ED Vasopressors – Core Concepts











Our body has 3 major classes of vasopressors
     - Catecholamines - ⍺/β receptor agonism
     - Vasopressin – Vasopressor receptor (V1) 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 (V1) 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)

LVAD evaluation in your ED - Think of "LVAD."
Look & Listen
Ventricles
Anticoagulation
Drive Line

​Although procedural sedation is a bread and butter component of emergency medicine, it is an area where we can introduce significant harm to our patients. Preparation and being facile with all components of the process if key to doing this safely and efficiently.
 
Level of Sedation

• Minimal Sedationis characterized by anxiolysis but with normal, although sometimes slowed, response to verbal stimuli. The person will be awake but relaxed.  Good for procedures that require patient cooperation and those in which pain is controlled by local or regional anesthesia. (Lac Repair, Abscess I+D)
• Moderate Sedation is characterized by a depressed level of consciousness and a slower but purposeful motor response to simple verbal or tactile stimuli. Patients at this level generally have their eyes closed and respond slowly to verbal commands. Dissociative Sedation is one type.   Moderate sedation can be used for procedures in which detailed patient cooperation is not necessary, and muscular relaxation with diminished pain reaction is desired. (dislocation reductions, chest tube insertions and cardioversions)
• Deep Sedation is characterized by a profoundly depressed level of consciousness, with a purposeful motor response elicited only after repeated or painful stimuli, so we might use it for procedures that are painful and require muscular relaxation with minimal patient reaction like burn wound care or open fracture reductions.

Prepare for Complications

• Hypotension and apnea are not uncommon when using the sedative agents discussed below
• Be prepared to emergently manage an airway or resuscitate a patient with fluids/pressors if needed
• Consider having airway cart, BVM, end tidal CO2, defibrillator and any other equipment you would need to take care of a crashing patient

 
Know Your Patient

• Detailed History: Experience with anesthesia, NPO time, current meds and allergies can help you choose right agent
• Focused Exam: ASA classification can help predict complications (Class III-V have much higher complication rate), Mallampati score can help you prepare for emergent intubation.

 
Choose Your Agent

• There are many agents to choose from, each with advantages and disadvantages
• Try to master as many as you can and become facile with all of your options

​During and Post Procedure

• Need two qualified professionals; one to administer drugs and/or do procedure, and another to watch vital signs for signs of complications
• Watch until patient can ambulate, eat and has mentally returned to baseline

Background:

• Lupus is more common than you think – 1/2000 people have it
• We will rarely diagnose lupus in ED – diagnostic criteria is intense and involves a blood test that takes days to come back.
• Must have 4/11 of the following
  • Malar rash, discoid rash, photosensitivity, oral ulcers, serositis, arthritis, renal involvement, neurological findings, hematological abnormality, AND at least one of the 4/11 must be a positive autoantibody.
• Lupus can affect every organ system in your body

 
Understanding Lupus – The Big Picture:

• People are constantly between Lupus flairs and remission
• Lupus medications have a ton of side effects
  • Steroids and Immunomodulators
• People are very pro-coagulableand immunocompromised
• Benign presentations may be more serious in patients with Lupus, even if they are taking their medications

 
Organ specific problems: Cardiac

• Patients with Lupus are 10x more likely to have ACS. Can present at younger ages too.
• Libman Sachs endocarditis gives you an increased risk of acute valve rupture
• Increased risk cardiac effusion, pericarditis, CHF, RHF

 
Organ specific problems: Respiratory

• Diffuse alveolar hemorrhage – very rare. 
• Increased risk pleural effusions, PE, PNA, pulmonary HTN, interstitial lung disease

 
Organ specific problems: Neuro

• Stroke, dural venous sinus thrombosis
• Seizure that may not respond to benzos – intubate and paralyze
• PRES - posterior reversible encephalopathy syndrome from immunomodulators
• Peripheral neuropathy with strange distributions – not a stocking glove presentation

 
Organ specific problems: Vasculitis
– resuscitate and give 1g methylprednisone, and suggest to the admitted team they should consider IVIG and/or plasmapheresis!

• Can cause any vessels to be inflamed/bleed
• Mesenteric = hematemesis, hematochezia, bowel necrosis, perforation 
• Lung = hemoptysis 
• Catastrophic antiphospholipid syndrome (CAPS) – presents with multiple arterial occlusions, cold clammy body parts. Do same as above plus add heparin.

 
Organ specific problems: Many others random presentations
​– if someone has Lupus and a weird problem it can likely be attributed to Lupus, but rule out other causes first.

Nasotracheal Intubation – Core Concepts

As with every sick patient – put on monitors, establish IV access, place on supplemental oxygen. Consider calling for physician backup including another ED provider, anesthesia, or even surgery if available to assist with procedure and possible transition to surgical airway
 

1. Examine
   1. Examine the mouth - look for posterior swelling, anatomical abnormalities
   2. Examine the nose – See if one nares appears more patent than the other
   3. Examine the neck – Identify surgical landmarks in case patient requires a surgical airway
2. Prep the patient
   1. Goal is analgesia and vasoconstriction of the nose
   2. Fill 10cc syringe with 5cc 4% lidocaine, 5cc oxymetazoline
   3. Alternatively use 5% liquid cocaine
   4. Inject with atomizer into the nares
3. Prep the patient – AGAIN
   1. Coat a nasal trumpet with visous lidocaine and insert into the nose
   2. Can dilate up 6 NPA -> 8 NPA (NPA = "Nasal Trumpet")
   3. Consider ketamine during this step, 0.5 – 1.0 mg/kg for pain control and sedation
4. Prep yourself
   1. Start with a 7.0 ETT tube but also grab a 6.5 or 6.0 as backup
   2. Prep your fiberoptic scope – check camera, attach suction
   3. Have available Yankhauer or other oral suction devices 
   4. Supplemental oral airway gear – laryngoscope blade or wooden tongue blade
   5. Surgical airway supplies OPEN at the bedside. If you are unable to perform nasotracheal intubation, patient will most likely require cricothyrotomy 
5. Load the tube
   1. Remove the nasal trumpet and insert your ETT first to ensure that it will fit as well as clear out gel and secretions to keep your camera view clear
   2. Advance ~ 15cm with bevel pointed laterally
6. Advance scope into preloaded ETT
   1. Identify epiglottitis, cords
   2. If no structures are obviously identifiable, withdraw ETT and endoscope 2-3cm at a time until you can recognize airway structures
7. Intubate
   1. Pass endoscope through cords and advance to carina
   2. If vocal cord spasm or spontaneous breathing makes advancement difficult, push paralytics ONLY if you have clearly identified the cords
8. Secure your tube
   1. Use either tape or even consider suturing tube to nose to ensure that it is not dislodged