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2/8/2019 0 Comments

Vasopressors in the ED


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ED Vasopressors – Core Concepts











Our body has 3 major classes of vasopressors
     - Catecholamines - 
⍺/β receptor agonism
     - Vasopressin – Vasopressor receptor (V
1) agonism
     - Angiotensin II – Angiotensin II Receptor (ATII-R) agonism


We use vasopressors to supplement our bodies own mechanisms to increase blood pressure.

VASOPRESSOR AGENTS

Norepinephrine
ONE LINER: THE “BEES KNEES” OF VASOPRESSORS
     - Mechanism: 
⍺/β agonism
     - Dose: Initial dose 5mcg/min (0.05mcg/kg/min)
     - Indication: Any shock, the best agent in (ALMOST) all circumstances: SOAP II (NEJM 2010) – 
Norepi vs dopamine for shock (primarily sepsis);
       Levy et al (JACC 2018) – Norepi vs epi for post 
AMI cardiogenic shock; VASST (NEJM 2008) – More norepi vs norepi + vasopressin
     - Good/bad: (+) Literally the best, (+) Safe for peripheral administration, (-) Can cause arrhythmias


Epinephrine
ONE LINER: NOT AS GOOD AS NOREPI, MAY HELP A DYING HEART
     - Mechanism: β/
⍺ agonism
     - Dose: Initial dose 5mcg/min (0.05mcg/kg/min)
     - Indication: Hypotension + bad heart – hypotension AND bradycardia; hypotension with poor
 contractility (titrate epi for heart function on
       POCUS + titrate norepi for BP); Periarrest phase 
(push-dose epi)
     - Good/bad: (+) Give a dying heart a better chance (maybe); (+) Can be used in push dose; (-) 
Lactate no longer reliable for monitoring shock;
       (-) Increased arrhythmias; (-) Limited evidence that epi is superior to norepi in most situations


Phenylephrine
ONE LINER: USE FOR IATROGENIC HYPOTENSION OR FOR A FAST HEART
     - Mechanism: Pure 
⍺
     - Dose: Initial dose 50mcg/min (0.5mcg/kg/min)
     - Indication: Sedation induced hypotension, hypotension with arrhythmia (Afib with RVR) - Good/bad: (+) Not arrhythmogenic;
       (-) Bad in heart failure


Dopamine:
ONE LINER: POOR MAN’S NOREPI
     - Mechanism: Dopa/β/
⍺ agonism - Dose: Dose dependent effects
       o Low Doses: 2 – 5 mcg/kg/minàDopa agonismo Mid Doses: 5 – 10 mcg/kg/minàβ agonism
       o High Doses: 10 – 20 mcg/kg/minà⍺ agonism
     - Indication: Bradycardia OR Hypotension. If both, use epi
     - Good/Bad: (-) Arrhythmias; (-) More adverse events compared to norepi


Vasopressin:
ONE LINER: SUPPLEMENTAL VASOPRESSOR, NEVER AS A SINGLE AGENT
     - Mechanism: Vasoconstriction via Vasopressin (V
1) receptor
     - Dose: Fixed dose 0.03U/min, no titration. Can use 20U as single bolus in cardiac arrest with 
steroids (VSE 2013)
     - Indication: Shock (septic, vasodilatory), renal failure
     - Good/bad: (+) No adrenergic activity – no arrhythmias, does not compete with catecholamines

       (+) Maybe decrease need for dialysis compared to norepi (VANISH Trial). (-) No mortality benefit compared to Norepi

THE OTHER AGENTS: Almost never used in ED
Dobutamine:
     - Mechanism: β agonism, no 
⍺
     - Indications: Bradycardia, cardiogenic shock
     - Dosage: Start at 2.5 mcg/kg/min (Max 20mcg/kg/min) 
     - Notes: Poor-mans milrinone. (-) Bad dysrhythmias. (+/-) Not a true “pressor”; Can cause 
vasodilation via β2 without ⍺ activity

Milrinone:
     - Mechanism: PDE inhibitor

       o Increased [Ca]i via cAMPàIonotropy + vasodilation
       o Lusitropiceffects–Increaseddiastolicrelaxation/filling
       o IncreasedPreload+Increasedcontractility+decreasedSVR=IncreasedCO
     -  Indications: Heart failure (with goals of transition to either transplant or assist device)
     -  Dosage: 0.25 – 0.5 mcg/kg/min
     -  Notes: (-) Causes arrhythmias. (+/-) Vasodilator. Needs continuous infusion through PICC

Methylene Blue:
     - Mechanism: Inhibit NO/cGMP vasodilation
     - Indications: Refractory vasodilatory shock
     - Dosage: 1-2mg/kg as bolus over 15min; Infusion 0.5mg/kg/hr x 4hrs - Notes: Used for refractory hypotension, used for salvage therapy


Angiotensin II
     - Mechanism: Binds Angiotensin-II receptors for direct vasoconstriction
     - Indications: Refractory vasodilatory shock
     - Dose: Start at 20ng/kg/min (Max 200ng/kg/min)
     - Notes: Hasn’t been looked at as solo vasopressor, just for refractory shock with other agents.

     - Very expensive without mortality benefit (ATHOS-3)

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