Critical Care Pearls

Mastering Vasopressor Management

Rules of Critical Care

1. Defend the blood pressure

  • “True” hypotension is an emergency
    • MAP<65 needs attention IMMEDIATELY
      • Hypotension →Decreased DBP → Decreased coronary blood flow → Cardiac ischemia →  Decreased CO → Hypotension (repeat)
    • Short durations hurt brain, kidneys, heart 
      • Longer durations of hypotension = worse outcomes
      • Push dose, immediate fluids, etc.
        • FIX IT!

2. You MUST diagnose shock

  • Always identify which type of shock!
    1. Stabilize/Defend BP
    2. Assessment of CO → Diagnose shock type
    3. Volume trial → Look for CO improvement

The choice of vasopressors is not always clear

  • The case for Vasopressin>NE: VASST trials
    • Are both studies underpowered? Is steroids+Vaso the magic solution for the truly sick?
      • No consensus solution
    • The comparison of NE to Dopa(SOAP II group)
      • Poorly dosed Dopa in the comparison group (not studying the physiological rationale)
      • NE maybe better for you (for cardiogenic shock)
    • Hypotension is due to a lack of catecholamines (just as HTN is due to an overabundance of them)

Alternative vasopressors: What is in the pipeline?

  • Selepressin 
    • Vasopressin targets V1a, V1b for vasoconstriction
      • Also targets Oxytocin and V2→ fluid overload and microvascular thrombosis 
    • Selepressin is a selective V1a agonist → targeted vasoconstriction
      • Improves free water clearance (lacks V2 targeting) → less lung injury/less lung edema
    • Less vascular leak(typical with Vasopressin)
  • Angiotensin II (Ang II)
    • First trial: 1961, then disappeared
    • Example: Distributive shock, s/p resuscitation, has INCREASED blood flow to kidneys → intraglomerular hypotension and AKI
      • Treatment with Ang II leads to improvements
        • NE leads to AFFERENT vasoconstriction
        • Ang II→ EFFERENT vasoconstriction (recruits capillary beds) 
        • ATHOS trial
          • Low doses of Ang II can causecatecholamine sparing
            • 2 outliers had HYPERtension (due to ARDS?) 
        • SEVERE ARDS causes Ang II deficiency
          • Pulmonary capillary endothelium damage can restrict conversion of Ang I to Ang II
        • Ang II Pilot data conclusions
          • IV Ang II has a role as a rescue vasopressor
          • IV Ang II may bemore useful in ARDS patients
      • Currently  undergoing a Phase III registration trial for Ang II as a vasopressor
        • First FDA trial for a drug AS a vasopressor
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