scenarios
  • Epinephrine will be first for anaphylactic shock and may be the third agent in septic shock
  • Think about phenylephrine in high-output states (patients with tachydysrhythmias), or with AS, though be cautious in patient with low cardiac output
  • The benefits outweigh risks for peripheral pressors in situations where you promptly have to increase blood pressure while you work on central access
  • Push-dose pressures can help you in a peritinbatuion or pericode situation because it is going to be one of the fastest ways we can boost BP while we work on other measures to stabilize the patient

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