Pressor-refractory Shock

• The pressors keep going up!

Mechanisms of Pressor-refractory Shock 🏴‍☠️

• Cardiogenic: all cardiac anatomic structures can be culprits. Progressive failure of the myocardium’s contractility can come in the form of the complication of acute illness (i.e. new stress cardiomyopathy), untreated myocarditis (i.e. uncontrolled inflammation), untreated ischemia (i.e. missed occlusion MI), or lack of ATP (i.e. thiamine deficiency). Myocardial support requires ⊕ inotrope, mechanical support, & addressing the underlying cause (i.e. immunosuppression, PCI, thiamine supplementation). Acute, flail mitral regurgitation is the primary valvulopathy to consider, which often requires TEE for higher-fidelity assessment of degree of MR

• Obstructive: progressive untreated tamponade results in massive external constriction of the cardiac chambers left untreated. LVOT obstruction can be fixed (e.g. HOCM) or dynamic (i.e. hyperkinetic LV), & it often worsens with ⊕ inotropy of vasopressors due to worsening of the outflow tract obstruction (i.e. turning up vasopressors paradoxically worsens the situation)

• Distributive: extreme, fixed vasoplegia can be the result of an exotoxin that requires surgical removal of the source (i.e. toxic shock syndrome), or lack of glucocorticoid-mediated vasoconstriction (i.e. adrenal insufficiency)

• Hypovolemic: the issue is “source control” of a missed bleed, which is most commonly occurring in the retroperitoneal space due to (supra)therapeutic anticoagulation or vasculopathy

• @ASanchez_PS @ArcieriMichael

• Graphic from this paper