Vasoplegic Syndrome Post-cardiopulmonary Bypass

[tab_nav type=”two-up”][tab_nav_item title=”Clinical Case” active=”true”][tab_nav_item title=”Answer” active=””][/tab_nav][tabs][tab active=”true”]A 65 year old male with a history of CAD, HTN, & HL initially presented to the ED with an NSTEMI was found on subsequent cardiac catheterization to have severe triple vessel disease.  He is brought to your ICU after a 3-vessel CABG (LIMA → LAD, SVG → OM1, & SVG → OM2).  His cross-clamp time was approximately 90 minutes with a total CPB time of 110 minutes.  He is currently intubated with the following vital signs:

T: 37.6     HR: 105   BP: 75/44  RR: 22  SpO2: 99%
CI: 3.5

The anesthesiologist tells you his SVR coming out of the OR was about 500 and was given a push-dose of phenylephrine 30 minutes prior to arrival for a similar BP.

Question: What is your first impression of the cause of this patients abnormal vital signs and what should your initial steps in management include?

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Vasoplegic Syndrome – Definition

• A severe SIRS response following open heart surgery that requires cardiopulmonary bypass (CPB)
• Form of vasodilitory shock that occurs in the early postoperative period (< 6 hours after weaning from CBP), manifested by:
  • Hypotension [MAP < 70 without vasoactive agents]
  • Tachycardia
  • Normal or increased cardiac output [CI > 2.5 L / min / m²]
  • Low systemic vascular resistance [SVR < 800 dynes-s · cm⁻⁵ · m⁻² ]

Possible/proposed causes

• Etiology incompletely understood, but multiple proposed causes
  • CPB pump related inflammatory response & activation of:
    • Platelets & Leukocytes
    • Compliment levels
    • Cytokine levels
    • Kininogen/Bradykinin pathways
    • Coagulation cascade
    • Fibrinolysis
    • Prostaglandins, catecholamines, corticosteroids
  • Vasopressin deficiency, endothelial dysfunction, & decreased myogenic reactivity to catecholamines
    • Arteriolar tone is a major determinant of SVR, regulated by the neurohormonal system and endothelial function.
    • An increase in SVR is often observed after CPB. Vasoconstriction may be related to a transient increase in several vasoactive hormones including catecholamines, serotonin, and vasopressin.
• Other potential causes
  • Blood product administration – Activation of PMNs & cytokine release
  • Surgical trauma
  • Protamine administration for heparin reversal – causing complement activation, histamine release, thromboxane and nitric oxide production, and antibody formation.

Possible Risk Factors

• Pre-operative ACE inhibitors: Inhibition of ACE results in a reduction of angiotensin II (one of the most potent endogenous vasopressor agents) and an increase in vasodilator bradykinin plasma levels
• Prolonged CPB time
  

Resuscitation goals

• Target MAP between 70-80 
  • Intravascular volume expansion – careful administration to avoid excessive volume loading
    • Limited evidence for use of specific crystalloid vs. colloid.  In general crystalloid first line
  • Early vasopressor use
    • Vasopressin: Infusion rates up to 0.06 units/min (maximum) – first line agent
    • Norepinephrine: Infusion rates starting at 0.05 mcg/kg/min – second line agent, as these patients may be refractory to refractory catecholamines.
  • Other suggested treatments
    • Methylene blue: 2 mg/kg IV
      • Potential salvage treatment
      • Mechanism: Inhibition of enzyme guanylyl cyclase which blocks NO & partially restores SVR
• Correct underlying causes for a metabolic acidosis

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